Infectious Diseases
Infectious Diseases: are the diseases being caused by pathogenic microorganism and parasites which
can infect people.
Characteristics
1.Have pathogens (syphilis spirochete、flu virus、measles virus, SARS-CoV-2)
2.Have infectivity
3.Have epidemiology feature
4.Have post infection immunity
Infection is the entry and multiplication of an infectious agent in the human body.
Diseases refer to the development of symptom and sign related to infection with an agent
Role of Pathogen （pathogenicity）
-number -virulence -invasiveness -toxin (endotoxin, exotoxin)
Infection spectrum includes Elimination of pathogen , Covert infection: sub-clinical infection
Overt infection: clinical infection, Carrier state, Latent infection
Covert infection = no symptoms, has infectivity
Overt infection = symptomatic, has infectivity
Carrier state = in body without producing evidence of any reaction in host, has infectivity
Latent infection state = asymptomatic, does not have infectivity ex; TB (no immune response)
Sources of Infection; Reservoir: source of organisms
the source may be:
Humans (covert infection, carrier state), Animals (zoonosis), Environment
Chain of infection:
● Causal agents, its reservoir（source of infection）
● The mode of transmission（route of transmission）
● Host （susceptibility of the population）
Three conditions must be met for infection that will spread from person to person
If any of these conditions is not met, the chain will be broken and the infectious disease will not spread.
1. One person must be infected with a microorganism (sources of infection)
2. The other person must be susceptible to infection with that microorganism
3. The microorganism must be able to leave the body of the infected person and enter the body of the
susceptible person
Routes of transmission: Respiratory tract, Gastrointestinal Tract, Urogenital tract, Parenteral (injection,
bite), Placenta
Susceptibility: Ability to become infected with an organism when exposed to it.
People may lose susceptibility (or become immune) once they have been:infected with the organism
Or Vaccinated (Medications may reduce susceptibility temporarily)
Stages of the Infectious diseases
• Incubation period:
Incubation period is the period between the
invasion of pathogens and the onset of disease.
• Prodromal stage:
the period between the onset of disease and apparent manifestation. Such as fever, headache,
fatigue, anorexia, myalgia.
• Stage of apparent manifestation:
typical symptoms and signs occur.
• Stage of Convalescence:
most of the clinical manifestations are subsiding.
Major common manifestation of infectious diseases
1.Fever
Fever is often regarded as the cardinal feature of infection.
2.Skin rash (eruption):
being seen in measles; rubella; epidemic hemorrhagic fever; vesicular-pustula rash in herpes
simplex.
3.Toxemic symptoms:
toxin causes a series of symptoms: malaise, anorexia, muscle and joint pains, mental
symptoms.
4.Septicemia:
Bacteria multiple in blood and produce toxin lead to a series of symptoms.
5.Monocytic-macrophagic system reaction:
leading to splenomegaly, hepatomegaly, lymphadenopathy.
The symptoms of infection depend on the type of the disease, some of infection affects the whole body
generally, such as fatigue, loss of appetite, weight loss, fever, night sweat, chills, aches and pains.
Other specifically affects individual body parts, such as skin rash, coughing or runny nose.
Rash
The time and sequence of appearance of rash have important reference value for diagnosis and differential
diagnosis.
Time of appearance:
1.chickenpox 2. scarlet fever 3.smallpox 4. measles 5. typhus 6. typhoid
The sequence and distribution of rash:
Chickenpox is mainly distributed on the trunk. The rash of measles starts behind the ears and on the face,
and then spreads to the trunk and limbs, and there are mucous spots.
Prevention of Infectious disease;
By breaking the chain of infection through
•
•
•
Elimination or containment of the resource of infection
Interruption in the important mechanism of transmission
Protection of susceptible host
EID (emerging infectious diseases)
EID are diseases whose incidence in humans has increased in the past 2 decades or threatens to
increase in the near future.The majority of emerging and reemerging infectious diseases are zoonotic.
Factors that contribute for EID:
= Mutation of organism to new serovar (antigenic type), Migration of humans and animals into new
environments, Travel, War and Natural disasters,Decline in vaccination rates, Climatic changes
Bioterrorism is also often included under the "emerging infectious disease" heading.
COVID-19
• Sources of infection: patients or asymptomatic
• Route of transmission: spread mainly via respiratory
• Susceptibility: population is generally susceptible
• Pathogen: severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
• Infectivity: can transmit from people to people
• Epidemiology feature: cases have been reported in all continents (pandemic)
• Post infection immunity: immunity
INFLUENZA
•
Influenza, commonly known as "the flu", is an infectious disease caused by an influenza virus.
•
Symptoms can be mild to severe. The most common symptoms include: a high fever, runny nose,
sore throat, muscle pains, headache, coughing, and feeling tired.
•
•
These symptoms typically begin 2 days after exposure to the virus and most last less than 1 week.
Influenza viruses are RNA virus that belongs to the family Orthomyxoviridae.
Classification
Influenza A virus:
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many different subtypes,
various sub-types infect humans, swine, horse, avian, marine animals
it can change frequently and dramatically, it can sweep across continents and around the world in
massive epidemics called pandemics,causes excess mortality and morbidity
Influenza B virus:
●
Restricted to humans, Can change slowly over time
●
More stable than Influenza A
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Has been associated with widespread illness among humans
●
Causes milder disease than Influenza A
Influenza C virus:
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Restricted to humans and dogs, pigs
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Relatively stable
●
Causes mild, sporadic illness among humans
●
Mild disease without seasonality
Routes of transmission: Influenza can be spread in three main ways:
by direct transmission: (when an infected person sneezes mucus directly into the eyes, nose
or mouth of another person);
the airborne route: (when someone inhales the aerosols produced by an infected person
coughing, sneezing or spitting)
through direct or indirect contact: hand-to-eye, hand-to-nose, or hand-to-mouth transmission,
or Contact with virus-contaminated goods.
Clinical findings of Influenza:
1- Uncomplicated Influenza; incubation period of 1 to 3 days, systemic symptoms predominate, mild
respiratory symptoms.
•
Fever, chills (which may be frank shaking chills), headaches, myalgia, malaise, and anorexia.The
systemic symptoms usually persist for 3 days.
•
Respiratory symptoms-particularly a dry cough, severe pharyngeal pain, and nasal obstruction and
discharge are usually also present at the onset of illness but are overshadowed by the systemic
symptoms.
•
Hoarseness and a dry or sore throat may also be present
2- Pneumonia Influenza:
• In the elderly ,children, or underlying diseases.
• (influenza viral pneumonia,bacterial infection or multiple pathogen infection).
3- Other types :
• encephalitis: (delirium, convulsions, disturbance of consciousness)
• gastrointestinal type: toxic type: circulation function impairment
Complications:
Primary influenza viral pneumonia
occurred predominantly among persons with cardiovascular disease, especially rheumatic heart disease
with mitral stenosis, and to a lesser extent in others with chronic cardiovascular and pulmonary disorders.
Secondary bacterial infection
The patients, who most often are elderly or have chronic pulmonary, cardiac, and metabolic or other
disease.
Other Pulmonary Complications
Croup Asthma Cystic fibrosis Chronic bronchitis, Exacerbation of chronic pulmonary disease
Diagnosis:
• Epidemiologic Data
Most cases have had close contact with influenza patients or been to endemic areas a week before the
onset of illness.
•
Clinical findings
fever, myalgia, cough, pulmonary and nonpulmonary complications
Laboratory: Significant lymphopenia and leucopenia, mild to moderate thrombocytopenia, and elevated
transaminase levels.
•
These abnormalities are poor prognostic signs.
•
Most patients have had negative bacteriologic cultures of sputum and blood.
•
Biochemical results: Abnormality of liver function:Myocardial enzyme abnormalities
Diagnostic imaging tests: (X-ray and CT )
• Virus Isolation Virus isolation from respiratory secretions.
• Rapid Diagnosis Detection of viral antigen (NP,M1) in respiratory secretions, the most rapid of
the ELISAs, can produce results in less than 1 hour. RT-PCR ( throat swab, nasal swab)
• Serologic Testing acute and convalescent serum specimens obtained 10 to 20 days after the
acute-phase serum specimen, four fold or greater rises in titer are considered diagnostic of
infection).
Treatment: isolation for 1 week, anti-inflammatory drugs, fever, anorexia, vomiting, intravenous fluid
infusion. Complicated patients: Pulmonary complications
Supportive care is important, including fluid and electrolyte management.（
hypokalemia,hyponatremia,hypochloridemia）
Supplemental oxygen, intubation, tracheotomy, assisted ventilation, and the use of positive
end-expiratory pressure (PEEP)
Prevention:
• Vaccine should be administered to allow time for the development of protective immunity prior to
the influenza season.
•
You should wash your hands frequently.
•
You should avoid going to areas that are dangerous zones.
•
You should avoid being around anyone that is infected with influenza.
•
You should eat right, sleep right, and have generally good health and exercise.
HEPATITIS
Pathogenesis:
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Acute viral hepatitis is characterized by acute necroinflammation of the liver
Liver injury is mediated by a strong cytotoxic T cell–mediated reaction against infected
hepatocytes that express viral antigens at their surface
Successful immune elimination may lead to viral clearance
The immune reaction is sometimes so potent that the patient develops subfulminant or
even fulminant hepatitis that requires liver transplantation
In some patients, the immune response fails and chronic infection is established
Typical course of acute viral hepatitis: Incubation phase, Preicteric Phase, Icteric Phase, Recovery
Phase
There are five types of viral hepatitis, hepatitis A, B, C, D, and E
• HAV and HEV are transmitted by fecal-oral route, while hepatitis B, C and D are transmitted
by percutaneous, perinatal mother-to-infant and sexual route
• The clinical course of acute hepatitis have four phases: inoculation, preicteric phase, icteric
phase and recovery phase
• Hepatitis B, C and D could progress to chronic disease and are important causes of liver
cirrhosis and liver cancer, while hepatitis A and E have an acute clinical course
• There is no specific treatment for acute viral hepatitis except acute hepatitis C which
requires antiviral therapy
• Effective vaccine for hepatitis A, B, and E has been developed, while HBV vaccine also
provides protection against HDV infection. No prophylactic method has been developed for
HCV
Acute hepatitis A- Fulminant: 0.1%, Transmission Route Fecal-oral
Ingestion of contaminated food or water, Person-to-person transmission
Clinical variants
• Relapsing hepatitis
• Cholestatic hepatitis
Treatment;
• No specific treatment is required
Restrict physical activity, High-calorie diet is desirable,Intravenous feeding is necessary if
patients has persistent vomiting, Avoid drugs capable of causing liver injury, Use of
cholestyramine if severe pruritus is present
• Hospitalization in severe cases
• Liver transplantation for fulminant hepatitis
Acute hepatitis B- Fulminant: 0.1%-1%
• Percutaneous transmission (Blood and blood products, Contaminated medical or surgical
materials,Injection drug use, Sharing scissors, razors and combs, Sexual transmission,
Perinatal mother-to-infant transmission)
• Patients with severe acute hepatitis B warrants antiviral therapy with a nucleoside or a
nucleotide analogue
⮚ Indication: patients with coagulopathy or persistent symptoms or marked jaundice for
more than 4 weeks
⮚ Entecavir [0.5 mg daily] or tenofovir [tenofovir disoproxil fumarate, 300 mg daily, or
tenofovir alafenamide, 25 mg daily], until the signs of severity regress
Acute hepatitis C- Fulminant: 0.1%
Standard precautions to limit exposures to infected persons
⮚ Screening of blood and blood products
⮚ Application of standard medical and surgical hygiene procedures
⮚ Safe use of syringes and materials for drug-users
Chronic:
Diagnosis
• Levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are usually
elevated
⮚ ALT and AST level may remain within the normal range for long periods of time in
patients with chronic viral hepatitis B or C
⮚ The ALT level is generally higher than the AST level
⮚ Both ALT and AST can reach 10 to 25 times the upper limit of normal during acute
exacerbations
• Alkaline phosphatase and γ-glutamyl transpeptidase levels are usually minimally elevated
• Serum bilirubin and albumin levels and the prothrombin time are normal
Liver ultrasound can determine the texture and size of the liver and spleen, exclude hepatic
masses, and assess the gallbladder, intrahepatic bile ducts, and portal venous flow
Computed tomography and magnetic resonance imaging of the liver are helpful if a mass or
other abnormality is found by ultrasound.
Results that suggest the presence of advanced fibrosis:
Platelet count < 160,000 ,AST levels higher than ALT levels, Elevation in serum bilirubin,
Decrease in serum albumin, Prolongation of the prothrombin time, Elevation in α-fetoprotein
levels, Presence of high globulin level
The natural history of chronic HBV infection consists of four phases:
• Immune tolerant phase
• Immune clearance phase
• Inactive carrier phase
• Reactivation phase
Diagnostic criteria of chronic hepatitis B
• HBsAg+ > 6 months
• Serum HBV DNA > 2×104 IU/mL (HBeAg positive) or serum HBV DNA > 2×103 IU/mL
(HBeAg negative)
• Persistent or intermittent elevation in ALT/AST levels
• Liver biopsy showing chronic hepatitis with moderate or severe necroinflammation.
Diagnostic criteria of chronic HBV carrier
• HBsAg + > 6 months
• HBeAg +
• High levels of serum HBV DNA
• Normal aminotransferase
• Mild or no liver necroinflammation and no or slow progression of fibrosis.
Diagnostic criteria of inactive HBsAg carrier
• HBsAg + > 6 months
• HBeAg - , anti-HBe +
• Serum HBV DNA < 2×103 IU/mL
• Persistently normal ALT levels
• Liver biopsy confirms absence of significant hepatitis
Goals of treatment
• Suppress HBV replication
• Reduce the histologic activity of chronic hepatitis
• Lessen the risk of cirrhosis and hepatocellular carcinoma
Indications of treatment
• Chronic Hepatitis B Without Cirrhosis
⮚ ALT >2×ULN
⮚ HBV DNA > 2×104 IU/ml in HBeAg-positive patients or HBV DNA > 2×103 IU/ml in
HBeAg-negative patients
• Compensated cirrhosis
⮚ Detectable HBV DNA
• Decompensated cirrhosis
⮚ Treat immediately, regardless of ALT or HBV DNA level
Pegylated IFN-𝛂
• Pegylated IFN-𝛂2a is administered subcutaneously at a dose of 180 μg/week for 48 weeks.
Side effects of pegylated IFN-𝛂 Flu-like syndrome, Fatigue, Bone marrow suppression:
neutropenia, thrombocytopenia, Anxiety, irritability, depression, suicide ideation,Thyroid
dysfunction,Exacerbation of autoimmune disease, Anorexia, weight loss, alopecia (hair loss)
Nucelos(t)ide analogues
• Administered orally once daily:
0.5 mg for entecavir, or 300 mg for tenofovir disoproxil fumarate, or 25 mg for tenofovir
alafenamide
• Nucelos(t)ide analogues are generally well tolerated
⮚ Renal impairment and decreases in mineral bone density are rarely seen with
tenofovir disoproxil fumarate, but not observed with tenofovir alafenamide.
Chronic Hepatitis C
Pathogenesis
• Acute HCV infection evolves into chronic infection in 50 to 80% of cases
• HCV is not a cytopathic virus
• Liver injury in chronic hepatitis C is related to the action of immune cells that recognize and
kill infected hepatocytes that express HCV antigens at their surface and the local production
of various cytokines and chemokines
• Chronic inflammation triggers fibrogenesis through the activation of hepatic stellate cells
• Chronic inflammation and progression of fibrosis predispose patients to cirrhosis
Clinical Manifestation
• HCV is the main cause of mixed cryoglobulinemia
• Low levels of circulating cryoglobulins, which contains, HCV RNA, anti-HCV antibodies,
rheumatoid factor, and complement, can be found in 50 to 70% of cases
• Elevated rheumatoid factor is found in 70% of cases
• Fewer than 1% of HCV-infected patients develop symptoms of cryoglobulinemic vasculitis,
including myalgias, arthralgias, rash, neuropathy, and membranoproliferative
glomerulonephritis
• Cryoglobulinemia can lead to end-stage renal disease or severe neuropathies and is related
to non–Hodgkin B-cell lymphomas
Diagnosis
• Chronic hepatitis C is defined as the persistence of HCV RNA for more than 6 months
• Chronic hepatitis C is diagnosed by the simultaneous presence of anti-HCV antibodies and
HCV RNA
• HCV genotype should be determined since it has important therapeutic implications
• Laboratory testing often reveals elevated rheumatoid factor and cryoglobulins
Treatment
• Chronic hepatitis C is curable by antiviral therapy
• The goal of treatment is to achieve a sustained virologic response, defined by undetectable
HCV RNA at 12 to 24 weeks after the end of therapy
• Sustained virologic response corresponds to a definitive cure of infection
• Indications of therapy: all treatment-naïve and previously treated patients with
persistent HCV infection should be treated, regardless of the severity of liver disease or
extrahepatic manifestations.
• Patients infected with HCV can be treated with one of seven oral anti-HCV drugs
• When available, the pangenotypic combinations (sofosbuvir/velpatasvir or
glecaprevir/pibrentasvir) should be preferred as first-line treatment options, regardless of the
HCV genotype
• Sofosbuvir/Velpatasvir/Voxilaprevir should be reserved for treatment of patients infected with
genotype 3 with cirrhosis and for retreatment of patients previously exposed to oral anti-HCV
drug.
Prognosis
• Hepatocellular carcinoma is rare in patients with chronic hepatitis C without cirrhosis
• In patients with cirrhosis, the incidence of hepatocellular carcinoma is 2 to 4% per year.
Chronic Hepatitis D
Epidemiology;
● HDV infection occurs in 10% of HBsAg carriers worldwide
● Only approximately 2% of patients acutely coinfected with HDV and HBV develop
chronic hepatitis D
● In chronic HBV carriers superinfected by HDV, however, 90% of patients become chronic
HDV carriers.
Clinical Manifestation;
● Chronic hepatitis D is generally severe, with more than 80% of patients developing
cirrhosis.
● Compared with patients who have chronic hepatitis B alone, patients with chronic
infection with both HBV and HDV are three times as likely to develop hepatocellular
carcinoma and twice as likely to die.
Diagnosis:
● Total anti-HDV antibodies remain at high levels in chronic HDV infection, and HDV RNA
is present
● Although all chronic HDV carriers also are chronic HBsAg carriers, chronic HDV carriers
generally have low or undetectable HBV DNA levels because HDV inhibits HBV
replication
Treatment:
● Pegylated IFN-α2a (180 μg once weekly) or pegylated IFN-α2b (1.5 μg/kg once weekly)
for 48 weeks is the only proven antiviral therapy for chronic HDV infection.
● The virologic response rate is approximately 50% on treatment, but only about 25% of
patients have undetectable HDV RNA 24 weeks after treatment.
Chronic Hepatitis E
Clinical manifestations and diagnosis:
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●
●
HEV infection is usually an acute self-limiting disease, but it causes chronic infection with
rapidly progressive cirrhosis in organ transplant recipients, patients with hematologic
malignancies that require chemotherapy, and immunosuppressed HIV-infected
individuals
Almost all cases of chronic infection have been in immunosuppressed patients
Immunosuppressed patients with chronic hepatitis E harbor repeatedly positive anti-HEV
antibodies and HEV RNA in blood
Treatment:
● There is no validated treatment of chronic HEV infection.
● Reducing the level of immunosuppression can result in viral clearance in approximately one
third of patients and potentially decrease the risk of subsequent cirrhosis
● Ribavirin (600 mg/ day) has been used in small case series. 95% of patients were observed
to have viral clearance for a median treatment duration of 3 months.
Summary
● The natural history of chronic hepatitis B can be divided into four phases: immune
tolerant phase, immune clearance phase, inactive carrier phase, and reactivation phase
● Diagnosis of chronic hepatitis B is based on HBsAg, serum HBV DNA, ALT/AST level
and liver biopsy. Treatment of chronic hepatitis B include pegylated interferon-α and
nucleo(s)tide analogues
● Chronic hepatitis C is diagnosed by the simultaneous presence of anti-HCV antibodies
and HCV RNA. The current standard treatment for chronic hepatitis C is orally
administered antiviral drugs
● HDV superinfection in patients with chronic hepatitis B results in increased severity and
risk of progression to cirrhosis. Patients with chronic hepatitis D should be treated with
pegylated interferon-α
● Chronic HEV infection only occurs on immunosuppressed patients. The reduction in
immunosuppression can lead to clearance of HEV in about one third of patients
HEMORHAGIC FEVER
INTRODUCTION: Acute viral zoonosis: Hanta virus. Reservoir host: rodents.Clinical
characteristics: fever, suffusion and bleeding, renal injury, shock.
Morphology: Circular or ovoid shape, Diameter: 78~210nm. Lipid bilayer
envelope Genome : Single-strand, antisense RNA. Segmented: Large (L),
Medium(M), Small (S)
TRANSMISSION: Vertical transmission: mother-infant. Fecal-oral: contaminated
food/surfaces. Human-human: Andes virus is the only transmissible strain
Pathophysiology of acute renal failure:
∙ GFR decreased
∙ Immune injury of kidney
∙ Cast obstruction of renal tubule
∙ Interstitial edema pressing renal tubule
Clinical manifestations
∙ Major cardinal symptoms: fever, suffusion and bleeding, acute renal insufficiency,
shock ∙ Incubation : 4-46 days (usually 7-14 days)
∙ Clinical stages: (phases)
1. Febrile stage: lasts for 3-7 days. Fever 39-40 C. infective intoxication
(nonspecific symptoms: Chills, malaise, headaches, nausea, vomiting, diarrhea,
abdominal,
backpain, orbital pain, blurred vision). Capillary damage sign(
suffusion/hyperemia, hemorrhage, exudative edema).Renal
injury(proteinuria, hematuria, cast,
membranoid substance).
2. Hypotensive phase: occurs 4th-6th day of illness. Lasts 1-3 days. Hypotension
(Systolic pressure <90mmHg) (Shock: Systolic pressure <70mmHg).
dizziness, debility, indifference or dysphoria, pale skin, cold clammy
limbs, superficial vein collapse, hypotension and urinary volume decrease.
3. Oliguric phase: occurs 5th-8th day of illness. Lasts 2-5 days. Oliguria: Urine
volume in 24h<500 ml. Anuria: Urine volume in 24h <50 ml. uremia.
Anorexia, nausea, vomiting, diarrhea, hiccup. Hemorrhage(petechia,
hemoptysis hematuria). Metabolic acidosis. Water and electrolyte imbalance.
4. Diuretic phase: occurs 9th-14th day of illness. Lasts 7-14 days. urine volume
>2000ml/24h.Water and electrolyte balance. Secondary infection, Secondary
shock.
5. Convalescent phase: lasts 1-3 months. Urine volume <2000ml
Complication:
Coagulation abnormalities Bleeding of internal organs, DIC
Complications of CNS: Meningitis or encephalitis, brain edema, intracranial bleeding.
Pulmonary edema: ARDS, Pulmonary edema due to heart failure
Other: Liver injury, Secondary infection, Spontaneous rupture of kidney
Lab findings:
Blood routine: WBC > 10×109/L or leukemoid. Thrombocytopenia <100×109/L. Heteromorphic
L >15%. RBC
Urine routine examination: proteinuria, hematuria, cast, membranoid substance, large
diffuse cells Serologic exam: IGM antibody, IgG antibody
Other exam: BUN, Cr, K, Na, Cl
Clinical types of hemorrhagic fever:
symptom
Type
renal injury Oliguri a/
T(℃)
hemorrh age
anuria
＜３８
no
No/
mild
proteinu ria
No
３８～
３9
petechia
e
mild
No/
hematu
ria
３９～
４0
obvious
obviou
s
obvious
＞４０
cavity
Seriou
s
anuria≤
２d or
Oliguri
a≤５d
Non-typical +- Mild +～++
Moderate +++ Severe ++++
Dangerous severe
shocks, etc.
Serious shock
viscera BUN＞
42.84
umol/L
anuria ＞２d or
Oliguri a＞５d
diagnosis:
Fever: Influenza,
septicemia, etc.
Shock: Other
infectious
Differential
Oliguria: Acute glomerulonephritis, etc.
Hemorrhage: Thrombopenia purpura, etc.
Abdominal pain: Surgical acute abdomen, etc.
Other causes of hemorrhagic fever: Yellow fever, Ebola, Septicemia, Dengue, Leptospirosis,
Severe fever with thrombocytopenia syndrome
Treatment:
Febrile stage: (infect control use ribavirin ) (decrease exudation by giving liquid treatment: salt
solution, vit c) (improv toxic symptom: fever—cooling and give dexamethasone ) prevent DIC:
dextran, heparin) Hypotensive phase: (supplement blood volume: crystalloid solution) (correct
acidosis 5% NAHCO3) (vasoactive agents:dopamine) (adrenocortical hormone: dexamethasone).
Oliguric phase: (Stabalize internal environment: maintain water-elec balance , maintain acid-base
balance, control azotemia by giving glucose 200-300g/day) (diuresis) ( blood letting therapy) (
dialysis therapy) Diuresis phase: ( supplement fluid and elec ) ( treatment and prevention of
secondary infection) Convalescent phase: ( supplement of nutrition ) ( rest 1-3 months )
Prevention:
Killing and preventing rats: host-reservoir control
Personal protective measures: human exposure prophylaxis intervention
Vaccination: prevents disease by 84-94%
EPIDEMIC ENCEPHALITIS B (JEV)
Introduction:
∙ Viral. Zoonosis. arboviruses flaviviridae flavivirus genus.RNA.
∙ JE patients typically present with high fever confusion or coma,convulsions,
pathological reflex, and meningeal irritation.
∙ Source: pig. Route : mosquitoes.
Etiology:
∙ The virus is thermolabile, and is inactivated by heating at 100℃ for 2 min or 56℃ for 30
min. ∙ However,JEV is resistant to low temperature and dry environment,it can be stored at 4
℃ for several years by freeze drying
Epidemiology:
JE occurs all year round in tropical areas.
In subtropical Asia, JE virus transmission is seasonal;
Human diseases usually peak in the summer and fall;
Virus transmission lasts from March to October and usually peaks during the rainy
season; JE is transmitted sporadically from July to September.
The most important vector is mosquitoe(Culex species).Transovarial transmission is the main
cause for infecting among mosquitoes.
The natural hosts of the Japanese encephalitis virus are birds, as maintenance hosts, and many
believe the virus will therefore never be completely eliminated.
Pigs act as an amplifying host and have a very important role in the epidemiology of the disease.
Infection in swine is asymptomatic, except in pregnant ones.
Human, cattle, and horses are incidental dead end hosts. JE virus can not spread directly from
person to person. Humans once infected do not develop enough concentration of JE virus in
their bloodstream to infect feeding mosquitoes.
Pathology:
Direct invasion of the nervous tissue by JEV and the resultant neuronal necrosis, gliocyte
hyperplasia, and infiltration of inflammatory cell result in brain tissue injury. Direct invasion of
the nervous tissue by
JEV and the resultant neuronal necrosis, gliocyte hyperplasia, and infiltration of inflammatory
cell result in brain tissue injury.
Clinical manifestations:
∙ The Japanese encephalitis virus (JEV) has an incubation period of 10 to 14 days.
Stage 1: initial:
∙ This stage is observed at the very beginning 1~3 days.
∙ Patients at this stage of infection present with high-grade fever, headache, and malaise. ∙ The
initial presentation usually begins with gastrointestinal symptoms of nausea,or abdominal pain.
∙ Vomiting and diarrhea or acute convulsions may be the earliest objective signs of illness, and
a few patients show stiff neck.
∙ This stage easily mistaken for upper respiratory tract infection.
Stage 2: fastigium
∙ This stage lasts for 4~10 days.
∙ Besides worsening of early symptoms, the major manifestation is impair brain
parenchyma. Including three kinds of prominent clinical manifestations:
1. Hyperpyrexia: High-grade fever usually lasts for 7~10 days, and lasts for more than 3 weeks
in severe cases. High fever aggravates the disease
2. Consciousness disturbance: includes sleepiness, delirium, coma, and
disorientation.Delirium presents early in the course of disease.
3. convulsions and seizures: Convulsions or seizures are due to hyperpyrexia, brain
parenchymal inflammation, and brain edema.
4.respiratory failure: Respiratory failure is caused by brain parenchymal inflammation,
hypoxia, brain edema, intracranial hypertension, and hernia.
5. circulatory failure
Stage 3: convalescence
∙ During convalescence stage, there is a gradual decrease in temperature, and
improvement in nervous systems and physical signs.
∙ The manifestations of this stage involve sustained low fever, hyperhidrosis,
insomnia, dementia, aphasia, dysphagia, facial paralysis, limb paralysis or
involuntary
Stage 4: sequela stage
∙ patients with JE have sequelae which mainly manifest as aphasia, limb
paralysis disturbance of consciousness, mental disorders, and dementia.
Lab finding:
.Hemogram：
White Blood Cell(WBC) counts usually range from 10x109/L to 20x109/L, and the
proportion of neutrophils is more than 80%. Some patients consistently exhibit normal
results.
2.CSF analysis：
∙ CSF appears clear or slightly turbid, and tension is elevated. WBC counts increase to
(50~500)x109/L and reach even as high as 1000x109/L, with a predominance of
neutrophils in the early stage followed by lymphocytes.
∙ Biochemical tests show normal glucose and chloride and elevated protein
levels. 3.Serological findings
① Determination of specific IgM antibody
∙ The IgM antibody arises in serum within 3 days and in CSF within 2 days of onset, which is
of diagnostic value in the earlystage.
Diagnosis:
1.Epidemiological materials The disease is strictly seasonal(summer and autumn) and occurs
mostly in children aged 2~7 years old. However, the number of adult cases has increased in
recent years. 2.Clinical characteristics Manifestations of acute onset include high fever,
headache, vomiting, consciousness disturbance, seizures， and positive pathological reflex.
3.Laboratory findings WBC analysis shows increased WBC and neutrophil counts. CSF test
reveals aseptic meningitis changes.
Serological examination,especially the determination of specific IgM antibody,
contributes to case confirmation.
The diagnosis can be verified by ①fourfold change in IgG antibody or neutralizing antibody
titers in serum during convalescence with respect to the levels in the acute phase, ②a positive
JEV IgM antibody in the acute phase,or③detection of specific JEV antigen and nucleic acids.
Differential diagnosis:
1 .Toxic bacillary diarrhea;
2.Bacterial meningitis;
3.Tuberculous meningitis;
4.Other viral encephalitis;
Prognosis:
∙ Most mild and ordinary cases of JE show a good recovery.
∙ Bad prognosis for pregnant and elderly
Treatment:
∙ Isolate: in anti mosquito ward
∙ General therapy:including the maintenance of water and electrolyte balance and
close observation can be used in the early stage. However, supportive care and
symptomatic
therapy should be adopted of patient conditions. Like assistance given for
feeding, breathing as required.
∙ Seizure give lorazepam, monitor vitals
Prevention: (control source of infec) ( interrupt transmission route ) ( Vaccination)
CHOLERA
Introduction: Vibrio cholerae. Gram -ve. H/O toxin. Cholera enterotoxin causes clinical manifestions.
Epidemiology/transmission: fecal-oral route.The cycle of transmission is closed when infected
humans shed the bacteria into the environment and contaminate water sources and food. Hot
seasons. O139 strand. Acute onset. Vaccines are not protective.
Clinical manifestations
Incubation period: generally 1 to 3 days (several hours - 7 days)
Diarrhea: Characteristic feces: "rice swill-like" feces with a small amount of mucus. No
abdominal pain. No tenesmus. No fever (O139 fever and abdominal pain are more common).
Symptoms last from hours to days.
Vomiting: frequently with watery emesis, is common. Vomiting may begin either before or
after the onset of diarrhea. Patients may have abdominal cramping but typically do not have
the frank abdominal pain classically associated with dysentery.
Dehydration: Hypovolemia and electrolyte loss. Dehydration. Muscle cramps. Hypokalemia.
Uremia, acidosis. Circulatory failure to 2-3 days.
Complications: acute renal failure. Acute pulmonary edema. Pneumonia.cholera sicca.
Lab diagnosis:
▪ Increased hemoglobin, increased white blood cells
▪ Decreased or normal serum potassium, sodium, and chloride
▪ Elevated blood urea nitrogen and creatinine
▪ bicarbonate drop
▪ Stool routine: Visible mucus and a little red and white blood cells
▪ Urine routine: a small amount of proteinuria, a few red and white blood cells, casts
▪ Fecal smear: Gram-negative Vibrio in a school-like arrangement
▪ Kinetic Test: Vibrio Shuttle Activity by Hanging Drop Microscope
▪ Brake test: agglutination with O1 group or O139 antiserum
Diagnosis:
When to suspect? ≥ 5 years old develops severe volume depletion from acute watery
diarrhea, even in an area where cholera is not known to be endemic.
Visible symptom:
∙ Sunken eyes and cheeks
∙ Decreased skin suppleness
∙ Dry mucous membranes
∙ Urine production is sharply decreased
∙ Renal failure is the most common
∙ Complications seen in recent outbreaks
∙ Gram -ve rods
∙ Culture result ( golden standard)
∙ Dark field microscopy
Treatment:
∙ Strict isolation
∙ Appropriate rehydration
∙ Antimicrobial and symptomatic therapy Report the epidemic
∙ After the symptoms disappear, the feces are cultured every other day, and the cultures
are negative for two consecutive times, and the isolation can be released
∙ Rehydration ( ORS Salt solution ) ( ringers lactate)
∙ Correct acidosis, shock, hypovolemia, pulmonary edema
∙ Anti microbial therapy: ciproflocacin, doxycycline, tetracycline
Prevention
∙ Vaccine
∙ Eliminate vectors: flies
∙ Isolate patients
∙ Strengthen water, food management
HIV
INTRODUCTION:
Human immunodeficiency virus (HIV) infection is caused by human immunodeficiency
virus 1 (HIV-1) and 2 (HIV-2).
MODE OF TRANSMISSION:
a. Sexual intercourse: unprotected sex. Multiple partners. Homosexuality,
b. Intervenous drug use: sharing noodles. Unsafe blood transfusion.
c. Vertical transmission: mother to infance ( in utero , child birth, breast
feeding) d. Occupational transmission: health care individual
NO TRANSMISSION OF HIV BY EATING, INSECT BITES, SHARING PHONE,
SHAKING HANDS.
ETIOLOGY:
HIV is an enveloped single-stranded RNA virus from the family
Retroviridae. HIV contains the 3 species-defining retroviral genes—
a. gag (group-specific antigen; the inner structural proteins)
b. POL (polymerase) contains integrase and protease -viral enzyme-and is produced
in the c terminal extension of gag protein.
c. env (envelope; the outer structural proteins responsible for cell-type
specificity). Clinicl manfifestation:
Phases
a. ACUTE : fever, soare throat, lymph node enlargement, joint pain, erythematous
rash, headache, oral anal vaginal ulcers, hepatosplenomegaly, stage lasts upto
6 months, highly infective stage
b. ASYMPTOMATIC: Persistent virus replication. Evasion of immune system
control. Reservoirs of HIV-infected cells: obstacles to the eradication of virus.
Viral dynamics. Clinical latency versus microbiologic latency.
c. AIDS (SYMPTOMATIC): divided into two phases
i. Early symptomatic: patient develops symptoms that have not yet met
the requirements of aids. Anemia, neutropenia, thrombocytopenia,
fever, weight loss, diarrhea.
ii. Advanced symptomatic: HIV infection can cause some sequelae,
including AIDS-associated dementia/encephalopathy and HIV
wasting syndrome (chronic diarrhea and weight loss with no
identifiable cause). AIDS manifests as recurrent, severe, and
occasionally life-threatening infections or opportunistic
malignancies. Opportunistic infections (toxoplasmosis, salmonella
septicemia, herpes)
Lab testing:
Screening assays - EIAs are the most frequently used screening assays.
Confirmatory assays - Western blot is regarded as the gold standard for serological diagnosis.
Diagnosis:
∙ The patient’s sexual history, history of drug use, history of blood transfusion, lifestyle
factors such as smoking and alcohol use, and exposure to certain diseases assist in the
diagnosis of HIV. ∙ When the absolute CD4 T-cell count declines to less than 200 cells per
cubic millimeter, the HIV infection is classified as AIDS.
Goals of anti retrovirals:
1. reduce morbidity and mortality
2. prolong life
3. improve life quality
4. restore immune function
5. suppress viral load
6. prevention of vertical transmission
When to initiate therapy?
1. CD4 T-cell count below 350 cells per cubic millimeter .
2. Patients with high viral load (eg, 100 000 copies per milliliter)
3. Pregnant woman
How to prevent infection of HIV?
Life style changes(decrease no. of sexual partners, engage in safe sex)
Adherence to drug therapy
AZT for pregnant women to prevent vertical transmission
Post exposure prophylaxis regimen for health care workers. lamivudine+tenofovir+
efavirenz/ lopinavir-ritonavir
Bic/3TC/FTC.
Classes of antiretroviral drugs
There are seven classes of antiretroviral (ARV) drugs currently approved. 1.
nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs),
2. non-nucleoside reverse transcriptase inhibitors (NNRTIs),
3. protease inhibitors (PIs),
4. fusion inhibitors (FIs),
5. CCR5 antagonists,
6. integrase inhibitors
7. entry inhibitor
preferred antiretroviral regimen:
∙ The preferred regimen of treatment consists of a combination of 2NRTIs+NNRTIs, 2NRTIs+
ritonavir boosted PI. Both of these regimens lead to a suppression of HIV RNA levels and
CD4 T cell level increases in most patients.
What does the regimen designed for each patient depend on ?
∙ Virologic efficacy
∙ Toxicity
∙ Pill burden
∙ Dosing frequency
∙ Drug-drug interaction potential
∙ Drug resistance testing results
∙ Comorbidity conditions
Keypoints from the ppt:
∙ Human immunodeficiency virus (HIV) infection is caused by human immunodeficiency
virus 1 (HIV-1) and 2 (HIV-2). It is marked by the extensive dysfunction of the immune
system. ∙ The routes of HIV transmission include sexual contact, vertical transmission,
intravenous drug use and occupational exposure (blood contact).
∙ The two most commonly used diagnostic modalities in HIV are enzyme immunoassay
(EIA) and Western blot test.
∙ Treatment of HIV infection includes the use of nucleoside reverse transcriptase inhibitors,
protease inhibitors (PIs), and non-nucleoside reverse transcriptase inhibitors.
∙ CD4 T-cell count and plasma HIV-RNA are used to monitor the patient’s response to
therapy. ∙ Several complications are associated with HIV infection, such as opportunistic
infections, malignancies, and gastrointestinal (GI) tract complications.
∙ Preventive measures, adherence to drug therapy, and lifestyle changes should be emphasized
to the patient.
Bacillary Dysentery (shigellosis)
> Diarrhea is defined as the passage of loose or watery stools, typically atleast three times
in a 24-hour period.
● Acute diarrhea- 14 days or lower in duration
● Persistent diarrhea - more than 14 days but less than 30 days.
● Chronic diarrhea - more than 30 days in duration
Infectious diarrhea - viruses , bacteria , Protozoa
No infectious diarrhea - more common in chronic diarrhea
> Shigella; once ingested it multiplies in the small intestine then enters the colon, where it
produces shigella enterotoxins and serotype toxin 1 which causes watery diarrhea .
> Escherichia coli comprises bacillary dysentery.
>Shigellosis is a clinical syndrome caused by invasion of the epithelium lining the terminal
ileum, colon, and rectum by Shigella species.
> Etiology ● dysentery bacillus, genus shigella
● non-spore-forming, small gram-negative rods
● nonmotile
● do not produce gas from sugars, decarboxylate lysine, or hydrolyze arginine.
● facultative anaerobic, but grow better under aerobic conditions
Pathogenicity :
1. Virulence - endotoxin (fever,shock) , exotoxin (cytotoxic,enterotoxin)
2. Invasiveness- (attach penetrate - multiply )
3. Resistance - Strong, 1-2 week in fruits,vegetables and dirty soil, heat for 60°C 10
min, and 30 min under the direct sunlight.
> Epidemiology:
✔ Source of infection: Only humans carry shigella. Patients and carriers are the source of
infection.
✔ Route of transmission: fecal oral route; direct person to person, sexual contact, indirectly
through contaminated food, water or formities
✔ Susceptibility of population:Immune protection after infection is serotype-specific, short
and weak, humans could be infected repeatedly.
✔ Epidemic characteristics: endemic in temperate and tropical climates.
Transmission of Shigella spp. is most likely when hygiene and sanitation are insufficient.
1
> Pathogenesis :
> Pathology :
● Within 12 hours---the bacteria transiently multiply in the small bowel abdominal pain,
cramping, fever
● Within a few days---a diffuse colonic localization of the bacteria urgency, tenesmus,
and passage of bloody mucoid stools
● Feature of pathology: acute: diffuse fibrinous exudative inflammation .
hyperemia, edema, hemorrhage, leukocyte infiltration; superficial necrosis, ulcer.
> Clinical manifestations :
● Incubation period - typically 2-4 day (hours to 7 days)
● Acute onset
● Fever
● Vomiting , diarrhea (initially diarrhea is watery but may contain blood,mucus and pus
)
● Abdominal pain , tesnesmus
> Major complications: are rare
● Intestinal complications - proctitis,intestinal obstruction , colonic perforation
● Systemic complications - bacteremia , reactive arthritis,hemolytic uremic
syndrome,metabolic disturbance: dehydration, hyponatremia
2
> laboratory findings:
● Blood routine examinations - WBC count increase,neutrophils increase
● Stool examination
● Bacterial culture and PCR testing
> Differential diagnosis:
● Amebic dysentery - entamoeba histolytica, low fever,abdominal pain
● Other bacterial diarrhea
● intussusception , acute hemorrhagic necrotizing colitis
> Treatment :
● Supportive therapy - rest, reasonable diet, hydration,electrolyte balance
● Antibiotic treatment:
1. Empiric treatment - first-line:ciprofloxacin, azithromycin, ceftriaxone
second choices: trimethoprim-sulfa methoxazole.
2. antimicrobial susceptibility: generally include fluoroquinolone, azithromycin, and a
third generation cephalosporin.
> prevention: Properly washing the hands can help,Food safety and regular drinking
Fill in the blanks:
1. Shigella is a common cause of bacterial diarrhea. It is transmitted by direct
______spread and, through ___and ____.
2. The incubation period ranges from __to _ days. Patients with Shigella gastroenteritis
typically present with ___, ___ and ____; Initially diarrhea is ____, but subsequently
may contain ___ , ___ & __;
3. Shigella gastroenteritis generally is ____, lasting no more than in an untreated
immunocompetent host.
4. Shigella should be suspected in patients with ___________, ___________, ______,
and ______, particularly if accompanied by fecal leukocytes. Definitive diagnosis is
made by _____. Antimicrobial susceptibility testing should be performed on all
isolates. If Shigella is identified by molecular testing, a stool sample should also be
sent for and ____ testing.
5. Antibiotic selection should be guided, if possible, by results of antimicrobial
susceptibility testing. Options generally include a _______,________, and a
________ . Trimethoprim-sulfamethoxazole and ampicillin are also options if
susceptibility is documented.
3
MCQ’S :
1. The pathogen of bacillary dysentery belongs to (A)
A. Shigella. B. Salmonella C. Vibrio D. Campylobacter E. Spirulina
2. The main factor of systemic toxemia of bacillary dysentery is caused by ()
A. Flora B. Endotoxin C. Exotoxin D. Immunity E. Number of bacteria
3. Regarding the clinical manifestations of acute dysentery, which is wrong ()
A. Protruding chills and fever B. Pus and blood in stool
C. Tenderness in the whole abdomen, mainly in the right lower abdomen
D. Often accompanied by tense
E. Dehydration and electrolyte disturbance may occur
4. The most reliable evidence for the diagnosis of bacillary dysentery is ()
A. Typical pus and blood stool B. Positive stool culture C. Obviously tense and heavy
D. Positive immunological examination
E. Stool microscopic examination found a large number of pus cells and phagocytes
5. Regarding the biological characteristics of Shigella, which of the following statements is
wrong ()
A. According to bacterial antigens, it can be divided into 4 groups: A, B, C, D
B. Strong survivability in the in vitro environment
C. Survive on fruits and contaminated items at room temperature for 10-20 d
D. The higher the temperature, the longer the survival time of Shigella E. Can produce
exotoxin.
6. The most important evidence for differentiating acute amoebic dysentery from acute
bacillary dysentery is()
A. Systemic poisoning symptoms B. Gross Appearance of Feces C. Abdominal tenderness
D. Pathogens detected in feces E. Intestinal mucosal lesions seen by sigmoidosco
7. Which of the following sources of infection is relatively more important in the epidemic of
bacillary dysentery ()
A. Acute typical patient B. Patients with Toxic Bacillary Dysentery C. Convalescent patients
D. Acute atypical patients, chronic patients and asymptomatic carriers. E. Chronic patients
8. Which of the following is the pathological change of the colon in the early stage of
bacillary dysentery? ( )
A. Diffuse fibrinous exudative inflammation of intestinal mucosa
B. Intestinal mucosa edema, thickening, ulceration
C. The intestinal wall forms a flask-like ulcer with a small mouth and a large bottom
D. Formation of eosinophilic granulomas
E. Swelling of endothelial cells in small blood vessels and exudation of plasma
4
Typhoid Fever
> Typhoid fever is an acute enteric infectious disease, and caused by Salmonella typhi
(S.Typhi).
> Etiology :
● rod,non-spore, no capsule,flagella
● Antigens: located in the cell capsule, H (flagellar antigen),O (Somatic or cell wall
antigen). Vi (polysaccharide virulence surface Vi antigen)
● Pathogenicity: endotoxin
> Epidemiology :
• Source of infection - carrier or patient is the only source.
Cases and chronic carriers are the main source of infection.
• Transmission - Fecal-oral route; Waterborne transmission ,Food-borne transmission,
Close contact transmission.
• Susceptibility and immunity - acquired immunity can keep longer, reinfection are rare
All seasons, usually in summer and autumn,most cases in school-age children and young
adults.
> Pathogenesis :
5
> Clinical manifestations :
1. The incubation period is usually 7 -14 days.
2. Typical infection : fever
● Nervous system symptoms - typhoid face, trinitius,hearing loss,typhoid meningitis
● Digestive system problems - loss of appetite, nausea, vomiting,abdominal
pain,diarrhea.
● Hepatomegaly ,splenomegaly
● Relatively slow pulse
● Rose spots - rosolea
● Relative bradycardia, apathies facial expressions.
> Complications: Intestinal hemorrhage, intestinal perforation, toxic myocarditis
> laboratory findings : blood culture, bone marrow and stool culture
> Widal tests - A test involving agglutination of typhoid bacilli when they are mixed with
serum containing typhoid antibodies from an individual having typhoid fever; used to detect
the presence of Salmonella typhi and S. paratyphi.
- How to Diagnose - early of the disease, previous infections,vaccination/nonspecific
memory reaction , typoid,paratyphoid A,paratyphoid B paratyphoid C
- Limitations of widal test 1. Tests done within 7 days of illness and after 4 weeks are usually negative.
2. Previous typhoid vaccination may contribute to elevated agglutinins in the
non-infected population.
3. Other infections of non-enteric salmonella infection such as Typhus, Immunological
disorders, chronic liver disease may cause false positive reaction.
4. Cross reaction between malaria parasites and salmonella antigens may cause false
positive Widal agglutination test.
-
polymerase chain reaction (PCR) based diagnostic have had limited sensitivity.
> Treatment :
● General treatment - disinfectant and isolation, diet (fluid and electrolytes), rest.
● Etiologic treatment - Antibiotics, such as ampicillin, chloramphenicol, fluoroquinolone,
trimethoprim-sulfamethoxazole, amoxicillin and ciprofloxacin etc used to treat typhoid
fever.
- Fluoroquinolones : penetrate well into macrophages, and achieve high
concentrations in the bowel and bile lumen. Norfloxacin (0.1~0.2 po. tid~qid/10~14
days) ,Ofloxacin (0.2 po. tid 10~14 days),ciprofloxacin (0. 5 po. bid 10days)
- Cephalosporins : third generations effective , 2g iv. Bid (adult)50mg/kg iv. Bid
(children) 10~14 days.
- Chloramphenicol : recommended dosage is 50 - 75 mg/kg/day for 14 days
●
Antibiotic resistance: as resistance to first line antibiotics, Typhoid resistant to these
agents is known as multidrug-resistant typhoid (MDR typhoid). Can be resolved
Azithromycin.
6
> Prevention: control source of infection - cases chronic carriers ,Cut of course of
transmission ,Vaccination.
- Food and hand washing precautions.
> Treatment of complication:
- Intestinal bleeding: Absolute bed rest, close monitoring of blood pressure and stool
bleeding ,Replenish blood volume, maintain water, electrolyte and acid-base balance
Hemostatic drugs, blood transfusion.
- Intestinal perforation:
● Patients with limited intestinal perforation should be given fasting and gastric tube for
gastrointestinal decompression.
● Strengthen antibiotic treatment.
● Patients with intestinal perforation complicated by peritonitis should undergo surgical
treatment in time.
MCQ’S
1.Which of the etiological characteristic of Typhoid bacillus is correct :
A. Group A of salmonella B. Negative gram staining, producing spores with sandwiches
C. There are bacterial (O) antigens, flagellar (H) antigens, and some bacteria have bacterial
surface (Vi) antigens
D. Vi antigenic antigen is strong, and the vi antibody titer is high and the duration is long
2. The main factor causing the disease of Typhoid bacillus is
A. Endotoxin B. Enterotoxin C. Exotoxins D. Neurotoxins E. Cytotoxin
3.The main source of infection causing the ongoing spread or epidemic of typhoid fever is
A. Patients with ordinary typhoid fever B. Patients with fulminant typhoid fever
C. Chronic carriers D. Recovery period for typhoid fever E. Incubation period of typhoid fever
4.The most valuable test is for patients who have used antibiotics and are suspected of
typhoid fever
A. Fecal culture B. Bone marrow culture C. Blood culture D. Fertilizer reaction
5.Which of the following is true in regard to prophylaxis against typhoid fever?
A. Typhim Vi is a live attenuated oral vaccine that should be given prior to travel in
areas of moderate to high risk for exposure
B. Vivotif is an inactivated oral vaccine that should be given prior to travel in areas of
moderate to high risk for exposure
C. Either vaccine will be >90% effective in preventing typhoid fever
D. Food and hand-washing precautions are recommended in addition to either of the
available vaccines
7
Malaria
> Malaria is a severe parasitosis caused by plasmodia which parasitize human hepatocyte
and red blood cells.
> Malaria: Plasmodia
•Infective stage: sporozoite
•Infective way : mosquito bite skin of human
>Causative organism: Plasmodia
P. Vivax: tertian malaria
P. Ovale: tertian malaria
P. Malariae: quartan malaria
P. Falciparum: malignant malaria
> Etiology :
- Two period ; Human-whole asexual reproduction
Parasitic position : liver and red blood cells exoerythrocytic stage ,erythrocytic stage
Mosquito-sexual parasitic stage
- Two host :Human-intermediate host Mosquito-final host
> Epidemiology :
● Source of Infection: Patient, parasite carrier
● Route of transmission: female mosquito biting person blood transfusion
● Susceptibility: universal susceptibility no-cross-immunity re-infection
● Epidemic features: sporadic or endemic, tropic or sub
> Pathogenesis :
> Pathology :
- Anemia (P. Vivax - retiform RBC,P. Malariae -mature RBC,P. Falciparum all ages RB)
- Hepatomegaly
- Splenomegaly - Proliferation of mononuclear phagocyte
- Cerebral edema & congestion -caused by P.falciparum
8
> Malaria also can be transmitted through:
1. inadvertent transfusion of infected blood
2. needle sharing among drug addicts
> Clinical manifestation : (Typical paroxysm)
● Chill: abrupt onset, shivering, pale face, cyanosis.Last 10 min or 1~2hr.
● High fever: T rise to 40oC with malaise, myalgia, thirsty. Last 2~6 hr.
● Sweating: profuse sweating with restlessness. Last 1-2hr.regular 48 hr. or 72 hr.
●
-
●
●
P.falciparum (small vessels are plugged) may produce :
Cerebral malaria: seizures and impaired consciousness. high fever, headache,
vomiting, convulsion, delirium, respiratory failure.
Renal failure - chill and fever , dard red or black urine,severe hemolytic anemia
causes : inadequate G-6-PD, toxin release by malarial parasite , Allergic reaction to
anti-malarial drug.(Acute glomerulonephritis)
Gastroenteritis
Serious anemia
Acute respiratory distress syndrome (ARDS)
Incubation period: tertian malaria: 13~15 days, quartan malaria: 24-30 days
malignant malaria: 7~12 days
Malaria caused by transfusion incubation period: 7~10 days ,no exoerythrocytic
phase, no relapse
> Laboratory diagnosis:
- Serological examination ELISA for P. antigen,DNA hybridization
- microscopic examination of a thin or thick smear, Giemsa's stain
> Differential Diagnosis : Influenza,Typhoid fever,Bacteremia/sepsis,Classic dengue fever
Acute schistosomiasis (Katayama fever), Leptospirosis,African tick fever, yellow fever
> Treatment :
Three principles: Control of clinical symptoms, Eradication of gametocytes, Prevent relapse
● Chloroquine, quinine, artemisinin and artemether----anti-erythrocytic stage drugs.
● Primaquine and pyrimethamine ----anti-exoerythrocytic stage drugs.
● Antimalarial drugs
● Chloroquine-resistant infection( mefloquine,artemisinine)
● Pernicious attack- Chloroquine: 10mg/kg iv drip in 4 hr. Then 5mg/kg, iv drip in 2 hr.
Quinine: 500mg iv drip in 4 hr.
● Radical therapy - Chloroquine (3 day) + primaquine ( 8 day )
● When to treat as chloroquine-resistant malaria?
- Falciparum known & patient from chloroquine resistant area
- Falciparum not known, patient is seriously ill and have symptoms of cerebral malaria
- (confusion, delerium, convulsions)
- Mixed infection,Benign tertian not responding to chloroquine
9
● Chloroquine resistant malaria- First line treatment:
Quinine/quinidine + doxycycline
Quinine/quinidine
Parenteral:
Loading dose: 20 mg/kg (up to 1.4 g) iv over 4 hrs Maintenance: 10 mg/kg (up to 700 mg) iv
8 hourly Oral: 600 mg TID for 5-7 days
Adv. Effects:Cinchonism (headache, dizziness, tinnitus, vertigo, fever) IV infusion may cause
hypotension, arrhythmias Can increase plasma levels of digoxin and warfarin
- Alternate regimens
a. Pyrimethamine & sulphadoxine (Fansidar)
b. Atovaquone & proguanil
c. Mefloquine
d. Artemether & lumefa
> Malaria during pregnancy Can be used:
Chloroquine non-resistant malaria ,Chloroquine ,Chloroquine resistant malaria
Chloroquine & proguanil,Quinine/quinidine,Mefloquine: avoid in 1st trimester
Atovaquone + proguanil (Malarone): use if necessary
Contraindicated:Doxycycline,Pyrimethamine and sulphadoxine combination
> Prevention:
● Chemoprophylaxis
● Malaria vaccine
● Prevention of mosquito bites by wearing long sleeve,Diethyl-toluamide lotion and
spray, coils and mats.
10
Meningococcal meningitis
> Meningococcal meningitis is a bacterial form of meningitis, a serious infection of the thin
lining that surrounds the brain and spinal cord.
- Neisseria meningitidis is the one with the potential to cause large epidemic.
- The meningitis belt of sub-Saharan Africa has the highest rates of the disease
- Neisseria meningitidis is a gram-negative diplococcus.
> Cultural condition :
❖ Optimal growth conditions are achieved in a moist environment at 35°C to 37°C under an
atmosphere of 5% to 10% carbon dioxide.
❖ The bacteria could grow well on the chocolate agar plate or the blood agar plate.
- The meningococcus will metabolize glucose and maltose to acid without gas
formation and fails to metabolize sucrose or lactose.
The organism contains cytochrome oxidase in its cell wall.
- The meningococcus has a rapid autolytic rate
> Pathogenesis of infection :
- The Pathogenesis of N. meningitidis involves a series of sequential steps. The
process begins when the bacterium colonizes the nasopharynx.
- The nasopharynx is a mixed epithelial surface containing ciliated secretory and
nonciliated, nonsecretory cells.
The airway epithelial surface is covered with a mucus layer that the organism must
penetrate.
- The meningococcus uses bacterial surface factors to adhere to nonciliated cells on
the airway surface.
Pili enhance attachment organelles
It has been shown that purified pili bind to a human cell surface protein CD46 that is
widely distributed and involved in regulation of complement activation
> Epidemiology :
❖ Source of infection: bacteria-carriers and patients.
❖ Transmission: The bacteria are transmitted from person-to-person through droplets of
respiratory or throat secretions from carriers and patients.
❖ The susceptibility of population: 6m-2y children are most common.
> Clinical Manifestations:
- The incubation period - The average incubation period is four days, but can range
between 2 and 10 days.
The most common symptoms: high fever, vomiting, headaches, a stiff neck,
sensitivity to
light and confusion.
- Petechial lesions are a common harbinger of this infection
- Generalized muscle tenderness may also be an important differential
sign.Occasionally, the pain from these myalgias is quite intense and causes the
patient considerable discomfort.
11
● Clinical Manifestations-four types
1. Common type Prodromal phase. 1-2 d. symptoms of upper respitory tract infection.
- Septic phase. 1-2 d.High fever, chill, headache, lassitude. Children-cry, apastia,
convulsion. >70%-Petechiae, ecchymosis.
- Meningitis phase. 2-5 days,Headache, lassitude, projectile vomiting, stiff
neck-meningeal irritation sign.severe:Delirium, convulsion, disturbance of
consciousness
4. Recovery phase. 1-3 w 10%-Herpes around mouth
2. Fulminant type - Shock type- High fever, chill, headache, vomiting , petechiae, ecchymosis -> signs of
shock such as blood pressure lower, heart rate higher.
Meningoencephalitis type- Damage of meninges and brain parenchyma.High fever,
chill, headache, lassitude, delirium, convulsion, disturbance of consciousness..
Severe-Cerebral hernia
- Mixed type-Mortality > 90%
3. Mild type - Most these patients could be seen at late epidemic season. The lesions are
mild. Low fever.
4. Chronic type - Not common,Most patients are adults,Easy to be misdiagnosed
MCQ’S
1.Neisseria meningitidis is a:
A.Gram-negative rod causing pneumonia and bacteremia
B.Gram-positive diplococcus causing primarily pneumonia
D. Gram-positive rod causing meningitis in immunocompetent patients
E. Gram-variable coccobacillus causing meningitis and otitis media
C. Gram-negative diplococcus causing epidemic meningitis and Septicemia
2.Serogroup A N. meningitidis:
A. Causes significant disease in the United States and Japan
B. Has been a major cause of epidemic meningococcal outbreaks
in subSaharan Africa
C. Expresses a sialic acid capsule
D. Has no effective vaccine
E. Is usually treated with sulfonamides
3.Which of the following is not true? The rash of invasive meningococcal disease:
A. Can be a blanching macular rash
B. Is typically petechial or purpuric
C. Can be confused with leukocytoclastic vasculitis, Rocky Mountain spotted fever, and
enteroviral infections
D. Is almost always present and easily detected
E. Is usually a single “bull’s-eye” lesion
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Case 2
Male, 15 years old, student.
He was admitted to the hospital on January 10.3 days ago, he had a sudden high fever of
39°C,accompanied by chills, severe headache, frequent vomiting, spitting out food and bile,
no upper abdominal discomfort, and normal bowel movements.
Past medical history: healthy,no history of stomach disease and tuberculosis, no history of
drug allergy, similar patients in school.
Physical examination:
T 39.1°C, P 110 beats/min, RR 22 beats/min, Bp 120/80mmHg, acute febrile symptoms,
conscious, scattered skin with a few bleeding points, superficial lymph nodes not palpable,
sclera not yellow, pharynx congestion (+) , no tonsil swelling, neck resistance. Heart, lung,
and abdominal examination showed no abnormality. Brudzinski sign (+), Kernig sign (+),
Babinski sign (-).
Laboratory tests:
blood routine: Hb124g/L, WBC14.4x109/L, N 84%, L 16%, plt 210x109/L, urine routine (-),
stool routine (-).
Question:
Q1)What is the most likely diagnosis? What is the diagnosis based on?
Diagnosis - meningococcal meningitis(common type)
1.Onset of the disease in winter and spring (January 10), this disease occurred locally
(similar patients in school)
2. Sudden high fever, severe headache, frequent projectile vomiting, skin hemorrhage and
meningeal irritation
3. The total number of WBC and the proportion of neutrophils in blood were increased
Q2)Which diseases need to be differentially diagnosed?
1. Purulent meningitis caused by other bacteria 2. Tuberculous meningitis
3. Viral meningitis
Q3) Further tests?
Lumbar puncture: pressure measurement, cerebrospinal fluid appearance, routine,
biochemical, bacteriological examination (culture and smear)。
Blood culture or skin petechiae smear。
Chest X-ray excludes pneumonia and tuberculosis.
Q4) What are the principles of treatment for this case?
1. Pathogen therapy:
- adequate dose, sensitive and can penetrate the blood-brain
barrier.
- High-dose penicillin is preferred, and chloramphenicol and third-generation
cephalosporins can be used.
2. Symptomatic treatment:
- mannitol lowers intracranial pressure
- physical cooling or antipyretics
13
> Complication of meningococcal infection- Pneumonia
- tympanitis
- suppurative arthritis
- endocarditis
- pericarditis
> laboratory diagnosis :
- Blood test-The blood regular test :WBC is very high, NE% become higher,CRP
become higher.
CSF test
❖ The median leukocyte count was about 1200, with a range of less than 10 to
65,000/mm3.
❖ About 75% had CSF glucose levels below 40 mg/dL.
❖ CSF protein levels ranged from 25 to more than
800 mg/dL, with the median value of about 150 mg/dL.
❖ the cell type in untreated cases is almost always
polymorphonuclear. Partially treated patients may have a pleomorphic spinal fluid.
-
PCR, which detects small quantities of bacterial DNA, has the potential to be an
important tool in the rapid diagnosis of meningococcal infection.
> the differences of CSF :
* What is pandy test?
- It is to detect protein in the CSF or other sterile fluid. the different level indicate
different meningitis.
*How do we get correct diagnosis?
- We should collect evidence as more as possible, include history+
Clinical signs +physical examination+ blood test + Bacteriological isolation from
sterile body fluid eg blood, CSF。 Only we get the correct diagnosis, the patient can
accept proper treatment.
14
> Sequela :
- Subdural effusion
- hydrocephalus
- acral necrosis
- deaf
- blindness
- seizure
- mental disorder
> Diagnosis ❖ Initial diagnosis of meningococcal meningitis can be made by clinical examination
followed by a lumbar puncture showing a purulent spinal fluid.
❖ The bacteria can sometimes be seen in microscopic examinations of the spinal fluid.
❖ The diagnosis is supported or confirmed by growing the bacteria from specimens of spinal
fluid or blood, by agglutination tests or by polymerase chain reaction (PCR).
❖ The identification of the serogroups and susceptibility testing to antibiotics are important
to define control measures.
❖ Clinically diagnosed case: clinical manifestations + CSF of purulent meningitis + petechia
or ecchymosis with/without septic shock
❖ Confirmed case: clinically diagnosed case + bacteriological or specific serum
immunological examination positive.
> Treatment :
-Meningococcal disease is potentially fatal and should always be viewed as a medical
emergency.
❖ Admission to a hospital or health centre is necessary, and isolation of the patient is
necessary.
❖ Appropriate antibiotic treatment must be started as soon as possible, ideally after the
lumbar puncture has been carried out if such a puncture can be performed immediately.
❖ If treatment is started prior to the lumbar puncture it may be difficult to grow the bacteria
from the spinal fluid and confirm the diagnosis.
❖ Mortality rates in patients with meningococcal meningitis are about 10% to 15% despite
antibiotic treatment
❖ Within 30 min The antibiotics - adequate dose, sensitive and can
penetrate the blood-brain barrier.
❖ Penicillins: Adult: 8MU q8h IV, children: total dose-200,000-400,000U/kg, q8h IV.(?)
❖ Cephalosporins: Ceftriaxone
❖ Chloramphenicol:(side effect)
> Prevention - Polysaccharide vaccines against A have been available to prevent the
disease for over 30 years.
15
1. Which of the following is not true regarding antibiotic treatment of meningococcal
meningitis? 20 seconds
A. It should be administered as soon as the diagnosis is considered.
B. It takes 10 to 14 days to be effective.
C. Options include ceftriaxone or cefotaxime, penicillin, or meropenem.
D. Quinolone resistance has been reported.
E. Sulfonamide resistance is now common.
2. Which of the following is not true regarding prevention of meningococcal disease?
A. Chemoprophylaxis is given to prevent secondary cases that occur usually 10 to 14 days
after the primary case.
B. Meningococcal polysaccharide-protein conjugate vaccines are a long-term control
measure of meningococcal disease.
C. Meningococcal vaccines have effectiveness in complement-deficient patients. D.
Rifampin, ceftriaxone, ciprofloxacin, and azithromycin are used for chemoprophylaxis.
E. Meningococcal polysaccharide vaccines are now preferred for prevention strategies
16
INFECTIOUS DISEASES
Communicable (contagious) diseases: diseases
whose causative agents may pass or be carried
from one person to another directly or indirectly.
four basic characteristics of infectious diseases
1. Have pathogens
2. syphilis spirochete、flu virus、measles virus、
SARS-CoV-2
3. Have infectivity
4. Have epidemiology feature
5. Have post infection immunity
Infectious Diseases: are the diseases being caused
by pathogenic microorganism and parasite which
can infect people.
1346 the plague known as the “Black Death,”
which killed up to one-third of the European
population
1566 people recorded the rabies
1817～1923 six worldwide cholera pandemic
1918～1919 spanish influenza killed 25 million
people
Patients with small pox can have lesions on palms
or soles. A.umblicated lesions, B.confluent lesions,
C.Panels
There is a clear difference between infection and
infectious diseases:
⚫ Infection is the entry and multiplication of an
infectious agent in human body.
⚫ Diseases refer to the development of symptom
and sign related to infection with an agent.
⚫
such as Epstein-Barr virus (EBV) infection and
Infectious mononucleosis (IM)
Three factors that determine outcome: Host, agent
and environment
Role of Pathogen （pathogenicity）
-number
-virulence
-invasiveness
-toxin (endotoxin, exotoxin)
⚫
Non specfic immunity- physical barrier,
phagocytosis, humoral barrier.
⚫
Specifc immunity- CMI, Humoral Immunity
Infection spectrum
elimination of pathogen
covert infection: sub-clinical infection
overt infection: clinical infection
carrier state
latent infection
Carrier state: Organism propagating at a rate
sufficient to maintain its numbers without
producing identifiable evidence of any reaction in
host.
Chain of infections
Causal agents, its reservoir（source of infection）
The mode of transmission（route of transmission）
Host （susceptibility of the population）
Three conditions must be met for infection that
will spread from person to person
1. One person must be infected with a
microorganism (sources of infection)
2. The other person must be susceptible to
infection with that microorganism
3. The microorganism must be able to leave the
body of the infected person and enter the body of
the susceptible person
Susceptibility
⚫ Ability to become infected with an organism
when exposed to it.
⚫ People may lose susceptibility (or become
immune) once they have been:
infected with the organism
Vaccinated
⚫ Medications may reduce susceptibility
temporarily
Basic characteristics of infectious disease.
⚫ Pathogen
⚫ Infectivity
⚫ Epidemiology feature
According to epidemic scale, there are 4 types
of epidemic:
⚫
Sporadic occurrence: occasional cases
Outbreak
Epidemic: local outbreaks
Pandemic: worldwide outbreaks
Post infection immunity
Signs of symptoms of infectious disease.
⚫ The symptoms of infection depend on the type
of the disease, some of infection affects the
whole body generally, such as fatigue, loss of
appetite, weight loss, fever, night sweat, chills,
aches and pains.
⚫ Other specifically affects individual body parts,
such as skin rash, coughing or runny nose.
Stages of infectious disease.(TIME)
Latency Period : the time between invasion of
infection agent and onset of infectiousness,
Latency period may not be the same as the
incubation period
Incubation period: Incubation period is the period
between the invasion of pathogens and the onset
of disease.
Prodromal stage: the period between the onset of
disease and apparent manifestation. Such as fever,
headache, fatigue, anorexia, myalgia.
Stage of apparent manifestation: typical
symptoms and signs occur.
Stage of Convalescence: most of the clinical
manifestations are subsiding.
Major common manifestation of infectious D
1.Fever- Fever is often regarded as the cardinal
feature of infection.
2.Skin rash (eruption): being seen in measles;
rubella; epidemic hemorrhagic fever;
vesicular-pustula rash in herpes simplex.
3.Toxemic symptoms: toxin causes a series of
symptoms: malaise, anorexia, muscle and joint
pains, mental symptoms.
4.Septicemia: Bacteria multiple in blood and
produce toxin lead to a series of symptoms.
5.Monocytic-macrophagic system reaction: leading
to splenomegaly, hepatomegaly,
lymphadenopathy.
RASH
The time and sequence of appearance of rash have
important reference value for diagnosis and
differential diagnosis.
Time of appearance:
1.chickenpox 2. scarlet fever 3.smallpox 4.
measles 5. typhus 6. typhoid
The sequence and distribution of rash:
Chickenpox is mainly distributed on the trunk. The
rash of measles starts behind the ears and on the
face, and then spreads to the trunk and limbs, and
there are mucous spots.
Lab diagnosis of infectious disease
Blood routine
Urinalysis
Fecal routine
Biochemica test
Etiological test
Immunoloic test- agg test, elisa,ppt test
Molecular biological technique- PCR
Endoscope
Imaging examination
HP examination
Treatment
Psychotherapy
General treatment
Immunotherpy
Etiologic treatment
Symptomatic treatment
Supportive treatment
Prevention
⚫ Breaking the chain of infection
⚫ Elimination or containment of the resource of
infection
⚫ Interruption in the important mechanism of
transmission
⚫ Protection of susceptible host
Emerging ID
EID are diseases whose incidence in humans has
increased in the past 2 decades or threatens to
increase in the near future.
⚫ Mutation of organism to new serovar
(antigenic type)
⚫ Migration of humans and animals into new
environments
⚫ Travel
⚫ War and natural disasters
⚫ Decline in vaccination rates
⚫ Climatic changes
⚫ Bioterrorism is also often included under the
"emerging infectious disease" heading.
These diseases include:
New infections resulting from changes or
evolution of existing organisms
Known infections spreading to new geographic
areas or populations
Previously unrecognized infections appearing in
areas undergoing ecologic transformation
Old infections reemerging as a result of
antimicrobial resistance in known agents
Causes of ILI
common cold
Influenza:tends to be less common but more
severe than the common cold.
Less-common causes include side effects of many
drugs and manifestations of many other diseases
KP
1. The conditions required for spreading of
infection (3):
Sources of infection, Susceptibility and Modes of
Transmission.
2.The basic characteristics of infectious (4)：
Pathogen, Infectivity, Epidemiology feature and
Post infection immunity
3.Major manifestations of the infection process (5):
Elimination of pathogen, Covert infection, Overt
infection, Carrier state, Latent infection.
COVID-19
⚫ Sources of infection: patients or asymptomatic
⚫ Route of transmission: spread mainly via
respiratory
⚫ Susceptibility: population is generally
susceptible
⚫ Pathogen: severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2)
⚫ Infectivity: can transmit from people to people
⚫ Epidemiology feature: cases have been
reported in all continents (pandemic)
⚫ Post infection immunity: immunity
INFLUENZA 2
Influenza like illness- flu, influenza virus
Fever-MC
Shivering
Chills
Malaise
Loss of appetite
Dry cough-MC
Runny nose
Sore throat
Body aches
Nausea
These symptoms typically begin 2 days after
exposure to the virus and most last less than 1
week.
⚫
⚫
⚫
Influenza viruses are RNA virus that belongs to the
family Orthomyxoviridae.
Electron microscopic- 80-120nm
The hemagglutinin (HA) and neuraminidase (NA)
proteins are shown on the surface of the particle. The
viral RNAs that make up the genome are shown as red
coils inside the particle and bound
to ribonuclearproteins (RNP).
Influenza virus strains are classified by their neucleoprotein
(A, B, or C)
A
many different
subtypes,
various sub-types infect
humans, swine, horse,
avian, marine animals
At least 16 highly
divergent, antigenically
distinct HAs have been
described in influenza A
viruses
(H1N1,H2N2,H3N2-MC)
as well as at least 9
distinct NAs
B
Restricted to
humans, Can
change slowly
over time
More stable
than Influenza A
C
Influenza C
virus:
Restricted to
humans and
dogs, pigs
Relatively stable
Has been
associated with
widespread
illness among
humans
Causes milder
disease than
Influenza A
Causes mild,
sporadic illness
among humans
Mild disease
without
seasonality
Pathogenesis of influenza A virus. The symptoms of
influenza are caused by viral pathologic and
immunopathologic effects, but the infection may
promote secondary bacterial infection.
ROUTES OF TRANSMISSION
Influenza can be spread in three main ways:
by direct transmission: (when an infected person
sneezes mucus directly into the eyes, nose or
mouth of another person);
the airborne route: (when someone inhales the
aerosols produced by an infected person coughing,
sneezing or spitting)
through direct or indirect contact: hand-to-eye,
hand-to-nose, or hand-to-mouth transmission, or
Contact with virus-contaminated goods.
CLINICAL FINDINGS OF I
1.Uncomplicated Influenza
⚫ Typical uncomplicated influenza often begins
with an abrupt onset of symptoms after an
incubation period of 1 to 3 days.
⚫ systemic symptoms predominate, mild
respiratory symptoms: Fever, chills (which may
be frank shaking chills), headaches, myalgia,
malaise, and anorexia.The systemic symptoms
usually persist for 3 days.
⚫ Respiratory symptoms-particularly a dry cough,
severe pharyngeal pain, and nasal obstruction
and discharge
⚫ Hoarseness and a dry or sore throat may also
be present, but these symptoms tend to
appear as systemic symptoms diminish
⚫ Cough is the most frequent and troublesome
of these symptoms and may be accompanied
by substernal discomfort or burning.
⚫ Influenza attack rates are higher in children
than in adults. Maximal temperatures tend to
be higher among children, and cervical
adenopathy is more frequent among children
than among adults.
⚫ Elderly individuals may present with only high
fever, lassitude, and confusion,Among elderly
persons, fever remains a very frequent
finding, . Pulmonary complications are far
more frequent in the elderly.
2.Pneumonia Influenza:
In the elderly ,children, or underlying diseases.
(influenza viral pneumonia,bacterial infection or
multiple pathogen infection).
3.Other types :
encephalitis: (delirium, convulsions, disturbance of
consciousness)
gastrointestinal type: toxic type: circulation
function impairment
Pulmonary Complications
⚫ Primary influenza viral pneumonia- occurred
predominately among persons with
cardiovascular disease, especially rheumatic
heart disease with mitral stenosis, and to a
lesser extent in others with chronic
cardiovascular and pulmonary disorders.
⚫ Secondary bacterial infection- The patients,
who most often are elderly or have chronic
pulmonary, cardiac, and metabolic or other
disease.
⚫ Other Pulmonary Complications
Croup Asthma,Cystic fibrosis, Chronic bronchitis,
Excerbation of chronic pulmonary disease
Nonpulmonary Complications
⚫ Myositis Cardiac complications Toxic shock
syndrome Central nervous complications
⚫ Reye’ Syndrome a change in mental status,
from lethargy to delirium, seizures, and
respiratory arrest
DIAGNOSIS
⚫ Epidemiologic Data
Most cases have had close contact with influenza
patients or been to endemic area a week before
the onset of illness.
⚫ Clinical findings
fever, myalgia, cough, pulmonary and
non-pulmonary complications
LABS
⚫ Significant lymphopenia and leucopenia, mild
to moderate thrombocytopenia, and elevated
transaminase levels.
⚫ These abnormalities are poor prognostic signs.
⚫ Most patients have had negative bacteriologic
cultures of sputum and blood.
⚫ Biochemical results: Abormality of liver
function:Myocardial enzyme abnormalities
⚫ Diagnostic imaging tests:
(X-ray and CT )
⚫ Virus Isolation
⚫ Virus isolation from respiratory secretions.
⚫ Rapid Diagnosis
⚫ Detection of viral antigen (NP,M1) in
respiratory secretions, the most rapid of the
ELISAs can produce results in less than 1 hour.
⚫ RT-PCR ( throat swab, nasal swab)
⚫
Serologic Testing- an acute and a convalescent
serum specimens obtained 10 to 20 days after
the acute-phase serum specimen, four fold or
greater rises in titer are considered diagnostic
of infection).
Treatment
⚫ Patients should rest and isolation and
treatment as soon as possible, the general
isolation 1 week or until the main symptoms
disappeared.
⚫ Ordinary patients had more drinking water;
high fever, headache were treated with
anti-inflammatory drugs (children avoid the
use of aspirin to prevent occurrence of Reye
syndrome);
⚫ fever, anorexia, vomiting- intravenous fluid
infusion;
⚫ should closely observe the patient's condition
in time detect and deal with all kinds of
complications.
Complicated patients：
Pulmonary complications
⚫ Supportive care is important, including fluid
and electrolyte management.
(hypokalemia,hyponatremia,hypochloridemia）
⚫ Supplemental oxygen, intubation,
tracheotomy, assisted ventilation, and the use
of positive end-expiratory pressure (PEEP) may
have a role depending on the severity of the
illness.
⚫ For patients with proven or suspected
bacterial infection, appropriate antibiotics for
the specific organism should be administered.
ANTI-VIRALS
Two classes：
M2 protein inhibitors and Neuraminidase
inhibitors.
Amantadine and Rimantadine
The antiviral activity of these drugs is due to
interaction with the M2 protein of susceptible
viruses.Binding of these drugs to the M2 protein
interferes with the function of M2 as an ion
channel.
Neuraminidase inhibitors：
Zanamivir is a highly potent and selective inhibitor
of the NA of influenza A and B virus, and can result
in an approximately 24 hour decrease in the
duration of symptoms when administered within
the first 48 hours of illness.
Oseltamivir (adult 150mg/per day, children
3mg/kg/per day, twice; five days)
Peramivir,Laninamivir
Priority: Hospitalized Patients with suspected or
confirmed pandemic H1N1 virus infectionTreatment recommended with Oseltamivir or
Zanamivir
Treat patients as soon as possible (duration: 5
days)
Outpatients with suspected or confirmed
pandemic H1N1 virus infection who are at high
risk for complications
Persons with chronic pulmonary, cardiac, renal,
hepatic, metabolic, hematological disorders;
immunosuppression, pregnant women, children <5
years; adults ≥65 years
treatment recommended with Oseltamivir or
Zanamivir
Treat patients as soon as possible (duration: 5
days)
EPI of influenza
⚫ Influenza occurs in distinct outbreaks of varying extent
every year.
⚫ This epidemiologic pattern reflects the changing nature
of the antigenic properties of influenza viruses, and
their subsequent spread depends upon multiple factors,
including transmissibility of the virus and the
susceptibility of the population.
⚫ Changes or mutations in the virus are referred to as
“antigenic variation”
⚫ Antigenic variation is referred to as drift or shift,
depending on whether the variation is small or great
⚫ The drift affects both Influenza A and B viruses and
occurs every 1-3 years within a subtype and can result in
significant epidemics
⚫ Antigenic shift affects the Influenza A virus only and
causes major changes within the virus. This can occur
every 10-40 years leading to a pandemic.
ACUTE VIRAL HEPATITIS-3
Pathogenesis
Acute viral hepatitis is characterized by acute
necro-inflammation of the liver
Liver injury is mediated by a strong cytotoxic T cell–mediated
reaction against infected hepatocytes that express viral
antigens at their surface
Successful immune elimination may lead to viral clearance
The immune reaction is sometimes so potent that the patient
develops subfulminant or even fulminant hepatitis that
requires liver transplantation
In some patients, the immune response fails and chronic
infection is established
Course
INCUBATION PHASE
Symptoms
-Asymptomatic
-Liver function test
Aminotransferase and bilirubin
levels normal
-Viremia: virus detectable in
blood
-Antibody: undetectable
-Duration: 2 weeks-6 months
Icteric phase
Symptoms
Jaundice appears
Nonspecific symptoms worsen
Hepatosplenomegaly may
develop
Liver function testaminotransferase levels > 10
times normal
Viremia: viral titers decline
Antibodies: appear
Duration: 1-3 weeks
PREICTERIC PHASE
Anoreixa
Nausea
Right UQ pain
Fever
Symptoms
Nonspecific symptoms
Fever, flu like symptoms
Liver function test
-Aminotransferase levels
begin to rise
Viremia: viral titers peak
Antibody:
detectable/undetectable
Duration: 3-10 days
Recovery phase
Symptoms
Resolve gradually
Liver function test
Aminotransferase and
bilirubin levels normalize
Viremia: undetectable
AntibodyIgM disappears after a period
of time
IgG last for a long time
Duration: 2-12 week
GENERAL EVALUATION
Liver function test
Coagulation test
First line diagnostic tests
Anti-HAV IgM
HBsAg, anti-HBc IgM
Anti-HCV antibodies
HCV RNA
Anti-HEV IgM
Second line diagnostic tests
HBsAg and anti-HBc IgM present: HDV RNA,
anti-HDV antibodies
Hepatits AV
Etiology
Classification: Picornaviridae, Hepatovirus
Nonenveloped
Nucleic Acid: 7.5 kb ssRNA
Acid and heat stable
Transmission Route
Fecal-oral
Ingestion of contaminated food or water
Person-to-person transmission
Clinical Manifestation
Incubation period(days): 15-45 (mean 30)
Acute HAV infection takes a mild course in most
cases
Fulminant: 0.1%
Progression to chronicity: None
Cancer: none
IgG antibodies appear early in the infection, persist
indefinitely, and confers protection against
reinfection
Clinical variants
Relapsing hepatitis
Recurrence of symptoms, aminotransferase
elevations and fecal excretion of HAV weeks to
months after apparent recovery from acute
hepatitis
Cholestatic hepatitis
Protracted cholestatic jaundice and pruritus
Diagnosis of acute hepatitis A is made by detection
of anti-HAV IgM in serum
Treatment
No specific treatment is required
Restrict physical activity
High-calorie diet is desirable
Intravenous feeding is necessary if patients has
persistent vomiting
Avoid drugs capable of causing liver injury
Use of cholestyramine if severe pruritus is present
Hospitalization in severe cases
Liver transplantation for fulminant hepatitis
Prevention
Active immunization - Hepatitis A vaccine
Two doses of the vaccine are recommended at a
6-month interval
Protective anti-HAV antibody titers persist for at
least 20 years
Passive immunization – Immunoglobulin
The administration of immunoglobulin (0.02 mL/kg)
is recommended as early after exposure as
possible
Hepatitis BV
Hepadnaviridae, Hepadnavirus
Classification:
Enveloped
Nucleic Acid: 3.2 kb DNA, the smallest known DNA
virus genome
Transmission Route
Percutaneous transmission
Blood and blood products
Contaminated medical or surgical materials
Injection drug use
Sharing scissors, razors and combs
Sexual transmission
Perinatal mother-to-infant transmission
CLINICAL MANIFESTATION
Incubation period (days): 30-180 (mean 60-90)
The manifestations are similar to those of other
causes of acute viral hepatitis
Jaundice has occurred one third of adult patients
with acute hepatitis B
Fulminant: 0.1%-1%
Progression to Chronicity: >90% (perinatal
acquisition) to <5% (adult infection)
Cancer: +
SEROLOGIC MARKERSHBsAg, Anti-HBs, HBeAg, Anti-HBe, Anti-HBc IgM,
Total anti-HBc
DIAGNOSIS
TREATMENT
Usually does not require antiviral therapy
Patients with severe acute hepatitis B warrants
antiviral therapy with a nucleoside or a nucleotide
analogue
Indication: patients with coagulopathy or persistent
symptoms or marked jaundice for more than 4 weeks
Entecavir [0.5 mg daily] or tenofovir [tenofovir disoproxil
fumarate, 300 mg daily, or tenofovir alafenamide, 25 mg
daily], until the signs of severity regress
Antiviral therapy does not cause hepatitis B to become a
chronic infection
PREVENTION
⚫ Active immunization - Hepatitis B vaccine
⚫ Universal infant vaccination programs have been
initiated in many countries
⚫ High-risk individuals should be screened for HBV
infection by HBsAg and anti-HBs antibody testing, and
seronegative persons should be vaccinated
⚫ Vaccination consists of the administration of
recombinant HBsAg in three injections at 0, 1, and 6
months
⚫ A titer greater than 10 IU/L is considered protective
⚫ The seroconversion rate is higher than 90% in healthy
individuals
⚫ One third to two thirds of vaccinated individuals lose
their anti-HBs antibodies after 10 to 15 years
Hepatitis CV
Classification: Flaviviridae, Hepacivirus
Enveloped
Nucleic Acid: 9.6 kb ssRNA
Genotypes: 1 to 6
Transmission Route
Percutaneous transmission
Intravenous drug use
Nosocomial transmission
Blood transfusion
Tattooing, piercing, acupuncture, accidental needle
exposure
Sexual transmission (unusual)
Mother-to-infant transmission (<5%)
CLINICAL MANIFESTATION
Incubation period (days): 15-160 (mean 50)
Nonspecific symptoms such as fatigue, low-grade
fever, myalgias, nausea, vomiting, or itching may
be present
Jaundice occurs in 20 to 30% of patients
Fulminant: 0.1%
Progression to chronicity: common (50-80%)
Cancer: +
50-80% patients with acute hepatitis C will
progress to chronic infection
During chronic infection, anti-HCV and HCV RNA
persists and serum amino-transferase fluctuates
DIAGNOSIS
TREATMENT
Patients with acute hepatitis C should be treated
with an all-oral combination of direct-acting
antiviral (DAA) drugs for 8 weeks
95-100% patients with hepatitis C could be cured
by DAA therapy
The cure of HCV infection should be assessed by
HCV RNA disappearance from serum at 12 and 24
weeks post-treatment
PREVENTION
No prophylactic vaccine is available
Standard precautions to limit exposures to infected
persons
Screening of blood and blood products
Application of standard medical and surgical
hygiene procedures
Safe use of syringes and materials for drug-users
Hepatitis DV
Classification: Deltavirus
Requires HBV to replicate and persist
Enveloped with hepatitis B surface antigen (HBsAg)
Nucleic Acid: 1.7 kb ssRNA, the smallest known
RNA virus genome
Transmission Route
Percutaneous transmission
Sexual transmission
Perinatal
mother-to-infant
transmission
(uncommon)
CLINICAL MANIFESTATION
HDV can be acquired at the same time as HBV
(coinfection) or by a chronic HBsAg carrier
(superinfection)
⚫ Coinfection is characterized by one or two
episodes of acute hepatitis; acute hepatitis can
range from mild to fulminant
⚫ In contrast, when chronic HBV carriers are
superinfected by HDV, acute hepatitis D is
generally severe, often fulminant, and
generally becomes chronic
Fulminant: 5-20%
Progression to chronicity
⚫ Coinfection with HBV: rare (2%)
⚫ Superinfection in chronic HBV carriers:
common (90%)
Cancer: HDV superinfection in chronic HBV carriers
will increase the risk of hepatocellular carcinoma
TREATMENT
No treatments are of proven benefit for acute
hepatitis D
DIAGNOSIS
PREVENTION
HBV vaccination is the most effective means of
preventing HDV infection
In chronic HBsAg carriers, standard hygiene and
behavioral precautions should be practiced to
avoid superinfection with HDV
Application of standard medical and surgical
hygiene procedures
Not sharing instruments such as toothbrushes,
razors, and combs
Safe use of syringes and materials for drug-users
Hepatitis EV
Classification: Hepeviridae, Orthohepevirus
Nonenveloped
Nucleic Acid: 7.5 kb ssRNA
Eight HEV genotypes (1 to 8)
Genotypes 1 and 2 appear to be strictly human
Genotypes 3 to 8 appear to be of animal origin but
can also infect humans.
One third of the world’s population has been
infected with HEV
It is the most common cause of acute hepatitis
worldwide
Transmission Route
Fecal-oral
Contaminated water supplies
Consumption of uncooked meat
Direct contact with infected animals (swine)
CLINICAL MANIFESTATION
Incubation period (days): 14-60 (mean 40)
HEV infection causes only mild, nonspecific
symptoms in the majority of cases
Fulminant: 1-2% (up to 20% in pregnant women)
Progression to chronicity: None
Cancer: None
HEV can be detected in stool for 1 week before the
onset of illness
Anti-HEV IgM antibody appears within 6 weeks and
persist for 3 to 12 months
Serum HEV RNA can be transiently detected
Anti-HEV IgG generally persists for life and confers
immunity
Diagnosis of acute hepatitis E is made by detection
of anti-HEV IgM in seru
TREATMENT
Treatment of acute hepatitis E is not
recommended because the vast majority of
patients recover spontaneously
Severe and fulminant cases should be referred to
specialized units and treated with ribavirin
monotherapy
PREVENTION
Improving public hygiene and eating well-cooked
meat are effective defenses against hepatitis E
Active immunization - hepatitis E vaccine
A prophylactic vaccine based on recombinant HEV
protein has been approved in China in 2011
Highly protective against HEV with 96% protective
efficacy over 12 months, and the efficacy remains
87% at 4.5 years
Not available elsewhere
Passive immunization
Immunoglobulin does not prevent infection
CHRONIC VIRAL HEPATITIS-4
Levels of alanine aminotransferase (ALT) and
aspartate aminotransferase (AST) are usually
elevated
⚫ ALT and AST level may remain within the
normal range for long periods of time in
patients with chronic viral hepatitis B or C
⚫ The ALT level is generally higher than the AST
level
⚫ Both ALT and AST can reach 10 to 25 times the
upper limit of normal during acute
exacerbations
Alkaline
phosphatase
and
γ-glutamyl
transpeptidase levels are usually minimally
elevated
Serum bilirubin and albumin levels and the
prothrombin time are normal
Results that suggest the presence of advanced
fibrosis:
⚫ Platelet count < 160,000
⚫ AST levels higher than ALT levels
⚫ Elevation in serum bilirubin
⚫ Decrease in serum albumin
⚫ Prolongation of the prothrombin time
⚫ Elevation in α-fetoprotein levels
⚫
⚫
⚫
Presence of high globulin level
Liver ultrasound can determine the texture
and size of the liver and spleen, exclude
hepatic masses, and assess the gallbladder,
intrahepatic bile ducts, and portal venous flow
Computed
tomography
and
magnetic
resonance imaging of the liver are helpful if a
mass or other abnormality is found by
ultrasound
HBV
PATHOGENESIS
⚫ HBV is not a cytopathic virus
⚫ Liver injury in chronic hepatitis B is a
consequence of the local immune response
⚫ In particular, liver injury is related to cytotoxic
T cells that recognize and kill infected
hepatocytes that express HBV antigens at their
surface and to the local production of
cytokines
⚫ Chronic inflammation triggers fibrogenesis
through the activation of hepatic stellate cells
⚫ Many patients with chronic hepatitis B have
progressive fibrosis, which may evolve into
cirrhosis
⚫ HBV integration and clonal hepatocyte
expansion occurs early in the course of chronic
HBV infection, indicating hepatocarinogenesis
is already underway
The natural history of chronic HBV infection
consists of four phases:
Immune tolerant phase,Immune clearance phase
Inactive carrier phase, Reactivation phase
Immune tolerant phase
Alanine
aminotransferase (ALT):
normal
HBV DNA: Elevated,
typically > 1 million
IU/ml
Hepatitis B e antigen
(HBeAg): +
Immune
clearance
phase
ALT: elevated
HBV DNA: Elevated, ≥
20, 000 IU/ml
HBeAg: +
Anti-HBe: Liver histology: minimal
inflammation
and
Anti-HBe: fibrosis
Liver histology: minimal Diagnosed
as
inflammation
and HBeAg-positive chronic
fibrosis
hepatitis B
Diagnosed as chronic
HBV carrier
INACTIVE
CARRIER
PHASE
ALT: normal
HBV DNA: low or
undetectable,
<2000
IU/ml
HBeAg: Anti-HBe: +
Liver histology: minimal
inflammation
but
variable fibrosis
Diagnosed as inactive
HBsAg carrier
Reactivation phase
ALT: elevated
HBV DNA: Elevated, ≥ 2,
000IU/ml
HBeAg: Anti-HBe: +
Liver
histology:
Moderate-to-severe
inflammation or fibrosis
Diagnosed
as
HBeAg-negative chronic
hepatitis
CLINICAL MANIFESTATION
Symptoms
Usually asymptomatic
Common symptoms include fatigue, sleep
disorders, difficulty concentrating, upper right
quadrant pain
Laboratory test
Elevated aminotransferase levels (only in immune
clearance and reactivation phase)
Mildly elevated alkaline phosphatase and
γ-glutamyl transpeptidase levels
Diagnostic criteria of chronic hepatitis B
HBsAg+ > 6 months
Serum HBV DNA > 2×104 IU/mL (HBeAg positive)
or serum HBV DNA > 2×103 IU/mL (HBeAg
negative)
Persistent or intermittent elevation in ALT/AST
levels
Liver biopsy showing chronic hepatitis with
moderate or severe necroinflammation
Diagnostic criteria of chronic HBV carrier
HBsAg + > 6 months
HBeAg +
High levels of serum HBV DNA
Normal aminotransferase
Mild or no liver necroinflammation and no or slow
progression of fibrosis
TREATMENT
Chronic HBV infection is not curable, but it usually
can be controlled by appropriate antiviral drugs
HCV infection is curable, and more than 95% of
patients who have access to new therapies are
cured
Suppress HBV replication
Reduce the histologic activity of chronic hepatitis
Lessen the risk of cirrhosis and hepatocellular
carcinom
Indications of treatment
Chronic Hepatitis B Without Cirrhosis
ALT >2×ULN
HBV DNA > 2×104 IU/ml in HBeAg-positive patients
or HBV DNA > 2×103 IU/ml in HBeAg-negative
patients
Compensated cirrhosis
Detectable HBV DNA
Decompensated cirrhosis
Treat immediately, regardless of ALT or HBV DNA
level
Pegylated IFN
Pegylated IFN-2a is administered subcutaneously
at a dose of 180 μg/week for 48 weeks
Pegylated IFN-α can provide a sustained virologic
response, defined as a sustained HBeAg
seroconversion (clearance of HBeAg, which is
replaced by anti-HBe antibodies) and an HBV DNA
level that remains below 2000 IU/mL after a
48-week course of treatment
Side effects of pegylated IFN
Flu-like syndrome
Fatigue
Bone
marrow
suppression:
neutropenia,
thrombocytopenia
Anxiety, irritability, depression, suicide ideation
Thyroid dysfunction
Nucleotide analogues, Three classes of have
been approved for HBV therapy:
Nucleotide analog prodrugs: tenofovir disoproxil,
tenofovir alafenamide and adefovir dipivoxil
Pyrimidine
L-nucleosides:
lamivudine
and
telbivudine
Guanosine analog: entecavir
Nucelos(t)ide analogues are generally well
tolerated
Renal impairment and decreases in mineral bone
density are rarely seen with tenofovir disoproxil
fumarate, but not observed with tenofovir
alafenamide
HCV
PATHOGENESIS
Acute HCV infection evolves into chronic infection
in 50 to 80% of cases
HCV is not a cytopathic virus
Liver injury in chronic hepatitis C is related to the
action of immune cells that recognize and kill
infected hepatocytes that express HCV antigens at
their surface and the local production of various
cytokines and chemokines
Chronic inflammation triggers fibrogenesis through
the activation of hepatic stellate cells
Chronic inflammation and progression of fibrosis
predispose patients to cirrhosis
CLINICAL MANIFESTATION
Symptoms
Fatigue
Laboratory test
Moderately
elevated
and
fluctuating
aminotransferase levels
Low titers of antinuclear and anti–smooth muscle
antibodies can be found
HCV-related cryoglobulinemia
HCV is the main cause of mixed cryoglobulinemia
Low levels of circulating cryoglobulins, which
contains, HCV RNA, anti-HCV antibodies,
rheumatoid factor, and complement, can be found
in 50 to 70% of cases
DIAGNOSIS
Chronic hepatitis C is defined as the persistence of
HCV RNA for more than 6 months
Chronic hepatitis C is diagnosed by the
simultaneous presence of anti-HCV antibodies and
HCV RNA
HCV genotype should be determined since it has
important therapeutic implications
Laboratory testing often reveals elevated
rheumatoid factor and cryoglobulins
TREATMENT
Pre-treatment assessment
⚫ Anti-HCV antibody, HCV RNA, HCV genotype,
liver function test, abdominal ultrasound or CT
⚫ HBsAg, anti-HBs antibody, anti-HBc antibody
◼ There is a potential risk of HBV
reactivation during or after HCV clearance
⚫ Noninvasive assessment of liver fibrosis
⚫
⚫
Renal function
Chronic hepatitis C is curable by antiviral
therapy
⚫ The goal of treatment is to achieve a sustained
virologic response, defined by undetectable
HCV RNA at 12 to 24 weeks after the end of
therapy
⚫ Sustained virologic response corresponds to a
definitive cure of infection
⚫ Indications of therapy: all treatment-naïve
and previously treated patients with persistent
HCV infection should be treated, regardless of
the severity of liver disease or extra-hepatic
manifestations
Classes of Anti-HCV drugs
Nucleoside NS5B inhibitor
Protease inhibitors
NS5A inhibitors
Non-nucleoside NS5B inhibitor
Prognosis
an estimated 20% of patients with chronic hepatitis
C develop cirrhosis after an average of 20 years of
progression in the absence of therapy
Hepatocellular carcinoma is rare in patients with
chronic hepatitis C without cirrhosis
In patients with cirrhosis, the incidence of
hepatocellular carcinoma is 2 to 4% per year
HDV
HDV infection occurs in 10% of HBsAg carriers
worldwide
Only approximately 2% of patients acutely
coinfected with HDV and HBV develop chronic
hepatitis D
In chronic HBV carriers superinfected by HDV,
however, 90% of patients become chronic HDV
carriers
CLINICAL MANIFESTATION
Chronic hepatitis D is generally severe, with more
than 80% of patients developing cirrhosis
Compared with patients who have chronic
hepatitis B alone, patients with chronic infection
with both HBV and HDV are three times as likely to
develop hepatocellular carcinoma and twice as
likely to die
DIAGNOSIS
Total anti-HDV antibodies remain at high levels in
chronic HDV infection, and HDV RNA is present
Although all chronic HDV carriers also are chronic
HBsAg carriers, chronic HDV carriers generally have
low or undetectable HBV DNA levels because HDV
inhibits HBV replication
TREATMENT
Pegylated IFN-α2a (180 μg once weekly) or
pegylated IFN-α2b (1.5 μg/kg once weekly) for 48
weeks is the only proven antiviral therapy for
chronic HDV infection
The virologic response rate is approximately 50%
on treatment, but only about 25% of patients have
undetectable HDV RNA 24 weeks after treatment
HEV
CLINICAL+DIAGNOSIS
⚫ HEV infection is usually an acute self-limiting
disease, but it causes chronic infection with
rapidly progressive cirrhosis in organ
transplant recipients, patients with
hematologic malignancies that require
chemotherapy, and immunosuppressed
HIV-infected individuals
⚫ Almost all cases of chronic infection have been
in immunosuppressed patients
⚫ Immunosuppressed patients with chronic
hepatitis E harbor repeatedly positive anti-HEV
antibodies and HEV RNA in blood
TREATMENT
There is no validated treatment of chronic HEV
infection.
Reducing the level of immunosuppression can
result in viral clearance in approximately one third
of patients and potentially decrease the risk of
subsequent cirrhosis
Ribavirin (600 mg/ day) has been used in small case
series. 95% of patients were observed to have viral
clearance for a median treatment duration of 3
months
EHF-5
Acute viral zoonosis caused by: Hantavirus
Reservoir host: Rodents
HV and their rodent hosts in China:
Field mice: Host of Hantann virus( type I)
Domestic rat: Host of Seoul virus(type II)
The clinical characteristic:
Fever
Suffusion and Bleeding
Renal injury
Shock
Clinical course:
Febrile/Toxic phase
Hypotensive phase
Oliguric phase
Diuretic phase
Convalescent phase
Morphology
Circular or ovoid shape, Diameter: 78~210nm
Lipid bilayer envelope
Genome
Single-strand, antisense RNA
Segmented: Large (L), Medium(M), Small (S)
VIRION PROPERTIES
Heat-labile: Survive 12 hours at 4 C, Survive
30mins at 56 C, Survive 1mins at 100 C, Survives
1-3 days after drying
Acid-sensitive: PH＜5.0 be inactivated
UV-inactivated: 10-15mins
Lipid solvents and nonionic detergents sensitive:
Ether, chloroform, phenol, formaldehyde, 70%
ethanol, and 0.5% iodine,etc.
EPIDEMIC FEATURES
Geographic distribution
Seasonal distribution
November~January, March~June
Fluctuates periodically
Distribution of population
20~50 years old
Male>Female
Farmer, worker in forest, soldiers
PATHOGENESIS
1.β3 integrins
2. HV is the initiating factor
Vascular leakage hypothesis
3. Immune factors:
Activation of innate immunity
Activation of complement
Activation of adaptive immunity
Overproduction of inflammatorycytokines
4. Host factors: The HLA-B8-DR3 haplotype, along
with others, has been associated with high
mortality rates.
CLINICAL MANIFESTATION
The major cardinal symptoms:
fever, suffusion and bleeding, acute renal
insufficiency, shock
Incubation period: 4~46 days, usually 7~14 days.
Clinical stages:
febrile (toxic), hypotensive, oliguric, diuretic,
convalescent
Febrile Phase：
Major cardinal symptoms
Fever, suffusion, hemorrhage, exudative
edema, renal injury
Three pains
Headache, lumbago, orbital pain.
Three reds (drunken face）
Flushing of face, flushing of neck,
flushing of upper chest
Renal injury
Hypotensive PHASE:
Occurs in 4th~6th day after illness ,
Last 1~3 days.
Hypotension: Systolic pressure <90mmHg;
Shock: Systolic pressure <70mmHg
Patients manifestate a series of
symptoms such as dizziness, debility, indifference
or dysphoria, pale skin , cold clammy limbs,
superficial vein collapse, hypotension and urinary
volume decrease.
OLIGRUIC PHASE:
Occurs in 5th~8th day, last 2~5days;
⚫ Oliguria: Urine volume in 24h<500 ml
⚫ Anuria: Urine volume in 24h <50 ml
⚫ Uremia:
⚫ Symptoms of digestive tract:
⚫ Anorexia, nausea, vomiting, diarrhea, hiccup.
⚫ Symptoms of nervous system:
⚫ Headache, lethargy, dysphoria
⚫ Hemmorhage
⚫ Metabolic acidosis
⚫ Disturbance of water and electrolyte balance
⚫ High blood volume syndrome
DIURETIC PHASE
Occurs in 9th~14th day after illness,
Last 7~14 days
Diuresis: urine volume >2000ml/24h.
* Water and electrolyte balance
* Secondary infection
* Secondary shock
Three periods according to the urine volume
Transitional phase-500~2000ml/24h
Early period of diuresis-2000ml~3000ml/24h
Late period of diuresis- >3000ml/24h
dehydration, hyponatremia, hypokalemia
Convalescent phase
Last 1~3m,Urine volume<2000ml
COMPLICATIONS
1. Coagulation abnormalities：
Bleeding of internal organs, DIC
2. Complications of CNS
Meningitis or encephalitis, brain edema,
intracranial bleeding.
3. Pulmonary edema:
ARDS, Pulmonary edema due to heart failure
4 . Other:
Liver injury, Secondary infection, Spontaneous
rupture of kidney
LABS
1. Blood routine examination
WBC > 10×109/L or leukemoid
Thrombocytopenia <100×109/L
Heteromorphic L >15%
RBC
2. Urine routine examination
Proteinuria
Hematuria
Cast
Membranoid substance
Large diffuse cell
3. Serological examination
Specific antibody
IgM antibody
IgG antibody
Specific antigen
Serum, WBC, cells in urine.
Direct immunofluorescence, ElisA
4. Pathagenic examination
Isolation of virus
PCR: RNA
5. Other examination
Bun, Cr, K, Na, Cl, liver function,
myocardial enzyme, blood glucose, clotting
mechanism, etc.
DDX
⚫ Fever: Influenza, septicemia, etc.
⚫
⚫
⚫
⚫
⚫
Shock: Other infectious shock, etc.
Oliguria: Acute glomerulonephriti, etc.
Hemorrhage: Thrombopenic purpura, etc.
Abdominal pain: Surgical acute abdomen,
etc.
Other causes of hemorrhagic fever: Yellow
fever, Ebola, Septicemia, Dengue,
Leptospirosis, Severe fever with
thrombocytopenia syndrome
1.FEBRILE PERIOD
Controlling infection:
ribavirin
Decreasing exudation:
Liquid treatment:
balanced salt solution,
1000~1500ml/24h
Vitamin C
20% mannitol
125~250ml
Improvement of toxic
symptoms:
High fever: physical
cooling ect.
Toxic symptoms:
dexamethason
Prevention of DIC:
Dextran
Heparin
0.5~1mg/kg/6~12h
2.HYPOTENSIVE PERIOD
Supplement of blood
volume:
Early, fast, suitable
volume, crystalloid
solution plus colloidal
solution
Correction of acidosis:
5% NaHCO3
Vaso-active agent:
Dopamine:
10~20mg/100ml; 654-2:
0.3~0.5mg/kg
Cardiotonics: cedilanid
Adrenocortical
hormone:
Dexamethason
10~20mg
4.Diuretic period :
5.Convalescent period:
Supplement of fluid
Supplement
and electrolyte
of nutrition;
Treatment or
Rest 1 - 3
prevention of secondary months.
infection .
3.OLIGURIC PERIOD
Stabilization of internal environment
Control of azotemia: Glucose 200g~300g/day
Maintaining fluid-electrolyte balance
liquid: urine volume + 500~700ml; electrolyte: K
Na Cl
Maintaining acid-base balance
Stabilization of blood pressure
Stabilization of internal environment
Diuresis
Bloodletting therapy and Catharsis
Dialysis therapy
PREVENTION
1. Killing and preventing rats
Host-reservoir control
2.Personal protective measures Human exposure
prophylaxis interventions
3.Vaccination- Prevention the disease: 88~94%.
EPIDEMIC ENCEPHALITIS B-6
Epidemic encephalitis B also is called as Japanese
encephalitis (JE).
JE is a vector-borne viral zoonotic disease that also
affects humans.
JE virus is belong to arboviruses flaviviridae
flavivirus genus, with similarities to several other
flaviviruses such as dengue f
JEV is a 20~40nm-sized spherical particle with
10976 base pairs of positive-strand RNA.
⚫ The positive-sense single-stranded RNA
genome is packaged in a capsid formed by
capsid proteins, and glycosylated protein(E
protein) and non-glycosylated protein(M
protein) are embedded in the membrane.
⚫ The E protein is the major antigen of the virus,
which is closely related to many important
biological activities.
⚫ The E protein also possesses blood coagulation
and neutralization activities.
PATHOGENESIS
⚫ JEV enters the human body following an
infective mosquito bite, first propagating in
the mononuclear-macrophage-system and
then transmitting into the blood circulation
resulting in virusemia.
⚫ The incidence and severity of JE after infection
with JEV depend on the virulence, number of
virus, and more importantly,on host immunity.
⚫
When host immunity is strong, the virus is
cleared soon after transient virusemia,and JEV
does not invade the CNS.The clinical
manifestations in these patients include
asymptomatic or mild infection.
⚫
When the immunity is poor, the virus cannot
be completely eliminated, and a part of the
virus will spread to the liver, spleen and other
places along with the blood circulation, and
continue to proliferate in the liver and spleen
mononuclear macrophage system.
⚫ After an incubation period of about 4 ~ 7 days,
a large number of viruses proliferated in the
liver and spleen are released into the
bloodstream again, becoming the second
viremia.
⚫
When the infected person has strong
immunity and the virus is weak, it may cause
no clinical symptoms or only mild symptoms,
such as fever, chills and general malaise.
⚫ However, when the infected person has weak
immunity, and the infected virus is large and
virulent, the virus will cross the blood-brain
barrier and invade the central nervous system,
causing brain parenchyma lesions.
⚫ Direct invasion of the nervous tissue by JEV
and other immune responses will result in
brain tissue injury.
PATHOLOGY
1. vasodilation congestion-irect invasion of the
nervous tissue by JEV and the resultant neuronal
necrosis, gliocyte hyperplasia, and infiltration of
inflammatory cell result in brain tissue injury.
2. Neuronophagia-Infected nerve cells become
degenerated, swollen, and focally necrotic,
surrounded by a large number of inflammatory
cells.
3. Cribriform encephalomalacia focus-In the
interstitium, inflammatory cells form a sheath
around blood vessels.
4. Formation of glial nodule-Microglia in the
mononuclear phagocytic system in the brain
parenchyma proliferate obviously, and microglia
nodules are formed near small blood vessels or
necrotic nerve cells.
LAB FINDINGS
1.Hemogram：
White Blood Cell(WBC) counts usually range
from 10x109/L to 20x109/L, and the proportion of
neutrophils is more than 80%. Some patients
consistently exhibit normal results.
2.CSF analysis：
CSF appears clear or slightly turbid,and tension
is elevated. WBC counts increase to
(50~500)x109/L and reach even as high as
1000x109/L, with a predominance of neutrophils in
the early stage followed by lymphocytes.
3.Serological findings
① Determination of specific IgM antibody
② Complement fixation test
③ Hemagglutinin inhibition test
4.Etiological Findings
① Isolation of virus
② Detection of virus antigen or nucleic acid
DIAGNOSIS
1.Epidemiological materials
The disease is strictly seasonal(summer and
autumn) and occurs mostly in children aged 2~7
years old. However, the number of adult cases has
increased in recent years.
2.Clinical characteristics
Manifestations of acute onset include high fever,
headache, vomiting, consciousness disturbance,
seizures， and positive pathological reflex.
3.Laboratory findings
WBC analysis shows increased WBC and neutrophil
counts. CSF test reveals aseptic meningitis
changes.
Serological examination,especially the
determination of specific IgM antibody,
contributes to case confirmation.
The diagnosis can be verified by ①fourfold
change in IgG antibody or neutralizing antibody
titers in serum during convalescence with respect
to the levels in the acute phase, ②a positive JEV
IgM antibody in the acute phase,or③detection of
specific JEV antigen and nucleic acids.
DDX
1.Toxic bacillary diarrhea;
2.Bacterial meningitis;
3.Tuberculous meningitis;
4.Other viral encephalitis
PROGNOSIS
Most mild and ordinary cases of JE show a good
recovery.
However, the mortality of patients with serious
disease can be as high as 20% primarily because of
central respiratory failure, and survivors present
with different degrees of sequelae.
TREATMENT
Isolate：
The patients should be isolated in wards with
anti-mosquito, until the temperature is normal.
There is currently no effective anti-viral drug to
treat epidemic encephalitis B.
Ribavirin and interferon can be used as early as
possible.
General therapy:
including the maintenance of water and electrolyte
balance and close observation can be used in the
early stage.
However, supportive care and symptomatic
therapy should be adopted of patient conditions.
Like assistance given for feeding, breathing as
required.
Symptomatic therapy:
Handling all body fluids.
Corticosteroids may be used to treat cerebral
edema.
Additional measures to reduce increased
intracranial pressure acutely include
hyperventilation and administration of mannitol.
Patients with seizures are generally treated
urgently with lorazepam or diazepam followed by
maintenance therapy with fosphenytoin.
PREVENTION
The key to epidemic encephalitis B prophylaxis is
comprehensive control measures, including
anti-monsquito methods and vaccination.
1. Control of infection source
2. Interruption of transmission route
3.Protection of susceptible populations
Vaccination is an effective method for longterm
protection.
The currently available vaccines in China are
inactivated vaccines or attenuated live
vaccines,which afford a protective rate of
60%~90%.
Vaccination targets children under 10 years and
people who move from non-endemic areas to
endemic areas.
1. Which of the following is not the cause of
peripheral respiratory failure of encephalitis B？
(THROAT BLOCKING)
2. What is the main source of infection of epidemic
encephalitis B?(
PIGS )
3. The clinical stage of Japanese encephalitis does
not include ( FEBRILE PERIOD )
4. The pathogens of Japanese encephalitis
are( RNA VIRUS
)
5. What is the route of transmission about
Japanese encephalitis virus?( CULEX )
6. The clinical manifestations of Japanese B
encephalitis in the second stage should be
excluded( DELAYED PARALYSIS )
Q1.What are the epidemic seasons and areas of
JE？
A1:Japanese encephalitis is transmitted
sporadically from July to September.
The disease is periodically epidemic in Southeast
Asia, China, and the Asian subcontinent.
Q2.Describe the source of infection of
encephalitis B please.
A2: Source of infection: Japanese encephalitis is a
zoonotic disease, people and many animals are the
source of infection.People are not the main source
of infection.Domestic animals, poultry and birds
can be infected with Japanese encephalitis virus,
among which the infection rate of pigs is the
highest.
Q3.Describe the route of transmission of
encephalitis B please.
A3：Transmission: Japanese encephalitis is mainly
transmitted by mosquito bites.
The Japanese encephalitis virus multiplies in
mosquitoes when they bite animals infected with
Japanese encephalitis virus, especially pigs.Then，
mosquitoes can cause disease in humans when
they bite.
Q4.Describe the vulnerable population of
Encephalitis B please.
A4：Vulnerable population: People are generally
suscep tible to Japanese encephalitis virus.Cases
occur chiefly in children between 2 and 10 years of
age,with a slight predominance of boys in endemic
areas, but the age of onset has recently been
reported to be increasing due to the application of
Japanese encephalitis vaccine.
Q5.Talk about the transmission cycle of JE Virus.
JE virus transmission is seasonal. Human disease
usually peaks in the summer and fall. In the
subtropics and tropics, transmission can occur
year-round, often with a peak during the rainy
season.
JEV is generally spread by infected mosquitoes,
specifically those of the Culex type. Pigs and wild
birds serve as a reservoir for the virus. The disease
mostly occurs outside of cities.
JE virus transmission is seasonal. Human disease
usually peaks in the summer and fall. In the
subtropics and tropics, transmission can occur
year-round, often with a peak during the rainy
season.
⑴The most important vector is mosquitoe(Culex
species).Transovarial transmission is the main
cause for infecting among mosquitoes.
⑵The natural hosts of the Japanese encephalitis
virus are birds, as maintenance hosts, and many
believe the virus will therefore never be
completely eliminated.
⑶Pigs act as an amplifying host and have a very
important role in the epidemiology of the disease.
Infection in swine is asymptomatic, except in
pregnant ones.
⑷Human, cattle, and horses are incidental dead
end hosts. JE virus can not spread directly from
person to person. Humans once infected do not
develop enough concentration of JE virus in their
bloodstream to infect feeding mosquitoes.
Q6.Describe the four stages of typical clinical
manifestations in Japanese encephalitis.
Typical clinical manifestations are divided into four
stages:
FIRST---Initial stage:1~3 days.Headache, nausea,
high fever, vomiting, somnolence.
SECOND---Fastigium stage:Day4~day10.
Persistent high fever, lethargy, convulsions and
coma. Respiratory failure, circulatory failure and
other conditions may occur in severe cases.
THIRD---Convalescence stage：Body temperature
drops and neurological symptoms and signs
improve.General patients in about 2 weeks to
complete recovery, and severe patients need 1-6
months to recover gradually.
FORTH---Sequela stage：If more than 6 months
some symptoms and signs still exist, it is called
sequelae. About 5-20% of patients have sequelae
that cannot be completely recovered after active
treatment.
CHOLERA-7
Vibrio cholerae
Intestinal infectious diseases
Class A infectious disease
Worldwide pandemics
International Quarantine Infectious Diseases
Typical clinical manifestations
Gram negative
Comma-shaped
Flagella
Fecal smears in a school-like arrangement
Hanging drop test by Dark field microscopy shows
shuttle movement
Pathogenicity of Vibrio cholerae
Flagellar motility, mucolytic enzymes, adhesins
Cholera toxin
Endotoxin
Cholera metabolites and other toxins
⚫ The antigenic structure: H antigen and O
antigen.
⚫ The O antigen is used to classify V. cholerae.
⚫ More than 200 serotypes have been identified.
⚫ Only the serogroups O1 and O139 are
associated with clinical cholera and have
pandemic potential.
EIPDEMIOLOGY
⚫ Cholera is spread through the fecal-oral route.
⚫
Vibrios have also been isolated from a variety
of fish and shellfish.
⚫ Either directly from person-to-person or
indirectly through contaminated fluids from an
environmental reservoir of varying duration,
food and potentially flies and fomites.
⚫ The cycle of transmission is closed when
infected humans shed the bacteria into the
environment and contaminate water sources
and food.
Risk factors
⚫ Poverty and lack of access to safe food, water,
and adequate sanitation.
⚫ Consumption of specific foods.
⚫ Blood group O.
⚫ Hypochlorhydria, partial gastrectomy.
PATHOGENESIS
Cholera enterotoxin (CT) causes the clinical
manifestations.
V. cholerae does not invade the intestinal wall.
Risk of getting infectiona: V. cholerae dose and
gastric acidity
V. cholerae need survive the acidic environment of
the stomach and then form colonies of bacteria on
the surface of the small intestine.
Pathophysiology:
Water and electrolyte disturbance
Metabolic acidosis
Severe dehydration
CLINICAL MANIFESTATION
⚫ Incubation period: generally 1 to 3 days
(several hours - 7 days)
⚫ Classical biotype and O139 type have severe
symptoms, El Tor biotype is often mild, with
more recessive infections.
⚫ Diarrhea
◼ (1) Characteristic feces: "rice swill-like"
feces with a small amount of mucus
◼ (2) No abdominal pain
◼ (3) No tenesmus
◼ (4) No fever (O139 fever and abdominal
pain are more common)
◼ (5) Symptoms last from hours to days
⚫ Other gastrointestinal symptoms
◼ Vomiting, frequently with watery emesis,
is common.
◼ Vomiting may begin either before or after
the onset of diarrhea.
◼ Patients may have abdominal cramping
but typically do not have the frank
abdominal pain classically associated with
dysentery.
◼ Diarhoea-vomiting
⚫ Manifestations of hypovolemia and electrolyte
loss
◼ Dehydration
◼ Muscle cramps
◼ Hypokalemia
◼ Uremia, acidosis
◼ Circulatory failurehours to 2-3 days
➢ CHILDREN ➢ PREGNANT ➢ ELDERLY
The clinical
Cholera in
Cholera in
manifestation
pregnant
elderly patients
of cholera in
women carries also carries a
children is
a bad
bad prognosis.
similar to that
prognosis and
in adults.
portends more Proper
severe clinical
rehydration
However,
illness,
may correct all
hypoglycemia, especially
electrolyte and
seizures, fever, when the
acid-base
and mental
disease is
abnormalities
alteration are
acquired at the in elderly
more common end of the
patients.
in children.
pregnancy.
Risk much
higher in
children 10x
greater than
adults
Fetal loss
occurs in as
many as 50% of
these
pregnancies.
COMPLICATION
Complications result from massive volume and
electrolyte loss as the Cholera stool contains high
concentrations of sodium, potassium, chloride, and
bicarbonate
Hypokalemia: causes arrhythmias, ileus, leg
cramps
Metabolic Acidosis: due to phosphate moving
out of cells
Hypoglycemia: mental status changes and
seizures
Hypotension: due to water loss
Hypofusion of critical organs
Acute renal failure:
Caused by hypovolemia and hypokalemia. Usually
occurs 7-9 days after illness
Acute pulmonary edema:
Metabolic acidosis, rehydration with plenty of
non-alkaline saline. Chest tightness, dyspnea,
cyanosis, pink frothy sputum.
GENERAL TESTS
➢ Increased hemoglobin, increased white blood
cells
➢ Decreased or normal serum potassium,
sodium, and chloride
➢ Elevated blood urea nitrogen and creatinine
➢ bicarbonate drop
➢ Stool routine: Visible mucus and a little red
and white blood cells
➢ Urine routine: a small amount of proteinuria, a
few red and white blood cells, casts
➢ Fecal smear: Gram-negative Vibrio in a
school-like arrangement
➢ Kinetic Test: Vibrio Shuttle Activity by Hanging
Drop Microscope
➢ Brake test: agglutination with O1 group or
O139 antiserum
PATHOGEN TESTS
➢ Isolation and culture
➢ Vibrio cholerae rapid auxiliary detection
➢ Colloidal gold rapid detection method
➢ Cholera toxin gene PCR detection
➢ Serum Immunology Test
➢ Epidemiological Retrospective Diagnosis
➢ Diagnosis of suspicious patients with negative
stool culture
DIAGNOSIS
➢ Cholera should be considered in all cases with
severe watery diarrhea and vomiting
➢ ≥ 5 years old develops severe volume
depletion from acute watery diarrhea, even in
an area where cholera is not known to be
endemic.
➢ In endemic areas, cholera should be suspected
in patients ≥ two years old with severe acute
watery diarrhea.
➢ Epidemiologic clues need to be collected
carefully.
VISIBLE SYMPTOMS
Sunken eyes and cheeks
Decreased skin suppleness
Dry mucous membranes
Urine production is sharply decreased
Renal failure is the most common
Complications seen in recent outbreaks
Specimens are collected
curved Gram negative rods
Untreated patients have 106 to 108 organisms mL
dark field or phase contrast microscopy
Culture results-golden standard
Additional methods of detection include PCR and
monoclonal antibody-based stool tests.
TREATMENT
Strict isolation- After the symptoms disappear, the
feces are cultured every other day, and the
cultures are negative for two consecutive times,
and the isolation can be released
Appropriate rehydrationOral Rehydration Salts (ORS)
Glucose 20g
Sodium chloride 3.5g
Sodium bicarbonate 2.5g
Potassium chloride 1.5g
Dissolved in 1000ml water
Intravenous rehydration
Principle - early, fast, sufficient amount, first salt
and then sugar, first fast and then slow, acid
correction and calcium supplementation, see
urinary potassium supplementation
Antimicrobial and symptomatic therapy
Antimicrobial Therapy
Quinolones:
ciprofloxacin, norfloxacin
Doxycycline
Cotrimoxazole
Purpose - to shorten the course of the disease,
reduce the frequency of diarrhea and rapidly
remove pathogenic bacteria from feces
Due to short duration of illness, antibiotics not
highly recommended:
High cost
-- Antibiotic Resistance
Limited gain from usage
What is the pathogen that causes cholera?
Vibrio cholerea.
How is cholera spread?
(B) Fecal-oral route.
What is the source of cholera infection?.
(C) Patients with cholera and carriers.
In the pathogenesis of cholera, what is the most
important?.
(B) Cholera enterotoxin.
What’s the core of the treatment of cholera?
(B) Rehydration therapy.
AIDS-8
Infection sources
Patient and asymptomatic carrier
HIV is located in
Contaminated Blood or blood products
Semen
Secretion of uterus and cunt
Other body fluid
Routes of transmission
Sexual transmission
Individuals who engage in unprotected sex
(penetrative sexual contact without the proper
use of a condom)
People who engage in unprotected sex with
multiple partners
Men who have sex with men
Men and women who exchange sex for money
or drugs or have sexual partners who do
Persons whose past or present sexual partners
were infected with HIV, were bisexual, or were
injection drug users
Persons being treated for sexually transmitted
infections （STIs）
blood transmission
Past or present intravenous drug use
Persons who share needles and syringes with
HIV-infected individuals
Persons with history of blood transfusion from
1978 to 1985
mother to child transmission,
Vertical transmission of HIV from infected
Mother to child may occur in utero , during
labor or through breast-feeding
In the absence of ART, HIV infect 25% to 30%
of infants born to HIV-infected mothers
the rate of vertical transmission can be
reduced to less 2% by treatment of mother or
infant with effective antiretroviral drugs.
Occupational transmission
vertical transmission
ETIOLOGY
HIV is an enveloped single-stranded RNA virus from
the family Retroviridae (subfamily, Lentivirinae).
HIV elaborates the enzyme reverse transcriptase. It
enables transcription of genomic RNA to proviral
DNA for integration into the host cell DNA.
HIV virion is a spherical particle.The virion is about
100nm in diameter and contains two copies of a
single-stranded RNA genomes.
HIV-1 is global in distribution, HIV-2 is found
primarily in western Africa.
HIV contains the 3 species-defining retroviral
genes—
➢ gag (group-specific antigen; the inner
structural proteins),
➢ pol (polymerase; also contains integrase and
protease—the viral enzymes—and is produced
as a C-terminal extension of the Gag protein),
and
➢ env (envelope; the outer structural proteins
responsible for cell-type specificity).
PATHOGENESIS
➢ After HIV enters the human body, it reaches
the local lymph nodes within 1-2 days, and the
virus can be detected in the blood within 5
days, leading to acute infection;
➢ Because the immune system of the body
cannot completely clear the virus, chronic
infection can be formed, including
asymptomatic infection and symptomatic
infection. About 8 years on average;
➢ The number of CD4+T lymphocytes decreased
continuously and slowly (mostly 800/ μ L to
350/ μ l)
➢ After entering the symptomatic stage, CD4+T
lymphocytes decreased rapidly again, and the
number of CD4 cells in most infected persons
was Less than 350/ μl, some patients with
advanced stage even dropped to 200/ μ L, and
rapidly reduce.
➢ Main reason for the decrease of CD4+T
lymphocytes caused by HIV infection.
➢ Hematopoietic system cells: T lymphocytes, B
lymphocytes, macrophages, NK cells, dendritic
cells, thymocytes, stromal fibro blasts, etc
➢ Brain: glial cells, ganglion cells, etc
➢ Intestine: columnar and goblet cells, colon
cancer cells, etc
➢ Skin: Langerhans cells, fibro blasts
➢ Others: myocardium and retina
PHASES
Clinical HIV infection undergoes 3 distinct phases:
1.Acute phase
40-70% HIV infected persons experience a
mononucleosis-like syndrome as following:
fever,
sore throat,
lymph node enlargement,
rash,
arthralgia (joint pain) and
headache
During the syndrome, HIV antibody is generally not
detectable, but HIV infection can be demonstrated
by plasma HIVRNA or p24 antigen assays, within
4-12 weeks after HIV infection, specific antibody
develop.
Common (found in more than 50% of patients)
Erythematous, maculopapular rash involving the
face, trunk, palms, and soles.
Meningeal signs
Pharyngitis (with or without exudates)Oral, vaginal,
or anal ulcers
Diffuse lymphadenopathy, Hepatosplenomegaly
Frequent (10% to 50%) Oral or vaginal candidiasis
that, in some cases, resolves without treatment.
Rare Cranial nerve palsies (especially involving
cranial nerve VII),Radiculopathy.
Encephalopathy .Guillain-Barre syndrome .
2.Asymptomatic infection
1、Persistent virus replication
2、Evasion of immune system control
3、Reservoirs of HIV-infected cells: obstacles to the
eradication of virus
4、Viral dynamics
5、Clinical latency versus microbiologic latency
3.AIDS (early and advanced symptomatic phase)
➢ The patient develops signs that indicate
disease progression but do not yet meet
requirements for the definition of AIDS.
➢ These include nonspecific dermatological,
haematological, and neurological
abnormalities, such as pancytopenia, anemia,
neutropenia, thrombocytopenia, dermatitis,
aseptic meningitis, and long-standing
headache or other neurological signs.
➢ In addition, patients frequently complain of
constitutional symptoms, such as fever, weight
loss, night sweats, chronic diarrhea, and
generalized lymphadenopathy
➢ The CD4 T-cell count reliably reflects the
current risk of acquiring opportunistic
infections
➢ For surveillance, a CD4 count below 200/μL is
considered AIDS-defining
➢ AIDS manifests as recurrent, severe, and
occasionally life-threatening infections or
opportunistic malignancies
➢ HIV infection can cause some sequelae,
including AIDS-associated
dementia/encephalopathy and HIV wasting
syndrome (chronic diarrhea and weight loss
with no identifiable cause)
LAB TESTS
➢ Serology is the usual method for diagnosing
HIV infection. Serological tests can be divided
into screening and confirmatory assays.
Screening assays should be as sensitive
whereas confirmatory assays should be as
specific as possible.
➢ Screening assays - EIAs are the most
frequently used screening assays. The
sensitivity and specificity of the presently
available commercial systems now approaches
100% but false positive and negative reactions
occur. Some assays have problems in detecting
HIV-1 subtype.
➢ Confirmatory assays - Western blot is regarded
as the gold standard for serological diagnosis.
However, its sensitivity is lower than screening
EIAs. Line immunoassays incorporate various
HIV antigens on nitrocellulose strips. The
interpretation of results is similar to Western
blot it is more sensitive and specific.
DIAGNOSIS
When the absolute CD4 T-cell count declines to
less than 200 cells per cubic millimeter, the HIV
infection is classified as AIDS.
Patients with AIDS become susceptible to
opportunistic infections and certain neoplasms,
known as AIDS-defining illnesses.
GOALS OF ANTI-RETROVIRAL TREATMENT
In order to achieve these goals, we also need to
pay attention patient’s
➢ Healthy lifestyle and nutrition as the basis
➢ Rational use of antiviral drugs
➢ Correct use of anti-opportunistic infection and
tumor drugs
➢ With appropriate support and symptomatic
treatment
➢ Ultimate objective：Improve quality of life and
prolong life
WHEN TO INTIATE THERAPY
Patients with high viral load (eg, 100 000 copies
per milliliter)
Patients with rapid CD4 T-cell count decline (100
per cubic millimeter per year)
Pregnant women
Patients with HIV-associated nephropathy
ANTI-RETROVIRAL DRUGS
There are seven classes of antiretroviral (ARV)
drugs currently approved.
1. nucleoside/nucleotide reverse transcriptase
inhibitors (NRTIs),
2. non-nucleoside reverse transcriptase inhibitors
(NNRTIs),
3. protease inhibitors (PIs),
4. fusion inhibitors (FIs),
5. CCR5 antagonists,
6. integrase inhibitors
7. entry inhibitor
The preferred regimen of treatment consists of a
combination of
2NRTIs+NNRTIs
2NRTIs+ ritonavir boosted PI.
Both of these regimens lead to a suppression of
HIV RNA levels and CD4 T-cell level increases in
most patients
PREVENTION
➢ The risk of contracting HIV increases with the
number of sexual partners. A change in the
lifestyle would obviously reduce the risk.
➢ The spread of HIV through blood transfusion
and blood products had virtually been
eliminated since the introduction of blood
donor screening in many countries.
➢ AZT had been shown to be effective in
preventing transmission of HIV from the
mother to the fetus. The incidence of HIV
infection in the baby was reduced by
two-thirds.
➢ For the management of health care workers
exposed to HIV through inoculation accidents
The CDC has recommended basic and
expanded HIV postexposure prophylaxis (PEP)
regimens.
➢ Vaccines are being developed at present but
progress is hampered by the high variability of
HIV. Clinical trials for several vaccines are in
progress.
Pre-exposure prophylaxis(PrEP)
The definition of PrEP: when people are at high risk
of HIV infection, they take (truvada entalbine
tenofovir) every day to reduce the probability of
infection. PrEP can reduce high risk
The risk of HIV infection in the population，adults
who do not use condoms continuously and are at
high risk of HIV infection should undergo
pre-exposure prevention
1. HIV cannot be transmitted through which of the
following ways: (HANDSHAKE)
2. Which of the following is not the main route of
transmission of AIDS: (digestive tract)
3. Which of the following is not a high-risk group
for HIV infection: (medical workers)
4. The incubation period of AIDS is generally: (8
yrs)
5. HIV is an enveloped single-stranded RNA
virus from the family Retroviridae.
6. HIV contains the 3 species-defining retroviral
genes: gag,pol,env
7. The loss of CD4 cells results in the development
of opportunistic infections and neoplastic
processes in HIV infectious patients.
8. Phases of HIV infection include Acute phase,
Asymptomatic phase, Early and advanced
symptomatic phase
SHIGELOSIS-9
Diarrhea is defined as the passage of loose or
watery stools, typically at least three times in a
24-hour period.
Acute diarrhea – 14 days or fewer in duration
Persistent diarrhea – more than 14 but fewer than
30 days in duration
Chronic diarrhea– more than 30 days in duration
Diarrhea illness caused by strains of invasive forms
of Shigella or invasive Escherichia coli
comprises bacillary dysentery.
Shigellosis is a clinical syndrome caused by invasion
of the epithelium lining the terminal ileum, colon,
and rectum by Shigella species
Pathogenicity:
- Virulence
endotoxin----fever, toxemia, shockexotoxin(shiga
toxin)----neurotoxic, cytotoxic , enterotoxin
- Invasiveness
(attach-penetrate-multiply)
Resistance:
Strong, 1-2week in fruits, vegetables and dirty
soil, heat for 60℃ 10 min,
and 30 min under
the direct sunlight.
EPIDEMIOLOGY
fecal-oral route
direct person-to-person
sexual contact
indirectly through contaminated food, water, or
fomites
Shigellosis is a clinical syndrome caused by
invasion of the epithelium lining the terminal
ileum, colon, and rectum by Shigella species
The pathogenesis of Shigella infection involves
invasion of colonic mucosal cells and induction of
an intense inflammatory response, leading to the
death of epithelial and immune cells and the
formation of colonic mucosal ulcerations and
abscesses.
PATHOLOGY
➢ Within 12 hours---the bacteria transiently
multiply in the small bowel
abdominal
pain, cramping, fever
➢ Within a few days---a diffuse colonic
localization of the bacteria
urgency,
tenesmus, and passage of bloody mucoid
stools
➢ acute: diffuse fibrinous exudative
inflammation
➢ hyperemia, edema, hemorrhage, leukocyte
infiltration;
➢ superficial necrosis, pseudomembrane
( cellulose, necrotic tissue, neutrophilic
leukocyte, red blood cell, bacterium );
➢ ulcer.
➢ Incubation period - typically 2-4 day(hours to
7 days)
CLINICAL MANIF
The spectrum of disease severity varies depending
on the serogroup of the infecting organism.
➢ Shigella sonnei commonly causes mild disease,
which may be limited to watery diarrhea,
while Shigella dysenteriae 1 or Shigella flexneri
commonly causes dysenteric symptoms
(bloody diarrhea) .
➢ However, Shigella of any species can cause
severe illness among people with
compromised immune systems
General features
➢ acute onset
➢ Fever – 30 to 40 percent, usually the first
manifestation
➢ Vomiting – 35 percent
➢ Diarrhea – Initially diarrhea is watery, but
subsequently may contain blood , mucus & pus
(stool frequency is typically 8-10 per day)
➢ Abdominal pain (tenderness) – 70 to 93
percent
➢ Tenesmus is a common complaint
COMPLICATIONS
➢ Intestinal Complication
➢ Proctitis or rectal prolapse: In infants and
young children
➢ Intestinal obstruction: more likely to be
infected with S. dysenteriae 1 and were more
severely ill
➢ Colonic perforation: extremely rare, occurs
principally in infants or severely malnourished
patients and is associated with infection due to
S. dysenteriae 1 or S. flexneri
➢
Toxic megacolon: occurs primarily in
the setting of S. dysenteriae 1 infection.
➢ Bacteremia: 0-7%, more common among
children than adults
➢ Reactive arthritis : Following S. flexneri
infection, reactive arthritis is an uncommon
complication that may be observed alone or in
association with conjunctivitis and urethritis.
➢ Hemolytic-uremic syndrome: Although
relatively uncommon, the hemolytic-uremic
syndrome (HUS) is the most frequent cause of
acute renal failure among infants and young
children worldwide. S. dysenteriae 1
➢ Neurologic disease: seizures, encephalopathy
with lethargy, confusion, and headache
➢ Metabolic disturbances: Dehydration,
hyponatremia
LAB FINDINGS
blood routine examination:
WBC count increase(10~20×109/L) or
occasionally decrease
neutrophils increase(a shift to the left)
Stool examination:
gross examination: stool mixed with mucus,
blood & pus.
direct microscopic examination:
WBC, RBC,
pus cells
Organism identification/Diagnostic assays
Bacterial culture: routine in most clinical
microbiology laboratories, the gold standard for
diagnosing shigella infection.
Molecular testing: PCR for Shigella-specific DNA
sequences in stool
SUPPORTIVE THERAPY
rest
reasonable diet
hydration
electrolyte balance
Intestinal antimotility drugs
Antibiotic treatment:
whether to use antibiotics or not?
➢ effective in shortening the duration of fever
and diarrhea
➢ shortens the duration of pathogen shedding in
stool
➢ Shigella infection is normally self-limited
➢ antibiotic resistance commonly develops in
populations after prolonged use of drugs
EMPIRIC THERAPY
first-line:
ciprofloxacin, azithromycin,
ceftriaxone
second choices:
trimethoprim-sulfamethoxazole
DIRECTED THERAPY
antimicrobial susceptibility:
generally include a fluoroquinolone, azithromycin,
and a third generation cephalosporin (cefixime or
ceftriaxone)
PREVENTION
There is no vaccine to prevent shigellosis.
Properly washing the hands can help.
Food safety and regular drinking water treatment
is best prevention
1.
2.
3.
4.
5.
6.
Shigella is a common cause of bacterial
diarrhea. It is transmitted by direct person to
person spread and, through feco-oral and
sexual contact.
The incubation period ranges from 2 to 4 days.
Patients with Shigella gastroenteritis typically
present with fever,vomitting and diarhoea;
Initially diarrhea is watery, but subsequently
may contain blood,mucus and pus
Shigella gastroenteritis generally is self
limited, lasting no more than 7 days in an
untreated immunocompetent host.
The pathogen of bacillary dysentery belongs
to (shigella)
The main factor of systemic toxemia of
bacillary dysentery is caused by (Endotoxin)
TYPHOID FEVER-10
Salmonella is a genus of the family of
Enterobacteriaceae.
Salmonellae are named for the pathologist Salmon,
who
first isolated Salmonella choleraesuis from porcine
intestine.
The organism classically responsible for the enteric
fever syndrome is S. enterica serotype Typhi
(formerly S. typhi).
Other Salmonella enterica serotypes that can cause
a similar clinical syndrome include but are not
limited to：
● Salmonella Paratyphi A
●Salmonella Paratyphi B
●Salmonella Paratyphi C
●Salmonella Choleraesuis
rod
non-spore
no capsule
Flagella
Antigens: located in the cell capsule
H (flagellar antigen).
O (Somatic or cell wall antigen).
Vi (polysaccharide virulence or
surface Vi antigen)
Pathogenicity: endotoxin
The carrier or patient is the only source of infection
for typhoid fever
cases
chronic carriers
TRANSMISSION: Fecal-oral route
Waterborne transmission
Food-borne transmission
Close contact transmission
CLINICAL MANIFESTATION
1.The initial period (early stage)
2.The fastigium stage
3.defervescence stage
4.convalescence stage
The incubation period is usually 7 -14 days.
Typical infection
➢ Fever, persistent high fever, last 10-14 days
➢ Nervous system symptoms
◼ yphoid face
◼ tinnitus, hearing loss
◼ Typhoid meningitis: delirium, stiff neck
and even coma
➢ Digestive system symptoms
◼ Loss of appetite
◼ Nausea/Vomiting
◼ Abdominal pain
◼ Constipation/diarrhoea
◼ Splenomegaly
◼ hepatomegaly
◼ toxic hepatitis
➢ Relatively slow pulse
➢ Rose spots
Recrudescence
In some patients, the temperature begins to drop
but has not returned to normal during the
remission period, and the temperature rises again
for 5 to 7 days before returning to normal, and
blood cultures may be positive during fever
Relapse
The fever resides for 1 to 3 weeks, clinical
symptoms reappear, and blood cultures are
positive. It is related to the complete destruction
of bacterial endings in the lesion and re-invasion of
the bloodstream. A small number of patients may
have more than 2 recurrences.
Intestinal hemorrhage: the most common
complication
Intestinal perforation: the most serious
complication
Toxic myocarditis
LAB DIAGNOSIS
Blood culture
Bone marrow
Stool culture
WIDAL TEST
➢ A test involving agglutination of typhoid bacilli
when they are mixed with serum containing
typhoid antibodies from an individual having
typhoid fever; used to detect the presence of
Salmonella typhi and S. paratyphi.
➢ Tests done within 7 days of illness and after 4
weeks are usually negative.
➢ Previous typhoid vaccination may contribute
to elevated agglutinins in the non-infected
population.
➢ Other infections of non-enteric salmonella
infection such as Typhus, Immunological
disorders, chronic liver disease may cause false
positive reaction.
➢ Cross reaction between malaria parasites and
salmonella antigens may cause false positive
Widal agglutination test
DIAGNOSIS
Epidemiology data
Typical symptoms and signs
Laboratory findings
Serologic evidence alone is not sufficient for
diagnosis.
GENERAL TREATMENT
Disinfection and isolation
Rest
Nursing
Diet: fluids and electrolytes should be
monitored
Etiologic treatment
Antibiotics, such as ampicillin, chloramphenicol,
fluoroquinolone, trimethoprim-sulfamethoxazole,
amoxicillin and ciprofloxacin etc used to treat
typhoid fever
Prompt treatment of the disease with the
antibiotics reduces the case-fatality rate to
approximately 1%.
fluoroquinolone
Optimal for the treatment of typhoid fever
penetrate well into macrophages, and achieve high
concentrations in the bowel and bile lumens
Cephalosporine
third generation effective
children and pregnant first choice
Chloramphenicol
The recommended dosage is 50 - 75 mg/kg/day for
14 days divided into four doses per day, or for at
least five to seven days after defervescence.
The disadvantages of using chloramphenicol
include a relatively high rate of relapse (57%), long
treatment courses (14 days) and the frequent
development of a carrier state in adults.
MDR TYPHOID,AB RESISTANCE
➢ Ciprofloxacin resistance is an increasing
problem.
➢ Where resistance is common, a
third-generation cephalosporin such as
ceftriaxone or cefotaxime is the first choice.
➢ Azithromycin has been suggested to be better
at treating typhoid in resistant populations
than both fluoroquinolone drugs and
ceftriaxone.
➢ Resistance to azithromycin has been reported
sporadically but it is not common as of yet.
➢ Carbapenems are only used for suspected
extensively drug-resistant (XDR) typhoid
infections.
TREATMENT OF COMPLICATIONS
Intestinal bleeding:
Absolute bed rest, close monitoring of blood
pressure and stool bleeding
Replenish blood volume, maintain water,
electrolyte and acid-base balance
Hemostatic drugs, blood transfusion
Intestinal perforation
Patients with limited intestinal perforation should
be given fasting and gastric tube for
gastrointestinal decompression.
Strengthen antibiotic treatment.
Patients with intestinal perforation complicated by
peritonitis should undergo surgical treatment in
time
PREVENTION
control source of infection: cases
chronic carriers
Cut of course of transmission
Vaccination
the live, but weakened strain of the Salmonella
bacteria, oral Ty21a vaccine (recommended only
people 2 years or older be vaccinated)
the injectable typhoid polysaccharide
vaccine (recommended for people 5 years or
older).
Both are efficacious and recommended for
travelers to areas where typhoid is endemic.
Boosters are recommended every five years for the
oral vaccine and every two years for the injectable
form.
MALARIA-11
Malaria： Plasmodia
Infective stage: sporozoite
Infective way : mosquito bite skin of human
Causative organism: Plasmodia
P. Vivax: tertian malaria
P. Ovale: tertian malaria
P. Malariae: quartan malaria
P. Falciparum: malignant malaria
Sporozoite: tachysporozite and bradysporozite
Clinical symptoms: erythrocytic stage
Pathogenicity: merozoite, malarial pigment &
products of
metabolism
Relapse: exoerythrocytic stage
Transmitted stage : gametocytes
Schizogonic cycle in red cells : 48 hrs/P.v and P. o;
36-48 hrs/P.f
ETIOLOGY
Two period
Human-whole asexual reproduction
Parasitic position : liver and red blood cells
exoerythrocytic stage
erythrocytic stage
Mosquito-sexual parasitic stage
Two host
Human-intermediate host
Mosquito-final host
Source of infection:
Patient, parasite carrier
Route of transmission:
female mosquito biting person
blood transfusion
Susceptibility:
universal susceptibility
no-cross-immunity
re-infection
Epidemic features:
sporadic or endemic, tropic or subtropic
Pathogenesis
LIFECYCLE
The female anopheline mosquito is responsible for
malaria transmission
➢
➢
➢
➢
➢
➢
➢
Hepatomegaly
Splenomegaly
Proliferation of mononuclear phagocyte
Cerebral edema & congestion
caused by P.falciparum (small vessels
are plugged)
P. falciparum is found primarily in tropical
regions and
➢ poses the greatest risk of death for
nonimmune persons
➢ because it can invade red blood cells of all ages
and is
➢ often drug-resistant.
➢ P. falciparum produces no dormant liver stages
➢ and thus dose not cause late relapse.
➢ P. vivax and P. ovale produce hepnozoites
➢ and may thus cause late relapse 6 or 11
months or more
➢ after the initial infection.
➢ P. malariae infections persist in blood stream
➢ at low levels for 30 years or more, they do not
produce
➢ hypnozoites and thus do not cause relapse
from persistent
liver stage.
CLINICAL MANIFESTATION
Typical paroxysm
1. Chill: abrupt onset, shivering, pale face, cyanosis.
Last 10 min or 1~2hr.
2. High fever: T rise to 40oC with malaise, myalgia,
thirsty. Last 2~6 hr.
3.Sweating: profuse sweating with restlessness.
Last 1-2hr.
regular 48 hr. or 72 hr. Cycle
Characteristic
1) . periodic; 2). repeated; 3). regular
P. FALCIPARUM
P.f: schizogony takes place in the capillaries of the
internal organs, the infected red cells tend to
adhere
to one other and the small vessels may become
plugged.
This may produce several fatal results:
Cerebral malaria: seizures and impaired
consciousness.
high fever, headache, vomiting, convulsion,
delirium,
respiratory failure
Renal failure
Gastroenteritis
Serious anemia
Acute respiratory distress syndrome (ARDS)
Shock
RENAL FAILURE
Black- water- fever:
cause:
1. inadequate G-6-PD
2. The toxin release by malarial parasite
3. Allergic reaction to anti-malarial drugs
feature:
1. chill & fever 2. dark red or black urine
3. severe hemolytic anemia
Acute glomerulonephritis
Malignant malaria (splenomegaly), The Kupffer
cells (macrophages) are loaded with black pigment,
which is malarial pigment (haemozoin).
Incubation period:
tertian malaria: 13~15 days
quartan malaria: 24-30 days
malignant malaria: 7~12 days
Malaria caused by transfusion
incubation period: 7~10 day
no exoerythrocytic phase, no relapse
Recrudescence occurs when the blood
schizonticide does not eliminate all parasites from
the blood stream, either because the dose was
inadequate or because the parasite is resistant to
the drug.
Relapse occurs in P. vivax and P. ovale infections
after the delayed development of liver stage
parasites that have not been treated adequately
with a tissue schizonticide.
P.f and P.m. have only recrudescence, but, P.v.
and P.o. both have relapse and recrudescence.
LAB DIAGNOSIS
➢ malaria is typically diagnosed by microscopic
examination of a thin or thick smear, Giemsa's
stain.
➢ Serological examination
➢ ELISA for P. antigen
➢ DNA hybridization
➢ Decreases in hemoglobin, hematocrit, and
haptoglobin, with increases in lactic
dehydrogenase and a vigorous reticulocyte
response.
➢ Thrombocytopenia is common.
➢ Renal disease, with proteinuria,
hemoglobinuria, and an elevated serum
creatinine level.
➢ Although liver involvement may occur, most
hyperbilirubinemia results from intravascular
hemolysis, and rises in serum enzymes such as
alanine aminotransferase may result from the
involvement of organs other than the liver.
DIAGNOSIS
Epidemiological data-endemic zone, blood
transfusion
Clinical manifestation
Laboratory findings
Diagnostic treatment:
chloroquine for 3 day
DDX
Influenza
Typhoid fever
Bacteremia/sepsis
Classic dengue fever
Acute schistosomiasis (Katayama fever)
Leptospirosis
African tick fever
East African trypanosomiasis (sleeping sickness)
Yellow fever
TREATMENT
➢ Three principles:
➢ Control of clinical symptoms
➢ Eradication of gametocytes
➢ Prevent relapse
➢ Chloroquine, quinine, artemisinin and
artemether----anti-erythrocytic stage drugs.
➢ Primaquine and pyrimethamine
----anti-exoerythrocytic stage drugs.
➢ Primaquine (anti-exoerythrocytic &
gametocyte)
➢ Anti-malarial drugs
➢ Chloroquine-susceptable infection
chloroquine : 1g /d, for 3 day, p.o. primaquine:
for 8day, p.o.
➢ Chloroquine-resistant infection
◼ mefloquine:
◼ artemisinine:
Chloroquine resistant malaria
When to treat as chloroquine-resistant malaria?
Falciparum known & patient from chloroquine
resistant area
Falciparum not known, patient is seriously ill and
have symptoms of cerebral malaria
(confusion, delerium, convulsions)
Mixed infection
Benign tertian not responding to chloroquine
First line treatment:
Quinine/quinidine + doxycycline
Quinine/quinidine
Parenteral:
Loading dose: 20 mg/kg (up to 1.4 g) iv over 4 hr
Maintenance: 10 mg/kg (up to 700 mg) iv 8 hourly
Oral: 600 mg TID for 5-7 days
Adv. Effects:
Cinchonism (headache, dizziness, tinnitus, vertigo,
fever)
IV infusion may cause hypotension, arrhythmias
Can increase plasma levels of digoxin and warfarin
Malaria during pregnancy
Can be used:
Chloroquine non-resistant malaria
Chloroquine
Chloroquine resistant malaria
Chloroquine & proguanil
Quinine/quinidine
Mefloquine: avoid in 1st trimester
Atovaquone + proguanil (Malarone): use if
necessary
Contraindicated:
Doxycycline
Pyrimethamine and sulphadoxine
combination
PREVENTION
Chemoprophylaxis
➢ Chloroquine / pyrimethamine
➢ used for prophylaxis of malaria
➢ Chemotherapy: 1 week before entry into the
➢ endemic area ; for 4 weeks after returning
from the endemic area.
➢ chloroquine: 0.3g once a week
➢ Malaria vaccines
MENINGITIS-12
➢ Meningitis is an infection/inflammation of the
brain and spinal cord surrounding membranes
known as the meninges. Meningococcal
meningitis is the term used to describe a
bacterial form of meningitis caused
by Neisseria meningitidis.
➢ This form of meningitis is associated with
high morbidity and mortality. Meningococcal
meningitis is a medical emergency for which
symptoms can range from transient fever to
fulminant bacteremia and septic shock.
➢ Meningococcal meningitis is a bacterial form
of meningitis, a serious infection of the
meninges that affects the brain membrane. It
can cause severe brain damage and is fatal in
50% of cases if untreated.
➢ Neisseria meningitidis is a gram-negative
diplococcus.
➢ Optimal growth conditions are achieved in a
moist environment at 35℃ to 37℃ under an
atmosphere of 5% to 10% carbon dioxide.
➢ The bacteria could grow well on the chocolate
agar plate or the blood agar plate.
➢ The meningococcus will metabolize glucose
and maltose to acid without gas formation and
fails to metabolize sucrose or lactose.
➢ the organism contains cytochrome oxidase in
its cell wall.
➢ The meningococcus has a rapid autolytic rate.
(?)
➢ The importance of iron in the survival of
microbes has stimulated interest in the
mechanisms that Neisseria organisms use for
iron acquisition.
PATHOGENESIS
➢ The Pathogenesis of N. meningitidis involves a
series of sequential steps. The process begins
when the bacterium colonizes the
nasopharynx.
➢ The only known reservoir for N. meningitidis is
the upper respiratory tract, although only a
few will develop invasive disease.
➢ The bacterium incubates for a period to 1 to
10 days and then further penetrates the
submucosa. In 10 to 20% of cases, the
bacterium invades the bloodstream. Once
present in the plasma, host defenses, which
include bactericidal antibodies, complement,
and phagocytic cells, may prevail and eliminate
bacteria.
➢ In cases, where host defenss fail to clear
bacteria, the patient enters the bacteremic
phase. Bacteria may now invade meninges and
other local sites, which can rapidly lead to
meningitis and fatal septicemia.
➢ The virulence factors: the expression of
capsular polysaccharide, the expression of
surface adhesion protein, iron chelating
mechanism and endotoxin.
➢ Bacterial pili and out memberane protein
could be virulence factor too.
EPIDEMIOLOGY
➢ Epidemics in Africa, New Zealand, and
Singapore indicate that this infection is still a
worldwide major public health problem.
➢ Children previously and presently account for
the greatest percentage of these cases. (?)
➢ The case-fatality rate varies depending on the
prevalence of disease, the nature of the
infection, and the socioeconomic conditions.
➢ serogroup A, B, and C strains have different
epidemic potential. (?)
➢ Source of infection: bacteria-carriers and
patients.
➢ Transmission: The bacteria are transmitted
from person-to-person through droplets of
respiratory or throat secretions from carriers
and patients.
➢ The susceptibility of population: 6m-2y
children are most common. (?)
➢ Although there remain gaps in our knowledge,
it is believed that 10% to 20% of the
population carries Neisseria meningitidis in
their throat at any given time. However, the
carriage rate may be higher in epidemic
situations. (?)
➢ The incubation period
The average incubation period is four days, but can
range between 2 and 10 days.
Clinical Manifestations
➢ The most common symptoms:
➢ high fever, vomiting, headaches, a stiff neck,
sensitivity to light and confusion.
➢ Even when the disease is diagnosed early and
adequate treatment is started, 5% to 10% of
patients die, typically within 24 to 48 hours
after the onset of symptoms.
➢ Bacterial meningitis may result in brain
damage, hearing loss or a learning disability in
10% to 20% of survivors.
➢ A less common but even more severe (often
fatal) form of meningococcal disease is
meningococcal septicemia, which is
characterized by a hemorrhagic rash and rapid
circulatory collapse
➢ he patient should be fully undressed to look
for petechiae and ecchymosis and to perform
a thorough skin exam. Meningeal irritability
can be confirmed by provocative tests like
Kernig and Brudzinki sign.
➢ the classic meningitis triad of fever, neck
stiffness, and altered mental status
➢ Petechial lesions are a common harbinger of
this infection
➢ The petechial lesions can coalesce and form
larger lesions that appear ecchymotic
1. Common type
1. Prodromal phase. 1-2 d.
The symptoms of upper respiratory tract infection.
2. Septic phase. 1-2 d.
High fever, chill, headache, lassitude.
Children-cry, apastia, convulsion.
>70%-Petechiae, ecchymosis.
3. Meningitis phase. 2-5 d
Headache, lassitude, projectile vomiting, stiff
neck-meningeal irritation sign
severe:Delirium, convulsion, disturbance of
consciousness
4. Recovery phase. 1-3 w
10%-Herpes around mouth
2. Fulminant type
1. Shock type.
High fever, chill, headache, vomiting ,
petechiae, ecchymosis -> signs of shock such as
blood pressure lower, heart rate higher.
2. Meningoencephalitis type.
Damage of meninges and brain parenchyma.
High fever, chill, headache, lassitude,
delirium, convulsion, disturbance of consciousness
Severe-Cerebral hernia
3. Mild type, MORTALITY >90%
Most these patients could be seen at late epidemic
season.
The lesions are mild. Low fever.
4. Chronic type
Not common.
Most patients are adults.
Easy to be misdiagnosed
LAB DIAGNOSIS
➢ Definitive diagnosis of serious meningococcal
infection has a prerequisite that the
bacteriologic isolation of N. meningitidis from
a usually sterile body fluid such as blood, CSF,
or synovial, pleural, or pericardial fluid. CSF
and blood are the most fruitful sources of
positive cultures.
➢ The ability to see or to culture meningococci in
petechial skin and mucosal lesions varies
widely.
➢ Skin biopsy may play a role in the diagnosis of
meningococcal infection.
The blood regular test :
WBC is very high, NE% become higher
CRP become higher
CSF TEST
The median leukocyte count was about 1200, with
a range of less than 10 to 65,000/mm3.
About 75% had CSF glucose levels below 40 mg/dL.
CSF protein levels ranged from 25 to more than
800 mg/dL, with the median value of about
150 mg/dL.
the cell type in untreated cases is almost always
polymorphonuclear. Partially treated patients may
have a pleomorphic spinal fluid.
➢ Pneumonia
➢ tympanitis
➢ suppurative arthritis
➢ endocarditis
➢ pericarditis
DIAGNOSIS
Initial diagnosis of meningococcal meningitis can
be made by clinical examination followed by a
lumbar puncture showing a purulent spinal fluid.
The bacteria can sometimes be seen in microscopic
examinations of the spinal fluid.
The diagnosis is supported or confirmed by
growing the bacteria from specimens of spinal fluid
or blood, by agglutination tests or by polymerase
chain reaction (PCR).
The identification of the serogroups and
susceptibility testing to antibiotics are important to
define control measures.
Clinically diagnosed case: clinical manifestations +
CSF of purulent meningitis + petechia or
ecchymosis with/without septic shock
Confirmed case: clinically diagnosed case +
bacteriological or specific serum immunological
examination positive.
TREATMENT
➢ Meningococcal disease is potentially fatal and
should always be viewed as a medical
emergency.
➢ Admission to a hospital or health centre is
necessary, and isolation of the patient is
necessary.
➢ Appropriate antibiotic treatment must be
started as soon as possible, ideally after the
lumbar puncture has been carried out if such a
puncture can be performed immediately.
➢ If treatment is started prior to the lumbar
puncture it may be difficult to grow the
bacteria from the spinal fluid and confirm the
diagnosis.
➢ Mortality rates in patients with
meningococcal meningitis are about 10% to 15%
despite antibiotic treatment
➢ Within 30 min
➢ The antibiotics - adequate dose, sensitive and
can penetrate the blood-brain barrier.
➢ Penicillins: Adult: 8MU q8h IV, children: total
dose-200,000-400,000U/kg, q8h IV.（？）
➢ Cephalosporins: Ceftriaxone （？）
➢ Chloramphenicol:(side effect)
PREVENTION
1.Polysaccharide vaccines against A have been
available to prevent the disease for over 30 years.
2. For group B, polysaccharide vaccines cannot be
developed, due to antigenic mimicry with
polysaccharide in human neurologic tissues.
Consequently, vaccines against B used in particular
in Cuba, New Zealand and Norway were outer
membrane proteins (OMP) and strain-specific to
control specific epidemics. Additional universal
group B protein vaccines are in late stages of
development.
3.Since 1999, meningococcal conjugate vaccines
against group C have been available and widely
used. Tetravalent A, C, Y and W135 conjugate
vaccines have been licensed since 2005 for use in
children and adults in Canada, the United States of
America, and Europe.
1.
Neisseria meningitidis is a: Gram-negative
diplococcus causing epidemic meningitis and
septicemia
2. Serogroup A N. meningitidis:Has been a
major cause of epidemic meningococcal
outbreaks in sub Saharan Africa
3. Which of the following is not true? The rash of
invasive meningococcal disease: D. Is almost
always present and easily detected
4. Which of the following is not true regarding
antibiotic treatment of meningococcal
meningitis? It takes 10 to 14 days to be
effective, Meningococci in cerebrospinal fluid
are killed within 3 to 4 hours after intravenous
treatment with an adequate dose of a
third-generation cephalosporin or penicillin.
5. Meningococcal conjugate vaccines are safe
and immunogenic in young children, induce
immunologic memory, and can decrease
nasopharyngeal carriage of meningococci.
Meningococcal conjugate vaccines have largely
replaced the older polysaccharide vaccines and are
now preferred for prevention strategies.
1、How do we get correct diagnosis：
We should collect evidence as more as
possible, include history+ Clinical signs +physical
examination+ blood test + Bacteriological isolation
from sterile body fluid eg blood, CSF。Only we get
the correct diagnosis, the patient can accept
proper treatment.
2. What is pandy test?
It is to detect protein in the CSF or other sterile
fluid. the different level indicate different
meningitis . REFER PICTURE
3.Clinical manifestation of fulminant type of
Meningococcal meningitis.
Three types:
1)Shock type.
High fever, chill, headache, vomiting , petechiae,
ecchymosis 。
signs of shock ：such as blood pressure lower,
heart rate higher.
2)Meningoencephalitis type.
Damage of meninges and brain parenchyma. High
fever, chill, headache, lassitude, delirium,
convulsion, disturbance of consciousness.
Severe-Cerebral hernia.
3)Mixed type.
The patients have both shock and
meningoencephalitis.
Mortality > 90%.
1）What is the most likely diagnosis? What is the
diagnosis based on?
Answer: meningococcal meningitis(common type)
Onset of the disease in winter and spring (January
10), this disease occurred locally (similar patients in
school)
2. Sudden high fever, severe headache, frequent
projectile vomiting, skin hemorrhage and
meningeal irritation
3.The total number of WBC and the proportion of
neutrophils in blood were increased
2)Which diseases need to be differentially
diagnosed?
1.Purulent meningitis caused by other bacteria
2. Tuberculous meningitis
3. Viral meningitis
3) FURTHER TESTS
Lumbar puncture: pressure measurement,
cerebrospinal fluid appearance, routine,
biochemical, bacteriological examination (culture
and smear)。
2. Blood culture or skin petechiae smear。
3. Chest X-ray excludes pneumonia and
tuberculosis
4) What are the principles of treatment for this
case?
1. Pathogen therapy:
adequate dose, sensitive and can penetrate the
blood-brain barrier.
High-dose penicillin is preferred, and
chloramphenicol and third-generation
cephalosporins can be used.
2. Symptomatic treatment:
(1) mannitol lowers intracranial pressure
(2) physical cooling or antipyretics
Kernig sign (+)
When flexing the hip 90 degrees and then
extending the leg, the patient feels subsequent
pain.
Brudzinskis sign +
When passively flexing the neck while supine,
patient involuntarily flexes his knees and hips
Babinski sign (-).
BREAST ANATOMY AND AUGMENTATION
❖ STRUCTURE OF BREAST:
Skin- nipple, areolar
Glandular- lobules, milk duct
Fat
Fibrous tissue- coppers ligament
❖ Breast innervations:
Lateral:
the lateral cutaneous branches of intercostal nerves (3-6).
Medial:
the anterior cutaneous branches of the intercostal nerves(2-6).
❖ Breast Augmentation Procedure Steps
•
•
•
•
The incision
Implant choice: Patients desired size, Skin elasticity, breast anatomy, body type.
Inserting and placing the implant
Closing the incision
❖ What decides the breast shape?
• TEPID SYSTEM
• The tissue characteristics (T)
• the envelope (E),
• the parenchyma (P),
• the implant (I)
• the dynamics (D) of implant and filler distribution
❖ COMPLICATIONS:
• Bleeding(hematoma)
• Infections
• Poor healing of incision
• Unfavorable scarring
• Changes in nipple or breast sensation
• Implant leakage or rupture
• CAPSULAR CONTRACTURE
❖ CAPSULAR CONTRACTURE:
Capsular contracture results from an exaggerated scar response to a foreign prosthetic material. All
surgical implants undergo some degree of encapsulation, but clinical problems arise when this scar
formation becomes excessive. Capsular contracture remains the most common complication of breast
augmentation, with rates reported between 0.5% and 30%.
REDUCTION MAMMAPLASTY
❖ describe the anatomy of the breast as it relates to reduction mammaplasty.
• GENERAL ANATOMY:
The base of the breast overlies the pectoralis major muscle between the second and sixth
ribs, and laterally from the edge of the sternum to the anterior axillary line.
The nipple is usually level with the fourth rib and just lateral to the midclavicular line.
•
The lower pole of the breast is fuller than the upper pole.
The circular areola surrounds the nipple and varies between 15 and 60 mm in diameter.
The breast parenchyma is made up of 15 to 25 lobes of glandular tissue, each emptying into
a separate milk duct terminating in the nipple.
MAIN ARTERIAL BLOOD SUPPLY:
internal mammary artery(IM)
lateral thoracic artery(LT)
•
•
intercostal artery (IC)
(3-8)
THE VASCULATURE OF NAC (nipple areolar complex) consists of:
Internal mammary perforators, Anteromedial and pectoralis major perforators, Anterolateral
intercostal perforators.
Nerves of NAC: 3-5 anterior and lateral cutaneous nerves.
The 4th intercostal nerve is the most important nipple innervation.
Innervation of Breast
intercostal nerves supply breast innervation (2-6)
Lateral:
the lateral cutaneous branches of intercostal nerves (3-6).
Medial:
the anterior cutaneous branches of the intercostal nerves (2-6)
❖ Definition of reduction mammaplasty and the indications for the surgery.
• Definition: Breast reduction can be defined as surgical reduction of breast volume to
achieve a smaller, aesthetically shaped breast mound with concomitant relief of the
potential symptoms of mammary hypertrophy.
• Indications:
❖ CLASSIFICATION OF BREAST HYPERTROPHY:
❖
❖ CLASSIFICATIONS OF BREAST PTOSIS:
The most commonly used systems are the following:
• Grade I : Mild ptosis – Nipple just below inframammary fold but still above lower pole of
breast
• Grade I I : Moderate ptosis – Nipple further below inframammary fold but still with some
lower pole tissue below nipple
• Grade III: Severe ptosis – Nipple well below inframammary fold and no lower pole tissue
below nipple; “Snoopy nose” appearance
❖ different procedures available for reduction mammaplasty?
• There are many surgical options for breast reduction. Often the choice of surgical
procedure is based on:
• patient morphology( breast volume and degree of nipple displacement)
•
surgeon’s choice( training and experience with certain procedures)
•
❖ Describe the common early and late complications following reduction mammaplasty.
•
Hematomas and Seromas
Hematomas manifest with increasing pain, swelling, and bruising of the affected side
and may be associated with evidence of vascular impairment to a previously viable nipple
or skin envelope secondary to tension-induced ischemia. 12 hours after the surgery.
Occurs first 12 hours after the surgery. Bleeding intercostal perforators are the most
common source.
Treatment involves surgical evacuation and sealing of the bleeding point.
Seromas are also rare, with an incidence between 1% and 5%. Aspiration is usually
adequate to deal with the problem.
•
Delayed Wound Healing
There are some background disease that may delay wound healing ,such as diabetes, poor
nutrition and smoking. Wound healing problems were directly proportional to the
preoperative breast size and quantity of fat within the breast.
Minimizing the size of the inferior dog-ear deformity and paying careful attention to
meticulous vertical incision coaptation are crucial to improved wound healing at this site.
•
Skin necrosis :
Skin necrosis is often tension related in Wise-pattern reductions and is virtually absent in
vertical techniques. In Wise-pattern closures, tension at the inverted T closure
compromises blood flow to the tips of the skin flaps, and necrosis follows.
•
Nipple Loss:
Nipple loss is uncommon, but it is reported in association with smoking.
Long pedicles or a thick pedicle folded in
vertical technique may also predispose to nipple loss from inadequate vascular perfusion.
It is more common in massive pedicled reductions. With vertical reduction, blistering
occurred in 3% with no nipple losses.
Nipple blistering is more likely than true full-thickness necrosis. If blistering occurs, it
should be allowed to heal secondarily, but patients should be warned that depigmentation
of the areola may result.
If frank necrosis occurs, it should also be allowed to heal before nipple reconstruction is
performed.
•
Nipple Numbness
Nipple numbness is common in most techniques to some degree; the tendency is for
feeling to return with time,but it may never return to normal levels.
•
Inability to Breast-feed: They should be warned that although some women are able to
breast-feed after reduction, many cannot; and of those who can, few are able to nourish
their children entirely from breast-feeding.
BREAST RECONSTRUCTION:
❖ Goal of Reconstruction:
The first is natural -appearing breast mound with adequate volume for projection and size .
The second goal is the optimal reconstruction of skin envelope. In skin -sparing mastectomies ,
the skin envelope may be intact .when no skin is resected (i.e.prophylactic mastectomy),the breast
mound must contoured to provide an inframammary fold and an anterior axillary line. In patients
with an inadequate skin envelope, a decision must be made as to the replacement of skin through
the use of expansion or with a regional or distant flap.
The third objective is symmetry. If necessary, a procedure is performed on the contralateral breast
to achieve symmetric projection and size or shape.
The final objective is the reconstruction of a nipple-areola complex that matches the opposite side
in color and projection.
❖ Techniques for reconstruction:
Implant-based reconstruction—Expender-implant/implant
• Flap-based reconstruction—Autologous tissues
•
The most common flaps for breast reconstruction are the deep inferior epigastric artery
perforator (DIEP) flap and the free transverse rectus abdominis musculocutaneous
(TRAM) flap.
• Flap related complications: Flap necrosis/loss
Donor-tissue-related complications
Hernia/bulge/laxity
Patient-reported outcomes
• Expender-implant/implant reconstruction
• Implant based complications:
Capsular contracture
Deflation of tissue expanders and saline implants
Rupture of silicone gel implants
Implant exposure
Malposition
Anaplastic large cell lymphoma
Breast implant illness
NEOPLASM
❖ Write down 10 names of common benign tumors on head and neck.
• Dermoid Cysts
• Pilomatrixoma
• Epidermal cyst
• Pyogenicgranuloma
• Teratomas
• Brachial cleft anomalies
• Hemangiomas
• Neurofibromas
• Lipomatosis
• Fibrous dysplasia
• Seborrheic keratosis
• Epidermal nevus
• Nevus sebaceous
• Epidermal nevus
• Rhinophyma
• Congenital Nevomelanocytic Nevus
•
❖ Write down 4 names of premalignant tumors on the skin.
• Actinic Keratoses
• Leukoplakia
• Xeroderma Pigmentosum
• Keratoacanthoma
• Bowen Disease
❖ 5 names of malignant tumors on the skin.
• Basal cell carcinoma
• Squamous cell carcinoma
• Pagets disease
• Sebaceous carcinoma
• Malignant Melanoma
• Soft Tissue Sarcoma:
FIBROSARCOMA
HEMANGIOPERICYTOMA
LIPOSARCOMA
LEIOMYOSARCOMA
MALIGNANT MESENCHYMOMA
ALVEOLAR SOFT PART SARCOMA
SYNOVIAL SARCOMAMalignant Bone Tumors
OSTEOSARCOMA
• FIBROSARCOMA
❖ The etiologic factors for malignant tumors on the skin.
Hereditary factors, infections (viral in particular), parental age, prenatal exposure to
certain drugs, and elevated birth weight have all been associated with various types of
neoplastic disease.
Ultraviolet Radiation
Exposure to Radiation
Immune Response
Chronic Wounds and Scars
❖ The ABCD Guidelines that can distinguish melanoma from nevus.
Melanoma:
A Asymmetry of the lesion as it grows from a round or oval lesion
B Border irregularity, which is a result of irregular growth rates of different parts of the lesion
C Color changes representing pigment granules deposited at varying depths in the dermis, depending on
the rate of invasion
D Diameter of the lesion becoming more than ¼ inch (>6 mm)
Nevus:
SCAR
❖ Histological classification of scars and their characteristics:
1. superficial scar: scar on the surface of the epidermis or dermis, local flat, generally no
dysfunction. Dermal shallow, because more than a mild scratch, shallow degree burns (Ⅰ ° ~
shallow Ⅱ °), superficial skin infections. Rough surface, may have pigmentation. Topical
palpation.
Treatment: no special treatment or general cosmetic medicine application.
2. hypertrophic scar: scar occurs in the deep dermis, which is prominent on the surface of the skin
but limited to the original scope of injury.
In deep Ⅱ ° and above burns or shallow Ⅱ ° burn infection, cut wounds, thick skin for skin in the area
around the scar is significantly higher than normal leather, such as ammonites of hard, boundaries
clear. Inchoate: capillary congest and show gules, flush or purple, acuteness SAO is urticant it is main
symptom. The duration was related to age and site. The hyperplasia period was longer in young adults
and sites with better blood supply, and shorter on the contrary. Outcome -- physiological scar (mature,
static)
3. Atrophic scar: occurs in the whole layer of the skin and subcutaneous scar. Have very big
contractive sex, can pull adjacent organization, organ, cause serious function obstacle. In
involving the full-thickness skin and subcutaneous tissue damage, such as large area Ⅲ ° burn,
traumatic tissue defect after healing with chronic ulcer and less subcutaneous tissue such as the
scalp, pretibial areas, etc. Scar hard, flat or slightly higher than the skin surface, with deep tissue
adhesion. Poor circulation, reddish or pale, extremely thin epidermis and no resistance to friction,
easy to collapse and not heal. Prone to cancer. It is easy to contract and pull, which affects the
function of surrounding tissues.
4. Keloid: most keloid usually occur 1 year after local injury, and generally present as a continuous
growth lump higher than the surrounding normal skin and beyond the original injury site, with
hard palpation, poor elasticity, and local itching or pain. It is now believed that -- skin fibrosis
tumor, whose pathological main points are large deposition of collagen and its mechanism
components in scar tissue, lesions and invasion of surrounding normal tissues, and short-term
non-healing tendency. Microscopically, a large number of immature fibroblasts were observed to
proliferate, and collagen fibers were hyaline, bulky and disordered, with rich mucus matrix. They
are most commonly seen in the anterior chest, neck, shoulder and upper brachial deltoid regions.
Good hair age 30 years old or younger. Appearance red, hard, prominent skin surface, can be a
crab foot (crab foot swelling).
❖ Differentiation of hypertrophic scar and keloid:
Both are collectively referred to as pathological scars
Similarities: the basic pathological forms are all based on the massive deposition of collagen fibers in the
dermis
Organizational characteristics
Difference:
hyperplastic lesions were limited to lesions -- hypertrophic scars
Hyperplasia extends beyond the lesion area -- keloid
Keloids can be classified as benign tumors of the skin
TREATMENT:
1) Pressure therapy: As an adjuvant therapy for surgery, laser, medicine, radiotherapy, etc., it can reduce
the dosage and reduce the recurrence rate. It is suitable for hypertrophic scar of various areas, or for
patients who are not suitable for radiotherapy and local drug therapy.Support with the last 6 months or
better. Indications: postoperative or new scar.
2）Silicone gel therapy: The most commonly used methods are skin care, scar deicide, silicone cream,
scar paste, etc. The methods are external paste, external coating, etc., easy to use, simple, no local
discomfort or slight discomfort. It is suitable for early application after operation or burn. In addition,
Chinese traditional medicine also has its own characteristics, such as scar antipruritic ointment. But the
effect is slow and the cure rate is low. New scar removal ointment is more suitable
3） Corticosteroid therapy:
4）Surgical treatment.
5）Radiation therapy
6）Anti-Inflammation.
FACIAL SOFT TISSUE TRAUMA:
❖ FACIAL NERVES:
❖ Facial Muscle:
• occipitofrontalis muscle: serves for facial expressions
• orbicularis oculi muscle: Closes the eye
• temporoparietalis muscle: distinct muscle above the auricularis superior.
• procerus muscle: The procerus arises by tendinous fibers from the fascia covering the
lower part of the nasal bone and upper part of the lateral nasal cartilage. It is inserted into
the skin over the lower part of the forehead between the two eyebrows on either side of
the midline, its fibers merging with those of The procerus helps to pull that part of the
skin between the eyebrows downwards, which assists in flaring the nostrils. It can also
contribute to an expression of anger
• nasalis muscle: whose function is to compress the nasal cartilages. It is the muscle
responsible for "flaring" of the nostrils
• corrugator supercili muscle: The corrugator draws the eyebrow downward and medially,
producing the vertical wrinkles of the forehead. It is the "frowning" muscle, and may be
regarded as the principal muscle in the expression of suffering. It also contracts to prevent
high sun glare, pulling the eyebrows toward the bridge of the nose, making a roof over
the area above the middle corner of the eye and typical forehead furrows.
• orbicularis oris muscle: This muscle closes the mouth and puckers the lips when it
contracts.
• risorius muscle: The risorius retracts the angle of the mouth to produce a smile, albeit an
insincere-looking one that does not involve the skin around the eyes.
• zygomaticus major muscle: . It is a muscle of facial expression which draws the angle of
the mouth superiorly and posteriorly to allow one to smile.
• zygomaticus minor: . It draws the upper lip backward, upward, and outward and is used
in smiling.
• levator labii superioris:
• levator anguli oris: facial muscle of the mouth arising from the canine fossa, immediately
below the infraorbital foramen. It elevates angle of mouth medially.
• buccinator muscle: Its purpose is to pull back the angle of the mouth and to flatten the
cheek area, which aids in holding the cheek to the teeth during chewing. This action
causes the muscle to keep food pushed back on the occlusal surface of the posterior teeth,
as when a person chews. By keeping the food in the correct position when chewing, the
buccinator assists the muscles of mastication. It aids whistling and smiling, and in
neonates it is used to suckle.
• depressor labii inferioris: This muscle helps to depress the lower lip.
• Mentalis: The primary effect of the mentalis contraction is the upward-inward movement
of the soft tissue complex of the chin, which raises the central portion of the lips in turn.
In the setting of lip incompetence (the upper and lower lips do not touch each other at
rest), the mentalis muscle contraction can bring temporary but strained oral competence.
• depressor anguli oris : The depressor anguli oris is responsible for pulling the angle of the
mouth downward.
Plastic Surgery
L5: Opthalmic Plastic Surgery
What are the five basic layer structures of the upper eyelid?
1. Eyelid skin
2. Subcutaneous tissues
3. Orbicularis Oculi Muscles
4. Tarsal plates
5. Conjunctiva
What are the anatomical differences between asian and whites to the upper
eyelid
1. the asian upper eyelid contains more prominent septal fat resulting in greater
lid fullness
2. The presence, position and depth of the superior eyelid fold are highly
variable in asians but in caucasians eyelids with a crease are thinner and
constant than asians
3. Many asian upper eyelids are characterized by a medial epicenthal fold
The advantages of suture and incision method:
1. the power of the levator muscle regarding the eye opening process is
transmited to pull up the entire lid margin, allowing the eyes to be easily
opened with minimal effort
2. There is a minimal surgical scarring when the eyes are are closed. When
they eyes are open, the double-eyelid line wouldn't be deep and is gently
and gradually formed
3. The difference between the left and right eyelid levels can be easily adjusted
Complications for blepharoplasty
Early complications
visual loss; retrobulbar hemorrhage, globe perforation, central retinal
artery occlusion
corneal abrasion
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eyelid hematoma
infection
swelling
Late complications
Eyelid malposition
Ptosis
Lagophthalmos
Over and under resection of skin
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Over and under resection of orbital fat
Eyelid crease abnormalities
Hypertrophic scaring
Dry eye syndrome
Definition of Blepharoptosis
It is the true ptosis of the eyelid which can be defined as a dropping of the eyelid
so that its margin falls below the normal anatomic position
Classification and Clinical manifestations of Blepharoptosis
1. Congenital ptosis; simple ptosis: ptosis of the upper eyelid caused by loss or
weakening of the levator muscle due to congenital dysplasia
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2. Acquired ptosis:
a. Neurogenic ptosis
b. Myogenic ptosis
c. Aponeurotic ptosis
d. Mechanical ptosis
e. Pseudeptosis
Blepharophimosis ptosis epicanthus inversions syndrome (BPES) (Komoto
syndrome)
Definition: its a condition where the patient has bilateral ptosis with reduced
lid size, vertically and horizontally. The nasal bridge is flat and there is
hypoplartic orbital rim
Main clinical manifestations:
1. Blepharophismosis: both the vertical and horizontal palpebral fissures
are shortened. normal 25 - 30mm but with BPES 20 - 22mm
2. Telecanthus: it refers to increased distance between the medial canthi of
the eyes, while the interpupillary distance is normal
3. Ptosis: cases are usually moderate to severe, its occurrence is mainly
caused by the dysplasia of levator muscle of upper eyelid
4. Epicanthus inverses
Treatment; the three techniques for one stage correction
mustards epicanthoplasty
fox’s lateral canthoplasty
ptosis correction by suspension of frontal muscle flap
L6: Skin Graft, Flap and Tissue Expansion
The classification of skin graft
Split-thickness skin graft: is when a graft includes only a portion of the
dermis
Full-thickness skin graft: is when the graft contains the entire dermis
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The indications of skin graft
Any traumatic wound that cannot be closed primarily
defects after oncologic resection
burn reconstruction
scar contracture release
congenital deficiencies of skin
hair restoration
nipple-areola reconstruction
The contraindications of skin graft
Absolute;
1. wounds with avascular beds
2. infected wounds
3. wounds due to malignant neoplasia
Relative:
1. Pressure sores
2. Wounds due to irradiation
3. Wounds due to vasculitis
4. Wounds due to arterial insufficiency
5. Wounds in cosmetically sensitive areas
6. Malnutrition
The common donor sites of skin graft
Split-thickness skin grafts can be taken from any area on the body. Popular
areas for split-thickness graft harvest include the thigh, trunk and buttocks
Common sites for full-thickness skin grafts of the head and neck include the
post auricular region, inner portion of upper arms, abdomen and inguinal
crease
The definition of flap
A flap consists of tissue that is mobilized on the basis of its vascular
anatomy. Flaps can be composed of skin, skin and fascia, skin and muscle,
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or skin, muscle and bone
The classification of flap
Can be classified by the circulation into:
Random flap: advancement flap, rotation flap, transposition flap
Axial flap: common axial flap, island flap, musculocutaneous flap, free flap
The composition of tissue expander
Its composition Is made of three parts: expander, catheter and injection port
The complications of tissue expansion:
Major complications involve infection, implant exposure and flap ischemia
Minor compilcations with expansion include transient pain with expansion,
seroma, dog ears at the sonar site and widening of scars
L7: Otoplasty
Microtia
Definition: its an incompletely formed ear. It’s the complete deficiency of the
auricle. The most common condition in which microtia is seen is hem facial
microsamia
Types of Microtia
Type 1: external ear is small and retains most of the normal structure of
the auricle. The external auditory meatus is usually present
Type 2: The anomaly of the external ear is moderately severe which will
be hook-shaped, S-shaped, or “question mark” in appearance
Type 3: The external ear is only a rudiment of soft tissue and the auricle
does not have any appearance of a normal pinna
Type 4: Anotia with all external ear structures absent
Surgical Techniques
1. Nagats Method:
a. Stage 1: Framework fabrication and insertion
b. Stage 2: Ear elevation
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c. Stage 3: Tragus construction
2. Expansion Method:
a. stage 1: implant tissue expander
b. stage 2: framework fabrication and insertion and lobule transposition
Postoperative course: the tubes are removed at 5th postoperative day and
antibiotic medicine will be used for 5 days. Patients should avoid sleeping on
their new ear for the first month
Prominent Ear
have these following features:
an underdevopled or flat antihelix
an overdeveloped or deep concha
a combination of both features
The operative procedure, an ellipse-shaped limited piece of skin was
removed from the posterior surface of the ear to provide access to the
anterior auricular aspect
Cryptotia
Defintion: also known as “pocket ear” is a congenital anomaly in which the
superior aspect of the helical cartilage is buried beneath the scalp, resulting
in an absence of the auriculocephalic sulcus
Surgical correction of crytotia attempts to achieve four goals:
1. Recreation of an auriculocephalic sulcus
2. Correction of any cartilaginous deformity
3. Release of abnormal auricular muscle insertion
4. Provision of additional skin as needed for coverage of exposed cartilage
or temporal scalp defects
Constricted Ear
Four aspects of the constricted ear:
1. Lidding: A deficiency of the scapha, superior crus, and fossa triangularis
creates a downward fold of the upper helix
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2. Protrusion. A deeper conchal fossa results from the flattened helix and
antihelix causing an anterior projection of the upper pole of the ear
3. Decreased ear size
4. Low ear position
Types of constricted ear
Group 1: Deformities are limited to a folding of the helix along the
superior edge, creating mild lidding and a mild decrease in the vertical
height
Group 2a: is defined as having a significant compression of the helix and
scapha with obvious loss of vertical height. Not necessitate the use of
local flats
Group 2b: is characterized as having a more severe compression of the
upper pole elements requiring both skeletal expansion and introduction
of the soft tissue for coverage
Group 3: contains deformities will severe tubular constriction that some
authors have deemed as a form of microtia requiring complete
autologous reconstruction with rib cartilage graft
Surgical correction of the constricted ear must incorporate the following
general principals
Do as little as possible to obtain an acceptable outcome. Every
correction does not require extensive dissection of the cartilage and soft
tissues.
Symmetry should be the major goal. Unilateral cases are undoubtedly
more challenging to obtain an acceptable degree of symmetry
Intra-auricular anatomy is secondary to vertical height. Although both
are important, asymmetric appearance of the vertical height and position
usually provides a satisfactory outcome.
No ear deformity is the same. Flexibility is required.
L10: Rhinoplasty
Anatomy of the nose
1. Definition and location of the keystone
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The nasal keystone region is an aptly named confluence of bone and
cartilage at the junction of the upper and middle thirds of the nose. Its
important for the stability and structure of the nose. The keystone region
consists of contributions from the paired nasal bones cephalic ally,
paired upper lateral cartilages (ULCa) caudally, quadrangular cartilage
anterior-inferiorly, and perpendicular plate of the ethmoid (PPE)
posteriorinferiorly
2. What is the cartilaginous structure of nasal septum composed of?
upper lateral cartilage: which is between the nasal bones and the alar
cartilage
lower lateral cartilage: u shaped, medial crus forms the columella and
lateral crus from the ala. It overlaps the upper lateral cartilage on each
side
septal cartilage: also known as quadrangular cartilage, separates two
nasal cavities. it supports the nasal dorsal and the tip of the nose
lesser cartilage: also known as sesamoid cartilages, interconnected by
the adjacent perichondrium and periosteum
3. 5 key points of anatomy of the nose
Nose has an upper, bony, cartilaginous middle and lower vaults
Layers of the nose are skin, fat, SMAS, muscle and bone
Blood supply from the facial and ophthalmic arteries
Sensation by ophthalmic and maxillary branches of trigeminal
Internal anatomy focuses on septum, internal valve and turbinate
4. Nasal base anatomy consists of:
columellar base
central columellar pillar
infralobular triangle
soft triangle (facet)
lateral wall of ala
alar base
nostril sill
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Aesthetic proportions of the nose
1. Front view: face is divided into upper, middle and lower thirds. Lower third is
further divided into upper third and lower two thirds by line between oral
commissures
2. Lateral view:
Tip projection; the tip projection of the nose should be proportional to the
nasal length. the ratio of nasal length to tip projection should be 1.0:0.67
or 3:2
Columellar-labial angle: is at the junction of the columella with the upper
lip, aesthetic id 90 to 100 degrees for men and 95 to 105 degrees for
female
3. Aesthetics proportions of the chin: the redial’s plane is a simple way to
assess the aesthetics of the chin. On a balances face, should touch the most
prominent anterior portion of the chin
Nasal implants
1. What is the common used type in rhinoplasty?
2. What are the pros and cons about costal cartilage
Pros:
larger quantity; when a significant amount of material is needed
be able to shape into straight flat strong piece
be used as caudal extension graft to improve nasal length and tip
projection
can be carved for nasal dorsal augmentation
Cons:
must be usable in older age group because cartilage has turned into
bone
has chance to become discernable resorption and become curve
Methods of Nose Augmentation
1. What kind of rhinoplasty incision do we have now?
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Closed rhinoplasty incision
Open rhinoplasty incision
2. If someone has a broad nasal tip, what kind of rhinoplasty do you suggest
he/she to do?
Open rhinoplasty; a tiplasty which is the suturing of the nasal cartilage to
produce a more refined tip
Risk and Complication
1. What kind of risk and complications does the rhinoplasty usually have?
Bleeding:
Infection
Nasal septum perforation:
Wound dehiscence:
Asymmetry:
Facial anti-aging
What are the signs of anti aging?
forehead lines
frown lines
drooping eyelid
brow sag
lateral cantus sag
crows feet
eyelid crease
droopy nose
check hollowing
enlarged earlobes
naso labial folds
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facial wrinkles
droopy chin
Anti aging Surgery
1. Raised eyebrow surgery: first surgical design. then correct the eyelid skin
flappy with eyebrow margin incision
2. Eye-pouch prosthesis: first cut the skin and separate the palpebral margin
skin from orbiculares oculi muscle. then open the orbital septum and remove
excess fat, third step suture skin
the two surgical methods are eyelid margin incision and second is
internal incision, no suture no scar.
3. Double eyelidplasty: surgeon will first evaluate the problem, the surgeon will
then use laser technique to open incision in upper eyelids. the surgeon will
determine the position of new double eyelids and sew the incision
4. Face lift: face wrinkle removing more skin, enhances the strength
Non surgical anti-aging
1. Special medical protein line to lift face: the protein thread has barbs that lift
the skin, the protein line is used to tighten the skin.
2. Botox-toxin A removes wrinkles: It gets rid of labellum wrinkles, also gets rid
of forehead wrinkles
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Important Qs from each ppt
L3:Physician-Patient Relationships
General rules about physician-patient relationship
Rule 1: Patient is number one
Rule 2: Always respond to the patient
Rule 3: Tell the patient everything even if he or she doesn't ask
Rule 4: Work on long-term relationship with patients, not just short term
problems
Rule 5: Listening is better than talking
Rule 6: Negotiate rather than order
Rule 7: Trust must be built, not assumed
Rule 8: Admit to the patient when you make a mistake
Rule 9: Never “pass off” your patent to someone else
Rule 10: Express empathy, then give control e.g ‘I’m sorry, what would you
like to do?’
Rule 11: Agree on problem before moving to solution
Rule 12: Be sure you know what the patient is talking about before
intervening
Rule 13: Patients do not get to select inappropriate treatments
Rule 14: Be sure who your patient is
Rule 15: Never lie
Rule 16: Accept the health belief of patients
Rule 17: Accept patients religious beliefs and participate if possible
Rule 18: Anything that increases communication is good
Rule 19: Be an advocate for the patient
Important Qs from each ppt
1
Rule 20: the key is not so much what you do, but how you do it
L4: Learning and Behavior Modification
Definition of classic conditioning
classic conditioning is defined as a conditioned response to a neutral stimulus
after having been paired repeatedly with an unconditioned stimulus, this
response is involuntary.
Operant conditioning
Definition of operant conditioning: it is a form of learning in which a response
increases in frequency as a result of its being followed by reinforcement.
Reinforcer: there are stimuli that increases the probability of the response
occurring again. Any stimulus is a reinforcer if it increases the probability of a
response
Reinforcement: this is the act of following a response with a reinforcer
Punishment: is used to reduce an undesired behavior
Reinforcement schedules: rules that control the delivery of reinforcement;
there are two types:
Continuous reinforcement: every response is followed by a
reinforcement
Intermittent or partial reinforcement: not every response is reinforced;
there are four types:
Fixed ratio schedule
Fixed interval schedule
Variable ratio schedule
Variable interval schedule
Therapy modification based on operant conditioning
1. Shaping
2. Extinction
Important Qs from each ppt
2
3. Stimulus control
4. Biofeedback (neurofeedback)
5. Fading
L5: Defense Mechanisms
Personality consists of three parts:
1. Id: which is the unconscious part of your personality.
childish and impulsive part
doesn't really think about the consequences
instinctive urges, sex and aggression
tries to increase pleasure and decrease pain
2. SuperEgo: the conscious part of your brain
super judgmental and moralizing, childish and impulsive part
behaves in a socially appropriate way
3. Ego: Rational and language based executers liking to reality
discern what is right or wrong based on context
How many subtypes of defense mechanism are there and what are they called?
There are four subtypes:
1. Narcissistic
2. Immature
3. Anxiety
4. Mature
Subtypes of narcissistic defense mechanisms
1. Projection
2. Denial
3. Splitting
Important Qs from each ppt
3
Subtypes of immature defense mechanisms
1. Blocking
2. Regression
3. Somatization
4. Introjection (Identification)
Subtypes of anxiety defense mechanisms
1. Displacement
2. Repression
3. Isolation of effect
4. Intellectualization
5. Acting out
6. Rationalization
7. Reaction formation
8. Undoing
9. Passive-aggressive
10. Dissociation
Subtypes of mature defense mechanisms
1. Humor
2. Sublimation
3. Suppression
L6: Psychologic Health and Testing
Type A traits
include:
impatient
competitive
preoccupied with deadlines
Important Qs from each ppt
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highly involved with their jobs
Definition of IQ and Formula as well as distribution and mean of IQ
IQ is a general estimate of the functional capacities of the person
Formula of IQ: (MA/CA) * 100 = IQ score
MA; mental age = median test score for a given age
CA; chronological age = actual age of the actual person taking the test
Mean is 100; standard deviation is 15
How many types of personality tests and what are they?
There are two types:
Objective tests
Projective tests
How many types of objective tests and what are they?
There are two types of objective personality tests:
criterion referenced: results are given meaning by comparing them with a
preset standard
norm referenced: results are given meaning by comparing them with a
normative group
How many types of projective tests and what are they?
there are four types:
Rorschach inkblot test
Thematic A perception test (TAT)
Sentence completion test
Projective drawings
L7: Sleep and Sleep Disorders
Sleep architecture
1. Awake, relaxed = alpha waves
2. Stage 1 sleep = theta waves
Important Qs from each ppt
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3. Stage 2 sleep = K-complexes
4. Stage 3 sleep = delta waves
5. Stage 4 sleep = delta waves
6. REM sleep = sawtooth waves
NREM sleep alternates with REM sleep throughout the sleep and is
characterized by:
1. slowing of the EEG rhythms
2. higher muscle tone
3. absence of eye movements
4. absence of “though like” mental activity
REM is characterized by:
1. An aroused EEG pattern
2. Sexual arousal
3. Saccadic eye movements
4. Elaborate visual imagery (dreaming)
5. Associated with pons
Sleep apnea syndrome complications
daytime fatigue
high blood pressure or heart problems
type 2 diabetes
metabolic syndrome
complications with medications and surgery
liver problems
sleep-deprived partners
Narcolepsy tetrad and treatment
The narcoleptic tetrad:
sleep attacks and excessive daytime sleepiness (EDS)
cataplexy
Important Qs from each ppt
6
hypnagogic hallucinations
sleep paralysis
Narcolepsy treatment:
CNS stimulants control the EDS; methylphenidate, dextroamphetamine
Tricyclic antidepressants control the cataplexy
Modafinil
L8: Organic Disorders
Delirium vs Dementia
Delirium
Dementia
History
Acute
Chronic
Onset
Rapid
Insidious
Duration
Days to Weeks
Months to Years
Course
Fluctuating
Chronically progressive
Level of consciousness
Fluctuating
Normal
Orientation
Impaired periodically
Disorientation to person
Memory
Recently markedly impaired
Recently remotely impaired
Perception
Visual hallucinations
Hallucinations less common
Sleep
Disrupted sleep-wake cycle
Less sleep disruption
Reversibility
Reversible
Mostly not reversible
Physiological changes
Prominent
Minimal
Attention span
Very short
Not reduced
Ten warning signs of Alzheimer disease
1. Memory loss that effects job skills
2. Difficulty performing familiar tasks
3. Problems with language
4. Disorientation to time and place
5. Poor judgment
Important Qs from each ppt
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6. Problems with abstract thought
7. Misplacing things
8. Changes in mood or behavior
9. Changes in personality
10. Loss of initiative
Alzheimers
Gross pathology:
diffuse atrophy of the brain on CT or MRI
flattened cortical sulci
enlarged cerebral ventricles
deficient blood flow in parietal lobes correlated with cognitive decline
reduction in choline acetyltransferase
reduced metabolism in temporal an parietal lobes
Microscopic pathology:
accumulation of amyloid beta-peptides
senile plaques
neurofibrillary tangles
granulovascular degeneration of the neurons
anatomic changes to amygdala, hippocampus, cortex, basal forebrain
Treatment:
supportive
symptomatic
reduce environmental changes
donepezil hydrochloride
Parkinsons disease
its decreased dopamine in substantial nigra
symptoms
Important Qs from each ppt
8
resting tremor; pill-rolling tremor
Bradykinesia
cogwheel rigidity; mask like facies; shuffling gait
Treatment:
L-dopa or deprenyl
Vascular dementia
Definition: decremental or patchy deterioration in cognitive functioning due to
severe cerebrovascular disease
Treatmen: Treatment of underlying condition such as; hypertension, diabetes
mellitus, hyperlipidemia
General measures for dementia
Left hemisphere
language
dominant in 97% of population, 60 to 70% in left handed persons
calculation-type problem solving
stroke damage to left id more likely to lead to depression
larger in size than is the right side and processes information faster
Right hemisphere
perception, artistic, visual-spatial
activated for intuition-type problem solving
stroke damaged to right is more likely to lead to apathy and indifference
prosody resides here
more 5-HT receptors
Functions of frontal cortex and lesions of dorsal prefrontal cortex
Key functions:
speech
critical to personality
abstract thought
Important Qs from each ppt
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memory and higher-order mental functions
capacity to initiate and stop tasks
concentration
Lesions of dorsal prefrontal cortex:
apathy
decreased drive, initiative
poor grooming
decreased attention
poor ability to think abstractly
broca aphasia if in dominant hemisphere
Functions and lesions of dominant lobe of temporal cortex
Functions of temporal cortex:
Language, memory and emotion
Lesions stem from stroke, tumor and trauma; herpes virus CNS
infections often affect temporal cortex
Bilateral lesions: dementia
Lesions of the postal left temporal lobe: deficits in recall or learning of
proper names
Lesions of dominant lobe:
euphoria
auditory hallucinations
delusions
thought disorders
poor verbal comprehensions (Wernicke)
Lesions of non dominant lobe:
Dysphoria
Irritability
Decreased visual and musical ability
Important Qs from each ppt
10
L9: DSM-5 Pt 1
Five major axes of diagnosis
1. Clinical disorders
2. Personality disorders and mental retardation
3. Physical conditions and disorders
4. Psychosocial and environmental problems
5. Global assessment of functioning (GAF)
What is clinical disorders?
They include: schizophrenic, affective, anxiety and somatoform disorders.
Also includes anorexia nervosa and bulimia nervosa, sexual disorders, sleep
disorders and autism
Criteria of schizophrenia
1. Bizzare delusions
2. Auditory hallucinations
3. Blunted affect
4. Loose associations
5. Deficiency in reality testing, distorted perception; impaired functioning overall
6. Disturbances in behavior and form and content of language and though
7. More than 6 months in duration
Definitions of bizarre delusions
Delusions: false beliefs not shared by culture
Illusions: misperception of real stimuli
Hallucinations: sensory impression, no stimuli
Severity of schizophrenia following what 5 symptoms?
1. delusions
2. hallucinations
3. disorganized speech
Important Qs from each ppt
11
4. abnormal psychomotors
5. negative symptoms
Positive symptoms (Type 1)
what schizophrenic person has that normal people do not e.g delusions,
hallucinations, bizarre behavior
associated with dopamine receptors
Negative symptoms (Type 2)
what normal people have that schizophrenic people do not have e.g flat
affect, motor retardation, apathy, mutism
associated with muscarinic receptors
L10: DSM-5 Pt 2
Neurochemical issues and other neurotransmiters
The dopamine hypothesis: the effectiveness of neuroleptic medications in
ameliorating the symptoms of schizophrenia.
the correlation of clinical efficacy with drug potency in dopamine receptor
antagonists
findings of increased dopamine receptor sensitivity in postmortem
studies
PET scan studies of schizophrenic patients compared with controls
Other neurotransmitters include:
Serotonin
Glutamine
Norepinephrine
Related excitatory amino acids
The neuropeptide cholecystokinin
Neurotensin
Attention and information processing deficits
smooth pursuit eye movement (SPEM)
Important Qs from each ppt
12
backward masking
event-related potentials (ERP)
prefrontal cortical (PFC) impairment
Mood disorders
Mild
Severe
Stable
dysthymia
Unipolar
Alternating
Cyclothymia
Bipolar
Basic subtypes of mood disorders
Dysthymia (nonsychotic depression)
Cyclothymia (nonpsychotic bipolar)
Seasonal affective disorde (SAD)
Unipolar disorder (major depression)
Bipolar disorder (manic-depression)
Dysthymia (non psychotic depression) key clinical manifestations
depressed mood
loss of interest or pleasure
chronic so at least 2 years
not severe enough for hospitalization
life time prevalence 45 in 1000
30% to 50% of alcoholics have secondary depression
Unipolar disorder (major depression) items that is associated with
1. anhedonia
2. feelings of worthlessness
3. weight loss or gain
4. recurent thoughts
Important Qs from each ppt
13
5. psychomotor agitation or retardation
6. somatic lantern
7. delusions or hallucinations
8. no motivation
9. decreased concentration
10. depressed mood
11. insomnia or hypersomnia
12. loss of sex drive
Bipolar disorder
Bipolar 1; mania is more prominent
Bipolar 2: recurrent depressive episodes plus hypomanic episodes
Neurochemical changes of bipolar disorder
increased norepinephrine (NE)
increased serotonin
slight increase in dopamine
Important Qs from each ppt
14
SOCIAL FAMILY LIFE-1
What’s reason for higher divorce rate ?
1.The changing of the basis for marriage from
economic to “love match”
2. Increased mobility and distance from
family supports
3. Fewer legal and religious constraints;
4. The lessening of economic dependence
of women.
What’s effect to children for divorce?
More behavior problems, delayed physical and
mental development.
However, staying in a hostile environment can be
harder.
Socioeconomic Status (SES)
SES: weighted combination of occupation and
education. Income is not used as a direct
determinant of SES, High SES people marry later
and have children later
LOWER SES, More sharply defined sex-role
expectations
More rigidity in expectations of individuals
And more action-oriented language rather than
conceptual language. LEADS TO SINGLE PARENT
FAMILY
SUICIDE
Between 10 and 20 suicide attempts for every one
that succeeds
Men commit suicide four times as often as women.
Women attempt three times as often as men
For people aged 15 to 24, suicide is the third
leading cause of death; for those aged 25 to 35, it
is the second.
What’s the factors that associated with high risk
for suicide ?
Clinical issues
a. Single best predictor of suicide: previous suicide
attempt
b. Other clinical signs
i. Sense of hopelessness
ii. Having a plan
c. Suicide threats are the clearest reason to
hospitalize someone for psychiatric reasons.
d. IMPORTANT: Suicide often occurs when a
person is feeling better after coming out of a deep
depressive episode (more likely just after
admission to hospital for psychiatric reasons).
e. Suicide common in patients faced with chronic,
painful, or hopeless condition
Hospitalization
Most admissions: psychiatric reasons
b. Most days in hospital: diseases of cardiovascular
system
c. Most days lost from work: disease of upper
respiratory system
d. Ambulatory clinics: back pain 30% of cases.
e. Most work-related disability: muscle/skeletal
problems
f. Most common for both males and females: back
pain; carpal tunnel is second for both
Health care payments
a. Capitation: prospective payment system.
Payments are made for number of people the
provider is responsible for, not care delivered.
b. Medicare: federal government program that
provides insurance payment for the elderly, the
disables, and dependents of the disabled.
i. Medicare does not generally cover routine
physical exams, nursing home care, or prescription
drugs.
ii. Medicare does cover ambulance transport,
dialysis, and speech and occupational therapy.
HIV/AIDS
About 1,000,000 adults and 200,000 children in the
U.S. are HIV positive ( male 1:100, female 1:800)
In some inner-city areas, as many as 50% of males
are HIV positive.
AIDS is now the fifth leading cause of death for all
men aged 25 to 44.
a. Better treatments have reduced mortality.
b. Unintended injuries is #1, heart disease is #2,
suicide is #3
AIDS is now the fifth leading cause of death for all
men aged 25 to 44.
a. Better treatments have reduced mortality.
b. Unintended injuries is #1, heart disease is #2,
suicide is #3
Most dangerous sexual practice: anal intercourse
HIV transmission rates
a. Risk from single sexual encounter with man who
is not a member of a risk group: 1 in 5 million
b. Risk from single encounter with man who is a
member of a high risk group: 1 in 20 to 1 in 2
c. Needle-stick (with HIV –positive blood): 1 in 100
to 1 in 1, 000 (average 1 in 250)
d. Seroconversion from blood transfusion: 2 of 3
CHILD DEVELOPMENT-2
1. INFANTS
Recent research has changed our past assumptions
about the capabilities of infants.
a. Reaching and grasping behavior
b. Ability to imitate facial expressions
c. Ability to synchronize their limb
movements
with speech of others (coupling or
entrainment)
d. Attachment behaviors, such as crying and
clinging
2. New born preferences
a) Bright objects with lots of contrast
b) Moving objects
c) Cuvres versus lines
d) Complex versus simple design
e) Evidence of a preference for facial stimuli
3. The fact that a neonate will demonstrate
defensive movements if an object looms
toward his or her face suggests the ability to
perceive a three-dimensional world.
4. Recent research also suggests that the
neonatal
nervoussystem
gives
special
attention to language versus nonlanguage
stimuli
5. At just 1 week old, the infant responds
differently to the smell of the mother
compared with the father.
6. Smiling
a) The smile develops from an innate reflex
present at birth (endogenous smile).
b) An infant shows exogenous smiling in
response to a face at 8 weeks.
c) A preferential social smile, e.g., to the
mother’s rather than another’s face,
appears about 12 to 16 weeks
7. Physical development
A.Hands and feet are the first parts of the body to
reach adult size.
B. Motor development follows set patterns
c. Capacity to copy shapes follows in alphabetical
order:
Circles, cross, rectangle, square, triangle
The exception is a “diamond,” which can generally
not be reproduced until age 7.
d. Earliest memories, roughly ages 2-4
e. First words (10 months), then first birthday, then
first steps (13 months)
8. Key developmental issues
Brain-growth spurt: “critical period” of great
vulnerability to environmental influence
Extending from last trimester of pregnancy
through
first 14 postnatal months
b. Earliest memories, roughly ages 2-4.
Separation anxiety: distress of infant following
separation from a caretaker
Appears at 8-12 months
Begins to disappear at 20-24 months
Continued separation, especially prior to 12
months leads to withdrawal and risk of anaclitic
Depression School phobia (Separation Anxiety
Disorder) is failure to resolve separation anxiety.
Treatment focuses on child’s interaction with
parents, not on activities in school.
Discipline, Be sure discipline is developmentally
age-appropriate. Abstract, cognitive reasoning
mean little to a child younger than 6 years.
If trying to stop a young child from hitting another,
don’t expect the child to understand how the other
feels.
Best application of discipline would be “time out.”
E. Attachment and loss
In childhood
A.Bowlby postulates three phases of response to
prolonged separation of children aged 7 months to
5 years
b. Psychological upset is more easily reversed in
stages of protest or despair than after detachment
has set in.
c.
Because
separation
has
behavioral
consequences, pediatric hospitalization must take
it into account through provision of parental
contact.
In adults
Adults who are bereaved or are mourning the loss
of a loved one also go through a series of phases.
b. Initial phase (protest, acute disbelief)
Lasts several weeks
Weeping
Hostility and protest
c. Intermediate phase (grief, disorganization)
d. Recovery (or reorganization) phase.
➢
➢
➢
➢
Be sure who your patient is.
Never lie
Accept the health beliefs of your patient.
Accept patients’ religious beliefs and
participate, if possible
➢ Anything that increases communication is
good
➢ Be an advocate for the patient.
➢ The key is not so much what you do, but HOW
you do it.
LEARNING AND BEHAVIOR
MODIFICATION-4
ABUSE
f. Clinical signs:
⚫ Broken bones in first year of life.
⚫ Sexually transmitted disease (STD) in young
children
⚫ 92% of injuries are soft tissue injuries(bruises,
burns, lacerations)
⚫ 5% have no physical signs.
⚫ Nonaccidental burns have a particularly poor
prognosis.They are associated with death or
foster home placement,If burn is on arms and
hands, it was likely an accident, if burn is on
arms but not hands, it is more likely abuse.
⚫ Shaken baby syndrome: look for broken blood
vessels in eyes
PHYSICIAN-PATIENT-3
General
Rules
about
physician-patient
relationship
➢ The patient is number one.
➢ Always respond to the patient
➢ Tell the patient everything
➢ Work on long-term relationships, not just
short-term problems.
➢ Listening is better than talking.
➢ Negotiate rather than order
➢ Trust must be built, not assumed.
➢ Admit to the patient when you have made a
mistake.
➢ Never “pass off” a patient to someone else.
➢ Express empathy, give control
➢ Agree on the problem before moving to a
solution
➢ Understand what the patient is talking about
before intervening
➢ Patients do not get to select inappropriate
treatments
The behaviorist definition of learning:
a relatively permanent change in behavior, not
due to fatigue, drugs, or maturation.
Two main types :
classic conditioning
operant or instrumental conditioning
classic conditioning
Classic conditioning is
defined as a conditioned
response to a neutral
stimulus after having
been paired repeatedly
with an unconditioned
stimulus,this response is
involuntary.
➢ The
pavlovian
experiment paired
the ringing of a bell
with the bringing of
food
so
that,eventually,the
sound of the bell
elicited
the
salivatory
response,which
previously occurred
only with the sight of
the food
➢ for
example,a
patient
receives
chemotherapy
(UCS),which induces
nausea(UCR),Eventu
ally,the sights and
sounds
of
the
hosiptal
alone(CS)elicit
nausea (now a CR).
Operant
operant conditioning is a
form
of
learning
described
by
many
behaviorists in which a
response increases in
frequency as a result of
its being followed by
reinforcement. To put it
more simply, a response
that is followed by a
reinforcing stimulus is
more likely to occur
again.
⚫ In
the
Skinner
experiment,pressing
a lever resulting in
the
delivery
of
food.After receiving
food,the bar pressing
behavior
increased.Because it
changed behavior,the
food is a reinforcing
event.
1.Reinforcer：there are
stimuli that increase the
probability of the
response occurring again.
Any
stimulus
is
a
reinforcer if it increases
1. a natural relationship
must exist between a
stimulus, such as an
object or an event, and a
reaction.
2.the stimulus that elicits
the reaction is repeated
paired with a neutral
stimulus, typically for
several
trials.
The
outcome is that the
previously
neutral
stimulus will, on its own,
elicit the conditioned
reaction
3.Stimulus
generalization:
an
organism's tendency to
respond to a similar
stimuli with the similar
response.
4.Extinction:
after
learning has occurred,
removal of the pairing
between the UCS and the
CS results in a decreased
probability
that
the
conditioned response will
be made.
the probability
of a response.
2.Reinforcement: this is
the act of following a
response
with
a
reinforcer.
3. Punishment: is used to
reduce an undesired
behavior.
4.Extinction ：
refers to the removal
of a reinforcer, resulting
in
Lower
response
frequency
and
strength.occurs when a
previously
reinforced
behavior is no longer
reinforced
with either positive or
negative reinforcement.
Types of reinforcement
a.Positive reinforcement：
occurs when a token or reward is given to
strengthen a desired behavior.
b.Negative reinforcement: also strengthens a
behavior, but it does so by removing something
that is unwanted.
Types of punishment
a.Positive punishment：
occurs when we introduce something to stop
an unwanted behavior.
b.Negative punishment：
when we take something away after an
undesirable behavior occurs.
Reinforcement schedules：
rules that control the delivery of reinforcement
⚫ Two types：
⚫ a. Continuous reinforcement: every response
is
followed
by
a
reinforcement
i:Results
in
fast
learning(acquisitions)
ii:Results
in
fast
extinction
when
reinforcement is stopped.
gave a chocolate every time he completes his math
homework
⚫ b. Intermittent (or partial) reinforcement: not
every response is reinforced
◼ i.Learning is slower
◼ ii.Responser is harder to extinguish
Four types
⚫ Fixed ratio schedule
Fixed ratio schedule delivers reinforcement after a
fixed number of responses.
Produces high response rate
Rewards a set of behaviors rather than a single
behavior
⚫ Fixed interval schedule
delivers reinforcement after a fixed period of
time elapses.
⚫ Variable ratio schedule
delivers reinforcement after a changing number of
responses.
⚫ Variable interval schedule
delivers reinforcement after a variable amount of
time has passed.
Therapy/modificatio
n
based on classic
conditioning
1.systematic
desensitization
⚫ often used to
treat anxiety and
phobias
⚫ Based on the
counter
conditioning or
reciprocal
Therapy/modification
based
on
operant
conditioning
1.Shaping (or successive
approximations)
⚫ achieves final target
behavior
by
reinforcing successive
approximations of the
desired responses
⚫ Reinforcement
is
gradually modified to
move behaviors from
inhibition
of
anxiety responses
⚫ when the person
is relaxed in the
presence of the
feared
stimulus,objectiv
ely,there is no
more phobia
⚫ note that this
works
by
replacing anxiety
with
relaxation,an
incompatible
response
2.exposure
⚫ simple
phobia
can sometimes
be treated by
forced exposure
to the feared
object
⚫ exposing
abruptly
and
directly to the
fear-evoking
stimulus itself
⚫ exposure
maintain
until
fear response is
extinguished
3.Aversive
conditioning
⚫ occurs when a
stimulus
that
produces deviant
behavior is paired
with an aversive
stimulus
⚫ key properties of
the
original
stimulus
are
changed
⚫ Used
in
the
treatment
of
alcoholism
the more general to
the specific responses
desire
2.Extinction
Discontinuing
the
reinforcement that is
maintaining an undesired
3.Stimulus control
sometimes stimuli
inadvertently
acquire
control
over
behavior.when this is
true,removal
of
that
stimulus can extinguish
the response
4.Biofeedback(neurofeed
back)
⚫ using
external
feedback to modify
internal
physiologic
states
⚫ used to be thought
that certain functions
of the autonomic
nervous system(heart
rate,blood
pressure,body
temperture)were
beyond the deliberate
control
of
a
person.biofeedback
involves providing the
person
with
information about his
internal responses to
stimuli and methods
to control and/or
modify them.
⚫ biofeedback works by
means
of
trial-and-error
learning and requires
repeated practice to
be effective
5.Fading
Father of classical- ivan pavlov
Father of operant- B.f skinner
DEFENSE MECHANISM-5
ID
➢ An unconscious part of your personality
➢ Childish and impulsive part
➢ Doesn't really think about the consequences
➢ Instinctive urges，sex，aggression，and other
➢ Primary process
➢ Try to increase pleasure and decrease pain
SUPER-EGO
➢ Conscience
➢ Super judgmental and moralizing childish and
impulsive part
➢ Behave in a socially appropriate way
EGO
➢ Rational and language-based executors liking
to reality
➢ Discern what is right or wrong based on
context
Defense mechanisms
➢ Defense mechanisms are techniques the
ego uses to avoid feelings of fear, uncertainty,
and shame.
➢ Ego attempt to resolve the conflict between Id
and Superego
➢ Operate in unconscious level
➢ It deny or distort reality in some way
Somatization
Psychic derivatives are converted into bodily
symptoms.
Feelings are manifest as physical symptoms
rather than psychological distress.
Doctor will rarely find a physical explanation for
the person’s symptoms
ANXIETY
Displacement
Changing the target of an emotion or drive, while
the person having the feeling remains the same
Allows the individual to act out their emotions in a
way that reduces the chances of negative
repercussions
A woman is berated by her boss ---yells at her
waitress over a small mistake on her order.
REPRESSION
Keeping certain thoughts, feelings, or urges out of
conscious awareness.
The goal is to prevent or minimize feelings of
anxiety.
Both a protective function, but can also be harmful
A person having no recollection of the abuse
suffered during childhood
Isolation of affect
Individual deals with emotional conflict or internal
or external stressors by the separation of ideas
from the feelings originally associated with them
A child who has been beaten discusses the
beatings without any display of emotions.
Intellectualization
Affect is stripped away and replaced by an
excessive use of intellectual processes.
Cognition replaces affect.The intellectual content is
academically, but not humanly, relevant.
A college going student who loses her father
worries about getting the right venue for her
father’s post-funeral gathering.
Acting out
Massive emotional or behavioral outburst to cover
up underlying feeling or idea. Strong action or
emotions to cover up unacceptable emotions.
For adolescents,substance abuse, overeating, or
getting into fights are “strong” actions that cover
up underlying feelings of vulnerability.
Rationalization
Rational explanations are used to justify attitudes,
beliefs, or behaviors that are unacceptable.
A person evades paying taxes and then rationalizes
it by talking about how the government wastes
money (and how it is better for people to keep
what they can).
Reaction formation
An unacceptable impulse is transformed into its
opposite.
Excessive over-reaction can often be a sign of
reaction formation.
A particular fetish feel is shameful, they condemn
fetish in order to demonstrate to others that they
are 'normal.'
A person who is angry with a colleague actually
ends up being particularly courteous and friendly
towards them
UNDOING
Trying to reverse or undo your feeling by doing
something that indicates the opposite.
When asked to recommend a friend for a job, a
man makes derogatory comments which prevent
the friend's getting the position; a few days later,
the man drops in to see his friend and brings him a
small gift. OCD
Passive-aggressive
Non performance or poor performance after
setting up the expectation of performance.
Regarded as a passive (indirect) expression of
hostility
The feelings of hostility are unconscious, and the
person using the defense is generally unaware of
them.
Student agrees to share class notes but goes home
without sharing them
Dissociation
Separates self from one's experience.
Third person rather than first person experience.
The facts of the events are accepted, but the self is
protected from the full impact of the experience.
A boy was involved in a very serious car
accident--his memory has frozen that memory.
Psychologic Health and Testing-6
TYPE-A, cluster of behavioral traits that has been
associated with increased prevalence and
incidence of coronary heart disease.
One major prospective study has shown that the
Type A behavior pattern is associated with a
twofold increase in incidence of coronary heart
disease, even after controlling for the major risk
factors (systolic blood pressure, cigarette smoking,
cholesterol).
Stressful life events: Holmes and Rahe scale used
to quantify stressful life events
IQ: a general estimate of the functional capacities
of the person
➢ Scaling intelligence: calculating an intelligence
quotient
➢ Mental age method
➢ Mental age (MA)=median test score for a given
age
➢ Chronological age (CA)=actual age of the
person taking the test
➢ Formula: (MA/CA) X 100 =IQ score
Commonly used IQ tests
a. Wechsler Adult Intelligence Scale, Revised
(WAIS-R) is for adults, aged 17 and older.
b. Wechsler Intelligence Scale for Children, Revised
(WISC-R) is for children aged 6 to 17.
c. Wechsler Preschool and Primary Scale of
Intelligence (WPPSI) is for children aged 4 to 6.
d. Stanford-Binet Scale is the first formal IQ test
(1905) and is used for children aged 2 to
18.Today,it's most useful with children younger
than 6, the impaired, or the very bright.
There are two types of objective personality tests:
⚫ Criterion referenced
Results are given meaning by comparing them with
a preset standard.
⚫ Norm referenced
Results are given meaning by comparing them with
a normative group.
High or low scores indicate deviation from that
group.
Minnesota Multiphasic Personality Inventory
(MMPI) revised 1989
Projective tests Classic examples
➢ Rorschach Inkblot Test
Major projective test .
10 inkblots, five in color and five not
Exner scoring method gives good reliability
➢ Thematic A perception Test (TAT)
Evaluates the conflicts, drives, motives, and
emotions that may be unconscious to the
individual
➢ Sentence Completion Test
Patient is asked to complete a set of sentence
stems with the first thing that comes to mind
Responses are scored for fears, desires, aspirations,
relationships
➢ Projective drawings
Patient given a sheet of paper and asked to draw a
house, a tree, a person, a family, or some other
subject
Neuropsychologic Tests
➢ Halsted-Reitan Battery
Tests for presence and localization of brain
dysfunction
Consists of five basic tests:
◼ category test,
◼ tactual performance test,
◼ Rhythm test,
◼ speech sounds perceptiontest,
◼ finger oscillation test.
➢ Luria Nebraska Battery
Tests level of impairment and functioning
Subscales: motor, rhythm, tactile, visual-spatial,
receptive speech, expressive speech, writing,
reading, arithmetic, amnestic, intellectual, right
and left hemisphere function
➢ Bender Visual Motor Gestalt Test
Screens for brain dysfunction
Nine designs are presented to the patient and
copied by him. The patient is then asked to recall
as many designs as he or she can
➢ Benton Visual Retention Test
Spatial construction, drawing task
10 designs that the patient copies as presented or
from memory
➢ Wechsler Memory Scale
Assess memory impairment
Subcomponents: recall of current and past
information, orientation, attention, concentration,
memory for story details, memory designs, and
learning
ORGANIC DISORDERS-7
Delirium:
acute onset, impaired cognitive functioning,
fluctuating and brief, reversible
Dementia:
loss of cognitive abilities, impaired social
functioning, loss of memory,
personality change; only 15% reversible; may
be progressive or static
Ten warning signs of Alzheimer disease
Memory loss that effects job skills
Difficulty performing familiar tasks
Problems with language
Disorientation to time and place
Poor judgment
Problems with abstract thought
Misplacing things
Changes in mood or behavior
Changes in personality
Loss of initiative
ALZHEIMER
➢ Most common, represents 65% of dementias
in patients older than 65
➢ Prevalence increases with age
➢ Women greater than men
➢ Family history confers greater risk
➢ Less risk for higher educated
➢ Linked to chromosomes 1 and 14 (mutations),
19 (apolipoprotein E),
➢ 21 (linked to Down syndrome)
PATHOLOGY
➢ Diffuse atrophy of the brain on CT or MRI
➢ Flattened cortical sulci
➢ Enlarged cerebral ventricles
➢ Deficient blood flow in parietal lobes
correlated with cognitive decline
➢ Reduction in choline acetyl transferase
➢ Reduced metabolism in temporal and parietal
lobes.
➢ Accumulation of amyloid beta-peptides
(protein fragment)
➢ Senile plaques
➢ Neurofibrillary tangles
➢ Granulovascular degeneration of the neurons
➢ Anatomic changes: to amygdala, hippocampus,
cortex, basal forebrain
TREATMENT
Supportive
Symptomatic
Reduce environmental changes
Donepezil hydrochloride
PARKINSONS
➢ Decreased dopamine in substantia nigra
➢ Annual prevalence is 200 in 100,000
➢ Resting tremor;Pill-rolling remor;
➢ Bradykinesia;
➢ Cogwheel rigidity;Masklike facies;Shuffling gait
➢ 40% to 80% develop dementia
➢ Depression is common;
➢ Treat
with
antidepressants
or
electroconvulsive therapy (ECT)
Treatment:
L-dopa or deprenyl
Vascular dementia
decremental or patchy deterioration in cognitive
functioning due to severe cerebrovascular disease
Most prevalent between ages 60 and 70
Appears earlier than does DAT
Men>women
Hypertension is predisposing factor
15% of all dementias in the elderly
Can often find some lateralizing neurologic signs
Treatment of underlying condition (hypertension,
diabetes mellitus, hyperlipidemia)
General measures for dementia
➢ Left hemisphere
Language
Dominant in 97% of population, 60% to 70% in
left-handed persons
Calculation-type problem solving
Stroke damage to left is more likely to lead to
depression
Larger in size than is the right side and processes
information faster
➢ Right hemisphere
Perception, artistic, visual-spatial
Activated for intuition-type problem solving
Stroke damage to right is more likely to lead to
apathy and indifference
Prosody resides here.
More 5-HT receptors
➢ FRONTAL CORTEX
Global orientation
Key functions
Speech
Critical to personality
Abstract thought
Memory and higher-order mental functions
Capacity to initiate and stop tasks
Concentration
Lesions of dorsal prefrontal cortex:
Apathy
Decreased drive, initiative
Poor grooming
Decreased attention
Poor ability to think abstractly
Broca aphasia (if in dominant hemisphere)
➢ Temporal cortex
Language; Memory; Emotion
Lesions stem from stroke, tumor, and trauma;
herpes virus CNS infections often affect temporal
cortex
Bilateral lesions: dementia
Lesions of the rostal (front) left temporal lobe:
deficits in recall or learning of proper names
Lesions of dominant lobe:
Euphoria
Auditory hallucinations
Delusions
Thought disorders
Poor verbal comprehension (Wernicke)
Lesions of non-dominant lobe:
Dysphoria
Irritability
Decreased visual and musical ability
➢ PARIETAL CORTEX
Key function: intellectual processing of sensory
information
Left: verbal processing (dominant)
Right: visual-spatial processing (nondominant)
Lesions of dominant lobe: Gerstmann syndrome
Agraphia
Acalculia
Finger agnosia
Right-left disorientation
Dysfunctions in this area account for aproportion
of learning disabilities
Lesions of nondominant lobe:
Denial of illness (anosognosia)
Construction apraxia (difficulty outlining objects)
Neglect of the opposite side (e.g., not washing or
dressing opposite side of body)
➢ OCCIPITAL CORTEX
Visual input
Recall of objects, scenes, and distances; PET scans
show activity in this area during recall of visual
images
Destruction: cortical blindness
Bilateral occlusion of posterior cerebral arteries:
Anton syndrome
Cortical blindness
Denial of blindness
Cannot see camouflaged objects
Occipital epileptic foci: visual hallucinations
SLEEP AND DISORDERS-8
NREM
➢ Divided into four stages on the basis of EEG
➢ The phase of sleep that is considered the quiet
or restful phase. During the three stages of
NREM sleep, a person falls asleep and then
moves from a light sleep into a deep sleep.
This is when a person's brain activity,
breathing, and heart rate slow down, body
temperature drops, muscles relax, and eye
movements stop.
➢ NREM sleep alternates with REM sleep
throughout the sleep period and is
characterized by:
◼ Slowing of EEG rhythm
◼ Higher muscle tone
◼ Absence of eye movements
◼ Absence of though-mental activity
REM
The phase of sleep in which most dreams occur.
During REM sleep, a person's brain activity,
breathing, heart rate, and blood pressure increase,
and the eyes move rapidly while closed. The
muscles in the arms and legs become temporarily
unable to move.
⚫ An aroused EEG pattern
⚫ Sexual arousal
⚫ Saccadic eye movements
⚫ laborate visual imagery (dreaming)
⚫ Associated with pons
SLEEP ARCHITECTURE
⚫ SLEEP LATENCY
Period between trying to sleep until sleep onset.
Insomniacs have long sleep latencies.
⚫ REM LATENCY
Period between falling asleep until first REM. In the
average adult, REM latency is 90 minutes.
⚫ SLEEP DEPRIVATION
The cerebral cortex
The rest of the body
shows the greatest seems
relatively
effects
of
sleep unaffected by sleep
deprivation but has the deprivation.
Physical
capacity to cope with restitution of the body
one night’s sleep loss.
comes
from
the
immobility that is a
by-product of sleep, not
from sleep itself.
⚫ Physiological function of sleep
REM:
memory consolidation
provides cerebral stimulation
prolonging of sleep
NREM
Promote growth :human growth hormone
Allaying tiredness
Serotonin (5-HT) rises
TSH inhibits
Initial REM cycle: approximately 90 minutes.
REM: 20% of sleep time
REM percentage remains constant(20%) up to
around 80 years of age
Total
sleeptime/24-hour
period
decreases
gradually with age
SLEEP DISRODERS
➢ Insomnia
⚫ Symptoms
Sleep disturbance:
Difficulty falling asleep Difficulty
Staying asleep throughout the night
Waking up too early in the morning
⚫
Daytime symptoms:
Daytime sleepiness
Low energy
Emotional problems
⚫
Possible reasons
Age
Sex
Emotional distress
Medical health problems: hypnotic
medication abuse
Disrupt Sleep architecture
⚫ Treatment
Behavior therapy:
Lifestyle changes
Medicines:
Triazolam (Halcion) is quick.
Zolpidem (new)
Nonbenzodiazepine (take 5 to 7 days only)
➢ Sleep apnea syndrome
a. Subtypes
Obstructive (upper airway) sleep apnea
Central (diaphragmatic) sleep apnea
Mixed sleep apnea
b. Possible reasons
Obstructive sleep apnea
Central sleep apnea
Being male
Being older
Family history
Use of alcohol，sedatives or tranquilizers.
Smoking
Nasal congestion
c. Complications
Daytime fatigue
High blood pressure or heart problems.
Type 2 diabetes
Metabolic syndrome.
Complications with medications and surgery
Liver problems.
Sleep-deprived partners
d.Treatment
Weight loss
Respiratory stimulants for purely central apnea.
Therapeutic efficacynot proven
Continuous
positive
airway
pressure
Most likely medical intervention
For severe obstructive and mixed apnea
tonsillectomy or tracheostomy
➢ Narcolepsy
a.The narcoleptic tetrad:
Sleep attacks and excessive daytime sleepiness
（EDS）
Cataplexy
Hypnagogic hallucinations
Sleep paralysis
b. Treatment
i.The pathophysiology is not well understood.
ii.CNS stimulants control the EDS
(methylphenidate,dextroamphetamine).
iii. Tricyclic antidepressants control the cataplexy
(imipramine)
iv. Modafinil (new): a nonamphetamine
alternative to CNS stimulants
E. Chemical and Psychiatric Correlates of Sleep
1. Dopamine
a. Any pharmacology that increase dopamine
increases wakefulness.
b. Dopamine blockers increase sleep somewhat.
2. Benzodiazepines
a. Limited decrease in REM and Stage 4 sleep,
much less than previously thought
b. Little rebound effect
c. Chronic use increases sleep latency
3. Moderate alcohol consumption
Early sleep onset
Increased wakefulness during the second half of
the night
4. Alcohol intoxication
a. Decrease REM
b. REM rebound (with nightmares) during
withdrawal
5. Barbiturates
a. Decreases REM
b. REM rebound, including nightmares, follows
stoppage of chronic use.
6. Major depression
a. Increase REM
b. Decreases REM latency
c. Decreased Stages 4 and 3 sleep
d. Increased sleep in multiple periods over 24
hours.
e. Early morning waking
f. Diurnal improvement
g. Sleep deprivation gives 60% remission from
symptoms
h. People who characteristically get a lot of REM
are more susceptible to onset of depression
DIAGNOSTIC AND STATISTIC
MANUAL-9
Axis I: Clinical disorders
➢ including schizophrenic, affective, anxiety, and
somatoform disorders. Also includes anorexia
nervosa, bulimia nervosa, sexual disorders,
sleep disorders, and autism
➢ including primary support group, social
occupation, education, housing, economics,
health care services, and legal issues
Axis II: Personality disorders and mental
retardation
Global assessment of functioning (GAF), scored on
a descending scale of 100 to 1, where 100
represents superior functioning, 50 represents
serious symptoms, and 10 represents persistent
danger of hurting self or others
Axis III: Physical conditions and disorders
Axis IV : Psychosocial and environmental
problems
Axis V: Global assessment of functioning (GAF)
Disorder usually diagnosed in childhood
Intellectual disability
Fetal alcohol syndrome (FAS) most common known
cause
Down and fragile-X syndromes most common
genetic causes
Autism spectrum disorders
a. Formerly pervasive development disorders
b. Usually diagnosed before the age of 3
c. Clinical signs
i.Problems with reciprocal social interaction,
decreased repetoire of activities and interests
ii. Abnormal or delayed language development,
impairment in verbal
and nonverbal
communication
iii. No separation anxiety
iv. Oblivious to external world
v. Fails to assume anticipatory posture, shrink
from touch
vi. Pronoun reversal
vii. Preference for inanimate objects
viii. Stereotyped behavior and interests
d. Male:female ratio=4: 1
e. Linked to chromosome 15, 11
f. Occurs in 1 of every 150 births
g. Monozygotic concordance greater than dizygotic
concordance
h. 80% have IQs below 70.
i. Potential causes
Association with prenatal and perinatal injury, e.g.,
rubella in first trimester
Failure of apoptosis (normal pruning of neural
circuits)
j.Treatment: behavioral techniques (shaping)
Attention deficit hyperactivity disorder (ADHD)
a.Problems
with
inattention,
impulsivity,
hyperactivity
b.Male to female ratio is 10:1.
c. AssocIated with lower doparmine levels
d.Treatment:methylphenidate,
dextroamphetamine, atomoxemotine
SCHIZOPHRENIA
⚫ Criteria
1. Bizarre delusions
Delusions: false beliefs not shared by culture .
Illusions: misperception of real stimuli .
Hallucinations: sensory impression, no stimuli
2. Auditory hallucinations (in 75%) .
Impaired concentration .
Note: not visual hallucinations
3. Blunted affect
4. Loose associations
5. Deficiency in reality testing, distorted perception;
impaired functioning overall
6. Disturbances in behavior and form and content
of language and thought
7. ﹥6 months in duration
⚫ b. Differential
1. Schizophreniform:
If symptoms less than 6 months
2. Brief psychotic disorder
If symptoms ﹥1 and ﹤ 30 days .
⚫ c. Epidemiology
1. Onset: male, age 15-24; female, age 25-34
2. Prevalence: 1% of population cross-culturally;
however, less chronic and severe in developing
countries than in developed countries
3. Downward drift to low SES
4. 50% patients attempt suicide, 10% succeed
5. Over 50% of schizophrenics do not live with their
families, nor are they institutionalized
⚫ d. Genetic contribution
1. Rates for monozygotic twins reared apart=rates
for MZ twins raised together (47%)
2. Dizygotic concordance: 13%
3. If two schizophrenic parents: 40% incidence
4. If one parent or one sibling: 12%
5. Heritability index: (MZ - DZ)/(100- DZ)
=proportion of conditions due to genetic factors
6. Risk in biologic relatives 10 times general
population (i.e., 10%)
2. Clinical presentation
⚫ A. Severity
DSM-5 does not include sub-types of schizophrenia.
Rather, current severity is documented from a low
of 0 to a high of 4 for the following 5 symptoms:
delusions
hallucinations
disorganized speech
abnormal psycho-motor activity
negative symptoms
⚫ B. Paranoid symptoms
Delusions of persecution or grandeur
Often accompanied by hallucinations (voices)
⚫ C. Catatonic symptoms
Complete stupor or may have pronounced
decrease in spontaneous movements
May be mute .
Often negativism,echopraxia,automatic obedience
Rigidity of posture; can be left standing or sitting in
awkward positions for long periods of time
Alternatively,can be excited and evidence extreme
motor agitation .
Incoherent and often violent or destructive
In their excitement, can hurt themselves,or
collapse in exhaustion
Repetitious, stereotyped behaviors
a. Positive symptoms (Type I)
1. What schizophrenic persons have that normals
do not,e.g.,delusions, hallucinations, bizarre
behavior
2.Associated with dopamine receptors
b. Negative symptoms (Type II)
1. What normals have,that schizophrenics do not,
e.g.,flaT affect, motor retardation, apathy, mutism
2. Associated with muscarinic receptors
PREDICTORS OF GOOD PROGNOSIS
a. Paranoid or catatonic
b. Late onset (female)
c. Quick onset
d. Positive symptoms
e. No family history of schizophrenia
f. Family history of mood disorder
g. Absence of structural brain abnormalities
The dopamine hypothesis
⚫ The effectiveness of neuroleptic medications
in ameliorating the symptoms of schizophrenia
⚫ The correlation of clinical efficacy with drug
potency in dopamine receptor antagonists
⚫ Findings of increased dopamine receptor
sensitivity in postmortem studies
⚫ Positron emission tomographic (PET) scan
studies of schizophrenic patients compared
with controls
Role of serotonin (5-HT)
⚫ Genes
involved
in
serotoninergic
neurotransmission are implicated on the
pathogenesis of schizophrenia.
⚫
Newer antipsychotics (e.g., clozapine) have
high affinity for serotonin receptors.
⚫ Serotonin rises when dopamine falls in some
areas of the brain.
Role of glutamate
⚫ Major neurotransmitter in pathways key to
schizophrenic symptoms
⚫ N-methyl-D-aspartate (NMDA) receptors .
Regulates brain development and controls
apoptosis, Phencyclidine and ketamine block the
NMDA channel: can create positive and negative
psychotic symptoms identical to schizophrenia
⚫ 2-(aminomethyl)
phenylacetic
acid
(AMPA)receptors .
Attention and information processing deficits
⚫ Smooth pursuit eye movement (SPEM)
The capacity of the eye to follow a slow moving
target is impaired in schizophrenic patients.
⚫ Backward masking
Two images shown in rapid succession
If shown one-half second apart, later image
"masks" the former for the schizophrenic
For normals, less than one-fourth second is
necessary for effect
⚫ Event-related potentials (ERP)
Schizophrenia is associated with diminished
amplitude of the auditory P300 ERP.
Abnormalities may be associated with impaired
selective attention; therefore, schizophrenic
patients do not conduct involuntary information
processing nOrmally.
⚫ Prefrontal cortical (PFC) impairment
⚫ Faced with a cognitive task, increased
activity is found in the prefrontal cortex of
normal individuals.
⚫ Schizophrenics
show
decreased
physiologic activity in prefrontal lobes
when faced with these tasks.
⚫ Impaired performance on the Wisconsin
Card Sort (WCST), a test sensitive to
prefrontal dysfunction
⚫ Clinical profile has similarities with
patients with frontal lobe injury (e.g.,
cognitive in
flexibility,problem-solving
difficulties, and apathy).
Cortical abnormalities
⚫ Larger ventricle size and ventricular brain
ratios (VBRs)
⚫ Cortical atrophy
⚫ Smaller frontal lobes
⚫ Atrophy of temporal lobes
⚫
Association with specific clinical and
cognitive correlates, including deficit
symptoms, cognitive impairment, and
poor outcome
⚫ Correlation between ventricle size, type,
and prognosis of illness
⚫ Subtle anomalies in limbic structures
⚫ Limbic system seen as the site of the
primary pathology for schizophrenia
⚫ Changes
in
hippocampus,
parahippocampal gyrus, entorhinal cortex,
amygdala, cingulate gyrus
⚫ Smaller volume of left hippocampus and
amygdala
⚫ also found in high-risk, nonsymptomatic
patients
⚫ Changes in parts of basal ganglia,
thalamus, cortex, corpus callosum, and
brainstem neurotransmitter systems
⚫ Loss of inhibitory neurons in second layer
of anterior cingulate gyrus
LONG TERM COURSE
Antipsychotic medications reduce acute (positive)
symptoms in 75% versus 25% with placebo
Relapse rates
40% in 2 years if on medication
80% in 2 years if off medication
Prognosis
33% of patients lead normal lives.
33% of patients experience symptoms but function
in society.
33% require frequent hospitalizations
If no first-year relapse and medications are taken,
10% relapse thereafter
Dysthymia (nonpsychotic depression)
Depressed mood
Loss of interest or pleasure
Chronic (at least 2 years)
Not severe enough for hospitalization
Life time prevalence 45 in 1,000
30% to 50% of alcoholics have secondary
depression.
May be associated with:
Increased or decreased appetite
Increased or decreased sleep .
Fatigue
Decreased self-esteem
Hopelessness
Lowered concentration
Cyclothymia (nonpsychotic bipolar)
Alternating states
Chronic
Often not recognized by the person (ego-syntonic)
Lifetime prevalence <1%
Seasonal affective disorder (SAD)
Depressive symptoms during winter months
Winter has shortest days/least amount of light
"Atypical"symptoms:
Increased sleep
Increased appetite
Decreased energy
Caused by abnormal melatonin metabolism
Treat with bright light therapy (not melatonin
tablets)
Unipolar disorder (major depression)
⚫ Symptoms for at least 2 weeks
⚫ Must represent a change from previous
functioning
⚫ Maybe associated with: Anhedonia ,
No motivation ,Feelings of worthlessness,
Decreased concentration,Weight loss or
gain ,Depressed mood,Recurrent thoughts,
Insomnia or hypersomnia, Psychomotor
agitation
OR
Retardation,Somatic
complaints Loss of sex drive,Delusions or
hallucinations (if mood congruent) .
⚫ Diurnal improvement as day progresses
⚫ Suicide:
⚫ 60% of depressed patients have suicidal
ideation.
⚫ 15% of depressed patients die by suicide.
⚫ Biologic correlates
⚫ PET scans show abnormally high glucose
metabolism in amygdala of depressed
people .
⚫ Smaller hippocampus, atrophy greater if
depressed longer .
⚫ Linked to abnormally high levels of
glucocorticoids
⚫ Sleep correlates
Increased REM in first half of sleep .
Decreased REM latency .
Decreased Stage 4 sleep .
Increased REM time overall
Early morning waking
Bipolar disorder (manic-depression)
Symptoms of major depression plus symptoms of
mania: a period of abnormal and persistent
elevated, expansive, or irritable mood
Alternates between depression and mania
Subtypes
(a) Bipolar I: mania more prominent
(b) Bipolar II: recurrent depressive episodes plus
hypomanic episodes
(c) If alternates within 48-72 hours, called "rapid
cycling bipolar disorder"
Manic symptoms
Increased self-esteem or grandiosity .
Low frustration tolerance .
Decreased need for sleep .
Flight of ideas .
Excessive involvement in activities
Weight loss and anorexia .
Erratic and uninhibited behavior
Increased libido
Neurochemical changes .
Increased norepinephrine (NE) .
Increased serotonin
Slight increase in dopamine
Sleep correlates .
Multiple awakenings
Markedly decreased sleep time
Ppt1 rehab introduction
Definition of rehab:
 Rehab med is an important branch of modern medicine.
 Restore ability lost :associated with disease, injury and disability
 The fourth medicine: prevention, clinical medicine ,health care and rehabilitation constitute a
comprehensive medicine.
Concept of rehab

Indications: Dysfunction or disability, including physical, psychological and social
dysfunction

Treatment measures: Various methods (including medical, psychological
,educational,social,vocational,engineering interventions ), to stimulate the potential ability of the
body to recover.

ultimate Goals: To improve the quality of life, enabling patients to return to society, community,
work place and family.

Although the pathological basis can not be eliminated, body function can be considerably
improved after rehabilitation.
What is a physiatrist?









Specialize in diagnosing and treating pain.
To an extend Restore lost function resulting from injury, illness or disability.
Treat the whole person not just the problem area
Lead a team of medical professionals
Provide no surgical treatment
Explain medical problem and treatment plan
Focus on treatment and prevention
They are nerve bone and muscle experts
Physiatrist have completed training in the medical specialty physical medicine and
rehabilitation (PM&R).
What does a multidisciplinary group consist of?










Physiatrist
Pt physical therapist
St speech therapist
Ot occupational therapist
Psychologist
Prosthetist and orthotist
Recreational therapist rt
Social worker sw
Nurse
Volunteer
What does a rehab program consist of?






Evaluation: we evaluate the disease or injury, its location and type and the survival function
Goal setting: set short term, medium and long term goals,
Programming: work out on the table with help of ot pt st.
Implementation: no. of team start work separately
Revaluation: reevaluate the state of illness so the rehab plan and treatment can be adjusted
Disposition setting: must go home and return to work place ; a few go to nursing home
Definition of disability?
Defects of the body's anatomical structure
psychological dysfunction
physiological dysfunction
(It can’t comepletly be solved even after rehabilitation and training ) The state limit and hinder their
normal life, work and study
Levels of disability example:
Various cause
Stroke-hemiplegia---------- cant walk-------------- cant go to work or school
Impairment
Organ level damage
disability
individual capacity level
handicap
social skill level
What is ICF?
The International Classification of Functioning, Disability and Health, known more commonly as ICF,
provides a standard language and framework for the description of health and health-related states.
It is a classification of health and health-related domains . domains that help us to describe changes in
body function and structure, what a person with a health condition can do in a standard environment (their
level of capacity), as well as what they actually do in their usual environment (their level of performance).
These domains are classified from body, individual and societal perspectives by means of two lists: a list
of body functions and structure, and a list of domains of activity and participation. The ICF is divided into
two parts. Part 1 deals with function and disability, while part 2 deals with surrounding environmental
factors.
What is the technology of rehab medicine?

Physical therapy (PT)

Occupational therapy (OT)

Speech Therapy (ST)

Psychotherapy (PsT)

Rehabilitation Engineering (RE)

Traditional Chinese Medicine (TCM)
Ppt2 rehab evaluation
What is rehab eval. Definition?
Also known as rehab assessment, refers to the use of various eval methods to have a thorough
understanding of the function(organic, psychological, social and living) of patient, assessing the types,
region, severity, and prognosis of dysfunction.so that the doctor and therapist
may design a rehab
program and choose proper rehab therapy and determine the effect of therapy.
Classification of rehav eval:
1.evaluation of motor function:
(a) muscle tone: is the resistance of muscle to stretch or passive elongation. It helps to maintain body
posture and perform movement.
I.
Hypermyotonia: is increased resistance to a passive stretch and flex of a limb, the
limbs are usually stiff. It is called “spasticity (or spasm) ” if velocity-dependent, and
“rigidity” if non velocity-dependent.
Hypomyotonia： is decreased resistance to a passive stretch and flex of a limb, the
limbs are usually floppy. It is often seen in peripheral nerve disease and cerebellum
disease.
Dysmyotonia: is a prolonged involuntary movement disorder characterized by
twisting or writhing repetitive movements and increased muscle tone. It may arise
after injury, inflammation, poison and heredity.
II.
III.
Eval of muscle tone (muscle spasticity) is done by modified Ashworth scale:
Grade
0
eval. standard
No increase in muscle tone.
1
Slight increase in muscle tone, manifested by a catch-and- release or minimal
resistance at the end of the range when the affected part is moved in flexion or extension.
1+
Slight increase in muscle tone, manifested by a catch followed by minimal
resistance throughout the remainder (less than half) of the ROM.
2
More marked increase in muscle tone through most of the ROM, but affected part
3
Considerable increase in muscle tone, passive movement difficult.
easily moved.
4

Affected parts rigid in flexion and extension.ROM, range of motion.
(b) muscle strength assessment: Muscle strength refers to the maximal force a muscle
or muscle group can exert during a contraction. Note not to test Don’t test after fatigue, sport or a
full meal.and the unaffected side should be tested first. Factors affect strength : gender, age,
fatigue, pain, swelling, spasm.
Method of eval for muscle strength
I.
Manual muscle test scoring:
Grade
0
standard
no contraction
1
muscle flicker, but no movement
2
movement possible, but not against gravity
3
movement possible against gravity, but not against
resistance by the examiner
4
movement possible against some resistance by the
examiner
5
II.
Isokinetic muscle test
III.
Isometric muscle test
IV.
Isotonic muscle test
normal strength
(c) ROM(range of motion): Range of motion refers to the distance and direction a joint can
move to its full potential.classified as Active range of motion（AROM: the individual moves the joint
themselves. Passive range of motion(PROM): therapist or equipment moves the joint through range of
motion (no effort from patient). Factors affecting rom are arthritis, pain, swelling of tissue around joint,
muscle spasm, muscle strength imbalance, scarring.
Purpose of rom test are:

Find out degree of limited ROM

Analyze cause of limited ROM

Offer a reference for treatment

Reassess of ROM to determine if treatment is effective
Factors affecting rom test:
 Bad posture of patient or examiner

Incorrectly location of goniometer

Pain

Patient’s lacking of understanding and cooperation

Age, gender, occupation, etc.
(d) gait analysis: gait refers to a repetitive sequence of limb movements to safely advance the
human body forwards. Gait Analysis: is a method used to assess the way we walk to highlight
biomechanical abnormalities and help to guide rehabilitation therapy.
Purpose of gait analysis:

Find out the key factors to cause abnormal gait by biomechanics and kinetics methods

Offer a guide for rehabilitation assessment and treatment

Medical diagnostics

Determine if the treatment is effective
Gait cycle: refers to the period from the foot contacts with the ground to the next contact with
the same foot.it is divided into two parts:
Stance phase: (60%)
 Early stance: Initial contact: The point when the heel strikes the ground. Loading
response: Body weight transfer onto stance limb.

Mid-stance : The whole foot of the stance limb contacts with the floor and the
opposite foot is at the swing phase

Terminal stance : The period to push off with the limb to propel body forwards,
start from heel rise and end by toe off
Swing phase: (40%)

initial swing: Hip and knee flexion in order to achieve foot clearance and
advancing of the trailing limb.

Mid-swing: Hip flexion, knee extension and ankle dorsiflexion. The clearance is
also the main task.


Terminal swing: The end of the swing phase before heel strike.
Clearance is lower extremity rises off ground during swing phase to guarantee
body moving forward.
Factors affecting gait:
 Disorders of bone and joint：sports injuries, amputee, deformity of trunk、
hip、knee or ankle caused by operation, pain, joint contracture, etc.

neuromuscular disorders: such as stroke, TBI,
SCI, CP, Parkinsonism ,spasm, muscle weakness, etc.
how is gait analyzed?


Kinematics analysis: involves analyze of center of gravity, clearance mechanism, temporal
parameters test and segmental motion test.

Kinetic analysis: Kinetics analysis involves a study of internal and external forces involved
in motion, and concerns the study of joint moments and powers.
Dynamic electromyography: Activation and control of muscles rely on electrical impulses and
Measuring electrical activity of a contracting muscle can give indirect indication of muscle action.
Neurological gait disturbances:
1. Hemiplegia gait: Hemiplegia patient has his common patterns of spastic
hypermyotonia: flexor spasm patterns of upper extremity and extensor spasm patterns
of lower extremity (hip extension, knee extension and ankle plantar flexion). So
circumduction gait is required for foot clearance.
2. paraplegia gait: The consequence of lower-level of SCI-patient is weakness of legs and
foot drop subsequently. Compensation is achieved through increased knee plus hip
flexion to aid clearance. It is called steppage gait.
3. Gait of cerebral palsy (CP)：because of thigh adductor spasticity in patient with spastic
CP, severe hip adduction and medial rotation may interfere with gait. Knees and thighs
hitting or crossing like scissors when walking. It is called scissors gait.
4. Parkinsonian gait：rigidity is the main symptom of patients with Parkinson's disease.
So people with Parkinson's tend to take small shuffling steps (called festination) as if
hurrying forward to keep balance. They may have trouble starting to walk, and may
have difficulty stopping or making a turn.
(e) balance evaluation: balance is the ability to attain or maintain a posture.
Classification:

static balance： is defined as balance in which the body maintains equilibrium
for one posture (sitting balance, standing balance).

dynamic balance : dynamic balance is described as maintaining equilibrium
while the body is in motion or changing from one balanced posture to another.
How can we keep balance?

Base of support is the region bounded by body parts in contact with a support surface. The
standing BOS is the square including two feet and the region between them.

Limits of stability are defined as the maximum distance an individual is able to lean in any
direction without loss of balance or changing the base of support.
a.
Center of gravity
Purpose of balance eval:

Find if balance disorders exist

Analyze cause of balance disorders

Determine if treatment is necessary (drugs or rehabilitation)

Reassess to determine if the treatment is effective

Estimate fall risk
Activities of daily life (ADL):

Definition: activities of daily living (ADL) are the things we normally do in daily living
including any daily activity we perform for self-care (such as feeding ourselves, bathing, dressing,
grooming), work, homemaking, and leisure.

purpose: ADL evaluations help to determine how independent patients are and what skills they can
accomplish on their own, as well as to gauge how independent each individual can become after
intervention of rehabilitation.
BARTHEL INDEX SCORING:
Item of ADL
dependent
independent
minor help
major help
Feeding
10
5
Bathing
5
0
0
0
Grooming
5
0
0
0
Dressing
10
0
0
5
0
0
Bowels
10
Bladder
5
10
Using the toilet
Transfer to bed
5
10
15
0
0
0
5
0
0
0
10
5
0
(bed to chair and back)
Mobility
15
10
5
0
Stairs
10
5
0
0
Barthel Index scoring:
the total score is 100
>60
self care of living, independent
60~40 need minor help
40~20 need major help
<20
dependent
Ppt3 techniques of rehab med
SECTION 1 Physical therapy

therapeutic exercise:
Goals
a. Functional ability
b. Ability of ADL
c. Social participation
d. Quality of life
Principles
a. Prevent impairments
b. Improve, restore or enhance physical function
c. Prevent or reduce health-related risk factors
d. Optimize overall health status, fitness or sense of well-being
What are the main techniques of therapeutic exercise?
a. ROM training: the arc through which movement occurs at a joint or a series of joints.
Classifications are:
AROM-active range of motion, A-AROM-active-assistive range of motion, PROMpassive range of motion
b. Joint mobilization techniques: Graded oscillation techniques: Grades I and II are
primarily used for treating joints limited by pain. Grades III and IV are primarily used as
stretching maneuvers.
c. Muscle strength and Endurance exercise: Muscle strength refers to the maximum strength
that a muscle can produce when it contract. muscle endurance refers to the ability of a
muscle to carry out a particular task on an ongoing basis
d. Balance exercise
e. Neurophysiological therapy: Techniques were developed specifically for patients with
central nervous system impairment, particularly impairment resulting from an acquired
cortical lesion
NPT commonly used
• Bobath technique:
1.
2.
3.
4.
5.
Bobath handshake
Control of key points
Improvement of abnormal muscle tension by reflexive mechanism
Noumenon and skin irritation
Promoting technique
• Brunnstrom technique: The basic principle is the common movement of limbs after
stroke (intergenerational movement), the appearance of primitive postural reflex and joint
reaction, which exist normally in the early stage of exercise
• PNF (proprioceptive neuromuscular facilitation) technique: activate or raise the
largest number of motor unit stop articipate in the activity through body, skin and audiovisual stimulation to promote the recovery of neuromuscular muscle.
• Rood technique: emphasizes controlled sensory stimulation and uses mild mechanical
stimulation or skin surface temperature stimulation in a specific skin area to affect the
skin receptors in this area in order to obtain local promoting effect to induce purposeful
response
f.
Motor relearning program:
1. Upper extremity function
2. Oral facial function
3. From lie on your back to sit up by the bed
4. Sitting balance
5. Stand and sit
6. Standing balance
7. Walk
What does an exercise prescription consist of?
A complete exercise prescription should include 4 aspects:
a.
b.
c.
d.

type of exercise
exercise intensity
frequency of exercise
duration of exercise
physical agent modalities
what are the therapeutic effects of physical agent modalities?
• decrease pain
• decrease inflammation or swelling
• increase range of motion
• improve overall function
classification of physical agent modality:

Electricity
• Photo
• Magnetic
• Sound
• Heat
• Cold
• Water
• Etc.
What are the biological effects of low frequency pulse electrotherapy?
1. Excite neuromuscular tissue
2. Analgesic effect
3. Improve local blood circulation
Used for patients with stroke, hemiplegia, cerebral palsy.
What are the thermal effects of high frequency electrotherapy?
1. Improve the local blood circulation, anti-inflammatory and loose swelling
2. Analgesia
3. Improve immunity
4. Promote tissue growth and repair
5. Reduce muscle tone
Manipulative therapy
SECTION 2. Occupational therapy:
Definition of occupational therapy:
Occupational therapy(OT) is a patient-centered health profession concerned with promoting
health and well being through occupation. The primary goal of occupational therapy is to enable people to
participate in the activities of everyday life.
Occupational therapeutic technology?
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
ADL TRAINING
IMPAIRMENT ORIENTED TRAINING
TASK ORIENTED TRAINING
BILATERL TRAINING
MIRROR THERAPY
ACTION OBSERVATION THERAPY
REPEATEDLY TRAINING
PRESSURE SUIT MAKING
WHEELCHAIR PRESCRIPTION
ENVIROMENT TRANSFORATION
SECTION 3 speech and language
Aphasia definition:
refers to the acquired communication disorder in individuals who were previously capable of using
language appropriately. loss of oral and written expression, comprehension ability.
Classification of aphasia:






Fluent aphasia
Non-fluent aphasia
Global aphasia
Anomic aphasia
Primary progressive aphasia(PPA)
Cognitive communication disorders
What are the content of aphasia therapy?
 Visual communication therapy (VIC)
 Visual action therapy (VAT)
 Melodic intonation therapy (MIT)
 Functional communication treatment (FCT)
 Promoting aphasics' communicative effectiveness (PACE)
 Constraint-induced language therapy (CILT)
 Group speech therapy
Section 4 cognitive rehab
Cognitive disorders:
 attention disorder




memory disorder
perception disorder
executive ability disorder
etc.
section 5 swallowing:
dysphagia definition:
A process in which food cannot be safely and effectively transported to the stomach due to structural
and/or functional impairment of the jaw, lips, tongue, soft palate, throat, esophagus and other organs.
Purpose of treatment:
o maintain the patient's basic nutritional intake
o prevent the occurrence of aspiration pneumonia.
Treatment of dysphagia:
compensations
• to allow patients to eat at least some foods orally without aspirating
exercises
• to build strength and coordination so that patients no longer need the
compensations and can return to full oral intake
treatment methods of dysphagia:
1. direct treatment:
•
•
•
•
Choice of body position
Selection of food characteristics
Bite size
Feeding environment
2. Indirect treatment:
 Training of facial and neck flexor muscles
 Tongue and pharynx training
 Stimulate pharyngeal reflex
 Closed glottis practice
 Swallowing on glottis
Section 6 rehab aids:
1. orthosis:
an orthosis is an external appliance worn to restrict or assist motion or to transfer
load from one area of the body to another.
2. Prosthesis:
 upper limb and lower limb prosthesis
 temporary and formal prosthesis
 decorative, functional, operational and athletic prosthesis
 endoskeleton and the exoskeleton prosthesis
 self-powered and external-powered prosthesis
ppt 5 REHAB FOR CEREBROVASCULR INJURY
Motor function rehab program:
Recovery
phase
Training
objective
Training programme
Flaccid
paralysis
stage
Prevent spasm
Association
reaction
Complication and
secondary lesion
Induce normal
motor pattern
Fine limbs position
Body position transfer
passive movement
Active movement
Spasm
stage
Inhibit spasm and
abnormal motor
pattern
Induce
Disjunctive
movement
Normal motor
pattern
Limb Extention and weight
loading
Trunk control
exercise for coordination
Motor coordination
Recovery
stage
Sufficient
Disjunctive
movement
Normal motor
pattern
Exercise for motor speed
Fineness movement training
Walking training





Therapeutic principle for cv injury:
inhibit abnormal and primitive reflex
pattern,to rebuild normal motor pattern.
Rehab goal for cv injury:
Pressure sore
Respiratory and urinary tract infections
Deep venous thrombosis
Joint swelling
Post stroke depression
(1) Acute phase
Clinical rescue is the main method. Rehabilitation measures should be early intervention, but
without affecting clinical rescue as a prerequisite. The duration of acute stroke is generally 1-3 weeks
Therapy at flaccid paralysis stage:
1. correct body position lie in bed:
 To lie in bed with uninjured side
 Functional electrical stimulation（FES）
 Biofeedback therapy
 Keep joint range of motion (ROM) passive movement
 Air pressure therapy
2. To turn the body over:
Bobath hand ; Grip; thumb ; to benefit ; shoulder ; Swinging ;
3. Bridge movement:


supporting the bed with both feet and raising the buttocks.
dynamic bridge movement
(2) Early recovery:



Subacute stage for 3-4 weeks
objective: to inhibit spasm, promote the recovery of segregation movement, active activity, and
avoid abnormal movement patterns.
Physical therapy project:
1. Bed and bedside activity:
1.1 upper limb lifting
1.2 sit by bed, stand by bed
1.3 alternate flexion and extension of lower limb
1.4 bridge movement
2. sitting activity: Sitting balance, upper limb weight bearing, upper limb and
lower limb functional activities
3. Standing activity: Standing balance, lower limb load, upper and lower steps
4. Walking in the Balance Bar
5. Indoor Walking and Outdoor Activities
6. Physical factors
7. Traditional Therapy
8. Occupational therapy
Walking Frame and Wheelchair
9. Speech Therapy
Therapy at spasm stage:






Spasm control and inhibit abnormal motor pattern. Facilitate the appearance of disjunctive
movement.
Utilize against spasm mode
Upper limb-elbow control training
Upper limb-elbow extension and elbow flexion control
Upper limb-shoulder flexion assist exercise
Active motion of upper limb-shoulder flexion




Upper limb-Elbow stretching resistance training
Hand-thumb anti-resistance supination training
Hand-thumb opposition training
The affected side of motor area stimulated by upper limb-transcranial magnetic
stimulation
Special clinical problems of stroke?
1. Shoulder: shoulder-hand syndrome, shoulder subluxation, soft tissue
2. Spasm and contracture
3. Swallow
4. Deep venous thrombosis
5. Pneumonia
6. Pressure sore
7. Post-stroke depression
To avoid pressure sore:
1. Keep skin clean and dry. Clean air cushion bed, water cushion, sponge cushion, soft pillow, turning
cushion in time.
2. Take a 30-degree low half-lying position and turn over periodically (2 hours) to relieve the pressure on
all parts of the body.
3. Master the skills of turning over and avoid dragging, pulling and pushing.
Ppt 6. CPR:
What are the rehab treatment for COPD?
1. Airway clearance technique: postural drainage, percussion, vibration, cough techniques,
manual hyperinflation, and airway suctioning.
2. Percussion: aimed at loosening retained secretions can be performed manually or with a
mechanical device.
3. Vibration: vibration is utilized in postural drainage positions to clear secretions from the
affected lung segments
4. Cough technique
5. Active cycle of breathing: The patient performs diaphragmatic breathing at normal tidal
volume for 5 to 10 seconds.
6. Mechanical aids for breathing: Inspiratory and expiratory mechanical aids are devices and
techniques that involve the manual or mechanical application of forces to the body or
intermittent pressure changes to the airway to assist inspiratory or expiratory muscle
function.
7. Manual hyper inflation and airway suctioning: Airway suctioning is performed routinely
for intubated patients to facilitate the removal of secretions and to stimulate the cough
reflex. Airway suctioning is indicated for patients with artificial airways who have excess
pulmonary secretions and the inability to clear the secretions from the airway.
8. Breathing exercises
9. Inspiratory muscle training: indicated for patients who exhibit signs and symptoms of
decreased strength or endurance of the diaphragm and intercostal muscles.Signs and
symptoms include, but are not limited to, decreased chest expansion, decreased breath
sounds, shortness of breath, uncoordinated breathing patterns, bradypnea, and decreased
tidal volumes.
What are the breathing exercise techniques?
1. Pursed lip technique
2. Paced breathingtechnique: defined as “volitional coordination of breathing during activity.”
During rhythmic activities, breathing can be coordinated with the rhythm of the activity. During
non-rhythmic activities, the patient can be instructed to breathe in at the beginning of the
activity and out during the activity.
3. Inspiratory hold techqinque: An inspiratory hold technique involves prolonged holding of the
breath at maximum inspiration. It can be used in conjunction with vibration techniques to aid in
airway clearance. It can also improve the flow of air into poorly ventilated regions of the lungs.
4. Stacked breathing: Stacked breathing is a series of deep breaths that build on top of the previous
breath without expiration until a maximal volume tolerated by the patient is reached. Each
inspiration is accompanied by a brief inspiratory hold.
5. Diaphragmatic controlled breathing: can be used to manage a patient’s dyspnea, reduce
atelectasis, and increase oxygenation. This technique has been described as “facilitating
outward motion of the abdominal wall while reducing upper rib cage motion during
inspiration.” Diaphragmatic controlled breathing (with or without manual facilitation) can be
used to manage a patient’s dyspnea, reduce atelectasis, and increase oxygenation.
6. Lateral costal breathing: Unilateral costal expansion or bilateral costal exercises address one
side or both sides, respectively, of the rib cage and corresponding intercostal muscles.
Unilateral costal expansion exercises may be more useful in the treatment session with a patient
who has a large incision from surgery on one side of the thorax.
7. Upper chest inhibiting technique: Inhibiting the upper chest can help a patient recruit the
diaphragm during inhalation. This technique should be used only after other techniques have
been attempted. The patient is positioned in side-lying, three-quarter supine or supine position.
8. Thoracic mobilization technique: If mobility of the thorax is restricted, it may be difficult for a
patient to improve his or her breathing pattern through controlled breathing alone. It may be
necessary to incorporate simple thoracic mobilization techniques to increase the ability of the
thorax to expand during breathing.
9. Butterfly: The butterfly technique is an upright version of the counter rotation technique and
can be used if the patient has good motor control. The patient sits unsupported, and the therapist
stands either in front of or behind the patient. The therapist assists the patient with bringing his
or her arms up into a butterfly position.
What are the phases of cardiac rehab?
Phase 1


STAGE: refers to acute myocardial infarction or acute coronary syndrome hospitalization.
Time:3 to 7 days.
INDICATION: patient vital signs were stable, no significant angina, resting heart rate <110
beats / min, without heart failure, severe arrhythmias, and cardiogenic shock, blood
pressure normal, normal body temperature
phase 2

STAGE: refers to patients discharged from hospital began to condition the stability of fully
established. Time:5 ~ 6 week
INDICATION: like patients of Phase 1 ，in stable condition, exercise capacity above three
metabolic equivalents (METs), no significant signs and symptoms while family activities.
(1METS = maximal oxygen uptake X3.5ml)

phase 3


STAGE: refers to the condition in a relatively long-term stability State, or from end stage Ⅱ
process , Including old myocardial infarction, stable Qualitative angina and coronary heart
disease hidden. Time: usually 2 to 3 months, since workout should last a lifetime
INDICATION: clinically stable condition, old myocardial infarction, coronary artery disease
with unstable angina ，after the acute myocardial infarction, surgical or interventional
treatment.
Rehabilitation evaluation of cardiac patients?
The patient refers to cardiac rehabilitation should have an individualized assessment before make
individual care plan and interventions.
1. Exercise test
1.1 Cardiopulmonary exercise test (CPET)：
1.Basis for formulating exercise prescription:
2 Early diagnosis of coronary heart disease:
3 Determine the severity and prognosis of atherosclerotic lesions:
4 Determine the risk of exercise:
5 Guide chronic disease management:
6 Others: According to the result of exercise test, assess the cardiopulmonary function and evaluate
the risk of surgery.
What are the treatment programs and goals of cardiac patients according to the cardiac phase?
Phase Ⅰ
Rehabilitation goal
Maintain existing levels of functionality and prevent the emergence of "disuse", relieve
anxiety and depression, transit to phase Ⅱ safely. The exercise capacity reaches 2～3 METs, and the low
level exercise test is negative, improve the daily activity of living. Patients and family members
understand the risk factors and precautions of coronary heart disease, adapt to the attack of the disease.
treatment program
a. Training on the bed:
b. Sitting training:
c. Walking training:
d. Defecation:
e. Walking up the stairs:
f. Respiratory training:
g. Rehabilitation program adjustment and monitoring:
h. Psychological rehabilitation and making a discharge plan:
i. Phase Ⅱ rehabilitation is not allowed if the following conditions exist: The
patients' clinical symptoms or social-environmental barriers limit their access to
phase Ⅱ rehabilitation (for example, the patients' social condition is very poor or
they live far away from the heart rehabilitation center).
Phase II
Rehab goal
Prevent heart function regression, gradually restore the ability of daily activities to restore
normal social life, start from low level physical exercise, restore physical strength to the level of preillness, obtain psychological recovery and change lifestyle. The exercise capacity reaches 4～6 METs, the
patient needs regular outpatient visits.
Treatment program:
a.
b.
c.
d.
e.
Aerobic exercise
Strength exercise
Flexibility exercise
Provide lifestyle education
Preparatory exercise:
f.
Main exercise: It includes aerobic, strength and flexibility exercise. Total time is about 30～90
minutes.
g. Relaxation exercise: Relaxation exercise helps to reduce a sudden increase in cardiac load to
avoid the cardiovascular accidents.
h. Treatment principles: General activities do not require medical monitoring, and remote ECG
monitoring systems can be used for greater intensity activities.
Phase III
Rehab goal:
Consolidate the results of Phase Ⅱ rehabilitation, develop intensive, high-level and
individualized exercise plan. Control risk factors, if necessary, combine drug therapy. Improve physical
activity and cardiovascular function. Maintain a good lifestyle, improve quality of life, and restore life and
work before the disease.
Treatment program
1.Exercise prescription: Every patient must have a personalized exercise prescription.
(a) Exercise prescription settings
(b) Safety factors affect the overall setting of exercise prescription and related
factors affect the composition of exercise prescription.
2. Training form: The training form can be divided into intermittent and continuous movement.
Intermittent exercise refers to a number of peak intensities during the basic training period and a
decrease in intensity between high intensities.
3. Amount of exercise: The amount of exercise is the key point of rehabilitation. A reasonable weekly
exercise is 2931～8374kJ (700～2000 kcal) (equivalent to walking or jogging 10～32 km). Both of too
much or too little exercise are bad for the body and cannot increase physical fitness. The basic elements
of the amount of exercise are intensity, time and frequency.
4. Exercise intensity, Exercise time: It refers to the time of each exercise. Exercise at target exercise
intensity typically lasts 10～60minutes.Training frequency: 3～5 days/week
5. Training implementation:
Preparatory exercise:
Main exercise: It refers to activities that reach the target exercise intensity. It includes
aerobic, strength and flexibility exercise. The main mechanism of low-intensity training is peripheral
effect, and the mechanism of high-intensity training is central effect.
6.Relaxation exercise:
Advice for exercise prescription: When the exercise prescription is made, the patient must
gradually reach the established exercise goal. There is no fixed template to achieve the goal. The exercise
prescription must be individualized, because different patient’s skeletal muscle status, enthusiasm and
physical fitness will affect the progress of exercise training
Why is health education important?
Health education is an important part of cardiac rehabilitation. CHD is a kind of chronic
disease, systemic management and continuous treatment are needed. After the patients return home
from the hospital, if they cannot get information about the disease from the doctor and understand how
to carry out effective self-management, the original bad habits will soon reappear. At the same time,
health education for family members, through social support and medical care support, enable patients
to develop a healthy lifestyle and get rid of the risk factors in the environment.
Ppt7 cervical spondylosis
Definition of CS?
A degenerative spinal disease that can involve any part of the Vertebra, the Intervertebral discs, and the
surrounding tissues such as nerve roots, spinal cord, blood vessels, sympathetic nerve and other
organizations
Classification of CS:
1. Cervical spondylotic pain:
 Neck pain
 Decreased rom
2. Cervical spondylotic vertebroarterial impairment
 Symptoms:
a. vertebrobasilar insufficiency (VBI): dizziness, headache, double vision, memory
loss
b. vertigo mostly caused by head rotation
 Signs:
a. Be dizzy when look down and rotate the neck
 Accessory examination:
a. X ray / CT: luschka joint hyperplasia
b. MRI: interveterbral disc herniation
c. Ultrasonography / MRA: narrowing, occlusion of vertebral artery.
3. Cervical spondylotic sympathetic imbalance
 Symptoms:
a. sympathetic nerve activation: headache, rapid heartbeat, high blood pressure, etc.
b. sympathetic inhibition: dizziness, bradycardia, low blood pressure,
gastrointestinal motility enhancement.
 Signs:
a. above symptoms when look down and rotate the neck
 Accessory examination: (same as type of VBI)
a. X ray / CT: luschka joint hyperplasia
b. MRI: interveterbral disc herniation
c. Ultrasonography / MRA: narrowing, occlusion of artery
4. Cervical spondylotic radiculopathy
 Symptoms
a. neck pain
b. radiating pain or numbness of upper limbs/fingers
 signs:
a. brachial plexus traction test (Eaton) positive
b. Intervertebral foraminal compression test (Spurling) positive
c. skin hypoesthesia/ anesthesia
d. tendon reflexes weak/ abscent: biceps, triceps, radial periosteal

Accessory examination
a. X ray: hyperostosis, intervertebral foramen stenosis
b. MRI: straight / lordosis, interveterbral disc herniation
5. Cervical spondylotic myelopathy
 Symptoms:
a. weakness and numbness of limbs
b. unsteady gait
 Signs:
a. dysfunction of movement, sensory, autonomic nerves (voiding dysfunction,
defecation disorder)
 Accessory examination:
a. MRI shows compression of spinal cord
6. Esophago-cervical spondylosis
 Symptoms & Signs:
a. Dysphagia when moving neck backward
 Accessory examination:
a. MRI shows compression of esophagus
b. VFSS (video fluoroscopic swallowing study) shows compression of esophagus
7. Mixed
Dysfunction
•
Physiological dysfunction
motor, sensory dysfunction, autonomic nerve
•
Psychological dysfunction
depression, anxiety, despair, frustration, etc.
•
Dysfunction of daily life and social abilities
decreased ability of social participation
rehab treatment for CS:
Rest in bed:
1.
Pillow
2. To relax neck muscle, release pain
Physical factor therapy:
1) high-, middle-, low-frequency electrotherapy: reduce pain
2) light therapy: improve local blood circulation, reduce edema
3) ultrasonic therapy: reduce pain and massage cells
4) static therapy: regulate autonomic nerve function
Traction therapy:

Traction angle
level
angle



C1-4
0°
C5-
C6-
6
7
15°
20°
25°
traction time: 10~30min, usually 15 to 20 minutes
traction weight: Body weight (kg) × (1/8 ~ 1/12) . 1/10 of the body weight for the
first traction.
Contraindications:
a. spinal cord is compressed severely
b. symptoms aggravated after traction trial
c. sympathetic imbalance of CS in acute phase
d. whiplash injury
e. cervical spine instability
i. Caution! artery insufficiency

Manual therapy:
McKenzie technique
Joint mobilization
Maitland technique
Chinese traditional massage
Exercise therapy:


C7-T1
relaxing muscles
Movement and resistant exercise in all directions


Chest expanding
Lead head upward and pull jaw backward
Orthosis therapy
Drug therapy:

Oral drug
a. release pain（NSAIDs ）；
b. repairing nerve（vitamin B1、B12 ）；


c. dehydration（mannitol）
External medication
a. liniments or plaster
Local injection
Surgery therapy:
a.
conservative treatment is invalid
b. spinal cord is compressed obviously
c. progressive muscle atrophy
d. syncope or cataplexy repeatedly
e. dysphagia caused by hyperostosis
f.
sudden paralysis
health education for CS:





pillow
change bad habits/keep good posture
keeping warm
join in leisure activities
watching TV correctly
When vertebral artery compressed, Cervical spondylotic vertebroarterial impairment &
sympathetic imbalance
When nerve roots were compressed, Cervical spondylotic radiculopathy
When spinal cord compressed, Cervical spondylotic myelopathy
When esophagus compressed, Esophago-cervical spondylosis
Ppt7 lumbar disc herniation
Definition of LDH:
a series of symptoms and signs caused by acute or chronic intervertebral disc herniate which can
lead to the nerve root compression or irritation on the basis of degeneration of lumbar vertebra or disc.
Symptoms:
a. low back pain
b. pain of lower limb (sciatic nerve / femoral nerve
Signs
a. Tenderness on spinous process, interspinous process and paraspinous tissue
b. Lasegue sign (+), even Brogard sign (+)
c. femoral nerve stretch test (+)
d. weakening or disappearance of tendon reflexes (patellar tendon, Achilles tendon
reflex)
e. weakness of muscle power and skin sensation of lower limb
f.
Urinary / defecation dysfunction
Rehabilitation treatment
a.
b.





Rest in bed
Physical factor therapy
High-frequency electrotherapy: relief of pain and nerve root edema
middle-frequency electrotherapy: to relieve pain, relax back muscles
low-frequency electrical stimulation: muscle relaxation, pain relief
Ultrasonic: to improve circulation and promote edema absorption, release adhesions
light therapy: to improve local circulation, relieve pain
c. Traction therapy

increasing the intervertebral space
 restore anatomical relationship among bones and joints
 push disc forward by increasing the tension of posterior longitudinal ligament
 traction position
 traction time: 20 min ~ 40 min
 traction weight: 25% ~ 70% of body weight
d. Manual therapy

McKenzie technology
 Joint mobilization
 Massage therapy
e.





Exercise therapy
Bridge Movement
Prone extension
Stretch like a bird
Sit-ups
Supine flexion
f.
g.



Orthosis therapy
Drug therapy/Surgery therapy
conservative treatment is invalid
severe disc herniation
sudden paralysis
1. Do
•
wear soft-soled and flat shoes
•
rotate the whole body
•
do exercise such as swimming, walking, jogging, etc
2. DON’T
•
sit and stand for long time (> 1h)
•
just turn around the upper body
•
hold your breath when you do exercise
ppt 7 spinal cord injury
definition:
caused by external direct or indirect factors. There are various motor, sensory and sphincter
dysfunction, dystonia and pathological reflex changes in the corresponding segments of SCI. The degree
and clinical manifestation of spinal cord injury depend on the location and nature of the primary injury.
Incomplete lesions of the spinal chord:
1.
2.
3.
4.
incomplete structural damage.
preservation of some motor or sensory function below the level of the injury. –
Sacral sparing (Perianal sensation, anal sphincter tone, and great toe flexor function).
subtypes ( syndromes ):
a) A-central cord syndrome (the most common) • Etiology: hyperextention injuries
Swelling in the center of the cord -> bony abnormality may be absent . • Symptoms : loss
of sensory and motor function below the level of the lesion • greater loss in arms than in
legs
b) B- anterior cord syndrome(common). • Etiology :acute anterior cord
compression,disruption of blood flow. • Symptoms: loss of motor function, loss of pain
temperature, crude touch ,crude pressure. Intact proprioception ,fine touch, fine pressure
,vibration.
c) C- posterior cord syndrome (rare) • Etiology: acute posterior cord compression . •
Symptoms :loss of proprioception ,fine touch ,fine pressure ,vibration . intact pain,
temperature, crude touch ,crude pressure.
d) D- Brown Sequard syndrome (uncommon) • Spinal tract involved: dorsal on same side ,
spinothalamic on the opposite side ,corticospinal on the same side. Etiology: transverse
hemisection of the cord • Symptoms: loss of motor function proprioception ,vibration
(epailateral) Loss of pain and temperature ( contralateral).
Complete spinal chord injury:
1. results in loss of all motor and sensory function below the level of the lesion.
2. shock is frequently the initial response resulting in loss of motor, sensoty, and reflex function
below the level the injury.
3. The patient may also develop neurogenic shock resulting in loss of autonomic function
High cervical injury:(C3 and above):


Motor and sensory deficits involve the entire arms and legs
Dependent on mechanical ventilation for breathing (diaphragm is innervated by C3-C5 levels)
Midcervical injury(C3-C):



Varying degrees of diaphragm dysfunction
Usually need ventilatory assistance in the acute phase
Shock
Low cervical injuries (C6-T1):


Usually able to breathe, although occasionally cord swelling can lead to temporary C3-C5
involvement (need mechanical ventilation)
The level can be determined by physical exam
Thoracic injuries (T2-L1):


Paraparesis or paraplegia
UMN (upper motor neuron) signs
Cauda equina injuries (L2 or below):



Paraparesis or paraplegia
LMN (lower motor neuron) signs
Thigh flexion is almost always preserved to some degree
SPINAL CORD ASSESSMENT:
Motor: how do you test each segment?
How do you determine the level? Key Sensory Landmarks
Reflexes:


Deep Tendon Reflexes:
a) Arm
b) Bicipital: C5
c) Styloradial: C6
d) Tricipital: C7
Leg
a) Patellar: L3, some L4
b) Achilles: S1

Pathological reflexes
a) Babinski (UMN lesion)
b) Hoffman (UMN lesion at or above cervical spinal cord)
c) Clonus (plantar or patellar)
What is and how do you determine the level of injury?
•
Motor level = the last level with at least 3/5 (against gravity) function(muscle grade)
•
Sensory level = the last level with preserved sensation
•
Radiographic level = the level of fracture on plain X Rays / CT scan / MRI
AISA impairment scale:
Cure and management:
Initial management:
•
Immobilization
•
•
a) Rigid collar
b) Sandbags and straps
c) Spine board
d) Log-roll to turn
Prevent hypotension
a) Pressors: Dopamine
b) Fluids to replace losses
Maintain oxygenation
Management in hospital:
•
•
•
NGT to suction
a) Prevents aspiration
b) Decompresses the abdomen
Foley
a) Urinary retention is common
Methylprednisolone: Only if started within 8 hours of injury
Cervical Spine Clearance:
•
•
•
•
Occiput to T1 need to be cleared
Neurosurgery or Orthopedics physician
If the patient
1. Is awake and oriented
2. Has no distracting injuries
3. Has no drugs on board
4. Has no neck pain
5. Is neurologically intact
6. then the c-spine can be cleared clinically, without any need for X－Rays
CT and/or MRI is necessary if the patient is comatose or has neck pain
Cervical Traction:
•
Provides temporary stability of the cervical spine
Surgical Decompression and/or Fusion:
•
•
Indications
•
Decompression of the neural elements
•
Stabilization of the bony elements (spine)
Timing
•
•
•
Emergent
Incomplete lesions with progressive neurologic deficit
Elective
•
Complete lesions (3-7 days post injury)
•
Central cord syndrome (2-3 weeks post injury)
Long term care:
•
Rehab for maximizing motor function
•
Bladder/bowel training
•
Psychological and social support
GOALS AND CONTENT:
ACUTE STAGE:
(goals)
•
keep respiratory passage cleaning and unblocked;
•
Keep ROM and paralyzed muscle length;
•
To strengthen paralyzed muscle and breathing muscle
•
to prevent sore or ulcer.
(content)
•
Good gesture position: body position : prostration>>>>>side-lying position>>>>>>sitting
position
•
breathing and sputum control:
I.
II.
III.
IV.
•
vertebral column fixed earlier period，to assist body
position changing
thoracic region knocking
manipulation assisted coughing
Passive Movement:
I.
II.
•
purpose： Keep ROM ，prevent contraction of articulation and muscle
start at earlier period（1-2times/day）
Blood vessel regulation training:
I.
II.
To sit at earlier period
Straighten ： ought to keep the stability of spinal ,and with waistline
III.
Use electric bed , the incline angle from 20 degree , then to increase gradually,
IV.
approximately to 90 degree 8 weeks later.
•
selectivity exercise for power:
I.
II.
Bare-handed resistive movement
Double PNF
mode
III.
sandbag and dumbbell
IV.
progressive resistive exercise.
V.
•
Suspension device
urination and defecation:
I.
II.
urinary retention:
i.
to last urethral catheterization---regular volley(300-400ml),2h/,water
enter:2500- 3000ml/day
ii.
cleaning intermission urethral catheterization independence- ------must
observe water go out and come in strictly
constipation: rectum lubricant or laxity
COVALESCENT STAGE:
•
Exercise for power
•
Muscle extension
•
psychotherapy
•
Mat exercise
•
Transfer and balance
•
walking
•
wheelchair
•
Orthotic using
•
ADL
Functional electrical stimulation
INTRO (ENT)
Anatomy of Nose has External nose, Nasal Cavity and Paranasal Sinuses.
External nose; the external nose is triangular-shaped projection in the center of the face, consists
of an osteocartilaginous framework covered by muscles and skin.
Nasal cavity; has nasal cavity proper and nasal vestibule. Nasal vestibule is the anterior and inferior part of the
nasal cavity. It is lined by skin and contains sebaceous glands,hair follicles and hair(vibrissae) easy to infect.
Nasal cavity has the roof and floor. Roof has anterior sloping part of the roof is formed by nasal bones; the
Posterior sloping part by the body of sphenoid bone;and the middle horizontal part, by the cribriform plate of
ethmoid. The floor of the nose is formed by the palatal process of the maxilla and the horizontal process of
the palate bones. Medial wall which has the nasal septum. Septum deviation can result in - Nasal obstruction,
Nasal bleeding, Headache, Anosmia, Sinusitis, External deformity.
Lateral Wall of the Nasal Cavity
➔ Nasolacrimal duct opens in the anterior part of inferior meatus.
➔ The anterior group of sinuses (frontal,maxillary and anterior ethmoidal sinuses) open to
infundibulum in the middle meatus.
➔ Posterior ethmoidal sinuses open into superior meatus.
➔ The opening of sphenoid sinus situate is sphenoethmoidal recess lies above the superior turbinate.
Ostiomeatal complex
The ostiomeatal complex is the sinus "hot spot," one of the most important anatomical regions with regard to sinus
health and disease. That comprises maxillary sinus ostia,anterior ethmoid cells and their ostia,ethmoid
infundibulum, hiatus semilunaris, and middle meatus.
Microanatomy of the Nasal Cavity (mucosal lining)
•
Respiratory epithelium
–
•
Columnar, goblet cells, mucus blanket, cilia
Olfactory epithelium
–
Small area near roof
Nerve Innervation
• Olfactory nerves (cranial nerve I), Trigeminal nerve (cranial nerve V), Parasympathetics,
Sympathetics.
Danger triangle of the face
Due to the special nature of the blood supply to the human nose and surrounding area, it is possible for retrograde
infections from the nasal area to spread to the brain. For this reason, the area from the corners of the mouth to the
region between the eyes, including the nose and maxilla, is known to doctors as the danger triangle of the face.
Paranasal Sinuses; The sinuses are air-filled bony cavities located in the face and skull adjacent to the nose.
• Maxillary sinus, Ethmoid sinus, Frontal sinus, Sphenoid sinus
Maxillary sinus is the largest one, present in the maxilla bone one either side of the nose and below the
eyes.The sinus drains into the nasal cavity through its ostium that is situated in the middle meatus.
Ethmoid Sinus; This sinus comprises a group of air cells, which form one of the most complex structures in
the body. Hence the sinus is rightly named the ethmoid ‘labyrinth’.
Frontal Sinus; The frontal sinuses are situated beneath the bone of the forehead and just in front of the bone
overlying the brain. And drains through the frontal recess to the middle meatus.
Sphenoid Sinus; The sphenoid sinuses are deep within the skull behind the ethmoid sinuses. The sinus opens in
the upper part of anterior wall and drains into the sphenoethmoidal recess.
Physiology of the Nose; Respiration, Airway, Heat exchange, Humidification, Self-cleansing, Protection
Nasal cycle
spontaneous reciprocating cycle of nasal congestion and decongestion . The nasal cycle is known to be regulated
by the sympathetic and parasympathetic branches of the autonomic nervous system (ANS).
Resonance to the voice
Rhinitis
It is an inflammation of the mucous membranes of the nose with excessive mucus production resulting in nasal
congestion and postnasal drip.
Acute Rhinitis
Cause: virual infection transmitted by droplets.
Latent Period: symptoms appear 1-3 days after the infection.
Course: 1-2 weeks
Clinical features: ●chill, low-grade fever,headache, malaise, myalgia.
● sneezing,nasal obstruction
● rhinorrhea(watery at beginning,mucopurulent later.
Treatment: ● Antivirotic, analgetic
● Nasal congestant
● Antibiotic for secondary bacterial infection and
Complication.
Chronic Rhinitis
Etiology: Recurrent or acute rhinitis, Persistence of nasal infection due to sinusitis,tonsillitis,and adenoids.
Nasal septum deviation. Chronic irritation from smoke,dust,toxic and irritant gas,e.g. Endocrinal or metabolic
factors,e.g. Medicamentous rhinitis.
Classification: Chronic Simple Rhinitis, Chronic Hypertrophic Rhinitis.
Pathological Change: Nasal mucosa edema and hyperaemia with seromucinous glands hypertrophy and
increasing secretion.
Clinical Features: 1. Intermittent or alternate nasal obustruction, usually worse on lying and affects the
dependent side of the nose. 2. Nasal discharge and post-nasal drip.
Sign: Nasal mucosa and turbinates swollen, pit on pressure and shrink with application of decongestant（e.g.
1% Ephedrine).
Treatment:1. Nasal decongestant drops or sprays to relieve nasal obstruction and improve sinus ventilation.
2. Treat the primary causes
Pathology:Hyperplasia of nasal mucosa,submucosa, seromucinous glands,periosteum and bone, especially on
the inferior turbinates.
Symptom: Persistent nasal obstruction with closed rhinolalia, Sticky nasal discharge, Headache & dizziness
Hyposmia.
Examination: Hypertrophy of turinates,little shrinkage for decongestant application. The inferior turbinate
may be mulberry shape.
Treatment: Submocoperiosteou resection of inferior turbinate is the best way.
Atrophic Rhinitis
Etiology: Primary atrophic rhinitis often occurred in young women，may associated with endocrinal
disturbance, nutritional deficiency, autoimmune disease and heredity. Secondary atrophic rhinitis may result
from infection,iatrogenic,and some specific infections like syphilis,lupus,leprosy.
Clinical Manifestation (Symptoms): Nosebleed, Hyposmia or anosmia, Nasal obstruction due to crust
formation, Headache, Foul smell from the nose (ozena)
Examination: Atrophic nasal mucosa & turbinates. Wide nasal cavity. Greenish or yellowish crusts in nasal
cavity.
Treatment:
Medical; Nasal irrigation and removal of crusts. Nasal drops(antibiotics and nebla-methol Co).Vitamin A and C
application.
Surgical; Narrowing the nasal cavities by submucosal insertion of cartilage ,bone or silica gel.
Allergic Rhinitis
•
Associated with atopy.
•
Atopy is an inherited predisposition to produce IgE to environmental allergens.
Allergic reaction:
●
Allergen encounters plasma cell
●
●
●
●
Antibody(IgE) is produced
IgE attaches to mast cell
Mast cell degranulates, releasing histamine and chemical mediators
Resulting inflammatory response
Allergens include: Pollen, House dust mites, Mold spores, Animal Allergens.
Classification: Seasonal(pollinosis /hayfever)
– Repetitive and predictable seasonal symptoms.
•
Perennial
– Symptoms that persist throughout the year. No seasonal pattern.
•
WHO suggestion- intermittent/persistent
Inspection: Examination - pale nasal mucosa - conjunctivitis long-standing - enlarged inferior turbinates
•
Blood tests - total serum IgE -RAST for specific IgE -Skin prick Test
Treatment: Allergen avoidance, Antihistamines, Intranasal Corticosteroids, Mast Cell Stabilisers,
Decongestants, Anti-cholinergic sprays, Immunotherapy.
Sinitus
Inflammation of the paranasal sinus caused by a bacterial or viral infection, or allergy.
Acute Sinitus
Causes:
●
Nasal cavity affection－acute and chronic rhinitis, allergic rhinitis ,septum deviation, nasal polyp
foreign body or tumor in nasal cavity,the ostiomeatal complex abnormality.
●
●
●
●
Adjacent infection－tonsillitis, adenoiditis, infection from molar or premolar teeth.
Nasal packing >48 hours.
Trauma ,Swimming and Diving.
Air pressure of the sinuses changed quickly.
●
Overtiredness
●
Nutrition and vitamin deficiency
●
Systemic disorders－diabetes, anemia,hypothyroidism ,immune deficiency, Atopy.
Symptoms: Fever, Headache, Nasal Discharge, Nasal Obstruction
Examination: 1.Nasal cavity inspection－pus in middle meatus or olfactory cleft. 2.Endoscopy
3.Palpation－tenderness in overlying bones 4.X-ray or CT scan.
Complication: 1.Otitis media, trachitis,bronchitis
2.Orbital cellulitis or abscess,retrobulbar neuritis
3.Osteomyelitis of maxilla or frontal bone.
4. Intracranial infeion－cavernous sinus thrombosis ,meningitis, subdural or/and epidural abscess,or brain
abscess.
Treatment: Broad-spectrum antibiotics. Intranasal vasoconstrictor or Corticosteroids. Postural drainage. Antral
lavage for maxillary sinusitis. Physiotherapy.
Chronic Sinusitis
Etiology: Recurrent acute sinusitis. Acute sinusitis can’t be cured thoroughly,and last for a long time.
Obstruction of osteomeatal complex region. Microbiology same as acute sinusitis
Symptoms: Purulent (yellow-green) rhinorrhea. Nasal obstruction. Headache (not marked). Hyposmia.Fatigue
,dizziness, low-grade fever, Cough, Halitosis.
Examination: Nasal cavity inspection. Endoscopy. Antral puncture and irrigation. X-Ray & CT scan.
Treatment: Steroid nasal sprays, Antihistamines, Antral puncture and irrigation. Displacement method
Endoscopic nasal surgery (FESS). Traditional radical operations- Caldwell Luc operation，Intranasal/External
ethmoidectomy, Trephination of frontal sinus, Intranasal sphenoidotomy.
Nasal Polyp
Nasal polyps are non-neoplastic masses of the nasal cavity and sinuses. They are formed when the soft tissue of
the sinuses becomes swollen and expands to fill the available space inside the nose. There may be one, or several
polyps in the nose.
The exact cause of nasal polyps is not known. Some medical opinions suggest that they are the result of an
allergy , while others believe they are caused by infection in the sinuses.
Symptoms: Nasal obstruction, Closed rhinolalia, snoring and apnea during sleep. Hyposmia or anosmia.
Obstructive sinusitis→purulent nasal discharge.Frog-shape nose because of long-term nasal polyp.
Treatment: Corticosteroids, Polypectomy,Ethmoidectomy, Functional Endoscopic Sinuses Surgery FESS.
Epistaxis (Nose bleed)
Reasons:
●
●
●
●
●
Vascularity of nose
Both external and internal carotids.
Anatoms are between arteries and veins.
Blood vessels run just under the mucosa-unprotected.
Larger vessels on the turbinate run in bony canals cannot contract.
(Kiesselbach’s) Little’s area is situated in the anterior inferior part of nasal septum and is supplied by branches
of both external and internal carotid arteries.
The four arteries, the branches of which anastomose richly and form a vascular plexus (Kiesselbach’s plexus) in
this region are:
1. Anterior ethmoidal.
2. Septal branch of superior labial.
3. Septal branch of sphenopalatine.
4. Greater palatine.
This vascular area is the most common site of nosebleed in children and young adults. It gets dried due to the
effect of inspiratory current and easily traumatized due to frequent picking (fingering) of nose.
Vessels involved: Anterior ethmoid, Posterior ethmoid, Greater palatine, Sphenopalatine, Superior labial.
Classification:
According to site
●
●
●
●
Anterior
Superior; Anterior ethmoid ( bleeding is from above ant. half of middle turbinate)
Inferior; Greater palatine,
Posterior; Sphenopalatine (Bleeding is from below anterior half of middle turbinate)
According to age
● Children:
○ Foreign body, nose picking .
● Adults:
○ Trauma, idiopathic.
● Middle age:
○ tumors.
● Old age:
○ Hypertension.
Local Causes:
As a result, trauma to the face can cause nasal injury and bleeding. The bleeding may be profuse, or simply a
minor complication.
1. Trauma: Finger nail trauma (obsessive compulsive disorder), injuries of nose (accidental,
homicidal, surgery), maxillofacial trauma, head injuries, nasal intubation, foreign bodies, rhinolith,
blowing of nose too hard and violent sneezing
Infections: Rhinitis, nasal vestibulitis, sinusitis, adenoiditis
2. Diphtheria, pyogenic granuloma, rhinosporidiosis, granulomatous lesions (tuberculosis, syphilis,
sarcoidosis, Wegener’s granuloma), atrophic rhinitis and rhinitis sicca, maggots and leeches,
neglected foreign body.
3. Idiopathic: “Spontaneous” is a better description.Usually initiated by minor ‘digital’ trauma
Often associated with atmospheric drying. Wegner's granulomatosis, Osler-Weber-Rendau's syn.
Atrophic rhinitis.
4. Neoplasms:
● Nasal cavity
● nasopharynx
● sinuses.
5. Benign neoplasms:
● Antrochoanal polyp
● “Inverting” papilloma
● Juvenile angiofibroma
6. Malignant neoplasms:
● Basal Cell Ca
● Squamous Ca
● Malignant Melanoma
● (Nasopharyngeal ca)
● (Adeno Ca /Adenoid cystic Ca)
7. Blood Vessels: Atherosclerosis, Collagen vascular diseases, Hereditary Haemorrhagic
telangiectasia, HHT, (Osler-Weber-Rendu disease)
General causes:
● Cardiovascular disease
- Hypertension, Atherosclerosis, Osler-Weber-Rendu disease
●
● Blood clotting problem
- Haemophilia, purpura, leukemias, aregenerative anemia.
●
● Vitamin C ,P & K deficiencies.
● Severe liver & kidney disease.
● Drugs – prescribed
- Anticoagulants - Warfarin / Heparin.
●
- Aspirin- platelet function inhibitor.
●
●
●
Toxicosis
Vicarious menstruation -during the period.
Environmental reason: High altitudes (drier and lower atm. pressure), Air-conditioning, Extreme changes in
temperature.
Site of bleeding: Nasal Septum - Little’s Area, 90% of epistaxis from this site. - Rest of septum spurs,
perforation, etc
Treatment:
●
●
●
First aid
○ Make the patient sit up, pinch or press nose, open mouth and breath.
○ Ice on forehead.
Definitive treatment
Prevention of recurrences
First Aid Position:
●
-
sitting upright
●
-
inclined slightly forward
●
-
mouth open
●
-
spit out any blood
●
-
vasoconstrictors
Treatment:
●
Look into the nose.
●
●
Assess blood loss.
○ Crystalloids or colloids
○ Transfusion
Locate the point after packing the nose with 4% xylocaine and 1:1000 adrenaline mixture.
●
Nasal endoscopy and electrocoagulation
Cauterization:
1) Chemicals;
●
●
Silver Nitrate stick,
chromic acid bead.
Electrical
●
Apply ointment and advise against blowing and nose picking.
Anterior Packing:
●
●
●
Unable to control bleeding.
Ribbon, tampon, splints.
Epistat balloon
Posterior Packing:
● Posterior packing if bleed is posterior.
● Foley's or other inflatable devices
● Removed as soon as possible.
● Antibiotics.
● Transfuse.
● Blood gases in children.
Nasal and Sinus Dressing
Special Cases:
●
●
Haemophilia;
○ Replace factor VIII, or fresh blood.
Other clotting deficiency;
●
○ FFP.
Purpura;
○ Platelets
Anticoagulants;
Stop drug or titrate.
Heparin is reversed with protamine sulphate,
warfarin with vitamin K
Unconscious head injury;
Dangerous to pack in suspected skull #.
Telangiectasia;
Septodermoplasty.
Other treatments:
●
●
●
●
Ligation of vessels
○ Maxillary artery
○ Ethmoid arteries
○ External Carotid artery
Embolization-DSA
Blood transfusion
Treatment of primary affection
Complication: Infection, Lose pack, Obstructing airway.
Nasal Trauma (Fracture of Nasal bone)
Nasal trauma is defined as any injury to the nose or related structure that may result in bleeding, a physical
deformity, a decreased ability to breathe normally because of obstruction, or an impaired sense of smell. The
injury may be either internal or external.
Symptoms:
●
●
●
●
●
●
●
●
●
●
●
●
Flattening or deformation of nasal shape
Infections of the cartilage or soft tissue
Epistaxis
Crepitus.
Pain and tissue swelling
Airway blockage from bleeding, fluid discharge, or tissue swelling
Rhinitis
Septal hematoma.
Bruising or discoloration (ecchymosis) of the tissues around the eye
Leakage of cerebrospinal fluid through the nostrils
Runny nose and watering of the eyes
Pain
●
●
●
●
Loss of the sense of smell
Nasal congestion and sneezing
Reddening and swelling of the mucous membranes lining the nose
Eventual destruction of the cartilage in the nasal septum and the tissues lining the nose
Etiology:
●
Traffic accident, Physical combat, Sports injury
Nasal bone--- Upper end: thick Lower end: thin
Signs:
●
●
●
●
●
●
●
●
Pain or tenderness, especially when touching your nose
Swelling of your nose and surrounding areas
Bleeding from your nose
Bruising around your nose or eyes
Crooked or misshapen nose
Difficulty breathing through your nose
Discharge of mucus from your nose
Feeling that one or both of your nasal passages are blocked
Diagnosis: X-ray in lateral view, CT, 3D.
Septal hematoma——puncture
Classification:
Treatment: Hemostasia, Cleaning & suturing wound, Restoring realignment.
Reduction of Nasal Bone:
●
●
●
●
Before soft tissue edema
7-14 days after injury
Walshan forceps
Nasal packing for 2-3d
Fracture of frontal bone:
Stringy, sunken and smashed fracture
Symptoms & Signs：Epistaxis, edema or sunken front.
Diagnosis：Frontal palpation, X-ray, CT scans
Treatment: stringy fracture
●
●
●
●
sunken fracture
smashed fracture
front & back wall fracture
base fracture (frontonasal fracture): restore the function of frontal sinus.
Principle：
●
●
●
To isolate the communication between frontal sinus and cranial cavity
to prevent rhinogenic complications
to keep the frontal part from deformation
Fracture of ethmoid bone:
Naso-orbito-ethmoidal fractures
Symptoms: increased intercanthal distance, diminished nasal projection, impaired nasofrontal and lacrimal
drainage.
Symptoms & Signs：
Edema of eyelid or nasal root, increase in the intercanthal distance. Sunken front, Vision disorder,
Diagnosis：X-ray film, CT scan
Treatment:
●
●
●
Vision disorder- depression of optic canal
Nosebleed- nasal pack or arterial ligation (ligation of ethmoidal artery)
Cerebrospinal fluid rhinorrhea (CSF) - surgical reparation
Fracture of zygomatic bone:
●
●
●
The management of zygomatic bone fractures depends on the degree of displacement and the
resultant aesthetic and functional deficits.
Surgery can be delayed until the majority of facial edema is gone.
Isolated zygomatic arch and zygomatic complex fractures with minimal or no displacement are not
managed surgically.
Blow-out fracture
Symptoms & Sign: Swelling and bruising, lid and infraorbital emphysema, Diplopia, restricted movement
of the eyes, vision disorder.
Diagnosis: Clinical manifestation, X-ray, CT scans
Treatment: Reduction after 7—10d post-wound.
Operation approach: via orbit, via maxillary sinus, external ethmoidectomy
RARE
Symptoms & Sign：
●
●
Protruding eye, swelling eyelids and zygoma
Palpation: orbital edge---“stairs-like”.
Maxilla Fracture
Cerebrospinal fluid rhinorrhea (CSF)
Etiology: Traumatic: Iatrogenic, external trauma
Location:Cribriform plate, Sphinoid, frontoethmoidal complex.
●
Nontraumatic: Spontaneous (or primary), direct erosion or increased intracranial pressure (tumors,
congenital or acquired hydrocephalus, or infections).
Diagnosis：History, laboratory test, endoscopic examination, ascertain the nature, fix the precise location
Treatment：1、Conservative treatment：To prevent from infection, To prevent from high cranial pressure
2、Surgery： transnasal repair; Intracranial approach
Otorhinolaryngology Head and Neck Surgery
Otolaryngology or ENT (ear, nose and throat) is the branch of medicine that specializes in the diagnosis and
treatment of ear, nose, throat, and head and neck disorders. The full name of the specialty is
otolaryngology-head and neck surgery. Practitioners are called otolaryngologists-head and neck surgeons, or
sometimes otorhinolaryngologists (ORL).
Characteristics: Intricate Anatomy, Wide patient variety, Medical and surgical management, Treating of
special and important senses, Cooperating of other experts.
Disorders related to the ear: THE E
•
hearing loss, infection of the ear, balance problem, tinnitus, Nerve pain, facial and carnial nerve
disorders.
Diseases of and related to the nose: THE N
•
Sinusitis, Allergy, Trauma, Tumor
Disorders of the throat: THE T
•
communication and speech, Larynx, Upper aerodigestive tract, Swallowing disorders
Disorders of the head and neck:
Infection diseases, tumor, trauma, Congenital deformities, Plastic and reconstructive surgery
Examination: Special instruments:
• Endoscopy ,microsopy,laryngoscopy.
Cochlear implant
Cochlear implants can improve hearing in people with severe hearing loss who are no longer helped by
using hearing aids. Cochlear implants can improve their communication and quality of life.
CHRONIC RHINITIS AND NASAL ALLERGIC DISEASE
❖ VIRAL RHINITIS (Acute Rhinitis):
1) COMMON COLD
➢ Etiology: it is caused by virus usually through airborne droplets.
• Adeno virus , picorna virus, rhino and coxsackie virus.
• Incubation period is 1-4 days and illness last for 2-3 weeks.
➢ CLINICAL FEATURES:
• Burning sensation of nose followed by nasal stuffiness , rhinorrhoea and
sneezing.
• Low grade fever.
• Nasal discharge is initially watery and profuse but may become mucopurulent
due to sec. bacterial invasion.
➢ Treatment:
• Bed rest
• Plenty of fluids.
• Antihistamine and nasal decongestant.
• Analgesics to relieve headache and antibiotics if secondary infection.
➢ Complications:
• Disease is usually self-limiting and resolves spontaneously after 2 to 3 weeks.
• Occasionally sinusitis, bronchitis, pharyngitis may occur.
❖ BACTERIAL RHINITIS (Acute rhinitis):
A) Non-specific infections:
• It may be primary or secondary.
• Primary bacterial rhinitis is seen in child usually infected by pneumococcus,
streptococcus or staphylococcus.
• A greyish white membrane may form in the nose , which with attempted
removal, cause bleeding.
B) Secondary bacterial rhinitis is result of bacterial infection supervening acute
viral rhinitis.
❖ IRRITATIVE (ALLERGIC) RHINITIS (Acute Rhinitis):
• Caused by exposure to dust, smoke and irritating gases like ammonia,
formalin etc.
• May result from trauma on nasal mucosa during intranasal manipulation.
➢ CLINICAL FEATURES:
• Immediate catarrhal reaction with sneezing, rhinorrhoea and nasal congestion.
• Symptoms may pass off rapidly with removal of offending agent .
❖ CHRONIC (SIMPLE) RHINITIS:
➢ Etiology:
• Recurrent attacks of acute rhinitis in presence of predisposing factors leads to
chronicity.
Predisposing factors:
• Persistence of nasal infection due to sinusitis , tonsillitis and adenoids.
• Chronic irritation from dust, smoke etc.
• Nasal obstruction due to synechia leading to persistence of discharge.
➢ PATHOLOGY:
Hyperemia
Edema of mucous membrane with hypertrophy of seromucinous glands
Increase in goblet cells.
Distend blood sinusoids of turbinates .
➢ CLINICAL FEATURES:
• Nasal obstruction
• Nasal discharge
• Headache
• Swollen turbinates- shrinkage with decongestant.
• Post nasal discharge.
➢ TREATMENT:
• Treatment of causative agent.
• Nasal irrigation with alkaline solution .
• Nasal decongestant help to relieve nasal obstruction and improves sinus
ventilation.
• A short course of systemic steroids helps to wean patients who have
addicted to excessive use of decongestant drops or sprays.
• Antibiotics are also commonly used.
❖ HYPERTROPHIC RHINITIS (CHRONIC):
It is characterised by thickening of mucosa, submucosa, seromucinous glands,
periosteum, and bone.
These changes are more marked on the turbinates.
➢ Etiology:
• Recurrent nasal infections.
• Chronic sinusitis , chronic irritation of nasal mucosa due to smoking and other
irritants
• Prolonged use of nasal drops , vasomotor agent and allergic rhinitis are also
pathogenic factors.
➢ SYMPTOMS:
• Nasal obstruction is main symptom.
• Nasal discharge is thick and sticky.
• Headache and transient anosmia are actually happen often.
➢ EXAMINATION:
• Hypertrophy of turbinates can present as the physical sign.
• Turbinate mucosa is thick and does not pit on pressure. Little shrinkage
with vasoconstrictor due to underlying fibrosis is the key feature.
➢ TREATMENT:
• Discovering the reason and remove it is the principle of treatment.
• Nasal obstruction can relieved, by reduction the size of turbinates via
various methods.
❖ PRIMARY ATROPHIC RHINITIS (CHRONIC):
• It is the chronic inflammation of nose characterised by atrophy of nasal
mucosa and turbinate bones . The nasal cavities are roomy and full of foulsmelling crusts.
• Atrophic rhinitis can be categorized into Two types
• Primary atrophic rhinitis
• Secondary atrophic rhinitis.
➢ ETIOLOGY:
• Hereditary factors.
• Endocrinal disturbance.
• Racial factors .
• Nutritional deficiency.
• Infective.
• Autoimmune process.
➢ PATHOLOGY:
• Ciliated columnar epithelium is lost and replaced by stratified squamous
type.
• Atrophy of seromucinous glands, venous blood sinusoids and some
nerve element.
• Turbinate undergoes resorption causing widening of nasal chambers.
➢ CLINICAL FEATURES
SIGN & SYMPTOMS
• Common occurs in female during the age of puberty.
• Foul smell from nose , but the patient remains unware is commonly
reported.
• Marked anosmia, epistaxis, nasal obstruction and the wide nasal
chambers due to larged crust formation.
These were the mainly clinical features.
➢ EXAMINATION:
EXAMINATION shows nasal cavity to be full of greenish or greyish
black dry crusts covering the turbinates & septum in nasal cavity.
• If attempt to remove them may cause bleeding.
After removed , nasal cavities appear roomy with atrophy of turbinates,
so much so that the posterior wall of nasopharynx can be easily seen .
• Nasal turbinates may be atrophy to mere ridges.
• Nasal mucosa appears pale .
• Nasal vestibule may be present saddle deformity.
• Atrophic changes may be extend to pharyngeal mucosa and larynx, with
cough and hoarseness of voice.
➢ RADIOGRAPHIC FINDINGS:
• Mucoperiosteal thickening of the paranasal sinuses.
• Loss of definition of the OMC due to resorption of the ethmoid bulla
and uncinate process.
• Hypoplasia of the maxillary sinuses.
• Enlargement of the nasal cavities with erosion and bowing of the lateral
nasal wall.
• Bony resorption and mucosal atrophy of the inferior and middle
turbinates.
➢ CURRENT THERAPIES:
• Goals of therapy: Restore nasal hydration , Minimize crusting
and debris
• Therapy options
Topical therapy
•
Saline irrigations
•
Antibiotic irrigations and Systemic antibiotics
•
Implants to fill nasal volume
•
Closure of the nostrils
Local therapy
• Irrigations Saline
• Mixtures
• Sodium bicarbonate
• Shehata: Sodium Carbonate 25g, Sodium Biborate 25g, and Sodium
Chloride 50g in 250ml water.
• Antibiotic solution
• Moore: Gentamycin solution 80mg/L
• Anti-drying agents
• Glycerin
• Mineral Oil
• Paraffin with 2% Menthol
• Other
• Acetylcholine
Systemic therapy:
• Oral antibiotics
• Tetracycline
• Ciprofloxacin
• Aminoglycosides
• Streptomycin injections
• Medication avoidance
• Vasoconstrictors
• Topical steroids *
• Other
• Vitamin A (12,500 to 15,000 Units daily)
• Potassium Iodide (Increases nasal secretions)
• Vasodilators
• Iron therapy
• Estrogen
• Corticosteroids *
• Vaccines
• Antibacterial (Pasturella, Bordetella)
➢ SURGICAL:
Young’s operation: is the most common procedure.
• Both the nostrils are closed completely within the nasal vestibules by
raising flaps. They could be opened after 6 months or later. In these
cases, mucosa may revert to normal and the crusting may be reduced.
• Circumferential flap elevation 1 cm cephalic to the alar rim during
operation.
Advantages
• Often provided relief of symptoms
Disadvantages
• Difficult to elevate circumferential flap
• Breakdown of central suture area common
• Difficult to cleaning
• Did not allow for periodic examination
• Recurrence after flap takedown
MODIFIED YOUNG’S OPERATION:
Advantages
• Technically easier than Young procedure
• No suture line breakdown
• No vestibular stenosis on takedown
Disadvantages
• Possible with large septal defects
• Does not allow for cleaning
• Does not allow for periodic examination
• Recurrence after flap takedown
NARROWING OF THE NASAL CAVITIES:
• Nasal chambers are very wide in atrophic rhinitis and air currents dry
up secretion leading to crusting . Narrowing the size of nasal helps
relieve the symptoms.
i. submucosal injection of teflon paste.
ii. insertion of fat, cartilage, bone or teflon strips under the
mucoperiosteum of the floor and lateral wall of nose and
mucoperichondrial of the septum
iii. Section and medial displacement lateral wall of nose.
❖ SECONDARY ATROPHIC RHINITIS:
• Complication of sinus surgery (89%)
• Complication of radiation (2.5%)
• Following nasal trauma (1%)
• Sequela of granulomatous diseases (1%)
• Sarcoid
• Rhino scleroma
• Sequela of other infectious processes
• Tuberculosis
• Syphilis
Were the pathogenic factors of secondary atrophic rhinitis.
❖ RHINITIS:
It is also a crust forming disease seen in patients who work in hot, dry and dusty
surrounding, e.g. bakers, iron and goldsmiths condition is confined to the
anterior third of nose particularly of the nasal septum. Here, the ciliated
columnar epithelium undergoes squamous metaplasia with atrophy of
seromucinous glands. Crusts form on the anterior part of septum and their
removal causes ulceration and epitaxis, and may lead to septal perforation.
➢ TREATMENT:
• Correction of the occupation surroundings
Application of bland ointment or one with an antibiotic and sterioid, to
the affected local membrane.
Nose pricking and forcible removal of crusts should be avoided.
• Nasal irrigation is a simple and well-tolerated procedure that has been
used by otolaryngologists for many years.
❖ RHINITIS CASEOSA:
• Caseosa rhinitis is an uncommon condition , usually unilateral and mostly
affecting male.
• Nose is filled with offensive purulent discharge and cheesy material . The
disease possibly arises from chronic sinusitis with collection of inspissated
cheesy material . Sinus mucosa becomes granulomatous.
• Bony walls of sinus may be destroyed, requiring differentiation from
malignancy.
➢ Treatment : Removal of debris and granulation tissue and free drainage
of the affected sinus is the key of treatment. Prognosis of this rhinitis type
is good.
❖ ALLERGIC RHINITIS: SYMPTOMS AND MANAGEMENT (EXAM)
Allergic rhinitis is clinically defined as a symptomatic
disorder of the nose induced by an IgE-mediated inflammation after allergen
exposure of the membranes lining the nose.
Inflammatory disorder of nasal mucosa, characterized by pruritus, sneezing,
rhinorrhoea and nasal congestion.
Adversely affects social life, school performance, and work productivity;
especially in patients with severe disease.
Loss of productivity, missed school and work days, and direct costs associated
with treatment create substantial costs to society.
MANAGEMENT:
Intra-nasal Steroids
First line drug in seasonal and perennial AR
Depending upon severity of disease, short courses of oral steroids in addition to
topical symptomatic relief
Fewer side effects
Intranasal antihistamines
Intranasal antihistamines are also proposed as first-line therapy.
The intranasal preparations targeted delivery that can increase dosage to nasal
tissues while decreasing systemic side-effects.
IMMUNOTHERAPY (AIT- ALLERGEN IMMUNO THERAPY)
•
Effective treatment of both AR & Asthma
•
•
Generally safe and well tolerated.
AIT represents a sole potentially curative and specific method of allergy
treatment.
•
AIT results in the restoration of immune tolerance toward the allergen of
interest.
•
Numerous studies have shown that the mechanisms underlying AIT include
desensitization effects, modulation of effector cell responses and related
antibody isotypes, modulation of migration of inflammatory cells.
RHINOLOGY:
❖ What are the 4 sinuses (name & function) :
• Anterior sinus: Maxillary sinus, Frontal sinus, Anterior ethmoid sinus
(Drainage in the middle meatus)
• Posterior sinuses: Posterior ethmoid sinus, sphenoid sinus (Drainage in
the superior meatus. The sphenoid sinus was drained to the sphenoid
ethmoidal recess.)
❖ Ostiomeatal complex (OMC):
Adjacent area structure centered on ethmoid infundibulum.
Including: Middle turbinate, uncinate process, ethmoid bulla Semilunar fissure,
natural ostium of anterior ethmoid sinus, frontal sinus and maxillary sinus.
❖ RHINOSINUSITIS:
➢ Anatomical characteristics of sinusitis：
1. Narrow ostium
2. The mucosa of the paranasal sinuses is continuous with that of the nasal cavity
3. Each ostium is adjacent to each other
4. Characteristics of each sinus and position of ostium
***The most important mechanism of sinusitis is the obstruction of drainage and
ventilation of ostium。
➢ GENERAL SYMPTOMS
Chills, fever, cough, anorexia, etc.
Local symptoms
1 nasal obstruction
2 Too much purulent mucus
Odor from anaerobic infection (odontogenic maxillary sinusitis)
3 Olfactory dysfunction
4 Headache
➢ TYPES OF PAIN: PAIN CHARACTERISTICS OF ACUTE
SINUSITIS:
➢
➢
➢ DIAGNOSIS:
➢ TREATMENT:
❖ WHAT ARE THE CLINICAL MANIFESTATIONS OF CHRONIC
SINUSITIS:
1 General symptoms：sometimes absent
2 Local symptoms：
① Too much purulent mucus：One of the main symptoms
② nasal obstruction：It is often caused by swelling of nasal mucosa and
polypoid change of turbinate.
③ Headache: It is mainly due to the absorption of bacterial toxins, resulting in
septic headache；Vacuum headache due to sinus ostium obstruction.
⑴ headache often accompanied by nasal obstruction, purulence and runny nose,
hypoesthesia.
⑵Headache often has time or regular parts.
⑶Headache can be relieved after nasal ventilation and drainage.
④ Loss or disappearance of olfactory
⑤
Visual dysfunction
❖ What are the clinical manifestations of maxillary carcinoma?
•
•
•
•
•
•
•
•
Purulent bloody snot
Nasal obstrustion
Pain and numbness in cheek
Protuberance of cheek
Molars pain and loosening
The hard palatal collapse and alveolar deformation
Eye syptoms: proptosis, diplopia, ocular pain and epiphora
Invasion of pterygopalatine fossa causes neuralgia and difficulty in
opening mouth
• Expansion of the skull base causes corresponding clinical features
• Cervical lymph node metastases are more common in the ipsilateral
submandibular lymph nodes
❖ Functional endoscopic sinus surgery(FESS) INDICATIONS AND
COMPLICATIONS:
• INDICATIONS:
Persistent disease despite medical therapy.
Recurrent RS with identifiable and related anatomical or acute pathological
abnormalities in the osteomeatal complex.
• COMPLICATIONS:
Losing your sense of smell. Some people report losing all or part of their sense of
smell.
Tearing eyes. FESS or sinus inflammation may cause your eyes to tear up.
Unusually heavy bleeding. While there’s little risk of heavy bleeding with FESS,
you may bleed more than usual. If that happens, your healthcare provider may
place packing in your nose and recommend you stay in the hospital so healthcare
providers can monitor your situation.
Leaking cerebral spinal fluid (CSF). This is a rare complication that affects fluid
surrounding your brain. If it leaks, you could develop meningitis or inflammation
of your brain.
Problems seeing. A few people have reported losing vision in one eye or having
double vision after their surgery.
NASOPHARYNGEAL CARCINOMA
❖ What are the Symptoms of Nasopharyngeal carcinoma (NPC)?
NPC is a squamous cell carcinoma (SCC) arising from the epithelial lining of the
nasopharynx.
• Symptoms of nose – Epistaxis, Nasal blockage, Nasal voice, Limitation
of mouth opening.
• Symptoms of the ear -- Block the Eustachian tube, Otitis media, Hearing
loss, Tinnitus, Aural fullness,
• Symptoms of the nervous system -- Invades the skull base,
Headaches(1/3), CNs involvement(neural paralysis), Bone erosion. 5th
Cranial nerve(loss of corneal reflex, mandibular deviation, facial sensory
disorder) ,6th Cranial nerve(oculomotor defect, diplopia), 12th Cranial
nerve(Difficulty in speaking, chewing, swallowing)
• Local spread(Swollen Superior deep cervical lymph node group,
painless,hard,moveless), Cervical lymph node rupture)
• Metastasis
❖ How to treat Nasopharyngeal carcinoma (NPC)?
1. Radiotherapy: initial
A combination of radiotherapy and chemotherapy: advanced disease
2. Surgical intervention:
Previous chemoradiation therapy has failed.
localized, well-defined, residual, or recurrent cancer.
Neck dissection in the setting of residual or recurrent nodal metastases that are not
responsive to nonsurgical treatment.
3. Interventional treatment
Through selective arterial cannulation the chemotherapeutic agents are injected
into the tumor in order to kill neoplastic cells and avoid injuring the neighboring
tissues as far as possible.
4. Biological treatment
Regulate patients’ immune system function.
ENT
Obstructive Sleep Apnea Syndrome
Definition of OSAHS
In OSAHS transient upper airway obstruction results in intermittent cessation
of air flow or breathing though there is normal respiratory effort. An apneahypopnea index is more than 5 events per hour of sleep. during the
episodes, oxyhemoglobin disaturation becomes less than 90%
Symptoms of OSAHS
Daytime symptoms:
waking up without feeling refreshed
morning headache, dry and sore throat
excessive daytime sleepiness
daytime fatigue
impaired concentration
irritability/ personality change
Night time symptoms:
snoring
witnessed apnea
gasping and choking sensations
restless sleep
Complications of OSAHS
1. cardiovascular consequences: hypertension, arrhythmia, coronary heart
disease, heart failure, sudden death
2. Neurocognitive effects
3. Traffic accidents
4. Divorce
Etiology
ENT
1
1. Age
2. Sex
3. Obesity
4. Social habits
5. Obstructie upper airway anatomy:
Obstruction of the nasal airway: turbinate hypertrophy, septal deviations,
nasal polyps, adenoid hypertrophy
Oral cavity: tonsillar hypertrophy, soft palate elongation
Craniofacial abnormalities: micrognathia
Diagnosis and Evaluation of OSAHS
For evaluation aim is:
1. identify if the patient has OSAHS
2. identify the potential causes and predisposing factors
3. locales the levels of obstruction in the upper airway
ESS scale (look at ppt)
Physical examination
Nasal examinations: nose and nasal cavity, nasopharynx
Oral and oropharyngeal examinations: palate, tongue, tonsil, mandibular
size, the position of the hyoid, the hyoid’s relationship to the mandible
Diagnosis of OSAHS
Polysomnograpthy (PSG): is the gold standard for diagnosis of OSAHS.
The technique entails an impatient study involving overnight assessment
of a number of measures
Grading the severity of OSAHS: the frequency of apnea and hypopnea is
used to grade the severity of OSAHS sd the apnea/hypopnea index (AHI)
Mild OSAHS (5 - 20 events per hr, 5<AHI<=20)
Moderate OSAHS (21-40 events per hr, 20<AHI<=40)
Severe OSAHS (More than 40 events per hr,AHI>40)
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2
the degree of oxyhemoglobin desaturation (SAO2): is less than 85% in
moderate OSA and less than 60% in severe OSA
Treatment of OSAHS
1. Non-surgical treatment:
Lifestyle modifications: such as behavioural changes, weight loss and
lifestyle changes
Nasal continuous positive airway pressure (CPAP): is the first choice.
the reason CPAP is so effective is that the pressure acts along the entire
upper airway so that all potentially occluding segments are stabilized
Intraoral devices: patients tolerate these devices more than CPAP, these
devices should be fitted and followed by an experienced dentist or
orthodontist
2. Surgical treatment:
Uvulopalatopharynoplasty (UPPP): this procedure involves
tonsillectomy, uvulectomy and excision of a variable segment of the soft
palate
Infectious Diseases of Larynx
Pediatric acute laryngitis
1. Clinical symptoms:
acute onset: progressive, rapid fever
hoarseness: barking cough
stridor: edema of subglottic portion, inspiratory dyspnea, three
depression signs
respiratory infection
2. Causes:
narrow laryngeal cavity, loose mucosa
soft laryngeal cartilages
abundant lymphatic and glandular tissues
week cough reflex
ENT
3
poor immunity resistance
laryngospasm
constrist laryngeal cavity
3. Differential diagnosis:
foreign body of trachea
laryngealspasm in children
congenital diseases of larynx
4. Treatment
Release laryngeal obstruction
Oxygen, spasmolysis
Supportive treatment
Decrease oxygen consumption
Adult acute epiglottis
1. Defintion: is an acute inflammation involved epiglottis and surrounding
supraglottic structures, there is marked edema and beta-hemolytic
streptococcus
2. Clinical features include:
Rapid progress
pale, fever
sore throat, dysphagia
dyspnea, stridor
epiglottic abscess
3. Physical examination: supraglottic portion diffused; hyperemia and edema
especially for epiglottis. Swelling of neck lymphatic nodes
4. Differential diagnosis:
acute laryngotrachelitis
laryngeal diphtheria
epiglottic cyst
ENT
4
5. Treatment:
anti infection: antibiotics and glucocorticoid, aerosol inhalation, abscess
drainage
airway: cricothyroid laryngotomy, tracheotomy, intubation
support
Anatomy of Larynx
Laryngeal obstruction
Definition
is a disease of the larynx or adjacent organ that makes the throat narrow to
the point of breathing difficulties, because the laryngeal obstruction can
cause hypoxia if it is not treated on time the patients life will be endangered
Etiology
Laryngeal obstruction can be cause by:
Inflammations: acute laryngitis, epiglottis, diperthia, tuberculosis, syphilis
Tumors: benign and malignant
Laryngeal paralysis: paralysis of one side of the larynx may cause very mild
obstruction or none at all. bilateral abductor paralysis produces a serious
obstruction to respiration
Foreign bodies
Congenital weakness of laryngeal structures, malformations
Edema: allergic reactions or instrumentation
Trauma
: heterogeneous
Symptoms and signs
symptoms of laryngeal obstruction include:
ENT
5
1. Inspiratory dyspnea: is the earliest symptom of a gradually developing
laryngeal obstruction
2. Inspiratory stridor: due to airflow sucked through narrow glottic area
causing vocal cord vibration
3. Retractive recession of the soft tissue: as dyspnea increases, retraction
of the supraclavicular and epigastric soft parts on inspiration is noted
due to the lower air pression in chest
4. Hoarseness
5. Cyanosis
Classifications
There are four grades:
1 degree: there is no dyspnea while the patient is quiet, but can appear mild
inspiratory dyspnea during moving or crying
2 degree: they could have slight inspiratory dyspnea combined with three
recession symptoms. the symptoms become serious after exercise. however
symptoms of cyanosis aren't obvious. Pulse is normal
3 degree: inspiratory dyspnea becomes more serious, three recession
symptoms are obvious. use of accessory muscles of respiration causes
characteristic retraction, which is most noticeable at the subrasternal fossa
but is also present at the intercostal space and above the clavicles. the
patient may become ashen. Restlessness is prominent in children.
symptoms of short of oxygen is obvious
4 degree: patients have reached extremely asphyxia
Treatment
Medication: for 1 and 2 degree dyspnea, medication has reliable affection in
reducing obstructive edema of an inflammatory process, such as antibiotics
penicillin and steroid
Tracheostomy: should be done especially for 3 to 4 degree laryngeal
obstruction
CASE: an elderly man has difficulty breathing for 2 weeks. smoking for 30 yrs,
alcohol for 60 yrs. Upon examination mild inspiratory dyspnea and inspiratory
ENT
6
stridor when sitting quietly and the dyspnea and stridor become worse when
exercising. no recession symptom
Tracheostomy
Definition
this is a procedure wherein an opening is made in the anterior tracheal wall
which is brought to skin by inserting a tube
Indication for tracheostomy
1. 3 to 4 degree laryngeal obstruction
2. retention of the secretions in the lower respiratory tract
3. preventative surgery for respiratory insufficiency before maxillofacial, oral,
pharyngeal and laryngeal operation
4. Mechanical ventilation for a long time
Postoperative complications
1. surgical emphysema of the neck and chest
2. displacement of tube
3. a high tracheostomy results subsequent subglottic stenosis
4. tracheomalacia
5. difficult decannulation
6. pulmonary infection
7. fatal hemorrhage
Care of tracheostomy
1. keep the correct position of trachestomy tube by selecting a proper sized
tube
2. removal of secretions
3. cleaning of tracheostomy tube
4. avoid infection
5. humidification and prevention of crusting
ENT
7
6. a trachesotomised patient cannot shout or call for help
Carcinoma of larynx
Etiology
smoking
drinking
viruous infection
sex hormone
environment
Classification
Classification of Laryngeal tumor:
1. Supraglottic
2. Glottic
3. Subglottic
4. Transglottic
Signs and symptoms
1. Subraglottic: patient complains of a sense of irritation as a foreign body in
his throat or senses of rawness or dryness which makes him discomfortable.
Poor prognosis
2. Glottic: free margin of the upper surface of tru vocal cord in its anterior twothird. Reaches to the anterior commissure and the other cord. rare lymph
node metastasis. Excellent prognosis
ENT
8
3. Subglottic: subglottic region is usually involved by the downward extension
of the glottic tumor and its very rare that a primary starts in the subglottis
itself. The spread occurs to pretracheal,paratracheal and mediastinallymph
nodes. Poor prognosis
The spread of laryngeal carcinoma
directly to the adjacent tissues
regional lymph nodes
lungs, liver and bone through the blood
Treatment
1. surgery
2. radiotherapy: retains the voice and the normal air passage
3. chemotherapy
For early stage T1 and T2 there are three options; carbon dioxide laser
surgery, open partial surgery and definitive RT
For advanced stage tumor extended partial laryngectomy or total
laryngectomy
Laryngeal function reconstruction after total laryngectomy includes artificial
larynx, electronic larynx and esophageal phonation
ENT
9
EAR (print ppt)
> Anatomy of ear :
● External ear - Collect sound waves
● Middle ear - Ossicular chain conduction
● Inner ear - Sensorineural conduction & balance
> External ear :
- It collect sound waves and channels them into the external auditory meatus where
the sound is amplified.the.the sounds waves travel toward the tympanic membrane
(ear drum).
- Tympanic membrane separates the outer ear from the middle ear.
Tympanic membrane and cavity : has 6 walls
1. Lateral wall formed by Tympanic membrane.
2. Medial wall - promontory wall (outer wall of inner ear) contains oval and round
windows.
3. The roof - tegment tympani
4. The posterior or mastoid wall
5. The floor (or jugular wall)
6. The anterior (or carotid) wall
> middle ear :
● Tympanic cavity
● Eustachian tube
- Connect tympanic cavity to the nasal pharynx
- Its posterior third is bony, and its anterior two thirds is cartilaginous
- It serves to equalize air pressures in tympanic cavity and nasal pharynx
● Ossicular chain - consists of three bones; the malleus, incus, and stapes joined by
two synovial joints, the incudomalleolar and incudostapedial joints
> inner ear :
● Cochlea
● Vestibule
● Function and test - audiogram , vestibular function
> disease of external ear and tympanic membrane:
- Chronic Otis media
- Pseudocyst of auricle
- Perichondritis of auricle
- Pseudocyst of auricle
- Anterior auricular fistula
- Furnucle of external auditory canal
- Acute Otis externa
- Cerulean of external auditory canal
- Cholesteastoma of external auditory canal
- Fungus of external auditory canal
- Tympanic membrane perforation.
1
Head and neck tumor
> Histology: > 90% squamous cell carcinoma Early-stage disease (l, ll) curable: > 80%
Locally advanced disease has poorer prognosis.5-yr survival rate:<40%
> Region affected by Cancer : most common type of cancer in the head and neck is
squamous cell carcinoma, which arises in the cells that line the inside of the nose, mouth
and throat.
- HNC includes cancers of the Mouth, Nose, Sinuse,Salivary glands,Throat, Lymph
nodes in the neck
> Factors Involved :
● Tobacco products: Smoking Tobacco,Cigarettes,Cigars,Pipes,Chewing Tobacco
● Alcohol
● Chemicals:Asbestos,Chromium,Nickel,Arsenic,Formaldehyde
● Other Factors: Ionizing Radiation,Plummer-Vinson Syndrome,Epstein-Barr Virus,
Human Papilloma Virus
> Symptoms ● A mass in the neck
- Persistent hoarseness in a smoker lasting more than several weeks
Pain in the ear (otalgia), pain in the throat on swallowing (odynophagia), or difficulty
swallowing (dysphagia)
- A lump below or in front of the ear
- A persistent oral ulcer
- Unilateral serous otitis media
● Oral cavity- white or red patch on the gums, tongue, swelling of the jaw.
● Nasal Cavity and sinuses :Sinuses that are blocked and do not clear,Chronic sinus
infections that do not respond to treatment with antibiotics,bleeding through the nose
frequent headaches, swelling or other trouble with the eyes, pain in the upper teeth
● Salivary glands - Swelling under the chin or around the jawbone; Numbness or
paralysis of the muscles in the face; Pain that does not go away in the face
● Pharynx - Sore throat and painful and/or difficult swallowing,Serous otitis
media,dysphagia, dysarthria, and otalgia, neck mass.
● Larynx - Hoarseness is common early in glottic cancers but is a late symptom for
supraglottic and subglottic cancers, Airway obstruction,otalgia, development of a
neck mass, or a "hot potato" voice.
> warning signs of neck and cancer - hoarseness,erythoplasia , serious Otis media , neck
mass, dysphagia,epistaxis and persistent sore throat.
> Factors Delaying HNC Diagnosis
- Two-thirds of oral cavity cancers and 77% of oropharyngeal cancers are not
diagnosed until they are larger than four centimeters in diameter.
- Reason can be:
• Patient procrastination in seeking medical attention
• Delayed diagnosis by physician
• Prolonged asymptomatic period all contribute to late diagnosis.
2
> Cancers spread in three main ways
- The first is direct extension from the primary site to adjacent areas.
- The second is spread through the lymphatic channels to lymph nodes.
- The third is spread through the blood vessels to distant sites in the body.
HNC, a spread to the lymph nodes in the neck is relatively common.
> T stage: The primary cancer(hypopharynx) invades in various directions, which are
color-coded vectors(arrows)
representing stage of progression: Tis,yellow; Tl, green; T2, blue; T3, purple; T4a,
red; and T4b, black
> Cervical lymph nodes :
3
4
> The risk of regional lymph node metastasis from a carcinoma of the true vocal cords is
exceedingly small.
- However, the risk increases with progression from the vocal cords to the false vocal
cords, aryepiglottic fold, pyriform sinus, and pharyngeal wall.
- Nearly two-thirds of patients with primary carcinomas of the hypopharynx present
with clinically palpable regional lymph node metastasis.
- The T stage usually reflects tumor burden or invasiveness and is correlated with risk
for nodal metastasis for any given primary site.
> OTHER NODAL FACTORS AFFECTING PROGNOSIS
● When enlarged lymph nodes are detected, the actual size of the nodal mass(es)
should be measured.
● It is recognized that most masses over 3 cm in diameter are not single nodes but are
confluent nodes or tumor in soft tissues of the neck.
● Careful clinical examination; radiologic assessment; and, in surgically treated
patients, detailed pathologic examination is necessary for documentation of tumor.
● Involvement of lower cervical lymph nodes (levels IV and VB) by metastatic cancer
usually is ominous.
● Lymphovascular invasion (LVI) and perineural invasion (PNI) by a tumor, as well as
the presence of tumor emboli in regional lymphatics, also has an adverse impact on
prognosis
> Diagnostic Test:
Physical examination , Endoscopy ,Laboratorytests,X-rays,CT scan, Magnetic resonance
imaging (MRI),PET-CT (positron emission computerized tomography)
Biopsy,FNAC(Fine-needle aspiration cytology)
5
> Neck Masses :
※The rules of neck masses 7 rule neck mases:
• 7 days: Inflammatory lesions • 7 weeks: Neoplasm
• 7 years: Congenital lesions
> Treatment : The treatment plan for an individual patient depends on a number of factors,
including the exact location of the tumor, the stage of the cancer, the person's age and
general health.
> SURGICAL TREATMENT
- Comprehensive Neck Dissection
applied to all surgical procedures in the lateral part of the neck that comprehensively remove
cervical lymph nodes from levels I to V.
• Classic radical neck dissection
• Extended radical neck dissection (i.e., resection of additional regional lymph nodes or
sacrifice of other structures such as cranial nerves, muscles, or skin)
• Modified neck dissection type I (MND-I), which selectively preserves one structure, the
spinal accessory nerve
• Modified neck dissection type II (MND-II), which preserves two anatomic structures, the
spinal accessory nerve and the sternocleidomastoid muscle, but sacrifices the internal
jugular vein
• Modified neck dissection type III (MND-III), which preserves three anatomic structures, the
spinal accessory nerve, internal jugular vein, and sternocleidomastoid muscle
- Selective Neck Dissection
Selective neck dissection operations remove only select groups of lymph nodes at risk of
micrometastasis in the clinically N0 neck. These operations include the following:
• Supraomohyoid neck dissection • Jugular node dissection
• Anterolateral neck dissection
• Posterolateral neck dissection
• Central compartment neck dissection
6
Foreign bodies of Air passages (print)
> Etiology :
> Nature of foreign bodies :
7
8
Hearing loss and vertigo
Q.1 Brief of auditory pathway (How we hear?)
Q.2 The main methods of evaluating hearing loss (tests)
1. Traditional Screening Tests
Watch test, Finger friction tests,Voice Tests (conversation and whisper)
2. Tuning Fork Tests (TFT)
3. Audiometric Tests(Impedance audiometry and pure tone audiometry)
4. Evoked Response Audiometry
5. Otoacoustic emissions
6. Central auditory tests
7. Hearing evaluation in infants and children
8. Rinne Test
• normal: AC>BC (positive Rinne)
• conductive HL: BC>AC (negative Rinne)
• sensorineural HL : AC>BC (positive Rinne or false negative
9.Weber Test
normal / symmetrical: loudness of tone equal in both ears
conductive hearing loss: tone louder in affected ear
- sensorineural hearing loss: tone louder in better ear
3.When we need the hearing evaluation?
- Type of hearing loss
- „Severity of hearing loss
- „Site of lesion
- „Cause of hearing loss
9
Q4. The classification of hearing loss.
1. Non-organic
Malingering (pretend to be ill )
psychogenic ( mental or emotional rather than physiological in origin)
2. Organic
Conductive hearing loss (CHL)
- Sensorineural hearing loss (SNHL)
peripheral : Cochlear (Sensory) ii. CN VIII (Neural).
Central : brainstem (medulla, pons, midbrain) ii. Thalamus iii. Temporal lobe
3. Mixed hearing loss
Q5. Managements of hearing loss.
- Medication : Antibiotics, glucocorticoids, drugs for improving circulation, drugs for
nourishing nerves.
- Surgery:Grommet Insertion. , Cholesteatoma resection of middle ear
- Artificial hearing device - hearing aids
- Cochlear implantation
Q6. Common causes of vertigo diseases.
Q7.The characteristics, diagnosis and treatment of BPPV ?
1.
-
-
Characteristics :
BPPV is the most common cause (20–40%) of peripheral vertigo.
Age: 11–84 years; mean age of onset fourth to fifth decades.
Incidence increases with age
It is a peripheral vestibular disease induced by changes in head position relative to
the direction of gravity, characterized by recurrent transient vertigo and characteristic
nystagmus.
It is often self-limiting and prone to recurrence
2. Diagnosis :
- Dix-Hallpike test: The BPPV is classified as active if rotatory nystagmus is elicited by
Dix-Hallpike test - Otolithiasis of posterior semicircular canal
- Roll test - Otolithiasis of horizontal semicircular
10
3.
-
Treatment :
consists of repositioning maneuvers; epley and barbecue maneuvers.
Oculomotor examination
Position test
Double temperature test
Video head pulse test
Vestibular evoked myogenic potential
Q8.Main features of MD?
- Ménière’s disease symptom complex consists of spontaneous episodic vertigo,
fluctuating sensorineural hearing loss (SNHL), tinnitus and often a sensation of
fluctuating ear fullness.
- 2 phases – early (almost always unilateral and symptoms episodic) and late
(symptoms present more or less all the time with episodes of exacerbation consisting
of an increased severity of symptoms)
- Clinical features : vertigo, deafness ,tinnitus, aural pressure.
- Treatment of Ménière’s disease :
> Medical treatment - recommending moderate sodium restriction (1-2 sodium/day),Diuretics
,Histamine (vasodilates labyrinth vasculature),vestibular suppressants
> Surgical Treatment : Hearing-conservative nonvestibular ablative surgery,
Hearing-conservative vestibular ablative surgery: Vestibular neurectomy;
Non-hearing conservative vestibular ablative
- diagnosis criteria :
A. Two or more spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours.
B. Audiometrically documented low- to medium- frequency sensorineural hearing loss in one
ear, defining the affected ear on at least one occasion before, during or after one of the
episodes of vertigo.
C. Fluctuating aural symptoms (hearing, tinnitus or fullness) in the affected ear.
D. Not better accounted for by another vestibular diagnosis.
11
COMPLICATIONS OF SUPPURATIVE OTITIS MEDIA
> Acute Otitis media (AOM) :
- An infection of the air-filled space behind the eardrum (the middle ear).
- An ear infection is usually caused by bacteria or viruses.
- It is most commonly seen in children between the ages of 6 to 24 months.
- The most common bacterial organisms causing otitis media are Streptococcus
pneumoniae.
●
If not treated the complications are : tympanic membrane (TM) perforation,
mastoiditis, labyrinthitis, petrositis, meningitis, brain abscess, hearing loss, lateral
and cavernous sinus thrombosis.
●
-
Pathophysiology :
Bacterial infection of the middle ear results from nasopharyngeal organisms causes
migrating via the eustachian tube.
Obstruction at the eustachian tube isthmus (i.e., the narrowest portion) results in
accumulation of middle ear secretions; secondary bacterial or viral infection of the
effusion causes suppuration and features of acute otitis media
-
●
Clinical features - fever, headache, ear pain , slight hear loss,cough,rhinitis
●
-
Treatment :
antibiotic therapy: Amoxicillin 80 to 90 mg per kg per day, given orally in two divided
doses (First-line drug)
Azithromycin,Cefpodoxime,cefdinir, ceftriaxone for children with penicillin allergy.
Analgesics such as Acetaminophen, Antipyrine and ibuprofen .
Management : High-dosage amoxicillin (80 to 90 mg per kg per day, divided into two
daily doses for 10 days) is recommended as first-line antibiotic therapy in children. In
children older than six years with mild to moderate disease, a five- to seven-day
course is adequate.
-
●
●
Factors affecting risk of AOM : age , breastfeeding , daycare attendance,
ethnicity,winter season, antibiotic treatment failure.
Assessment - hearing and language testing is recommended for recurrent effusion.
12
> Otitis media with effusion (OMR):
- Is a collection of non-infected fluid in the middle ear space. It is also called serous or
secretory otitis media (SOM). This fluid may accumulate in the middle ear as a result
of a cold, sore throat or upper respiratory infection.
●
●
●
-
Symptoms - A feeling of fullness in the ear,Muffled hearing,Fluid that drains from the
ears (if the eardrum has ruptured),Some pain inside the ear
If your child’s otitis media with effusion develops into an infection, he or she may
have other symptoms. These include:Pain in the
ear,Fever,Irritability,Listlessness,Trouble hearing,Not feeling like eating or sleeping
Etiology :
Risk factors for OME include passive smoking, bottle feeding, day-care nursery, and
atopy.
Both children and adult can develop OTE.
As the Eustachian tube is positioned more horizontally in younger children. As the
child develops into an adult, the tube elongates and angles caudally. Therefore, OME
is more common in children, and the position of the head at this age can influence
the development of OME.
●
Pathophysiology : After an acute otitis media in children, fluid builds up in the middle
ear, it places pressure on the tympanic membrane. The pressure prevents the
tympanic membrane from vibrating properly, decreases sound conduction, and
therefore results in a decreased hearing.
●
-
Treatment and management:
generally resolves spontaneously with watchful waiting. However, if it is persistent,
myringotomy with tympanostomy tube insertion is considered an effective treatment.
Hearing aids non invasive treatment
If not, surgery should be considered.
-
13
CHRONIC SUPPURATIVE OTITIS MEDIA and Cholesteatoma
> Cholesteatoma :
In normal persons, there is no keratinizing squamous epithelium in the middle ear
cleft and its presence (skin in the wrong place) is called cholesteatoma.
● Structure of Cholesteatoma:
• Cholesteatoma is an epidermal inclusion cyst
• It contains desquamated debris (mainly white-yellow keratin flakes resembling cholesterol
crystals) from its keratinizing squamous epithelial lining.
• Cholesteatoma has two parts—matrix and central white mass
◆ Matrix: It is made up of keratinizing squamous epithelium, which rests on a thin stroma of
fibrous tissues.
◆ Central white mass: It consists of keratin debris, which is produced by the matrix.
●
-
Types of Cholesteatoma
Congenital cholesteatoma - It arises from the embryonic epidermal cell rests
(keratinizing epithelium) entrapped in the middle ear cleft or temporal bone. important
sites : middle ear, petrous apex and the cerebellopontine angle.
◆ Clinical features: A middle ear congenital cholesteatoma presents with conductive hearing
loss and a white mass that can be seen behind an intact tympanic membrane. It may rupture
through the tympanic membrane and present with a discharging ear. Then it becomes
indistinguishable from CSOM.
- Acquired cholesteatoma
◆ Primary acquired cholesteatoma: In primary acquired cholesteatoma, there is neither
history of previous otitis media, a preexisting perforation, nor otorrhea.
◆ Secondary acquired cholesteatoma
> Pathogenesis of Acquired Cholesteatoma :
• Invagination theory : this theory explains primary acquired cholesteatoma.
Invagination of tympanic membrane from pars flaccida (attic) or posterosuperior part of pars
tensa occurs in the form of retraction pocket.
• Epithelial invasion or migration theory :This theory explains secondary acquired
cholesteatoma.The keratinizing squamous epithelium of tympanic membrane or deep canal
wall migrates into the middle ear through a tympanic membrane perforation.
• Basal cell hyperplasia theory : • Under the influence of infection, basal cells of germinal
layer of skin can proliferate and lay down keratinizing squamous epithelium.
- Prickle epithelial cells of pars flaccida can invade the subepithelial tissue by means of
proliferating columns of epithelial cells. Basal lamina disruptions have been
documented.
- These basal lamina breaks allow invasion of epithelial cones into the subepithelial
connective tissue and the formation of microcholesteatomas, which may enlarge and
perforate an intact tympanic membrane and present as primary acquired
cholesteatoma.
14
• Squamous metaplasia theory :
- Middle ear mucosa, like respiratory mucosa elsewhere, can undergo metaplasia due
to repeated infections and transform into squamous epithelium.
- Such a change has also been reported in OME. Middle ear mucosa can undergo
metaplasia due to repeated infection through a preexisting perforation and result in
secondary acquired cholesteatoma.
The simple squamous or cuboidal epithelium of middle ear cleft can undergo a
metaplastic transformation into keratinizing epithelium.
- The pluripotent epithelial cells, stimulated by inflammation, can become keratinizing,
which would enlarge because of accumulated debris and contact with tympanic
membrane.
- With infection and inflammation, cholesteatoma results in perforation of the tympanic
membrane and present as primary acquired cholestea.
> Genesis of primary and secondary cholesteatomas :
• Primary acquired cholesteatoma
- Invagination of pars flaccida.
- Basal cell hyperplasia.
- Squamous metaplasia.
• Secondary acquired cholesteatoma :
- Migration of squamous epithelium
- Metaplasia.
> CHRONIC SUPPURATIVE OTITIS MEDIA :
- CSOM is a long-standing infection of a part or whole of the middle ear cleft
characterized by ear discharge and a permanent perforation.
- A perforation becomes permanent when its edges are covered by squamous
epithelium and it does not heal spontaneously. A permanent perforation can be
likened to an epithelium-lined fistulous track
- Incidence is higher in poor socioeconomic classes, poor nutrition and lack of health
education.
> Epidemiology:
- It affects both sexes and all age groups.
- Chronic suppurative otitis media is the leading cause of hearing impairment in rural
population
> Assessment:
• Examination under microscope It is essential in every case and provides useful information
regarding presence of granulations, in-growth of squamous epithelium from the edges of
perforation, status of ossicular chain, tympanosclerosis and adhesions.
• Audiogram. It gives an assessment of degree of hearing loss and its type.
• Culture and sensitivity of ear discharge. It helps to select proper antibiotic ear drops.
Aerobic organisms: Pseudomonas aeruginosa (most common), Proteus, Escherichia
coli and Staphylococcus aureus.
Anaerobes: Bacteroides fragilis (most common) and anaerobic streptococci
• Mastoid x-rays/CT scan temporal bone
15
> CSOM examination :
• Suction clearance and examination under operating microscope forms an important part of
the clinical examination and assessment of any type of CSOM
> Types of CSOM:
> Classification of CSOM:
1. Mucosal disease :
- active chronic suppurative otitis media
- Inactive (permanent perforation)
- Healed (adhesive otitis media)
2. Squamosal disease :
- Retraction pockets in pars flaccida or in pars tensa
- Active (cholesteatoma with discharge)
16
> TUBOTYMPANIC (MUCOSAL) CSOM OR CSOM WITHOUT CHOLESTEATOMA :
● Aetiology - The disease starts in childhood and is therefore common in that age
group.
1. It is the sequela of acute otitis media usually following exanthematous fever and leaving
behind a large central perforation.
2. Ascending infections via the eustachian tube. Infection from tonsils, adenoids and infected
sinuses may be responsible for persistent or recurring otorrhoea. Ascending infection to
middle ear occurs more easily in the presence of infection.
3. Persistent mucoid otorrhoea is sometimes the result of allergy to ingestants such as milk,
eggs, fish, etc.
●
-
Pathology Perforation of pars tensa. It is a central perforation and its size and position varies
Middle ear mucosa
Polyp.
Ossicular chain
Tympanosclerosis.
Fibrosis and adhesions.
● Clinical features - ear discharge ,hearing loss ,perforation, middle ear mucosa.
• Active (wet perforation) : In the presence of inflammation of mucosa and mucopurulent
discharge, the disease is called active
• Inactive (dry perforation): In the absence of inflammation of mucosa and mucopurulent
discharge, the disease is called inactive.
• Healed chronic otitis media :Healing of perforation leads to its closure with thin membrane
(fibrous layer absent). It may be associated with tympanosclerosis or some conductive
hearing loss.
●
-
Assessment Examination under microscope
Audiogram. It gives an assessment of degree of hearing loss and its type.
Culture and sensitivity of ear discharge. It helps to select proper antibiotic ear drops.
Mastoid x-rays/CT scan temporal bone
● Treatment - Medical therapy
• Aural toilet: Removal of discharge and debris from the EAC can be done by dry
mopping with absorbent cotton buds and suction clearance under microscope.
• Antibiotic or steroid ear drops: Antibiotic or steroid ear drops 3–4 times a day in wet and
running ears have local antimicrobial and anti-inflammatory effects
• Systemic antibiotics: They are prescribed only in cases of acute exacerbation. There is no
role of systemic antibiotics in the treatment of uncomplicated CSOM.
• Treatment of source of infection: Treatment of contributory diseases (infections of tonsils,
adenoids, nose and paranasal sinuses and allergy) is important.
17
- Surgical treatment:
•Removal of ear polyp or granulations: They facilitate ear toilet and treatment
with local antibiotics
•Tympanoplasty: In a dry ear, myringoplasty or tympanoplasty restores hearing and checks
repeated infection from the external ear canal.
● Patient’s instructions
• Water should not enter in the ear while bathing, swimming and hair wash. The ear plugs
and rubber inserts may be employed.
• Avoid forceful nose-blowing as it can push the infection from nasopharynx to middle ear.
• Avoid self-cleaning of the ear.
• Stop the ear drops once the ear becomes dry.
• Take treatment of upper respiratory infections at the earlier,
> CHRONIC OTITIS MEDIA WITH CHOLESTEATOMA :
● Pathology :
• cholesteatoma
• osteitis and granulation tissue. Osteitis involves outer attic wall and posterosuperior margin
of the tympanic ring. A mass of granulation tissue surrounds the area of osteitis and may
even fill the attic, antrum, posterior tympanum and mastoid. A fleshy red polypus may be
seen filling the meatus
• ossicular necrosis. It is common in atticoantral disease. Destruction may be limited to the
long process of incus or may also involve stapes superstructure, handle of malleus or the
entire ossicular chain. Therefore, hearing loss is always greater than in disease of
tubotympanic type. Occasionally, the cholesteatoma bridges the gap caused by the
destroyed ossicles and hearing loss is not apparent (cholesteatoma hearer).
• cholesterol granuloma. It is a mass of granulation tissue with foreign body giant cells
surrounding the cholesterol crystals. It is a reaction to long-standing retention of secretions
or haemorrhage, and may or may not coexist with cholesteatoma. When present in the
mesotympanum, behind an intact drum, the latter appears blue.
● Clinical features:
• Symptoms:
- No symptoms: Patients may remain asymptomatic in initial stages of disease.
- Ear discharge
- hearing loss.
- bleeding
Signs:
• Perforation. It is either attic or posterosuperior marginal type .A small attic perforation may
be missed due to presence of a small amount of crusted discharge. Sometimes, the area of
perforation is masked by a small granuloma.
• Retraction pocket. An invagination of tympanic membrane is seen in the attic or
posterosuperior area of pars tensa.
• Cholesteatoma. Pearly-white flakes of cholesteatoma can be sucked from the retrac tion
pockets. Suction clearance and examination under operating microscope forms an important
part of the clinical examination and assessment of any type of CSOM
18
● Assessment :
• examination under microscope.
• tuning Fork tests and audiogram.
• x-ray mastoids/CT scan temporal bone
• culture and sensitivity of ear discharge
● Features Indicating Complications in CSOM :
• Pain. Pain is uncommon in uncomplicated CSOM. Its presence is considered serious as it
may indicate extradural, perisinus or brain abscess. Sometimes, it is due to otitis externa
associated with a discharging ear.
• Vertigo. It indicates erosion of lateral semicircular canal which may progress to labyrinthitis
or meningitis. Fistula test should be performed in all cases.
• Persistent headache. It is suggestive of an intracranial complication.
• Facial weakness. indicates erosion of facial canal.
• A listless child refusing to take Feeds. and
easily going to sleep (extradural abscess).
• Fever, nausea and Vomiting.
• Irritability and neck rigidity. (meningitis).
• Diplopia. (Gradenigo syndrome) petrositis.
• Ataxia. (labyrinthitis or cerebellar abscess).
• Abscess round the ear. (mastoiditis)
● Treatment :• Surgical Treatment :The mainstay of treatment is surgical removal of cholesteatoma and
rendering the ear safe. The secondary part of the surgery includes preservation and
reconstruction of hearing system. In presence of complications, surgery should be performed
at the earliest possible
• Atticotomy: Transcanal.
• Canal-wall-up procedure (intact posterior meatal wall or closed procedure): •
Canal-wall-down procedure (open procedure):
• Tympanoplasty:
●
Factors determining extent and type of surgery:
• Hearing status of both the ears • Extent of cholesteatoma
• Mastoid pneumatization.
• Function of ET
• Presence of complications
• Patient factors: Age, occupation and general medical status
19
Ppt 1 oral and maxillofacial examination:
Routine examinations of Oral:
Equipment’s and their uses
Mouth mirror
•
Reflect and focus light to increase the lighting of the inspected part
•
Reflect the image of the inspected part and see the part that cannot be directly reached by the
sight
•
Pull or press soft tissues such as lips, cheeks and tongue
Probe
•
Explore tooth surface defects
•
Detect the feeling of the affected teeth and find the sensitive parts of the teeth
•
Special periodontal probe (with scale and blunt head) for checking the sensory function of skin or
mucosa
Tweezers
•
Test the tooth mobility
•
Remove corrupt tissue and foreign matter
•
Clamping supplementary and drugs
•
Percussion examination
Dental Unit
•
It is mainly used for oral surgery and examination and treatment of oral diseases.
Interrogation


1)
2)
3)
4)
5)

main suit
History of Present Illness
Time of onset, inducement and reason
The location, nature, time and degree of pain
The evolution of pathological changes
Are there any complications？
What examinations and treatments have patients undergone？
Past history
1) Heart disease, hyperglycemia, diabetes, blood disease
2) History of drug allergy (especially history of anesthetic allergy)
WHAT ARE THE INSPECTIONS OF THE ORAL CAVITY?
Inspection
•
tooth —Occlusal relationship, color, caries, calculus, loss
•
gingiva — swelling, hyperplasia, abscess, bleeding, overflow
•
oral mucosa —Color, herpes, ulcer, hyperkeratosis, lump
•
tongue —Ulcers, motor or sensory abnormalities
•
salivary glands —Catheter mouth redness and swelling Salivary overflow during salivary gland
extrusion
Probing (dental probe)
•
Determine the location and scope of the lesion
•
Check tooth movement
•
To explore whether the edge of the filling is close to the tooth and whether there is secondary
caries
•
Find the sensitive sites
•
Probing the depth of periodontal pocket
•
Detect the condition of subgingival calculus
•
Sense the direction of the fistula
Percussion
•
Vertical percussion — periapical lesion
•
Lateral percussion — lesions on one side of the periodontal ligament
Palpation
•
Whether there is gingival abscess - toothache or fluctuation
•
Perception of jaw force —With or without traumatic occlusion
Bite diagnosis
•
Observe the bite marks of wax or occlusal
paper, or blue dots on the tooth surface to
find the early contact point
Olfactory examination
•
Gangrenous pulp
•
Necrotizing pulpitis
Tooth mobility test:
Depending on the degree of tooth loosening：
I Degree looseness:
 Buccal-lingual direction (internal and external direction) was less than 1mm, but
there was no movement in other directions.
II Degree looseness:


a.the buccal-lingual (internal and external) motion between 1 and 2mm;
b.the buccal-lingual (internal and external) and mesial-distal (left and right) motion.
III Degree looseness:


a.the buccal-lingual (internal and external) motion more than 2mm;
b.The motion of buccal lingual direction (internal and external direction), mesial and
distal direction (left and right direction) and vertical direction (up and down
direction)
Routine examination of the maxillofacial:
Inspection
•
Facial expression and conscious expression ( Patients with facial injury often have brain injury if
they have changes in consciousness and sense )
•
Changes of skin color, wrinkle and elasticity of face and neck
•
Whether the maxillofacial shape is symmetrical, whether there are mass deformity and tissue
defect, etc
•
Observe the color and luster of skin and mucous membrane for abnormal changes
•
Observe the mouth opening of TMJ
1. Normal mouth opening ：3-4.5cm; Slightly restricted ：2-3cm,
2. Moderately restricted <1cm; Excessive mouth opening >4.5cm
palpation
•
Pay attention to skin temperature
•
Whether there is tenderness, mass, etc. if there is a mass, check its size, shape, hardness, location,
depth, adhesion fluctuation, etc
•
For bone masses, we should pay attention to whether there is ping-pong elasticity in the range of
bone swelling or hyperplasia·
•
Trauma patients should be examined for signs of fracture
Probing (when there is fistula sinus in frontal and facial region)
•
The depth and direction of the mandible should be explored
•
Is it through the mouth
•
Can you touch rough bone surface or movable dead bone, foreign body, etc
•
If necessary, dye was injected into the fistula or fistulography was performed
Maxillofacial injuries



The effect of the shape and size of bilateral pupil on light reflex
Is there cerebrospinal fluid otorrhea or rhinorrhea
Is there any external auditory canal bleeding
Maxillary sinus


Nasal obstruction or bloody secretion on the affected side
Exophthalmos, dyskinesia, diplopia
Examination of facial bones





symmetry
Bone continuity
Is there any step or depression defect
Is there any tenderness
Is there any bone fricative or abnormal activity
Examination of maxillofacial and cervical lymph nodes





Check body position
Inspection sequence
Pay attention to its hardness and mobility
Pay attention to tenderness or wave motion
Pay attention to whether it adheres to the skin or the base
Temporomandibular joint examination







Symmetry of bilateral joint area
Is the motion of both sides consistent
Do you have tenderness
Contractility of masticatory muscles
Mouth opening
Open mouth type
Occlusal relationship
Salivary gland examination



Facial symmetry
Salivary gland secretion
The thickness and texture of catheter (from proximal end to catheter mouth)
i. Does facial nerve branch function have obstacle
ii. Tongue movement (leaning to one side or tongue muscle tremor)
iii. Does pharynx side and soft palate have bulging
What is the order of examination?
•
outside → inside, front → back, superficial → deep
•
Healthy side should be compared with the affected side
•
the oral vestibule examination
Lip, cheek, gingival mucosa, lip-buccal groove, and lip-buccal frenulum. pay
attention to Color anomaly and texture changes.Fistulas, sinus tracts, ulcers, pseudo membrane, tissue
necrosis, mass, Whether there is redness, swelling and discharge at the mouth of the parotid duct.
Special examinations of oral and maxillofacial:

Periodontal exploration periodontal pocket measurement: One of the chief signs of gum
disease is the presence of periodontal ("peri" – around "odont" – tooth) pockets that is, spaces
around the teeth, below the gum line, that have become infected.
 Periodontal exploration periodontal pocket measurement:
 periodontal probe: Insert the probe between the tooth and gum, and then
measures from the top of the gum to the bottom of the sulcus or pocket. Six
measurements, in millimeters, are taken around each tooth: three on the outer
(lip) side and three on the inner (tongue) side.
 1-3 mm is normal space below the gum tissue
 3-5mm is early or mild periodontitis
 5-7mm is moderate periodontitis
 7-10mm is advanced periodontitis
 Pulp vitality test:
 Thermal /Cold Test
• Normal: The response of control teeth and tested teeth to stimulation is the same
• Sensitivity: The pain response is stronger than that of the control teeth and lasted for
a period of time
• Dullness: The pain response is milder or duller than that of the control teeth
• Tardy pain: After stimulation is removed, pain reaction will appear in affected teeth
for a while, lasting for a period of time
• No response: No response to stimulation
 Electrical activity test
•
•
•
•
Current intensity = control teeth: pulp vitality is normal (electrical test response is
normal)
Current intensity > control teeth: pulp reaction is slow, pulp mostly is degeneration
Current intensity < control teeth: pulp reaction is sensitive
Pulp necrosis intensity: no reaction
 Examination of salivary secretion function:
• the patients were given acidic substances to increase the reflex secretion of glands;
According to the changes and secretion of the gland itself, judge the secretory
function of the gland and the patency of the duct.
Imaging examinations of oral and maxillofacial :
•
•
•
•
•
•
•
•
•
•
•
X-ray plain film
Intraoral photographs
Panoramic radiographs
Radiographs anteroposterior and lateral view of the head
CBCT
MRI
Radionuclide examination
Ultrasonic examination
Puncture and cytological examination (forbidden for suspected carotid body tumor or aneurysm)
Biopsy
Laboratory inspection
Ppt 2 local anesthesia
Mode of action of local anesthesia:
the voltage-gated sodium channel:
•
•
•
As the entry of sodium into the nerve cell during the firing cycle is the chief driver
producing depolarization, blockade of sodium transfer causes inhibition of neural
activity.
Knowledge of the structure of the sodium channel is essential for an understanding of
the action of local anesthetics.
The sodium channel is not a singular structure and that at least nine different variations
have been identified
Techniques of local anesthesia for oral and maxillofacial surgery:
1. Topical anesthesia
• useful when applied to the oral mucosa
• available in a number of formulations including creams, ointments and sprays
• anesthesia of the teeth and jaws is not at present possible by this method.
2. Infiltration
• useful in providing localized skin and mucosal anesthesia and can also be used
to provide anesthesia for some teeth and part of the jaws.
• When used intraorally, access to the point of needle penetration is easiest when
the patient has the mouth only partly open.
• Slow injection has a number of advantages. It reduces discomfort and increases
success. In addition a slow rate of injection may lessen the effects of systemic
problems
• This method allows about 45 minutes of anesthesia of the dental pulps when a
solution containing a vasoconstrictor (such as lidocaine with epinephrine) is
used; soft tissue anesthesia is longer and the patient may have subjective
anesthesia of the soft tissues for 1.5 hours.
3. Regional block anesthesia
• Mandibular anesthesia:
i.
Inferior alveolar nerve block (Halstead technique): This method
anesthetizes the teeth and bone on one side of the mandible along with
the soft tissues on the buccal aspect anterior to the mental foramen. this
injection usually anesthetizes the lingual nerve that supplies the
anterior two thirds of the tongue on one side.
ii.
Gow-Gates technique:anesthetize the lingual, long buccal, mylohyoid
and auriculotemporal nerves. anesthetizes the lingual nerve that
supplies the anterior two thirds of the tongue on one side.
iii.
Mental and incisive nerve block: anesthetizes the teeth and jaw from
the premolars anteriorly as well as the soft tissues of the lower lip and
chin to the midline on one side.needle is inserted at the depth of the
buccal sulcus between the premolar teeth and advanced to a zone
below the premolar apices.
iv.
Long buccal nerve block:depositing 0.5 ml of solution in the region of
the coronoid notch of the mandible.
v.
vi.
• Maxillary anesthesia:
i.
Maxillary nerve block: anesthetizes the teeth and bone of the maxilla
on one side together with the buccal and palatal mucosa, the skin and
mucosa of the upper lip, the lower eyelid, and the lateral aspect of
the nose. Tuberosity approach(by depositing solution high in the
buccal sulcus in the plane of the distal surface of the maxillary
second molar tooth. The needle is advanced at an angle of 45).
Greater palatine foramen approach(needle is inserted into the greater
palatine foramen and advanced at an angle of 45)
ii.
Posterior superior alveolar nerve block: This injection anesthetizes
the maxillary molar teeth, associated bone and buccal gingivae.
iii.
Infraorbital nerve block: involves inserting a long needle high into
the buccal sulcus between the premolar teeth and advancing towards
the infraorbital foramen, anesthetizes the teeth and associated bone
from the second premolar to the central incisor.
iv.
Greater palatine nerve block:anesthetizes the soft tissues of the palate
from the foramen anteriorly to the canine region.soft tissues of the
hard palate up to the canine region on one side will be anesthetized.
v.
Nasopalatine nerve block: anesthetizes the tissues of the hard palate
adjacent to the incisor teeth bilaterally.
4. Supplementary intraoral techniques of local anesthesia
• Intraligamentary (periodontal ligament) anesthesia: a specific version of an
intraosseous technique.
• Intrapulpal anesthesia: This method has limited indications, as exposure of the
tooth pulp is essential. This is the most localized form of anesthesia described
here and in theory could be used to anesthetize one pulp canal of a multirooted
tooth.
Local anesthesia drugs:
1) Lidocaine: the gold standard drug. When a vasoconstrictor is added to 2% lidocaine then satisfactory
anesthesia is provided for the teeth.
2) Mepivacaine
3) Prilocaine
4) Articaine
5) Etidocaine:not effective for infiltration
6) Bupivacaine: a long-lasting local anesthetic
7) Levobupivacaine
8) Ropivacaine
Complications of local anesthesia in the orofacial region:
Localized complications:
•
•
•
•
Nerve damage
Trismus
Motor nerve paralysis
Intravascular injection
Systemic complications
•
•
•
•
Allergy
Infection
Toxicity
Drug interaction
Ppt3 salivary gland disease
Salivary gland anatomy:
•
•
•
Parotid: salivary gland is situated around the external ear.Parotid’s saliva is secreted through
Stensen’s ducts, the orifices of which are visible on the buccal mucosa in the vicinity of the
maxillary first or second molar.
Sublingual salivary gland: is located below the tongue lying on opposite sides of the lingual
frenulum, superior to the mylohyoid muscle. * 3 sets of minor salivary glands of
tongue: - Weber, border of the lateral tongue; - Von Ebner, surrounding the circumvallate
papillae; Blandin and Nuhn, anterior lingual glands.
Submandibular salivary gland: is situated in the digastrics triangle of neck. Submandibular
gland saliva is secreted through the submandibular duct (Wharton’s duct).horse shoe shaped.
Salivary gland function:
•
•
•
•
•
•
Produce saliva
Keeps your mouth moist and comfortable.
Helps you chew, taste, and swallow.
Fights germs in your mouth and prevents bad breath.
Has proteins and minerals that protect tooth enamel and prevent tooth decay and gum disease.
Helps keep dentures securely in place.
Salivary gland dysfunctions:
1) xerostomia( oral dryness):
1.1. lips: dry with cracking, peeling and atrophy
1.2. buccal mucosa may be pale and corrugated
1.3. dorsal tongue may appear smooth due to a loss of papillation and erythematous or may
appear fissured
1.4. dental caries： carious lesions often affect the root surfaces and cusp tips of teeth
1.5. Candidiasis:
- Erythematous form of candidiasis, appearing as red patches on the mucosa
- Angular cheilitis, persistent cracking or fissuring of the oral commissures
2) Sjogren syndrome:
Symptoms:
•
Xerostomia
- Professional dry mouth
- Rampant dental caries
- Adult parotitis
- Tongue pain, dry and cracked tongue surface, atrophic and smooth tongue papilla
- Oral mucosal ulcers or secondary infections
•
Keratoconjunctivitis sicca
- dry eyes
•
foreign body sensation
lack of tears occur
System performance
-
Skin: allergic purpura-like rash, leave brown pigmentation
Joints Arthralgia
Kidney damage
Lung, no respiratory symptoms
*Digestive system, atrophic gastritis, decreased gastric acid, indigestion
Nerves, A few of them involve the nervous system
Blood system, decrease in white blood cell count or(and) thrombocytopenia
Treatment:
There is currently no cure for this disease. It is mainly to take measures to improve symptoms,
control and delay the progression of tissue and organ damage caused by immune response and
secondary infections.
Management of xerostomia:
- preventive therapy
- symptomatic treatment
- local or topical salivary stimulations
- systemic salivary stimulation
- therapy directed at an underlying systemic disorder
3) salivary gland infections:
- caused by bacteria or viruses
- commonly affects the parotid salivary glands, submandibular salivary glands.
- Purulent infection:acute suppurative mumps, chronic recurrent mumps, chronic
obstructive mumps, salivary stones , submandibular glands inflammation.
- Viral infections:mumps is a viral infection
- Specific infection: tuberculosis, actinomycosis, and HIV-related salivary gland diseases.
Sign and symptoms of infection:
(mumps)
- the primary sign of mumps is swollen salivary glands that cause the
cheeks to puff out.
-
Pain in the swollen salivary glands on one or both sides of your face
Pain while chewing or swallowing
Fever
Headache
Muscle aches
-
Weakness and fatigue
Loss of appetite
4) Salivary gland tumors:
-
I.
Most salivary gland tumors (80%) arise in the parotid gland.
Malignant Tumor of salivary gland include
(1) ulceration of the overlying mucosa,
(2) fixation of the mass to deeper tissue plants
(3) induration,
(4) invasion
(5) cervical lymphadenopathy
Warthin tumor(adenolymphoma):
-
Benign
the posterior lower pole of the partoid gland
the male to female ratio is 6:1 to 70 years old
a history of growth and decline related to the lymph node
grows slowly, rarely exceeding 3-4cm in diameter
prone to inflammation
multiple, bilateral
round or oval, with smooth surface, soft texture, sometimes elastic ,and cystic change
purple-brown, with cysts in the cross section, containing cheese-like or viscous
liquid
treatment:
If it occurs in the lower pole of the parotid gland, after confirming neck and facial trunk of the facial nerve,
perform a regional parotidectomy in normal tissues more than 0.5cm outside. The other parts of the partoid
gland should be removed with the superficial lobes or whole lobes of the facial nerve.
II.
Mucoepidermoid carcinoma:
-
Malignant
the most common malignant tumor of the salivary glands
they are divided into two types: highly differentiated and poorly differentiated
there are more women with mucoepidermoid carcinoma than men
the parotid glands, the palate and submandibular glands, posterior glands of molars
III.
Well
poor
- It is a painless mass
and grows
-slowly
- vary in size
- the borders can be
clear or unclear
- the texture is medium
to hard
- the surface can be
nodular
- adhere to the facial
nerve
- Symptoms of facial
paralysis are rare
- Cervical lymph node
metastasis is rare
It grows faster, may be painful
- unclear borders
- adheres to surrounding tissues
- often involve the facial nerve
- lymph node metastasis
- hematological metastasis
- easy to relapse
- the patient’s prognosis is poor
adenoid cystic carcinoma:
- it is a common tumor of the submandibular and sublingual glands.
- early stage, painless masses
- The course is longer, months or years
- generally small, mostly 1 - 3 cm
- round or nodular, and smooth
- unclear boundaries, poor mobility, adhere to surrounding tissues
- spread along the nerves
- Invade adjacent bone tissue
Treatment:
- Surgical resection
- To expand the normal boundary of the operation
- Postoperative radiotherapy and chemotherapy
- The preservation of the facial nerve should not be overly considered
- Submandibular triangle dissection
- There is no need for selective lymph node dissection
- For some cases that have lost the opportunity for surgery, radiotherapy can also be
used to control the development
5) Salivary gland stones:
-
is a calcified structure that may form inside a salivary gland or duct. It can block the flow
of saliva into the mouth.
-
85% occurs in the submandibular gland, followed by the parotid gland, and the
sublingual gland is rare.
Charactristics:
- the submandibular glands are mixed glands, the saliva is more viscous, and the calcium
content is 2 times higher.
- The submandibular gland duct runs from bottom to top.
Diagnosis:
- If you have symptoms of a salivary gland stone, your doctor will first check for stones with a
physical exam. Sometimes tests may also be ordered, such as X-ray, CT scan, or ultrasound.
- More and more, doctors are using a newer and less invasive technique called sialendoscopy to
remove salivary gland stones.
Treatment:
- If a stone is detected, the goal of treatment is to remove it.
- For small stones, stimulating saliva flow by sucking on a lemon or sour candies may cause
the stone to pass spontaneously.
- In other cases where stones are small, may massage or push the stone out of the duct.
- For larger, harder-to-remove stones, make a small incision in the mouth to remove the stone.
6) Salivary gland mucous cyst:
•
Parotid cyst
- retention cyst
- rare
- painless mass in the parotid area
- colorless transparent liquid
•
Congenital cyst
- dermoid cyst
- branchial cleft cyst
- congenital parotid duct cyst
•
Sublingual gland cyst
- sublingual area above the mandibular - hyoid muscle
- light purple-blue
- soft and wavy- extra tongue
- slightly yellow or egg white-like liquid
- remove the sublingual gland
oral mucocele (small salivary gland mucocyst)
- extravasated mucinous cyst
80% lower lip & ventral side of tongue
blue vesicles resemble blisters
Egg white-like viscous liquid
•
7) Lesions:
-
may mimic the presentation of salivary gland tumors:
Inflammatory diseases, infections,
Nutritional deficiencies
may present as diffuse glandular enlargement.
Salivary gland-Diagnosis:
-
CT is considered the gold standard in the evaluation of inflammatory disease of the salivary
gland. Landmark adjacent structures such as the retromandibular vein, carotid artery, and
deep lymph nodes can also be identified on CT.
CT can define the characteristic hypervascular wall, it is possible to distinguish fluidfilled masses from abscesses.
Sialometry
Sialochemistry
Salivary Diagnostics
Salivary Gland Imaging :
Plain film radiography
Sialography
Ultrasonography
Radionuclide imaging
Magnetic resonance imaging (MRI)
Computered and Positron emission tomography(PET)
PPT 4 ORAL MUCOSAL DISEASE
Disease 1: Lichen planus


Lichen planus is an inflammatory disease of the skin or oral mucosa, characterized by
glistening angulated papules.
When the disease is confined to the skin it may be acute, subacute or chronic; oral involvement is
usually chronic.
Causes:
- The etiology is not known, but psychosomatic factors seem to be involved in a large percentage
of cases.
- It affects about 1 percent of the population, mainly women, and usually it appears during the
fifth or sixth decade.
- Possible causes of oral lichen planus include non-steroidal, anti-inflammatory drugs
(NSAIDS), iodides, tetracycline, gold, streptomycin, dental fillings containing mercury in the
form of amalgam (if the patient is allergic to mercury), and rough fillings.
- Causes may have an allergic reaction, particularly following exposure to dyes and color film
developers.
Signs and symptoms:
- Lichen planus may occur only in the oral cavity or on the skin, but in most cases lesions
eventually develop in both locations.
-
The most common locations are the buccal mucosa in relation to the occlusal plane of the
teeth, the tongue, the facial surface of the gingiva, hard palate and lower lip.
The lesions are usually symmetrical and tend to be dendritic and popular.
The dendritic lesions consist of grayish white, linear, lacelike elevations composed
of individual papules.
The papules are usually the size of a pinhead. The lesions frequently present erosion at the
sites of frictional trauma. These areas are bright red,and apt to cause symptoms such as
dryness and pain.
-
Differential diagnosis:
- Linear leukoplakia
- White sponge nevus
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Treatments:
Lichen planus tends to resist treatment, and oral lesions may persist for years.
The possibility of psychogenic etiology should be explored.
Vitamins and antibiotics have also been used with some success.
Corticosteroids, such as thymic peptide, are systemically and topically applied.
Disease 2 acute moniliasis ( thrush ):
Definition of the disease
It is belong to fungus infection.
Cause and mechanism
It is infected by fungus
Symptom and sign
•
•
The oral lesions may appear anywhere on the mucosal surface as a simple patch, but usually the
lesions are multiple.
The characteristic lesions are creamy-white, simulating milk, adherent and when removed, give
rise to bleeding points.
Diagnosis
The diagnosis is based upon the history, clinical appearance of the lesions and microscopic study
of smears of scrapings from them.
Disease 3 pemphigus vulgaris:
Definition of the disease:
It is a severe chronic autoimmunity disease appear in oral mucosa and skin. Pemphigus is an acute
or chronic skin disease that usually presents oral lesions. Of the several types of the condition,
pemphigus vulgaris is the most common. Pemphigus vulgaris is an autoimmune disorder, where the
body's immune system attacks some of the proteins in the skin. Pemphigus usually occurs in
middle-aged or older people. This picture shows a close-up of lesions in the mouth.
Cause and mechanisms:

Pemphigus is an autoimmune disorder. The immune system produces antibodies against specific
proteins in the skin and mucous membrane. These antibodies create a reaction that cause skin cells
to separate.
The exact cause is unknown.


Sometimes pemphigus is caused by certain medications, although this is rare. Medications that may
cause this condition include:
Blood pressure medications called ACE inhibitors
Chelating agents such as penicillamine, which remove certain materials from the
blood

Pemphigus is uncommon. It occurs almost exclusively in middle-aged or older people.
Signs and symptoms:
1) Oral lesion
•
The characteristic feature is that of primary bullous lesions in the mucous membrane.
•
The thin-walled lesions rupture promptly, leaving a raw area that is subsequently,leaving a raw
area that is subsequently covered with a membranous exudates.
2) The initial bullae are usually as large as the thumb nail.
•
•
•
•
•
In the early stages of the disease, they tend to be discrete and few; individual lesions
usually heal within ten days to two weeks.
As the disease progresses, the oral lesions coalesce with deeper ulcerations, so that relatively
little normal mucosa remains.
Involvement of the pharynx, larynx and trachea may ensue.
Pain is severe; chewing and swallowing are extremely difficult.
Differential diagnosis:
1.
2.
The oral lesions of erythema multiform and frequently similar to those seen in pemphigus.
Bullous lichen planus must also be considered in the differential diagnosis.
Treatment:
•
•
•
•
•
Severe cases of pemphigus are treated similarly to severe burns.
Treatment may require hospitalization, including care in a burn unit or intensive care unit.
Treatment is aimed at reducing symptoms and preventing complications.
Patients can be maintained and the lesion controlled with systemic corticosteroids, but the drug
side effects may be severe.
Treatment may involve:
a. Fluids, proteins, and electrolytes given through a vein (IV)
b. IV feedings if there are severe mouth ulcers
c. Anesthetic (numbing) mouth lozenges to reduce mouth ulcer pain
d. Antibiotics and antifungal medications to control or prevent infections
disease4 recurrent aphthous ulcers:
Definition of the disease:

They are painful and can occur anywhere inside the mouth.

They are the most common type of mouth ulcer.

At least 1 in 5 people develop aphthous mouth ulcers at some stage in their life.

Women are affected more often than men.
Symptom and Sign

In its most characteristic form RAU presents the picture of a number of small ulcers( 1 to 5 ),
appearing on the buccal mucosa, the labial mucosa, the floor of the mouth, or the tongue.
There is usually a sensation described as burning or pricking for a short period before the
ulcers appear.
Following this phase, ulceration occurs directly by loss of the epithelium; some cases have
been described in which an initial vesical has been seen.
The ulcers are usually less than 1 cm in diameter and, in most instances, their size is about 4
or 5 mm.
The appearance of the ulcers is grey-yellow, often with a red and slightly raised margin and
they are round and oval round.
The ulcers are painful, particularly if the tongue is involved, and may make eating or
speaking difficult.
Lymph node enlargement is seen only as a response to secondary infection in severely
affected patients and is not a routine finding.
The course of these ulcers varies from a few days to a little over 2 weeks, but by far the most
common duration is about 10 days.
In RAU healing occurs without scar formation.





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

Treatment
 The strict oral hygiene.


This is of importance on two counts:In the first instance, it is obvious that the ulcers
may be exacerbated and made more painful in the presence of local sepsis and
resulting secondary infection. The second factor is the possiblility of enhancement of
the auto-immune process by the stimulating effect of local sepsis.
The use of covering agents.


There are a number of available pastes and gels which can be used to coat the
surface of the ulcers and to form a protective barrier against secondary infection and
further mechanical irritation.
The use of topical antibiotics.
 A much effective measure in relief of symptoms caused by secondary infection is
application of topical antibiotics.
 The use of topical steroids.
•
•
When properly used topical steroids are effective drugs in the treatment of RAU.
However, the patient response is variable and there are some individuals who gain
little or no relief from their use.
 . The use of topical anesthetics.

Local anaesthetics may be used as a last resort to give a patient a brief period of relief
from pain when, for instance, he or she is eating a meal
Disease5 White Patches ( Leukoplakia )
Definition
 The definition of white patch is that a white patch on the oral mucosa cannot be away and is not
susceptible to any other clinical diagnosis.
 Some oral white patch can transform to cancer.
Cause and Mechanism
 The most important cause is the use of tobacco.
Diagnosis
•
•
According to clinical feature and biopsy, easy to give a diagnosis.
White patch is belong to precancerous lesion, the following may suggest cancerous
transformation.










The age is above 60 years old.
A long history smoker.
The incidence of male is higher than that of female.
Candidal infection.
A long-case history.
White patch is in the dangerous areas if it is in the marginal tongue,
floor of mouth, and mouth corner.
Epithelial hyperplasia abnormally
It appears ulceration and erosion.
Stimulating pain or automatic pain.
Treatment
 1. Remove the stimulating factor, such as smoking.
 2. Use Vitamin in the local area.
 3. Operation and biopsy.
Disease6 Herpetic Stomatitis
Cause and Mechanism
 Herpetic stomatitis is caused by the herpes simplex virus.
 The infection is characterized by ulcers, blisters and inflammation.
 The condition is more prevalent in children than adults and is contagious.
Symptom and Sign
 This illness affects patients in two main age groups, young children (the most in 2 mouth-2 years)
and young adults.
 An acute herpetic stomatitis represents the primary infection and it is only rarely that a second
acute attack follow.
 The patient with acute herpetic stomatitis often gives a history of recent exposure to a patient with
a herpetic lesion; the incubation period is about a week.
 The initial symptom are of malaise with tiredness, muscle aches, and, sometime, a sore tender.
Treatment
 The treatment of acute herpetic stomatitis depends almost entirely upon the elimination of
secondary infection.
Important Qs
L5: Periodontal disease
What is gingitivitis?
it is the inflammation of gums they are dark red, blood vessels are dilated
and bleeding. For recovery oral hygiene practiced well, the bacterial plaque
removed regularly and it can develop into periodontitis
What is periodontal disease?
It is when the inflammation continues the root surface covered with bacterial
film (dental plaque and tartar), a deep pocket develops along the teeth, loss
of the anchoring fibers and the bone tissue. Teeth is loose, displaced. Has to
be pulled
What is chronic periodontitis?
Long lasting inflammatory disease affecting the soft and hard tissues of the
teeth
Pathogenesis of chronic periodontitis
Plaque, or microbial biofilm: is a sticky secretion comprised of bacterial cells
in a polysaccharide media, which is attached to the teeth and other nonshedding surfaces by a glycocalyx.
A result of a complex interplay, between microbial challenge, host response,
and other modifying factors.
Risk factors of chronic periodontitis
Important Qs
1
1. Bacterial plaque: major cause of gum inflammation. Some bacteria can
further promote the development of periodontitis
2. Tartar: is calcified dental plaque that can form below or above the gum line.
tartar must be removed professionally on a regular basis
3. Smoking: reduces resistances of the gums to harmful bacteria
4. Systemic diseases: such as diabetes. have higher risk of developing
periodontitis. as well as patients with periodontitis having higher risk for
diabetes
5. Diet: unhealthy diet has a higher risk of developing both diabetes and
periodontitis
6. Stress: reduces the gums resistance to harmful bacteria
7. Genetic disposition: cause the differences in the immune system, the
condition can be different from person to person
8. Age: in chronic disease, age factor is more obvious
Anatomy of periodontium
The paeriodontium is composed of:
Gingiva facing the tooth; this is divided into:
free marginal gingiva: the edge or border, distance of 0.5-2mm from
margin of gingiva
Attached gingiva: firm, resilient, tightly bound to underlying
periosteum of alveolar bone
Interdental areas: concical shape referred as interdental papilla
periodontal ligament: is a soft, fibrous specialised connective tissue, it is
mainly composed of fiber bundles. Fibers of PDL attach on one side to
the root cementum, on the other side to the alveolar bone of the tooth
socket
cementum: is a mineralized dental tissue covering the anatomical part of
the teeth-root. it begins from the cementoenamel junction to the apex. a
medium for the attachment of collagen fibers, binding the tooth to the
surrounding structures
alveolar bone: the supporting bone consists of two parts. The first part is
cortical plates, made of compact bone. Second part is the spongy bone,
Important Qs
2
filling the area between plates and the alveolar bone
Characteristics of chronic periodontitis
Bleeding gums: the first signs of inflamed gums are redness and slight
swelling at the gum line, and possibly bleeding when brushing the teeth, or a
checkup with the probe
Bad breath: only professional teeth cleaning can help
Problems chewing and after eating: which includes tooth being loss, gingival
recession and bone resorption
Attachment loss
Gum pocket anf tooth loss: cause the anchoring structure of the teeth to
break down. This results in the deep gum pockets and the treatment effect s
very poor; for healthy sites probing depth is less than 3mm and when
periodontitis occurs probing depth is more than 4mm
X ray finding: periodontitis can be definitely confirmed only with the
necessary X-rays. When the tooth with greater probing depth, yourequre
additional assessment with an x-ray. It makes it possible to estimate the
severity of bone loss
Periodontal examination
Communication: need a comprehensive history including the complete
medical history, a dental history and a social history including tobacco and
recreational drug use
Oral hygiene instruction: observation of the patients plaque control
techniques at the outset of the examination prior to the intramural evaluation
An intraoral examination: including probing depths, attachment loss,
bleeding, tooth mobility, plaque levels, an occlusal analysis, photographs
intramural and extra oral, a complete series of periodical radiographs
Diagnosis of periodontal diseases
Gingivitis: defined as an infection of the gingiva caused by the toxins from
dental plaque, there is no attachment loss to bone loss
Periodontitis: bacterial infection of gingiva, the periodontal ligament, alveolar
bone, and cementum, which causes attachment and bone loss in an apical
direction and the attachment loss is not reversible. It is the immune system
and how the host responds to these toxins
Important Qs
3
Peri-implant mucositis: it is similar to gingivitis around natural teeth, its a
bacterially caused inflammation of the soft tissue surrounding an implant and
doesn't cause bone loss. its reversible with treatment
Peri-implantitis- is an infection, which causes bone loss and threatens the
longevity of the implant fixture, as well as being systemically challenging to
the patient
Therapy of chronic periodontitis
Treatment Goals for chronic periodontitis:
1. Control bacterial plaque biofilm t a level that is compatible with
periodontal health
2. Alter or eliminate any local or systemic contributing risk factors for
periodontitis
3. Arrest the disease progression
4. Prevent the recurrence of periodontitis
Phasing of therapy of periodontitis:
1. Phase 1 therapy: removing and controlling the etiologic factors
contributing to dental disease as well as patient education in preventive
dentistry techniques
2. Phase 2 therapy: Surgical services
3. Phase 3 therapy: fabrication of permanent dental and prosthetic
restorations
4. Phase 4 therapy: maintenance therapy services
Phase I Therapy
1. Patient plaque control technique instructions
2. Identify and remove calculus deposits
3. Remove diseased altered cementum
4. Reduce periodontal pathogens
5. Resolve inflammation
6. Arrest attachment loss.
Important Qs
4
Recommended intervals for reevaluation of
phase I therapy:
1. For patients with gingivitis received a dental prophylaxis,
reevaluation occurs 4–6 weeks after treatment.
2. For patients with periodontitis and received scaling and
root planing, an 8–10 weeks reevaluation is recommended.
Four possible decisions should be made according to reevaluation:
1.Refine phase I therapy.
2.Proceed with phase II periodontal surgical services.
3.Commence with phase III restorative therapy if no further
active periodontal therapy is needed.
4.Refer clinically healthy patients to the maintenance therapy
program (phase IV therapy).
Surgical treatment:
In situations with very advanced periodontitis, the deeper gum
pockets that remain can generally be successfully reduced only
with surgical treatment.
Periodontal tissue regeneration: To reconstruct bone structure and function,
periodontal tissue regeneration is the ultimate treatment.
Need surgical treatment (GTR,GBR,.etc).
Professional long-term care (aftercare, recall):
1. For the optimal long-term success, it is also important to
continue to have ongoing professional care
2. The interval should be short, between 2 and 3 months, for 1–
2 years.
L6:Extraction of Tooth
Indications for extraction
1. caries
2. periodontal disease
3. before radiation therapy
4. crown and root fractures
Important Qs
5
5. malposition of teeth
6. teeth in bone fracture lines
7. impacted teeth
8. supernumerary teeth
9. orthodontic or prosthetic indications
Contraindications for extraction
1. systemic contraindications
all general health factors and mental factors
hemophilia or other coagulopathies
uncontrolled metabolic diseases such as diabetes, severe uncontrolled
hypertension and cardiac diseases
Ongoing radio and or chemotherapy is also a relative contraindication be
aware of the medications patients
2. local contraindications
the most common local contraindiatio is an ongoing acute inflammatory
or infectious process
One of the most important is radiation therapy, past and present,
involving the jaws
teeth within the area of a tumor, especially if it is malignant, should not
be removed
Control of anxiety and pain
Sedation: although pain associated with extractions is managed effectively
through the administration of local anesthesia, patients are anxious because
of the fear of pain.
Local anesthesia: profound local anesthesia results in loss of all pain,
temperatur and touch sensations but it doesn't anesthetize the
proprioceptive fibers
Technique for extraction
1. Principles of simple (closed) extraction: extraction of a tooth requires
expansion of the alveolar socket and separation of the attachment of the
periodontal and attaching gingival soft tissues. controlled force is delivered
Important Qs
6
with dental elevators and forceps to expand and, in a controlled way, fracture
the alveolar process, roots or crown of the tooth.
The first step in extraction is gently expanding the alveolar bone. The
dental elevator is used for lever transmitting from a long lever arm with
moderate force into a short lever arm with high force. The appropriate
dental forceps can then be applied as far apically as possible by acting
as a wedge in the socket. A steady grip must be obtained and lunation
pressure is applied in linguinal and buccal directions continuing with
dental applied persistent force to expand the alveolus. The center of
rotation should be kept as apical as possible
2. Surgical (open) extraction of teeth or roots: This should be done if:
failure to remove a tooth with forceps or closed extraction
presence of thick dense bone, particularly buccocortical bone as
assessed preoperatively
presence of short clinical crowns with signs of severe attrition as a result
of bruxism or habitual grinding
hypercementosis
teeth with long and divergent roots
presence of large pneumatized maxillary sinus with the roots of maxillary
molars extending into the sinus especially in the case of isolated molars
teeth with extensive caries, root caries, or that have large amalgam
restorations are candidates for surgical extraction
deciduous teeth occasionally present problems for the surgeon and
should not be underestimated
erupted mandibular third molars with limited access
endodontically treated teeth
Technique for surgical extraction:
surgical extractions should be carries out under high-standard aseptic
conditions. irrigation by sterile saline should be carried out when cone
and teeth are cut by bur. The flaps used with tooth extractions are
envelope or sulcular flaps, which are developed along the cervial necks
of the teeth. Bone is removed by rongeur or by a surgical bur to provide
access to the tooth which can be removed ain a more controlled
Important Qs
7
manner. A straight dental elevator is used to expand the periodontal
ligament space. teeth with two roots can be either sectioned into two
halves and then removed similarly to two premolars.
Postextraction care: no debridement or curettage of the socket is
necessary unless there is a pathologic process seen on a
radiograph preoperatively. Obvious debris, such as tooth fragments,
amalgam or calculus may be present in the tooth socket after
extraction and should be carefully removed with a curette or suction.
Gentle digital pressure with the index finger and thumb should be
applied to the buck-lingual walls of the extraction socket to
compress the usually expanded buck-lingual plates after extraction
restore the original crest dimension
Postoperative instructions:
Important Qs
8
Oral and Maxillofacial Infections
Q1. Characteristics of Oral and Maxillofacial Infections :
● Anatomy:
1. Maxilla/Mandible
2. Muscle
3. Blood Vessel
4. Lymph Vessel
5. Nerve
6. Salivary Glands
● Factors conducive to infection development :
1. Exposed to the outside;
2. the Special Anatomical Structure and Suitable Environment; 3. Unique Odontogenic
Infection (Children origin);
4. Latent facial space and loose connective tissue;
5. Rich blood circulation;
6. Rich lymphatic circulation;
7. Symptoms can be detected early;
8. Easy to treat
● Oral and maxillofacial anatomy:
- facial bone: Latent facial space, loose connective tissue
- There are totally 14 bones making up the maxillofacial bony framework:
Single bone: mandible, vomer
Pairing bones:maxilla ,zygomatic bones ,palatine bones, inferior nasal congcha, nasal
bones, lacrimal bones
- Muscles : The superficial muscle called mimetic muscle; The deep muscles
called masticatory muscle.
- facial blood vessels - artery, vein , capillary ;rich blood circulation
- The lymphatic system has 3 functions:Removal of excess fluids from body
tissues,Absorption of fatty acids to the circulatory system, Production of immune
c
● Oral and Maxillofacial Infection :
Infectious diseases will be divided into bacterial, fungal and viral infections
1. Bacterial Infections:
- Syphilis
- Chlamydia and Gonorrhea - Actinomycosis
1
- Tuberculosis
2. Fungal infections: Blastomycosis, Histoplasmosis
3.Viral infections: Viral Hepatitis, Oral hairy leukoplakia (OHL)
Q2. Maxillofacial dangerous triangle?
● Concept:
from the corners of the mouth to the root of the nose, called the dangerous triangle of
the maxillofacial area.
● Anatomical Features:
. the deep facial venous network communicate with the orbit and the cranial cavernous
sinus;
. No valve in the venous cavity;
. when muscles contract, blood can flow back
- Because of venous communication via the ophthalmic veins between the facial vein
and the cavernous sinus.
- For retrograde infection from the nasal area to spread to the brain, causing
communication
venous cavernous sinus thrombosis, meningitis or brain abscess.
Q3. Maxillofacial Furuncle and Carbuncle
>Furuncle:Acute suppurative inflammation that causes a single hair follicle and its
accessories
>Carbuncle:adjacent hair follicles and their accessories at the same time acute
suppurative inflammation.
- The cause of Furuncle and Carbuncle
* Pathogenic bacteria: Staphylococcus aureus * Local factors: Unclean skin,Skin
abrasion
* Systemic factors:
- Decreased systemic immunity
- Systemic failure
- Wasting diseases
- Diabetes
- Treatment principles
* Local Therapy: - 2% iodine tincture coated ,Hypertonic saline wet compress
* System Therapy: - Antibacterial drugs ,Hypoglycemia treatment
* Surgical Therapy: - Incisions and drainage
2
Q4. Pericoronitis of the Third Molar of the Mandible?
Definition: Inflamed and swollen gum tissue overlying impacted wisdom tooth;
● Pathogenic factor:
1. impacted
2. blind pouch formation
3. retention of food residue
4. local trauma
5. decreased body resistance
Inflammation of soft tissue around the crown when the third molar erupts incomplete
and impacted
● Clinical symptoms: -Fever and chills - Leucocytosis
- General malaise Local symptoms: - Local pain
- Red and swollen gums with pus - Limitation of mouth opening
- Dysphagia
● Examination:
- Incomplete or impacted wisdom teeth
- Pericoronal soft tissue hyperemia and swelling - Tenderness
- Redness and swelling in the maxillofacial region
● Treatment principles:
* Local Therapy:
- Remove food debris, necrotic tissue and pus in blind pouch
- Rince the gum pockets repeatedly with NS, 1%-3% H2O2,0.1% Chlorhexidine, Until
the overflow is clear.
- Wipe dry, Put the iodine glycerin into the gum pocket.
* System Therapy: Antibacterial drugs, Systemic support therapy
* Surgical Therapy:Incision and drainage,Gingival flap resection, Wisdom tooth
extraction
Q5. Infection of Masseteric Space ?
- Masseteric space infection : refers to a purulent infection of the masseter muscle
space.
3
The main clinical manifestations are acute inflammatory redness, throbbing pain, and
tenderness centered on the masseter muscle.
- Clinical Features:
-The masseter region centered on the mandibular ramus and mandibular angle was
swollen, hardened and tender, and the mouth opening was obviously limited.
- The masseter muscle is thick and firm, the abscess is difficult to rupture on its own,
and it is not easy to feel a sense of fluctuation.
- If the inflammation is more than 1 week, the tender points is limited or there is pitting
edema- Withdraw viscous pus;The patient has an increase in the total number of white
blood cells and an increase in the proportion of neutrophils.
- Principles:
- Determine severity
- Evaluate host defenses
- Decide: inpatient vs. outpatient - Treat surgically
- Support medically
-Choose antibiotic
- Administer antibiotic appropriately - Reevaluate frequent
Temporomandibular Joint Diseases
> Anatomy of TMJ:
4
The TMJ is formed by the mandibular condyle and the mandibular fossa of the temporal
bone, into which it fits. The articular disc separates these two bones from direct
articulation. The TMJ is classified as a compound joint. By definition, a compound joint
requires the presence of at least three bones, but the TMJ is made up of only two.
Functionally, the articular disc serves as a nonossified bone, which permits the complex
movements of the joint. Since the articular disc functions as a third bone, the
craniomandibular articulation is considered a compound joint.
● Mandibular condyle ● Joint surface of temporal bone
● Articular disc
● TMJ capsule
● TMJ ligament
> Normal function of TMJ :
● Many anatomy texts show the disc within the TMJ to be superior and slightly anterior
to the condylar head when the teeth are in occlusion, with the two main ridges of the
disc placed one behind and one in front of the condyle.
● During mouth opening the condyle rotates against the disc and the disc slides
forwards and downwards along the articular eminence, but the ridges on the disc
remain on either side of the condylar head.
● This forward slide in the upper joint space is called translation.
● In general, much of the early part of mouth opening occurs as a hinge movement in
the lower joint space and later in opening a greater part of the movement is translatory
> Temporomandibular Disorders(TMD): it is a group of orofacial disorders characterized
by:
● Pain in the preauricular area, TMJ, or muscles of mastication
● Limitations/deviations in mandibular range of motion
● TMJ sounds during jaw function
> Epidemiology of TMD :
● TMD pain has been estimated to affect 10% (5-12%) of the population
● It is at least twice as common in women as in men
● It occurs more frequently in people 20-50 years old
>Etiology of TMD :
Causes of TMD are unclear as TMD usually involves more than a single symptom and
rarely has a single cause. TMD is believed to result from several factors acting together,
including :
- jaw injuries (trauma)
- tooth clenching and grinding (bruxism) joint disease (arthritis)
5
-
improper bite
emotional unstability.
- Overuse injury :
● Dental Procedures
● Patient’s mouth must be opened quickly and widely in order to achieve the treament.
● The jaw may remain open and fixed in place for a prolonged period of time.
● This can lead to an overuse injury of the jaw joint.
- Bruxism:
● Clenching or Grinding
● When you grind or clench your teeth, you can wear away the cartilage that lines the
temporomandibular joint. As this happens, bone rubs create the symptoms of TMD.
● This behavior may occur when you are sleeping, and you might not even realize you
are doing it. Grinding and clenching tend to be frequent if you are stressed
- Joint disease :
● Arthritis
● Degenerative arthritis, such as osteoarthritis, can lead to the displacement or
dislocation of the disk.
● This dislocated disk can lead to clicking, grating or popping sounds.
● It can limit jaw movement and cause pain when open and close mouth.
- Occlusal factors
● Improper Bite
● If the teeth do not properly line up when biting, the chewing muscles may be under
excessive pressure.
● If this goes untreated, you may experience pain and spasms in the muscles around
the jaw.
● In addition, the ligaments that hold the jaw in place can become overstretched and
may be unable to stabilize jaw movement
> Psychological factors
● Anxiety, tension, anger: → masticatory muscle spasm → bruxism
6
● Substance P increase: →vasodilation and inflammation → pain
● Psychological survey: TMD – paranoia , depression
> Clinical feature of TMD
● Pain :
- Pain of muscular origin is often described as aching, but may also be throbbing
or sharp, or described as ‘burning’, ‘stiffness’, ‘tightness’, ‘pressure’, ‘fullness’ or
even ‘numbness’.
- It may be unilateral, but is the only common pain of the head and neck
experienced bilaterally.
- Muscular pain may be clearly localized to a ‘trigger point’ centred in one muscle,
or may be less well defined in distribution in the preauricular or temporal areas.
- Activities involving stretching or use of the masticatory muscles, such as
chewing, yawning, laughing or singing, usually worsen the pain.
> tenderness of muscle and joints - Sites of origin of pain are often tender to gentle palpation.
- Masseter and temporalis muscles are accessible to palpation over most of their
surfaces.
- Medial pterygoid can only readily be felt on the midpoint of its anterior border.
Lateral pterygoid is found by passing a small finger between the maxillary
tuberosity and the coronoid process of the mandible.A major difference between
the sides of the face is usually of diagnostic value.
● Limitations in mandibular range - This can take the form of "stiffness" or pain when opening the mouth, which limits
mobility.
- In cases associated with muscle problems, the onset is usually slow and varies
in severity.‘Locking’ is very sudden in onset and, if relieved, recovery is also fast.
- A reasonable measure of the lower limit of interincisal opening for an adult with a
class 1 occlusion is 40 mm, measured between the upper and lower incisal
edges.
- Lateral excursive and pro-trusive movements may be less affected. Lower limits
for these measures are approximately 7 mm.
●
-
Noise ---- Clinical feature of TMD
The most common noise associated with the TMJ is clicking (or snapping,
cracking, bumping or popping).
7
-
Clicking TMJ is common which possibly affecting one-third of the adult
population.
The noise may be experienced by the sufferer only or may be audible to others,
but is always associated with joint movement.
The clinician may detect inaudible sounds by palpation or auscultation over the
joints.
Most people who have clicking TMJ are not "suffering" from joint noise to seek
help.
> Temporomandibular disorders Clinical stages:
Stage I. Muscular dysfunction - Types:
1. Lateral pterygoid muscle hyperfunction
- Symptoms: Clicking (articular disc is pulled excessively over the articular
eminence),overextended opening→subluxation, Deviation
- Treatment: Adjust muscle function( 0.5-1% procaine 5ml, block therapy, once a
day, 5-7 times as a course), Muscle training: the suprahyoid muscle group.
2. Lateral pterygoid muscle spasm
- Symptoms: Pain when opening or chewing, Dull pain, no spontaneous pain,
Moderate opening limitation, Passive opening is larger than natural
opening,Unilateral →mandibular movement deviation
- Treatment: Relieve spasms (physiotherapy, block therapy, herbs hot dressing,
massage)
3. Masticatory muscle groups spasm
- Symptoms: more common in closed muscle groups, severe limited opening
(Trismus), no pain
- Identification:opening difficulties← tumors, tetanus, hysteria
- Treatment: Relieve spasms (physiotherapy, block, herbal hot compress,
massage), Mental relaxation, rest, sedation(diazepam), muscle relaxants,
analgesics (aspirin)
4. Myofascial pain dysfunction
- Symptoms: Localized, persistent dull pain, opening pain
● It is primarily a disease of young patients and is morecommon in women than men.
● Muscle pain, especially during use or in the morning.
● Specific tender spots (trigger points) may be found in individual muscles, or
tenderness in many muscles.
8
● The condition usually lasts from a few weeks to a few months, but the severity can
vary somewhat during that time.
● Mouth opening is often restricted, but interincisal opening is rarely less than 15 m
- Treatment:
1. Reassurance and explanation to patients
2. Jaw rest and soft diet
3. Sedation (diazepam), analgesic (aspirin)
4. Tenderness - physiotherapy , block therapy
5. Use the soft vinyl mouthguard (for about 6 weeks)
> Trigger point
- A trigger point is an area of hyperirritability in a tissue that, when compressed, is
locally tender, hypersensitive, and gives rise to referred pain and tenderness.
- Trigger point development may be due to trauma, sustained contraction, or acute
strain.
- When a needle penetrates this area it may cause a twitch response and referred
pain.
- Trigger Points and Muscle Injections :
● Injection of local anesthetic agents without epinephrine may cause a temporary
anesthesia, which enables the clinician to stretch the muscles in the affected area.
● A vasodilator effect of the local anesthetic may improve perfusion to the area, thus
allowing harmful metabolites which may induce pain to be more readily removed by the
vasculature.
Stage II. Internal derangement
● Internal derangement
● Secondary to muscle disorder
● Types:
1. Disc displacement with reduction - Two clicks
● The disc is anteriorly displaced when the teeth are in occlusion.
● At the opening, the disc moves backward and the condyle moves relative forward,
resulting in a clicking sound and "normal" relationship between the condyle and the disc
during the sudden movement.
● When the individual with a reducing disc displacement closes their teeth together the
disc is again displaced anteriorly and lead to the click again.
9
- Diagnosis :
● Plain radiographs are no value in determining the position of the disc.
● Arthrography, arthroscopy, or MRI are performed to complete the diagnosis.
● But for almost all cases, diagnosis based only on clinical is quite satisfactory.
- Principal clinical features of disc displacement with reduction:
• Click in the temporomandibular joint on opening.
closing or both
• Possible association with myofascial pain dysfunction
• Possibly pain free
• Possible normal opening
• Often deviation on opening to side of click beforeclicking. with straightening
afterwards.
- Treatment
● A clicking joint may be considered normal.
● No treament other than reassurance and explanation can be given to the patient with
symptomless click.
● Where disc displacement with reduction appears to be the cause of suffering, it can
be treated with relatively conservative methods.
● The anterior repositioning appliance, occlusal splints, to interfere with parafunction
may offer some help.
● Physiotherapy
2. Disc displacement without reduction - Symptoms :
● History of joint pain associated with the clicking, worsens over weeks to years and
leads to locking, often as a sudden event.
● In these situations, the disc remains anteriorly displaced despite the patient’s best
effort at opening;in other words, there is no reduction.
● In unilateral cases, lasting deviation on opening.
● Opening could not be increased by passive stretching
● Pain may be present in front of the ear.
- Principal clinical features :
●Limited mouth opening
●History of click which was ceased
●Possibly painful
●Limited translatory movement
10
- Treatment
● Explanation of the condition and reassurance
● Muscle relaxants and physiotherapy
● Manipulation under anaesthetic
● Lubrication: articular injection of 1% sodium hyaluronate
● Arthroscopy reduction
● TMJ surgery---Meniscoplasty, Meniscectomy.
3. Expansion of the joint capsule & loosening of disc attachments
- Symptoms:
● Capsular laxity, large opening→subluxation
● Recurrent dislocation, with synovitis
- Treatment:
● Articular injection → sclerotherapy: 5% cod liver oil Sodium (extracapsular - damage
facial N)
Prognosis of internal derangement - Up to 50% of those who develop a closed lock
eventually do return to normal, comfortable mobility, without clicking, and many more
will see their symptoms improve over a few years.
Stage III. Degenerative disease
- Clinical features
● In general onset is in middle age.
● The joints are often painful, especially during exercise, and often tender when
palpated at the lateral pole or inside the ear.
● Limitation of movement, particularly translational movement, is often severe with
interincisal opening often around 20 mm and sometimes less than that.
● There is often a grating or crackling crepitus on joint movement and the patient will
often describe a ‘grinding’ or ‘grating’ noise in the joint.
- Diagnosis
● Radiography helps to confirm the diagnosis.
● There may be erosion, osteophytes or traction spurs inactive disease and marked
irregularity of the condylar surface in the resolving phase.
-
Principal clinical features of degenerative joint disease:
11
• Pain centred in the joint
Tender joint
• Crepitus
• Limitation of mouth opening
• Limited translatory movement
• Radiological signs (erosion, traction spurs remodelling)
- Types:
1. Articular disc perforation or rupture - Symptoms:
● Develops in bilaminar area
● Breaking noise, opening deviation, joint pain
- Treatment:
● 1. Conservative treatment & comprehensive treatment of
● 2. Meniscoplasty, Menisectomy : repeated onset, pain and restricted opening
→surgery (perforation repair, disc excision)
2. OsteoarthrosisTypes: Sclerosis, destruction, cystic change, hyperplasia, osteophytes
● Symptoms:Continuous friction sound, crepitus, rubbing bass.
- Treatment
● Explanation and reassurance
● Anti-inflammatory drugs
● Physiotherapy
● Restore deficiencies in the posterior occlusion to reduce loading on TMJ
● Intra-articular steroid injection (advanced disease)
● Surgery (advanced disease, final option) to smooth irregular condylar head where
there are osteophytes or irregularities.
3. Combination of the above.
> TMJ DISLOCATION :
- The condyle of the dislocated joint is in front of the articular eminence
- The mandible is rotated downwards, leaving the posterior surface of the condyle
resting against the anterior aspect of the eminence
-
Clinical features
12
● The patient's jaw is "out" and will not close, usually following a yawn, or perhaps after
laughing, a dental extraction, jaw trauma.
● The patient has difficulty speaking and may have severe pain anterior to the ear.
● A depression can be seen or felt in the preauricular area and the jaw may appear
prominent.
● If only one joint is dislocated there is a marked jaw deviation to the opposite side
- Treatment
● The short-term treatment is manual reduction.
● The patient should be warned to keep the mouth shut for 24 hours after reduction.
- Reduction of dislocation of the TMJ. *
• Have the patient supine
• Stand behind the head
• Place the thumbs on the posterior teeth and the fingers under the chin
• Press increasingly firmly on the posterior teeth while pulling gently up anteriorly
• If there is great resistance concentrate on one side at a time
• When reduced hold the mouth shut for 30 seconds OrSO
• Advise restricted mouth opening for at least 24 hours
> Manual reduction:
● Have the patient sit on a low stool, his back and head braced against something
firm--either against the wall, facing you, or with the back of his head braced against your
body, facing away from you.
● With gloved hands, wrap your thumbs in gauze, seat them upon the lower molars,
grasp both sides of the mandible, lock your elbows, and bending from the waist, exert
slow, steady pressure down and posteriorly. The mandible should be at or below the
level of your forearm.
● In a bilateral dislocation, attempt to reduce one side at a time.
● If the jaw does not relocate easily or convincingly, you may want to reassess the
dislocation with x rays, and try again using intravenous midazolam to overcome the
13
muscle spasm and 1-2ml of intra articular 1% lidocaine to overcome the pain. Inject
directly into the palpable depression left by the displaced condyle.
-
Bimanual mandibular manipulation in a downward-posterior direction to
disengage the condyle from its open-locked position posterior to the articular
eminence
> Recurrent dislocation
Surgery techniques fall into several categories:
● prevention of forward condylar movement by placing a block (bone, cartilage,
alloplast) on the articular eminence, in front of the condyle
● prevention of condylar movement by tightening the constraints of the capsule
● limitation of the forward pull of lateral pterygoid (by section)
● permitting easier reduction of the dislocation by reduction of the height of the emin
14
(1-4)
UVEITIS
❖ Anterior uveitis:
• The anterior chamber is the primary site of inflammation in anterior uveitis.
• Symptoms: pain, photophobia, blurred vision.
• Examination:
• circumcorneal redness
• keratic precipitates(KP)
• aqueous flare or
• anterior chamber cells
• small or irregular pupil
• Iris nodules
• posterior synechiae
• circumcorneal redness
KP: are composed of inflammatory cells such as lymphocytes, plasma cells and
macrophages. KP is usually evident in patients with active inflammation. The left
photograph shows KP in anterior uveitis. The left one shows a highly magnified
view of fresh KP in early anterior uveitis.
Then what cause KP?
During inflammation, because the blood-aqueous barrier and endothelium have
been destroyed,
This photograph shows endothelial cellular ‘dusting’ and early KP formation.
Aqueous flare:
We all know the vascular wall of the iris has the function of blood-aqueous barrier,
so the content of protein and cell in normal aqueous humor is very less. The
presence of flare indicates active inflammation with a resultant higher risk of
complications over the longer term. This photograph shows a white opacity in the
anterior chamber when observed by slit-lamp microscope that indicates aqueous
flare. We can also see inflammatory cells floating in the anterior chamber.
❖ WHAT IS POSTERIOR SYNECHIAE OF IRIS?
Iris bombe: Due to blockade of communication between anterior and posterior
chambers, aqueous humor can’t flow from the posterior chamber to the anterior
one to retain in the posterior chamber, the iris is pushed forward with a shape of
bulging.
❖ WHATS SECLUSION OF PUPIL:
if posterior synechiae is extensive, the whole papillary margin firmly adhered to
the surface of the lens, antero-posterior flow of aqueous humor is obstructed.
❖ WHAT ARE THE PRESENTATIONS OF ANTERIOR UVEITIS?
Symptoms
pain, photophobia, decreased vision.
Signs
circumcorneal redness
KP.
aqueous flare or inflammatory cells
small or irregular pupil
Iris nodules
posterior synechiae.
❖ WHAT ARE THE SIGNS OF POSTERIOR UVEITIS?
Signs
cells in the vitreous humor.
white or yellow-white lesions on the retina or choroid or both.
retinal detachment.
optic disk edema
Retinal detachment, although infrequent, occurs most commonly in posterior
uveitis and may be tractional, rhegmatogenous, or exudative in nature.
❖ DIFFERENTIAL DIAGNOSIS OF UVEITIS:
acute conjunctivitis
acute angle-closure glaucoma
keratitis
acute conjunctivitis: superficial injection, normal anterior segment
anterior uveitis: corneal redness, KP, and aqueous flare
acute angel-closure glaucoma: elevated intraocular pressure, corneal edema and
very shallow anterior chamber.
anterior uveitis: small pupil, the anterior chamber isn’t shallow; normal or low
intraocular pressure.
Keratitis: epithelial staining or defects, or stromal thickening or infiltrate. anterior
uveitis: normal cornea.
❖ WHAT ARE THE COMPLICATIONS OF UVEITIS?
•
•
•
•
•
•
•
•
•
•
•
•
Synechiae - commonest , if numerous can cause blockage of aqueous flow
leading to glaucoma
Cataract
Cystoid macular edema
Retinal detachment
Synechiae
•
Anterior synechiae : at the chamber angle and
cause glaucoma.
•
Posterior synechiae : pupillary seclusion and
forward bulging of the iris.
Cataract
Inflammation promote lens thickening and opacification.
Cystoid macular edema
a common cause of visual loss in uveitis.
Longstanding or recurrent cause permanent loss of vision due to cystoid
degeneration.
Retinal detachment
tractional, rhegmatogenous and exudative forms.
exudative retinal detachment suggests significant choroidal inflammation.
•
exudative retinal detachment most commonly in association with VogtKoyanagi- Harada disease, sympathetic ophthalmia, and posterior scleritis or
in association with severe retinitis or retinal vasculitis.
❖ Fuchs uveitis syndrome (type of anterior uveitis)
Fuchs uveitis syndrome is also called Fuchs heterochromic iridocyclitis. It is a
chronic non-granulomatous condition diagnosed at an average of 40 years old.
❖ INTERMEDIATE UVEITIS:
The hallmark of intermediate uveitis is vitreous inflammation. Intermediate uveitis
is typically bilateral and tends to affect patients in their late teens or early adult
years. Men and women are affected equally.
The hall mark of intermediate uveitis is vitreous inflammation. The most striking
finding on examination is vitritis often accompanied by vitreous condensations,
either free-floating as “snowballs” or layered over the pars plana and ciliary body
as “snow-banking.” The left photograph shows clumps of white cells that form the
globular yellow-white 'snowballs' in the inferior peripheral vitreous. The right
photograph shows yellow-white exudates band to form 'snowbanks'. Adjacent
retinal vasculitis is common in intermediate uveitis. Anterior chamber
inflammation is mild and posterior synechiae are uncommon. If anterior chamber
inflammation is significant, the inflammation is more appropriately termed diffuse
uveitis or panuveitis.
The most common complications of intermediate uveitis include Cystoid
macular edema is the most common cause of decreased vision.
❖ POSTERIOR UVEITIS (TYPE OF INTERMEDIATE UVEITIS):
the first sign important in the diagnosis of posterior uveitis is hypopyon. Disorders
of the posterior segment that may be associated with significant anterior
inflammation and hypopyon include syphilis, tuberculosis, sarcoidosis,
endogenous endophthalmitis, Behçet disease. When this occurs, the uveitis is more
appropriately termed diffuse or panuveitis.
Glaucoma(SIGNS)-Acute ocular hypertension in association with posterior uveitis
can occur with toxoplasmosis, ARN syndrome due to herpes simplex virus or
varicellazoster virus, sarcoidosis, or syphilis.
GLAUCOMA
❖ CLINICAL CHRACTERISTICS OF POAG?
• Insidious in onset, Slowly progressive and painless.
• Bilateral but can be quite asymmetric.
• Fluctuate pressure: unreliable on single measurement of IOP
• Glaucomatous optic disc.
• Peripheral vision is affected first.
• Eventually the entire vision will be lost.
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OCULAR HYPERTENSION?
Elevated intraocular pressure with no visual damage.
Considered glaucoma suspects.
Retinal ganglion cell damage not detectable with currently available
techniques.
• The rate develop glaucoma is approximately 1–2% per year.
• Patients should undergo regular monitoring (once or twice a year) .
• Overestimation of intraocular pressure for other reasons besides CCT.
❖ NORMAL TENSION GLAUCOMA?
• Progressive visual field loss with no IOP elevation.
• Inherited predisposition to IOP.
• Associations with vasospasm and low intracranial pressure.
❖ MEDICATION OF POAG
• Prostaglandin analogues
• Alpha-adrenergic agonists
• Carbonic anhydrase inhibitors
• Beta-adrenergic blockers
❖ LASER THERAPIES AND SURGERIES FOR GLAUCOMA
• YAG laser iridotomy for PACG
• Cataract extraction
• FOR POAG:
• Trabecular ablation
• Viscocanalostomy
• Trabeculectomy
❖ NORMAL IOP:
average intraocular pressure is between 15-16 mmHg and about 95% of people
have an intraocular pressure between ten and 21.
❖ DEVIATION OF ESTIMATION OF IOP BY CCT:
❖ NORMAL STRUCTURES UNDER GONIOSCOPY:
❖ SIGNS OF A GLAUCOMATOUS OPTIC DISK:
❖ EXAMINATIONS FOR GLAUCOMATOUS NEUROPATHY: (LOOK FOR)
• OCT
• Angio disc scan
❖ DIFFERENCE BETWEEN GLAUCOMATUS AND OTHER OPTIC NERVE
DAMAGE? (LOOK FOR)
Ophthalmology
Lens and Cataract
Typical vision problems of different subtypes of age related cataract
1. Cortical cataract; symptoms include:
bilateral, often symmetric
both far vision and near vision are affected
visual function is variably affected depending on pupil area
intumescent lens: angle closure
2. Nuclear cataract; symptoms include:
Lenticular myopia
poor hue discrimination
monocular diplopa
3. Posterior subcapsular cataract(PSC): symptoms include:
earlier vision problem
worse near vision
hemeralopia
monocular diplopia
Differentiation of PSCs include trauma, corticosteroid, inflammation and
radiation
Different stages of cortical cataract
1. Incipient-cataract; they are peripheral, wedge-shape opacities
2. Immature-cataract; intumescent cataract, narrow anterior chamber angle
3. Mature cataract; detumescence
4. Hyper mature cataract; morgagnian cataract (secondary glaucoma)
Treatment of cataract
1. Medical treatment: includes B vitamins, multivitamins and carotenoids
Ophthalmology
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2. Surgery: Phacoemulsification
Indications of cataract surgery
1. Difficulty with driving, reading, walking, daily life
2. Difficulty with funds examination or treatment
Retinal and Optic Nerve disease
Screening of Diabetic Retinopathy
Patients with type 1: ophthalmologic examination within 3 years after
diagnosis, reexamine annually
Patients with type 2: annually
Diabetic woman during pregnancy: every 3 months
Digital fundal photography is an effective and sensitive screening method
Classification of DR
Nonproliferative diabetic retinopathy: Mild NPDR is characterized by at least
one microaneurysm. In moderate NPDR, there are numerous micro
aneurysms, intraretinal hemorrhages, venous beading, and/or cotton-wool
spots. Severe NDPR is characterized by cotton-wool spots, venous bleeding
in two quadrants and intraretinal microvascular abnormalities (IRMA) either
in four quadrants or severe in one quadrant
Diabetic maculopathy: manifests as focal or diffuse retinal thickening
(edema), caused primarily by a breakdown of the inner blood-retinal barrier
at the level of the retinal capillary endothelium that allows leakage of fluid
and plasma constituents into the surrounding retina
Proliferative diabetic retinopathy: causes most severe complications. Its
characterized by new vessels on the optic disk (NVD) or else where in the
retina (NVE)
Clinical manifestations of CRVO
Afferent pupillary defect
Opacification of the superficial retina
Cherry-red spot
Ophthalmology
2
Cilioretinal artery
Clinical manifestations of RVO
Sudden painless loss of vision
Clinical appearance varies from a few small scattered retinal hemorrhages
and cotton-wool spots to a marked hemorrhagic appearance with both deep
and superficial retinal hemorrhage
Major complications of CRVO
Macular edema
Neovascular glaucoma secondary to iris neovascularization
Retinal neovascularization
Definition of Retinal Detachment
Separation of the sensory retina from the retinal pigment epithelium
Classification of Retinal Detachment
The three main types are:
Rhegmatogenous detachment
Traction detachment
Exudative (serous) or hemorrhagic detachment
Clinical features of typical optic neuritis
subacute loss of vision developing over 2-7 days
reduced visual acuity
visual field defect
reduced color vision
reduced pupillary response to light shone in the affected RAPD
Periocular pain in 90%, exacerbated by eye movement in 50%
Optic disk
normal during acute phase in two thirds (retrobulbar optic neuritis)
mildly swollen in acute phase in one third
in children, swollen optic disk in acute phase in two thirds
Ophthalmology
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Retinal exudates and cotton wool spots do not occur and are suggestive
of an infectious illness
No associated systemic illness
Usually spontaneous recovery of vision with visual acuity better than 20/30
within 2 weeks
Ophthalmology
4
OCULAR TRAUMA
> Ocular trauma - Any mechanical, physical and chemical external factors acting on the eye,
causing damage to the structure and function of visual organs.High risk groups:
Male, children and young adults.
• Visual harm:
– The primary cause of monocular blindness.
– The second leading cause of blindness after cataract.
Q.1 Classification of mechanical ocular trauma ?
Q.2 Anterior and posterior segment complications of blunt trauma ?
● Anterior segment complications of blunt trauma
– Corneal abrasion
– Acute corneal edema
– Hyphema
– The anterior uvea contusion – Lens contusion
– Rupture of the globe
● Posterior segment complications of blunt trauma :
– Vitreous haemorrhage – Commotio retinae
– Choroidal rupture
– Retinal breaks
– Optic nerve contusion
1
Q.3 Classifications of corneal and scleral lacerations?
- Corneal lacerations Classifications:
• Small shelving corneal lacerations - May not require suturing as they often heal spontaneously
or with the aid of a soft bandage contact lens.
• Medium-sized corneal lacerations - Usually require suturing, especially if the anterior chamber
is shallow or flat.
• Corneal lacerations with iris involvement
• Corneal lacerations with lenticular damage.
- Scleral laceration classification :
• Anterior scleral lacerations - May be associated with serious complications such as iridociliary
prolapse and vitreous incarceration.
• Posterior scleral lacerations - Frequently associated with retinal breaks unless very superficial.
The scleral wound is exposed and sutured starting anteriorly and working posteriorly.
Q.4 Clinical features of corneal foreign bodies and intraocular foreign bodies?
● Corneal foreign bodies – Extremely common and cause considerable irritation.
– Leukocyte infiltration may also develop around any foreign body
of some duration.
– If a foreign body is allowed to remain, there is a significant risk of secondary infection and
corneal ulceration.
– Mild secondary uveitis is common with irritative miosis and photophobia.
– Ferrous foreign bodies of even a few days’ duration often result in rust staining of the bed of
the abrasion
●
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Intraocular foreign bodies May traumatize the eye mechanically, introduce infection or exert other toxic effects on
the intraocular structures.
May be located anywhere from the anterior chamber to the retina and choroid.
Notable mechanical effects include cataract formation secondary to capsular injury,
vitreous liquefaction, retinal haemorrhages and tears.
Stone and organic foreign bodies are particularly prone to result in infection.
Q.5 Emergency treatment of chemical injuries?
- Copious irrigation is crucial to minimize duration of contact with the
chemical and normalize the pH in the conjunctival sac as soon as possible. Normal saline
should be used to irrigate the eye for 15-30 minutes or until pH is normalized.
- Double-eversion of the eyelids should be performed to any retained particulate matter
trapped in the fornices, such as lime or cement, may be removed.
- Debridement of necrotic areas of corneal epithelium should be performed to allow for
proper re-epithelialization.
2
C-12 STRABISMUS
> Effects of strabismus :
- Abnormal sensory phenomena
Diplopia
- Visual confusion
- Abnormal retinal correspondence
- Suppression
- Amblyopia
Eccentric fixation
> Brown syndrome : Superior oblique tendon sheath syndrome
● Causes :
❖ Brown syndrome is due to fibrous adhesions of SO tendon and trochlea
❖ May be from congenital and acquired factors.
● CLINICAL FEATURES:
Major signs of Brown syndrome are:Elevation was limited when the eye is in the adduction
position.
● Clinical signs :
(a) Downshoot in adduction.
(b) Hypotropia in primary position.
(c) Anomalous head position with ipsilateral head tilt and chin up.
3
Match
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1 Bulging of descemet’s membrane. Descemetocele
2 corneal epithelium desquamate and damage to Bowman’s membrane, Localized necrotic material
of superficial layers of cornea falls off. Corneal ulcer
3 Weak area of ulcer is unable to support the increased IOP. Perforation
4 repeated healing and perforation. Fistula
5 iris remains adherent to corneal scar. Anterior synechia
6 the pupillary border of iris prolapse through opening, exudation takes place on prolapsed tissue.
Adherent leukoma
7 anterior chamber anatomy is lost , angle of anterior chamber is occluded Secondary glaucoma
8 a ectasia of the adherent leucoma, an ectatic cicatrization with incarceration of iris . Staphyloma
9 Result of purulent iridocyclitis, endophthalmitis and panophthalmitis. Atrophia bulbi
10 Newly formed fibres are laid down irregularly. Corneal scar
11 Mild corneal scar，iris can be seen easily through scar. Nebula
12 Moderate corneal scar. Macular
13 Severe corneal scar. Iris cannot be seen through scar. Leucoma
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1.Symptoms of Corneal Ulcer
Symptoms are usually marked, they are:
1. Diminution of vision, depending on location of corneal ulcer
2. Pain and foreign body/ gritty sensation
3. Photophobia ( difficulty in opening eyes especially in bright light )
4. Watering /lacrimation
5. There may be discharge (Mucopurulent / purulent)
2. Signs of active corneal inflammation
1.
Visual acuity may be affected, depending on location of corneal ulcer
2.
Edema of lids of affected eye in severe cases
3.
Blepharospasm
4.
Ciliary and conjunctival congestion
5.
Hypopyon ( pus may be present in anterior chamber)
6.
Iridocyclitis
7. cellular infiltration of the stroma, edema, neovacularization(superficial or deep)，necrosis
Cornea: loss of transparency.
yellowish/ grayish pale
varying shape /size
breach in continuity of corneal surface
irregular floor and margins
floor appears grayish / grayish pale/ grayish yellow
projecting swollen edges
ground glass like due to corneal edema
3.Why photophobia when keratitis?
• The result of painful contraction of an inflamed iris
•
Dilation of iris vessels is a reflex phenomenon caused by irritation of the corneal nerve endings
4. Properties of hypopyon
• a collection of inflammatory cells that appears as a pale layer in the inferior anterior chamber
•
characteristic of both bacterial and fungal central corneal ulcers.
•
sterile in bacterial corneal ulcers unless there has been a rupture of Descemet’s membrane
•
may contain fungal elements in fungal ulcers .
5. Rules of Therapy
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Remove etiological factor
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Control infection
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Promote healing
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Decrease cicatricle
6. Functions of cycloplegic
prevent ciliary spasm
relieve pain
prevent dangerous results of iridocyclitis
breaks adhesions
prevent synechia formation.
Signs of cornea of baterial keraitits
Gram-positive bacteria
well-circumscribed Oval or round local abscess lesion
Stromal infiltration in the central 2/3 of cornea
severe stromal abscess and corneal perforation
accompanied hypopyon and keratic precipitates
The cornea surrounding the ulcer is often clear
Gram-negtive bacteria
• Rapid development of liquefactive necrosis of the cornea
•
unclear border of ulcer
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extensive stromal loss, corneal perforation, and intraocular infection.
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a large hypopyon that tends to increase in size as the ulcer progresses
First line treatment of Corneal Ulcer
First line treatment : topical fluoroquinolones
eg, ofloxacin, moxifloxacin
Second line treatment of Corneal Ulcer
Second line treatment :
Topical cefuroxime(fortified 5%) gentimicine(fortified 1.5%)
Signs of fungal keratitis
• The lesion may mimic bacterial and herpetic infections or even may co-exist with them
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The fungal corneal ulcer is indolent and typified by an infiltrate with irregular edges, typically
appears as white or gray white elevated hard superficial ulcer with dot-like satellite opacities around
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the satellite lesions are usually infiltrates at sites distant from the main area of ulceration
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Often a hypopyon, marked inflammation of the globe and minimal vascularization may appear
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Underlying the principal lesion, and the satellite lesions as well, there is often an endothelial plaque
associated with a severe anterior chamber reaction
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Corneal abscesses frequently occur
Signs of Dendritic ulcer
Most characteristic lesion, occurs in corneal epithelium
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Typical branching, linear pattern with feathery edges and terminal bulbs at ends.
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Visualized by fluorescein staining
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Signs of Disciform ulcer
Most common form of stromal disease in HSV infection.
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Edema is most prominent sign.
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Edematous stroma in a central, disk- shaped area, without significant infiltration and usually
without vascularization.
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Folds in descemet’s membrane
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Keratic precipitates(KP) may lie directly under disciform lesion but may also involve the entire
endothelium.
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First line and Second line treatment of Disciform ulcer
First line treatment is topical acyclovir or ganciclovir，5 times daily for 1week then 3 times daily
for a week
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Second line treatment is topical trifluorothymidine
Types of Keratitis
1 white or gray white elevated hard ulcer with dot-like satellite opacities around
Fungal keratitis
2 Typical branching, linear pattern with feathery edges and terminal bulbs at ends Dendritic Keratitis
3 stroma is edematous in a central,disk-shaped area,without significant infiltration and usually without
vascularization Disiform Keratitis
4 local abscess lesion or severe stromal abscess and corneal perforation
positive)
Bacterial Keratitis(gram
5 Rapid development of liquefactive necrosis of the cornea Bacterial Keratitis(gram negtive)
1 Please change ：+1．00DS／+2．00DC×90 to another form （ ）
A．+1．00DS／+2．00DS×180
B．+3．00DS／-2．00DC×180
C．+3．00DS／-2．00DC×90
D．+2．00DS／+2．00DC×180
E．+2．00DS／-2．00DC×90
(1) algebraically sum the original sphere and cylinder;
(+1．00)+( +2．00)= +3．00
(2) reverse the sign of the cylinder;
the sign of the cylinder here is “+”, so we change it to “-”
(3) change the axis of the cylinder by 90°.
the axis of the cylinder here is “90”, change the axis of the cylinder by 90°, so we change it to “180”
2 In one patient, the near point lies at 0.2 m and the far point at 2 m. The range of accommodation is （ ）
A 5D
B 4.5 D
C 4D
D 5.5 D
Range of accommodation:
In mathematical terms , the range of accommodation is obtained by subtracting near-point refractive
power from far-point refractive power.
near-point: Shortest distance that allows focused vision
far-point: Farthest point that is still discernible in focus
near-point refractive power 1/0.2m=5D
far-point refractive power 1/2m=0.5D
Range of accommodation
5D-0.5D=4.5D
1 . What is moderate degree of myopia?
A 〈-3.00 D
B -3.00--- -6.00D
C -3.00--- -5.00D
D 〉-6.00D
Degree of myopia:
mild〈-3.00 D
moderate -3.00--- -6.00D
high 〉-6.00D
2. What is astigmatism with the rule?
A the meridian with the greater refractive power is horizontal
B the meridian with the greater refractive power is vertical
C the principal meridians do not lie within 20° of the horizontal and vertical
D the power or orientation of the principal meridians changes across the pupillary aperture
Astigmatism with the rule (most common form, commonly in younger patients ): the meridian with the
greater refractive power is vertical
Astigmatism against the rule (commonly in older patients): the meridian with the greater refractive power
is horizontal