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Pathophysiology Exam 3

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Chapter 29
● Anemia
○ A medical condition in which the RBC or hemoglobin is less than normal.
○ Causes: decreased in production of RBCs or hemoglobin to the increase of loss
(typically bleeding acute or chronic) or destruction of RBC or a combination of
these factors
■ You can have a normal RBC count with decreased hemoglobin
○ Clinical Manifestations:
■ Reduced oxygen carrying capacity: hypoxia *
■ Reduced oxygen levels in the blood: hypoxemia
■ Dyspnea (shortness of breath), palpitations, dizziness, fatigue, pallor
■ Neurological and GI changes
● Organ dysfunction
■ Increased rate and depth of breathing in order to increase oxygen
○
Acute Blood Loss:
■ Loss of RBC exceeds production of new RBC
● Blood loss is the most common cause of acute anemia
■ Posthemorrhagic anemia
● A normocytic-normochromic anemia caused by acute blood loss
from the vascular space
● Major cause is trauma **
○ Gi hemorrhage
○ Ruptured ectopic pregnancies
○ Ruptured aneurysms
○ DIC
■ Restoring blood volume by plasma expanders or transfusions can
diminish some symptoms of anemia but the hemoglobin restoration can
take 6-8 weeks
■ Clinical manifestations
● Depends on severity of blood loss
● Large volume loss reduced systemic filling pressure,resulting in
decreased venous return
● Low BP, dizzy, lose consciousness
○
Anemias of blood loss
■ Anemia from chronic blood loss only occurs if the loss is greater than the
replacement capacity of the bone marrow. If iron stores are depleted, iron
deficiency anemia can occur
■ Cancer, non hodgkin's lymphoma, inflammatory disorders, etc.
○
Pernicious Anemia
■ The most common macrocytic anemia
■ Is caused by vitamin b12 deficiency
■
■
■
■
■
■
○
Lacks intrinsic factor from the gastric parietal cells
● Required for B12 absorption
May be congenital or autoimmune disorder
● Autoantibodies against intrinsic factor
Conditions that increase risk include:
● Genetics
● Endocrine disorders
● Gastrectomy, ileal resection, tapeworms, demand of vitamin b12
● Chronic gastritis and H. Pylori
● Proton pump inhibitors
Clinical manifestations
● Early symptoms are commonly overlooked because they are
nonspecific
● Weakness, fatigue
● Tingling or prickling (paresthesias) of the feet and fingers, difficulty
walking
● Loss of appetite, abdominal pains, weight loss
● Sore tongue that is smooth and beefy red, secondary to atrophic
glossitis
Evaluation
● Blood tests, bone marrow aspiration, serologic studies, gastric
biopsy, clinical manifestations
Treatment
● weekly/monthly injections or high oral doses of vitamin b12
● If left untreated, death will result
○ Untreated PA is fatal, usually because of heart failure
Iron Deficiency Anemia (IDA)
■ Most common type of nutritional anemia worldwide
● Without iron body can not produce hemoglobin
■ Causes:
● Pregnancy
● Chronic Blood loss (assess for any source of blood loss i.e. blood
in stool); once the source of blood loss is identified and corrected,
oral iron replacement therapy can be initiated
● Dietary lack and eating disorders
● Impaired absorption
● Increased requirement
● Chronic blood loss
● Medications (that cause Gi bleeding)
● Some surgeries
■ Highest Risk: toddlers, adolescent girls, women of childbearing age, those
living in poverty, infants consuming cow's milk, older adults on restrictive
diets, teenagers on junk food diets
■
■
○
●
Vitamin C is good for iron absorption so should be given along with iron
supplements
Clinical Manifestations
● Fatigue, weakness, shortness of breath
● Pale earlobes, palms and conjunctivae
● Brittle, thin, coarsely ridges, and spoon shaped (concave or
koilonychia) nails
● Burning mouth
● Angular stomatitis; dryness and soreness in the corners of the
mouth
● Become symptomatic: when hemoglobin (Hgb) 7-8 g/dL
Hemolytic Anemia
■ Occurs when the bone marrow isn't making enough red cells to replace
the ones that are being destroyed
■ Hemolytic anemias may either be congenital or acquired
● Can happen due to viral of bacterial infections, medications, blood
cancers, overactive spleen, mechanical heart valves that damage
red blood cells as they leave the heart, transfusion reactions
● Can go away and come back
■ Of the acquired forms, autoimmune reaction (immunohemolytic) and
drug-induced hemolytic anemia are the most common
■ Symptoms
● Weakness, paleness, jaundice, dark-colored urine, fever, inability
to do physical activity and heart murmur
■ Clinical Manifestations
● May be asymptomatic
● Jaundice (icterus)
○ Arises from excess of bilirubin
● Aplastic crisis
● Splenomegaly
○ Enlargement of the spleen
Disorder of Platelets
○ Thrombocytopenia
■ Platelet count <100,000/ mm^3
● <50,000/ mm^3. Hemorrhage from minor trauma
○ Falls
○ Can not get an epidural without platelet count of at least
100,000
○ Can not received port for chemo without high enough
platelets
● <15,000/mm^3: spontaneous bleeding
● <10,000 mm^3: severe bleeding that can be fatal
■
■
■
●
Example: Heparin-induced: immune-mediated, adverse drug reaction
caused by IgG antibodies against the heparin=platelet factor 4; can lead
to thrombosis, must stop heparin
Signs: superficial bleeding, easy bleeding, prolonged bleeding, bleeding
from gums or nose
Decreased platelet production, increased consumption
● Viral infections, drugs, chemo, nutritional deficiencies (b12, folate)
renal failure, radiation
Disorders of Coagulation
○ Disorders of coagulation usually are created by defects or deficiencies in one or
more of the clotting factors. We are going to discuss coagulation disorders that
are attributed to pathologic conditions that trigger coagulation inappropriately
○
Disseminated intravascular coagulation also known as DIC
■ A complex syndrome of coagulation resulting in formation of fibrin clots in
medium and small vessels throughout the body
■ Clotting and hemorrhage simultaneously occur
● Abnormally spread and ongoing
● Sepsis (most common), cancer or acute leukemia, trauma, blood
transfusion
■ Cause: variety of clinical conditions that release tissue factor
● Inflammation, infection, cancer
■ Clots can clog vessels and cut off supply to vital organs hence damaging
them OR the clotting proteins can be consumed which increases chances
of bleeding with out without injury
■ Clinical Manifestations
● Bleeding of eyes, nose or gums
○ Bleeding at three or more non linked sites
● Bleeding from venipuncture sites
● Bleeding from arterial lines
● Bleeding from surgical wounds
● Purpura, petechiae, and hematomas
● Symmetric cyanosis of the fingers and toes
○
Thromboembolic Disease
■ Blood clots! (develop clots spontaneously)
● Thrombus: fixed
● Embolus: moving
● Arterial thrombi: defects in proteins involved in hemostasis
○ High blood flow
○ Can stop blood from reaching important organs
● Venous thrombi: variety of clinical disorders or conditions
○ Low blood flow
■
■
■
When a thrombus detaches from the vessel wall and circulated in the
bloodstream it is referred to as an embolus
Treatment
● Prevention is key!
● Anticoagulants (heparin, coumadin)
○ Better for venous not arterial
● Thrombolytic (streptokinase, urokinase)
Virchow Triad (why blood clots develop within the veins)
● Injury to the blood vessel endothelium: atherosclerosis, many
others
● Abnormalities of blood flow
● Hypercoagulability of the blood
Chapter 28
● Cellular Components of the Blood
○ Erythrocytes: red blood cells; are the most abundant cells of the blood; primarily
responsible for tissue oxygenation; they contain hemoglobin
○ Leukocytes: white blood cells; fight infection and remove debris
■ Classified by structure (granulocyte or agranulocyte) or function
(phagocytes or immunocytes)
■ Granulocytes include neutrophils, basophils, and eosinophils and are all
phagocytes; mast cells are also classified as granulocytes
● Neutrophil: most numerous granulocyte; more than 50% of total
leukocyte count; reach full maturity in bone marrow; first
responders
Ingest and destroy organisms
● Eosinophils: highly destructive to parasites and viruses
● Basophils: often increase during an allergic inflammatory reaction
and parasitic infections (particularly ticks)
● Mast Cells: similar to basophils but generated differently in the
bone marrow in which they migrate in immature form into tissues;
play central role in inflammation
■ Agranulocytes:
● Monocytes: largest; horseshoe nucleus
● Macrophages: remove old and damaged cells and molecular
substances from blood
○ Also remove contaminating microorganisms from liver and
spleen
● Lymphocytes: primary cell of immune response
● Natural Killer Cells: Killer Cells
○ Tumors and viruses
○
●
Do this without being induced to previous pathogens
Quantitative Alterations of Leukocytes
○ Leukocytosis occurs as normal protective response to physiologic stressors, such
as infection, strenuous exercise, emotional changes, temperature changes,
anesthesia, surgery, pregnancy, and some drugs, hormones and toxins
■ It is also caused by pathologic conditions such as malignancies and
hematologic disorders
○
Leukopenia is never normal and is defined as an absolute blood cell count less
than 4000 cells/uL
■ Leukopenia is associated with a decrease in the number of neutrophils,
which increases the risk for infection
● Bad because neutrophils are our first responders and can go
anywhere in the body
■ Leukopenia can be caused by radiation, anaphylactic shock, autoimmune
disease (e.g., systemic lupus erythematosus), immune deficiencies, and
exposure to certain drugs such as glucocorticoids and chemotherapeutic
agents
○
Granulocytosis
■ A result of an increase in the number of neutrophils
● Occurs in response to infection
■ The marrow releases immature cells, causing a shift to the left when
responding to an infection that has created a demand for neutrophils that
exceeds the supply in circulation
○
Neutrophilia
■ Another term that may be used to describe granulocytosis because
neutrophils are the most numerous of the granulocytes
■ Early stages of inflammation or infection
○
Neutropenia
■ A condition associated with a reduction in the number of circulating
neutrophils
■ Due to severe and prolonged infections
○
Eosinophils
■ Results most commonly from parasitic invasion and ingestion of from
inhalation of toxic foreign particles
■ Allergies, asthma , hay fever, drug reactions and parasites
○
Eosinopenia
■ Decrease of eosinophils in blood
■
●
From migration to inflammatory sites
○
Basophilia
■ Seen in hypersensitivity reactions and hypersensitivity reactions because
of the high content of histamine and subsequent release
■ RARE
■ Associated with leukemia
○
Monocytes
■ Occurs during the late or recuperative phase of infection when
macrophages (mature monocytes) phagocytose surviving microorganisms
and debris
● Monocytosis is often seen in chronic infections, usually with
intracellular bacteria, such as tuberculosis (TB), brucellosis,
listeriosis, and subacute bacterial endocarditis (SBE)
● Peripheral monocytosis has been found to correlate with the
extent of myocardial damage following myocardial infarction,
increased numbers of monocytes also may indicate marrow
recovery from agranulocytes
○
Granulocytopenia
■ A significant decrease in the number of neutrophils, can be a life
threatening condition if sepsis occurs
■ It is often caused by chemotherapeutic agents, severe infection and
radiation
○
Lymphocytosis
■ Associated with viral infections, like epstein barr virus and mono
Diseases and Disorders
○ Infectious Mononucleosis
■ Acute, self-limiting viral infection of B lymphocytes
■ Commonly caused by the EBV- 85%
● EBV is a type of herpes virus
■ Transmission: usually by saliva through personal contact (kissing)
● May be present in mucosal secretions of genital tract, respiratory
tract and blood
■ Incubation Period: 30-50 days
● 3-5 day onset of fever and joint pain
■ Clinical Manifestations
● Malaise (feeling icky!), arthralgia (joint pain)
● Classic triad of symptoms: fever, pharyngitis (pain or irritation of
the throat) and lymphadenopathy of the cervical lymph nodes
■ Diagnostic test
■
●
● Monospot qualitative test for heterophilic antibodies
Treatment
● Rest and alleviation of symptoms with analgesics and antipyretics
and penicillin or erythromycin
○ Fatigue is the most common complaint and can last 1-4
months
● Ibuprofen, not aspirin, for children and adolescents because of
reported incidence of reye syndrome
Leukemias
○ Malignant disorders of the blood and blood-forming organs
○ Exhibit uncontrolled proliferation of malignant leukocytes
■ Overcrowding of bone marrow
■ Decreased production and function of normal hematopoietic cells
■ Accumulation disorder as well ad proliferation disorder
● Leukocytes in the bone marrow and blood - causes overcrowding
of the bone barrow and decreases production of other blood cells
(RBC, WBC and platelets)
○ Classification
■ Predominant cell of origin: myeloid or lymphoid
● Myeloid cells develop into RBC, Platelets and basophils,
eosinophils and neutrophils
● Lymphoid cells develop into lymphocytes and natural killer cells
■ Rate of progression: acute or chronic
● Acute- malignant cells (blasts) are immature and incapable of
performing their immune system functions
● Chronic- develop in mature cells and they can perform some of
their duties but not well
○ Develop at slower rate
■ Pathophysiology:
● Common features: T cells, B cells or NK cells
○ Majority B cells, then T cells
○ NK is rare
● Accumulation and proliferation
● Accumulate in liver, spleen, lymph nodes or other organs
● Increased leukemic cells in blood are the most dramatic indicator
BUT it is primarily disruption of bone marrow!
○ Overfill bone marrow and spill into blood
○
Acute leukemia
■ Most common childhood leukemia
● Leukemia overall is more common in adults
■ Acute myelocytic leukemia (AML)
● Myeloblasts- bone marrow
■
■
■
○
●
○ Myeloid differentiation stops, decreased rate of apoptosis
● Blast cells
● Eight different subtypes
● More common acute leukemia in adults
○ Anemia, infections and bleeding
Acute Lymphatic Leukemia (ALL)
● Most common childhood leukemia
○ Rare in adults
● Lymphoblasts
● More B lymphatic cells than T cells
○ B cells help germs not enter body; t cells destroy germ
cells
○ Chromosomal alterations- replaces healthy cells with
cancer cells that carry cancer to organs and grow and
divide
● Abrupt onset
● Liver enlargement
Presence of undifferentiated or immature cells, usually blast cells
Rapid onset and short survival
● Abrupt and stormy onset
Chronic Leukemia
■ Chronic Myelogenous Leukemia (CML)
● Found mostly in adults
● Begins in the blood-forming vells of the bone marrow
● Caused by a chromosome mutation that occurs spontaneously
■ Chronic lymphocytic leukemia (CLL)
● Most common leukemia in adults and the western world
○ Typically peaks in fifth to sixth decades
● Most B cell origin
● Somewhat genetics
● Increased infection due to reduced neutrophil levels
■ Predominant cell is mature but does not function normally
■ Slow progression
● Don't interfere with blood cell production to the extent of acute
leukemias
■ Symptoms:
● Infections
Leukemia Risk Factors
○ Family linked
○ Down syndrome disorders
○ Cigarette smoke
○ Benzene
○
Ionizing radiation
●
Clinical Manifestations
○ Very similar for all types
● Fatigue
○ Caused by anemia
● Bleeding
○ Result of thrombocytopenia (reduced circulating platelets)
● Fever
○ Caused by infection (normally in mouth, throat, respiratory
tract, urinary tract, etc)
● Anorexia
○ Weight loss because most people have diminished taste
○ Muscle atrophy, difficulty swallowing
● Liver, spleen and lymph node enlargement
○ More common in AML
● Abdominal pain
● Pain in bones and joints
○ Due to inflammation/ stretching or periosteum
● CNS involvement
●
Lymphadenopathy
○ Enlarged lymph nodes
○ Increase in size and number
○
■ Normal- non palpable
■ Enlarged- palpable and tender or painful to touch
Localized versus generalized
■ Localized- drainage of area that was infected
■ Generalized- result of a malignant or non malignant disease
● Particularly in adults
●
Malignant Lymphomas
○ Male up a diverse group on neoplasma that develop from the proliferation of
malignant lymphocytes in the lymphoid system
■ Lymphoma is the most common blood cancer in the US
■ Malignant transformation produces a cell with uncontrolled and excessive
growth that accumulated in the lymph nodes and other sites, producing
tumor masses
■ Lymphomas usually start in the lymph nodes or lymphoid tissues of the
stomach or intestines
■ Lymphatic system made up of lymphocytes (T and B cells)
● B cells make antibodies that help protect the body against germs
● T cells destroy germs. Abnormal cells in body
○ Bosot or slow other immune system cells
■ Classifications of lymphomas are base don the type of cell it originated
from
● Hodgkin’s lymphoma
● Non-hodgkin's lymphoma
●
Hodgkin vs Non Hodgkin Lymphoma
○ Two major categories
■ Hodgkin Lymphoma
● Linked to EBV
● Presence of B cells called Reed-Sternberg cells
○ Can also find in other illnesses and cancers
○ Must have Reed Sternberg cells in order to be diagnosed
with Hodgkin Lymphoma
● Not very common
● Higher in males
● Median age of diagnosis 64 years
● Clinical Manifestations
○ Enlarged painless neck lymph nodes
■ First sign
○ Lymphadenopathy, causing pressure and obstruction
○ Mediastinal mass
■ Found on X ray
■ Clinical Manifesations:
●
■
Fever, weight loss, night sweats, pruritus
(itchy skin), fatigue
■ If accompanied with weight loss, poor prognosis
● Incidence rates for HL have declined, especially among older
adults
● Denmark, the Netherlands, and the US have the highest incidence
of HL and Japan and Australia have the lowest incidence
● HL peaks at two different stages: early in life in the second and
third decades and later in life during the sixth and seventh
decades
Non-Hodgkin Lymphoma
● B cells, T cells, NK cells
● Slightly more common than hodgkin’s
○ Cause unknown, predict weakened immune system
● Is now called B cell neoplasia and includes T-cell and NK
neoplasms
○ Lymphocytes don't die, just continue to grow and divide
which causes cells to grow and cause inflammation
● Is linked to chromosome translocations
● Clinical Manifestations:
○ Localized or generalized painless lymphadenopathy
○ Nodal enlargement and transformation over months or
years
○ Retroperitoneal and abdominal masses with symptoms of
abdominal fullness and back pain
○ Ascites (fluid in the peritoneal cavity) and leg swelling
○ Persistent fatigue
○ fever/night sweats
○ Unexplained weight loss
Alterations of Hematologic Function in Children
●
●
Disorders of Erythrocytes
○ Anemia: most common blood disorder in children
■ Causes:
● Ineffective erythropoiesis
● Premature destruction of erythrocytes
● Most common cause: iron deficiency
● Inherited, congenital or both
■
Hemolytic Anemia
● Premature destruction caused by intrinsic abnormalities of the
erythrocytes
○ Intrinsic- destruction of RBC is due to flaw within RBC
themselves, inherited
■ RBCs don't live as long
■ Ex: sickle cell anemia
○ Extrinsic- destruction of RBC is from an cause outside the
cell
■ Ex: Infections, autoimmune, penicillin, medication,
cancers, etc.
● Red blood cells destroyed faster than the bone marrow can make
them
● Damaging extra-erythrocytic factors
● Inherited, congenital, or both
■
Iron Deficiency Anemia
● Due to dietary insufficiencies, absorption problems, blood loss,
increased iron requirement
○ Cows milk
● Iron deficiency anemia is common in children because of their
extremely high need of iron for normal growth
● Clinical manifestations
○ Irritability, decreased activity tolerance, weakness, lack of
interest in play, pica
○ May impact attention span, alertness, learning
● Treatment:
○ Iron with vitamin C
○ Cows milk restricted
Practice!
○ Iron Deficiency Anemia..
■ Is caused by reduced hemosiderin after birth
■ May be associated with the ingestion of cows milk
●
■
■
Cows milk contains a heat-sensitive protein that produces
gastrointestinal inflammation that may cause chronic blood loss
Produces detectable lethargy and fatigue
Is commonly associated with reduced dietary iron in school-aged children
●
Hemolytic Disease of the Fetus and Newborn (HDFN)
○ Can occur only if antigens on fetal erythrocytes differ from antigens on maternal
erythrocytes
■ A blood problem in newborns where RBCs break down at a fast rate
● Alloimmune disease
■ Causes:
● The antigenic properties of erythrocytes are determined
genetically: they may be type A, B, or O and may or may not
include Rh antigen D
● Erythrocytes that express Rh antigen D are Rh-positive; those that
do not are Rh-negative
● Maternal-fetal incompatibility exists if mother and fetus differ in
ABO blood type or if the fetus is Rh-positive and and mother is
Rh-negative
○ Most often happens at birth when placenta breaks away,
but can happen anytime mother and babies blood mix
■ During a fall, miscarriage, etc.
■ Hyperbilirubinemia occurs after birth because excretion of lipid-soluble
unconjugated bilirubin through the placenta is no longer possible
■ Called erythroblastosis during pregnancy (when moms body attacks
second baby due to blood type)
■ If mother is Rh-negative she will be given RhoGAM during pregnancy and
at delivery
● 2nd pregnancies most often affected
●
Sickle Cell Disease
○ Disorders are characterized by the presence of an abnormal hemoglobin (Hb S)
■ Mutation causes valine to be replaced by glutamic acid
○ Is autosomal recessive
○ Deoxygenation and dehydration: red blood cells solidify and stretch into an
elongated sickle shape
○ Sickle cell trait: child inherits Hb S from one parent and normal hemoglobin (Hb
A) from the other; the heterozygous carrier rarely has symptoms
■ Different from the disease!
■ Have both normal and sickle cell blood cells- most have no symptoms
■ 50% chance of passing on to children
Chapter 23: Alterations of Cardiac Functions
●
Overview of Cardiovascular Diseases
○ Cardiovascular disease is the leading cause of death in both the US and
worldwide
○ Disorders of the veins, arteries, and heart wall comprise the scope of
cardiovascular disease
●
Diseases of the Veins
○ Varicose Veins
■ Aka varicosities; occur when veins become enlarged, dilated, and
overfilled with blood.
■ Typically appear swollen and raised and often have purple or bluish color
■ Causes: incompetent valves, venous obstruction, muscle pump
dysfunction of a combination of them
■ Twisted enlarged vein, most common in legs but can happen in any
superficial vein
■ Concern: cosmetic, aching, pain, discomfort
■ Risk factors: women are at higher risk, pregnancy, increased weight,
increased age, leg trauma, sitting or standing for long periods of time and
family history
■ Symptoms: include visible distended veins; itching, burning or throbbing
around lower leg veins; and muscle cramping or pain in the lower legs..
■ Prevention/treatment: lose weight, decrease time standing or sitting, leg
elevation, physical exercise and compression stockings
○ Practice: If a person wants to reduce the risk of developing varicose veins, that
does the healthcare professional advise of this person?
■ Avoid standing for long periods of time
■ Maintain a healthy weight
■ Drink plenty of fluids
■ Wear compression stockings
○
Deep Venous Thrombosis (DVT)
■ Venous thromboembolism (VTE) includes deep venous thrombosis (DVT)
and pulmonary embolism (PE)
■ DVT is a blood clot that remains attached to the vessel wall, usually in a
single side of a lower extremity
● Mostly deep veins of legs, can cause swelling and pain or be
asymptomatic
● Most thrombi will dissolve without treatment, but if untreated it can
detach and travel to the lung resulting in PE
■
■
■
■
■
●
● Everyone hospitalized and over the age of 60 are at risk for DVT!
A detached thrombus is a thromboembolism
● Very serious as can get stuck in lungs (PE), brain, gastrointestinal
tract, kidneys, etc.
● Significant cause of mortality
Venous thrombi are more common than arterial thrombi because blood
flow and pressure are lower in the veins than arteries
Three factors (triad of Virchow) promote venous thrombosis:
● (1) Venous stasis (associated with immobility, obesity, prolonged
leg dependency, age, congestive heart failure (CHF)
○ When develop in lower extremities has a higher chance of
breaking off and causing PE
○ Common causes: paralysis, varicose veins, surgery of hips
and knees, traveling for long periods without moving
extremities, heart failure
● (2) Venous endothelial damage (related to trauma, venipuncture,
IV medications)
○ Common causes: IV drugs, venipuncture, dwelling
catheters, trauma, injury, surgery
● (3) Hypercoagulable States (from inherited disorders, smoking,
malignancy, liver disease, pregnancy, oral contraceptives,
hormone replacement, hyperhomocysteinemia, antiphospholipid
syndrome)
○ Common causes: diseases processes (cancer, severe
illness, sepsis), estrogen birth control, postpartum period,
dehydration
● Can remember by acronym SHE
Symptoms:
● Often absent
● If a symptom is present it is typically pain
● Unilateral leg swelling, dilation of superficial veins, calf
tenderness, skin that is mottled or cyanotic
Because DVT is usually asymptomatic and difficult to detect, prevention
of DVT is a high priority
● I.e.- being mobilized as soon as possible after surgery, injury or
illness, additional prophylactic treatment for individuals at low risk
can include aspirin or pneumatic devices
Diseases of the Arteries
○ Hypertension
■ Hypertension (HTN) is consistent elevation of systemic arterial blood
pressure
● A systolic blood pressure (SBP) of 130 mmHg or greater or a
diastolic blood pressure (DBP) of 80 mmHg or greater
○
■
■
■
■
■
■
More blood heart pumps and circumference of arteries is
measured
○ Systolic: pressure when heart beats
○ Diastolic: pressure between beats
Is the most common primary diagnosis in the US- approx ⅓ adults older
than 20 have hypertension
Primary (essential) hypertension
● Genetic and environmental factors
● 95% (no identifiable cause)
● Develops gradually over many years
● Risk factors: age, ethnicity, family history of hypertension and
genetic factors, lower education and socioeconomic status,
tobacco use, psychosocial stressors, sleep apnea, dietary factors,
glucose intolerance (diabetes mellitus) and obesity
● Hypertension + dyslipidemia + glucose intolerance = metabolic
syndrome
Secondary hypertension
● Is caused by altered hemodynamics from an underlying primary
disease or drugs
○ Raises peripheral vascular resistance or cardiac output
○ Underlying disorder
■ I.e.- renal vascular or parenchymal disease,
adrenocortical tumors, adrenomedullary tumors
(pheochromocytoma) and drugs (oral
contraceptives, corticosteroids, antihistamines)
● BP returns to normal if the cause is identified and removed before
permanent structural changes occur
Affects the entire cardiovascular system
● Systolic hypertension: most significant factor in causing organ
damages
Increases the risk for myocardial infarction (MI), kidney disease, and
stroke
Pathophysiology:
●
■
■
■
○
Hypertension is caused by increases in cardiac output, total
peripheral resistance, or both
○ Cardiac output is increased by any condition that increases
heart rate or stroke volume, whereas peripheral resistance
is increased by any factor that increases blood viscosity or
reduced vessel diameter (vasoconstriction)
Complicated hypertension: chronic hypertension that damages the
walls of systemic blood vessels
● Target organs include the kidney, brain, heart , extremities, and
eyes
Hypertensive Crisis (or malignant hypertension): rapidly progressive
hypertension in which diastolic pressure is usually greater than 140
mmHg
● It can occur as an uncommon complication of primary
hypertension.
○ Other causes: pregnancy, cocaine or amphetamine use,
reaction to certain medications, adrenal tumors, and
alcohol withdrawal
● High arterial pressure renders the cerebral arterioles incapable of
regulating blood flow to the cerebral capillary beds. High
hydrostatic pressures in the capillaries cause vascular fluid to be
excluded into the interstitial space. If blood pressure is not
reduced, cerebral edema and cerebral dysfunction
(encephalopathy) increase until death happens.
○ Can also cause: cardiac failure, uremia (high levels of
waste in blood due to failing kidneys), retinopathy, or
strokes
Hypertension treatment
● Reducing or eliminating risk factors
● Dietary approaches to stop hypertension (DASH)
● Cessation of smoking
● Exercise program that promotes endurance and relaxation
Orthostatic (postural) hypotension
■ Refers to a decrease in systolic blood pressure of at least 20 mmHg or a
decrease in diastolic blood pressure of at least 10 mmHg within 3 minutes
of moving to a standing position
● Often chronic and more common in older adults due to slowing of
reflexes
■ Lack or normal BP compensation in response to gravitational changes in
circulation, leading to pooling and vasodilation
■ Primary versus secondary orthostatic hypotension
● Primary: risk factor for falls, death, coronary artery disease, heart
failure, and stroke
○
■
■
Treatment: thigh high stockings, administer
vasoconstrictors when necessary, not lying down flat
● Secondary: acute, altered body chemistry, drug interaction,
prolonged immobility, physical exhaustion, potassium/ sodium
depletion, pregnancy, adrenal deficiency etc.
○ Treatment: correcting underlying disorder
Clinical manifestation: orthostatic hypotension often is accompanied by
dizziness, blurring or loss of vision, and fainting
Treatment: focused on correcting the underlying disorder
●
Aneurysm
○ Localized dilation or outpouching of a vessel wall or cardiac chamber
○ True vs false
○ Most commonly occur in the thoracic or abdominal aorta
○ Arteriosclerosis and hypertension are found in more than half of all individuals
with aneurysms.
■ Chronic hypertension results in mechanical and shear forces that
contribute to remodeling and weakening of the vessel wall.
■ Atherosclerosis is a common cause of aneurysms because plaque
formation erodes the vessel wall
○ Infections such as syphilis, collagen disorders (Marfan syndrome) and traumatic
injury to the chest or abdomen can also cause aortic aneurysms
○ Clinical manifestations:
■ Heart- dysrhythmias, heart failure, embolism of heart to vital organs
(brain)
■ Aortic- asymptomatic until they rupture; pain, difficulty swallowing,
breathlessness
■ Abdominal- impair flow to extremities, cause ischemia
●
Arterial Thrombus Formation
○ Tend to develop wherever intravascular conditions promote activation of the
coagulation or clotting cascade
○ In the arteries, the activation of the coagulation cascade is most often caused by
roughening of the tunica intima by atherosclerosis
■ Another important cause is anatomic changes of an artery (such as
aneurysm) that can stimulate thrombus formation, particularly if the
change results in pooling of arterial blood
■ Thrombi also form on heart valves altered by calcification or bacterial
vegetation
■ Valvular thrombi are associated most commonly with inflammation of the
endocardium (endocarditis) and rheumatic heart disease
■ Widespread arterial thrombus formation can occur in shock, particularly
shock resulting from septicemia
●
■
●
In septic shock, systemic inflammation activates the intrinsic and
extrinsic pathways of coagulation, resulting in microvascular
thrombosis throughout the systemic arterial circulation
Arterial thrombi pose two potential threats throughout the circulation:
● (1) the thrombus may grow large enough to occlude the artery,
causing ischemia in tissue supplied by the artery
● (2) the thrombus may dislodge, becoming a thromboembolism that
travels through the vascular system until it occludes flow into a
distal systemic vascular bed
Embolism
○ The obstruction of a vessel by an embolus- a bolus matter that is circulating the
bloodstream
○ The embolism may consist of a dislodged thrombus (often a DVT), an air bubble,
an aggregate of amniotic fluid, an aggregate of fat, bacteria or cancer cells; or a
foreign substance
○ An embolus travels in the bloodstream until it reaches a vessel through which it
cannot fit
■ No matter how tiny it is, an symbolism eventually will lodge in a systemic
or pulmonary vessel
■ The source of the embolus determines whether the embolus will lodge in
a vessel of the pulmonary or systemic circulation
○ Clinical manifestations may vary depending on location:
■ Pulmonary artery embolism causes chest pain and dyspnea; renal artery
embolism causes abdominal pain and oliguria (Decreased urinary
production); mesenteric artery embolism causes abdominal pain and
paralytic, ischemic bowel. Embolism to a coronary or cerebral artery can
result in MI or stroke
○ Thromboembolism
■ Vascular obstruction from dislodged thrombus
■ Pulmonary emboli originate in the venous circulation (mostly in the deep
veins of the legs) or in the right heart
■ Arterial emboli most commonly originate from thrombi in the left heart that
form as the result of an MI, valvular disease, left heart failure,
endocarditis, and dysrhythmias. More than half of these thromboemboli
lodge in the lower extremities (in the femoral and popliteal arteries) others
lodge in the coronary arteries and the cerebral vasculature.
○ Air embolism
■ Room air that enters the circulation
■ Room air that enters the circulation through intravenous lines is a
common cause of air embolism
■ I.e. - air from lungs enters blood stream in traumatic injuries such as a
gunshot wound to the chest
○ Amniotic fluid embolism
○
■ Amniotic fluid that is forced into the mother’s bloodstream
■ Treatment: dialysis
Bacterial embolism
■ Cause: infectious endocarditis (clumps of bacterial vegetarian is
dislodged from infected cardiac valves and ejected into pulmonary or
systemic circulation)
■ Treatment: bed rest, supplemental oxygen, antibiotics to help infection
●
Peripheral Vascular Disease
○ Raynaud phenomenon and Raynaud disease
■ Raynaud Phenomenon is secondary to systemic diseases, such as
collagen vascular disease (e.g. scleroderma), chemotherapy, cocaine
use, hypothyroidism, pulmonary hypertension, thoracic outlet syndrome,
serum sickness, vasculitis or malignancy.
● May reflect progression of the underlying diseases
■ Raynaud Disease: primary vasospastic disorder of unknown origin
● Associated with female gender, family history, smoking, manual
occupation, migraine and cardiovascular disease
○ Triggered by emotional distress and cold temperatures
○ Clinical Manifestations: pallor, numbness, sensation of cold in the digits
(especially in fingertips and feet– ischemia can lead to gangrene in chronic
conditions), attacks tend to be bilateral, cyanotic skin but returns to normal after
attack
○ Treatment: avoidance of stimuli that triggers attack, arm exercises or vasodilators
●
Atherosclerosis
○ A build up of fats, cholesterol, and other substances in and on the artery walls
○ Is a form of arteriosclerosis in which thickening and hardening of the vessel are
caused by accumulation of lipid-laden macrophages within the arterial wall, which
leads to the formation of a lesion called plaque
○ Not a single disease but rather a pathologic process that can affect vascular
systems throughout the body, resulting in ischemic syndromes that can vary
widely in their severity and clinical manifestations
○ Atherosclerosis is the leading cause of coronary artery and cerebrovascular
disease
○ CAD caused by atherosclerosis the major cause of myocardial ischemia
■ Major cause of stroke!
○ Causes: aging, smoking, hypertension, diabetes
○ Signs and symptoms
■ Partial: transient ischemic events associated with exercise or stress
■ Complete: tissue infarction, pain
●
Cholesterol
○ HDL: good cholesterol
○
LDL: bad cholesterol
●
Question: which elevated value may be protective of the development of
atherosclerosis?
○ Very low-density lipoproteins (VLDLs)
○ Low-density Lipoproteins (LDLs)
○ High-density lipoproteins (HDLs)
○ Triglycerides
●
Peripheral Artery Disease
○ Refers to atherosclerotic disease of arteries that prefuses the limbs, especially
the lower extremities
■ The risk factors for PAD are the same as those for atherosclerotic
disease, and it is especially prevalent in individuals who smoke and with
diabetes
●
Coronary Artery Disease (Coronary Heart Disease)
○ Any vascular disorder that narrows or occlude the coronary arteries
○ Results in an imbalance between coronary supply of blood and myocardial
demand for oxygen and nutrients
■ Reversible myocardial ischemia or irreversible infarction may result
○ Most common cause: atherosclerosis
○ Modifiable conventional risks include:
■ Dyslipidemia
■ Hypertension
● 2-3 fold increased risk of CAD
■ Cigarette smoking
● Increased heart rate to do epinephrine and norepinephrine
(increases LDL decreases HDL)
■ Diabetes and insulin resistance
● Also associated with dyslipidemia
■ Obesity and sedentary lifestyle
■ An atherogenic diet
● If individuals get appropriate preventative care, modification of
these factors can significantly reduce the risk of CAD
○ Nonmodifiable Risk Factors: conventional or major risk factors for CAD that are
nonmodifiable:
■ Advanced age
■ Male gender or women after menopause
■ Family history
●
Dyslipidemia
○ Triglyceride and LDL levels normally too high and HDL too low
■ RISK FOR HEART ATTACK AND STROKE
○
○
○
○
○
An increased serum concentration of LDL is an indicator of coronary risk,
however, the relative risk of elevated LDL depends on the presence of other risk
factors
LDL is responsive for the delivery of cholesterol into the tissues
Low levels of HDL cholesterol also are a strong indicator of coronary risk
■ HDL is responsible for “reverse cholesterol transport” which returns
excess cholesterol from the tissues to the liver, where it binds to hepatic
receptors (including the LDL receptor) and is processed and eliminated as
bile ot converted to cholesterol-containing steroids
■ HDL can remove excess cholesterol from the arterial wall through several
pathways
Other lipoproteins associated with increased cardiovascular risk include elevated
levels of serum VLDL (triglycerides) and increased lipoproteins
Triglycerides are associated with an increased risk for CAD, especially in
combination with other risk factors such as diabetes
●
Questions
○ Atherosclerosis is the leading cause of coronary heart disease
○ The risk of CAD increases with heavy smoking and decreases once smoking is
stopped
○ Hypertension is responsible for a two- to threefold increase risk of atherosclerotic
cardiovascular disease including MI.
●
Transient Myocardial Ischemia
○ Diminishes myocardial blood supply leading to ischemia
■ Myocardial cells can become ischemic within 10 seconds of coronary
occlusion and within several minutes the heart loses the ability to contract
and cardiac output decreases
■ Can also cause conduction abnormalities that cause changes in EEGs
and initiate dysrhythmias
■ Can be benign
○ Can be reversible
○ Clinical Manifestations
■ Stable Angina
● Angina pectoris-chest pain
○ Transient chest discomfort (pressure or pain)
○ Often people clench fist over left chest, can be mistaken
for ingestion
■ Prinzmetal Angina
● Unpredictable and at rest (chest pain)
○ Pain caused by vasospasm with or without atherosclerosis
● Nighttime
■ Unstable Angina
● New onset
●
●
●
●
■
■
Occurs at rest
Increases in severity/frequency
Shortness of breath, sweating, anxiety
Signals that there is artherosclerotic plaque that has ruptured and
can lead to an infarction soon after
Silent Angina
● No symptoms
In women:
● Atypical chest pain, sense of uneasiness, severe fatigue,
palpitations
●
Acute Coronary Syndromes
○ When there is a sudden coronary obstruction caused by thrombus formation over
a ruptures or ulcerated atherosclerotic plaque, acute coronary syndromes result
○ Include unstable angina and myocardial infarction
■ Unstable angina is the result if reversible myocardial ischemia and is a
harbinger of impending infarction
■ Myocardial infarction (MI) results when prolonged ischemia causes
irreversible damage to the heart muscle (heart attack)
■ Sudden cardiac death can occur as a result of any of the acute coronary
syndromes
●
Myocardial Infarction (Heart Attack)
○ When coronary blood flow is disrupted for an extended period of time necrosis
can occur
○ Thrombus is less likely to move than in unstable angina
○ STEMI- or Non-STEMI
○ The first symptom of acute MI is usually sudden, severe, chest pain
○ It is not possible to distinguish between angina and MU by symptoms alone,
although the pain associated with MI tends to be more severe and prolonged. It
may be described as heavy and crushing, such as an elephant sitting on my
chest
○ Radiation the the neck, jaw, back, shoulder, or left arm is common
○ Some individuals (especially older adults or those with diabetes) experience no
pain, thereby have a “silent” infarction
○ Infarction often stimulates a sensation of unrelenting indigestion
○ Nausea nad vomiting may occur because of reflex stimulation of vomiting centers
by pain fibers
○ Vasovagal reflexes from the area of the infarcted myocardium also may affect
gastrointestinal tract
●
Infective Endocarditis (IE)
○ A general term used to describe infection and inflammation of the endocardium,
especially the cardiac valves.
○
○
○
○
The incidence of IE is increasing in the US, in large part because of the increase
in the implantation of prosthetic valves
Bacteria are the most common cause of IE with staphylococcus aureus the most
common causative agent worldwide
■ Other causes include: streptococci, enterococci, viruses, fungi, rickettsia,
and parasites
Risk factors: implantation of prosthetic heart valves, congenital lesions
associated with highly turbulent flow (ventricular septal defect), acquired valvular
heart disease (mitral valve prolapse), previous infective endocarditis, intravenous
drug use, long term indwelling intravenous catheterization ( for pressure,
monitoring, feeding, hemodialysis), implantable cardiac pacemakers, heart
transplant with defective valve
Clinical manifestations
■ Fever
■ New or changed cardiac murmur
■ Petechial lesions of the skin, conjunctiva and oral mucosa
■ Osler nodes: painful erythematous nodules on the pads of the fingers and
toes
■ Janeway lesions: non painful hemorrhagic lesions on the palms and soles
■ Weight loss, back pain, night sweats, heart failure, emboli
●
Heart Failure
○ Defines as the pathophysiologic condition in which the heart is unable to
generate an adequate cardiac output such that inadequate perfusion of tissues or
increased diastolic filling pressure of the left ventricle, or both, occurs;
consequently, pulmonary capillary pressures are increased
○ Risk factors include ischemic heart disease and hypertension
■ Others include age, smoking, obesity, diabetes, renal failure, heart
disease, congenital heart disease, excessive alcohol use
○ Types:
■ Left heart failure aka congestive
● Fluid goes back into lungs and causes shortness of breath
● Most causes of heart failure result in the dysfunction of the left
ventricle
■ Diastolic heart failure
● Left ventricle cant fill fully
■ Right heart failure
● Fluid can back up into lungs, abdomen, feet and cause swelling
■ High Output failure
●
Dysrhythmias
○ A-fib most common
■ Disorganized electrical impulses in heart
■ 4-5 fold increase of risk of stroke
■
2-3 fold increase risk of heart failure
The Pulmonary System
● Alterations of Pulmonary function
○ Upper structures: nose, pharynx
○ Lower structures: trachea, bronchi bronchioles, alveoli
●
Key Terms
○ Cough: protective reflex to help clear airway with explosive expiration
○ Sputum: mucus that is coughed up; can be examined to aid with diagnosis
○ Hemoptysis: coughing up blood
○ Hypoxemia: reduced levels of arterial oxygen (reduced PaO2)
○ Hypoxia: reduced oxygenation of cells in tissues
○ Hypercapnia: CO2 retention
○ Dyspnea: subjective sensation of uncomfortable breathing
○ Dyspnea on exertion: shortness of breath with activity
○ Orthopnea: shortness of breath when lying down
●
Abnormal Breathing Patterns
○ Normal breathing rate: 20 breaths per minute
○ Kussmaul Respirations: deep rapid breathing pattern seen in patients with
metabolic acidosis
■ Causes: severe acidemia, diabetic ketoacidosis and kidney failure
○ Cheyne Stokes Respirations: alternating periods of deep and shallow breathing
and apnea
■ Causes: carbon dioxide build up in system, stroke, brain tumors, carbon
dioxide poisoning, high altitude sickness, morphine administration
●
Signs and Symptoms of Respiratory Distress
○
●
Patients with respiratory distress will often use accessory muscles of breathing,
have retracting intercostal spaces, flaring nostrils, and assume “tripod”
positioning (hands on knees, bent over)
○ Other signs of respiratory distress can includeL hypoxemia, hypoxia,
hypercapnia, tachycardia, tachypnea (increased respiratory rate), slow
respiratory rate, hyper or hypotension, cyanosis, confusion, etc.
Acute Respiratory Failure
○ Inadequate gas exchange leading to either hypoxemia/hypoxia (poor
oxygenation) OR hypercapnia (poor ventilation)
○ Multiple different etiologies including trauma, injury, infection of lungs, airways,
chest wall, brain, spinal cord, heart, liver etc or from sedation and or surgical
procedures
■ Patients with history of smoking, chronic renal failure, chronic liver failure,
underlying lung disease, and infection have increased risk of developing
post-op respiratory failure
○ Patients may require oxygenation or ventilation support with non-invasive or
invasive devices
●
Lung Pleura Abnormalities
○ Affect the tissues that cover the outside of the lungs and lines the inside of your
chest cavity
■ The pleural space is the space between the two thin layers of pleura, itis
filled with a small amount of fluid that helps the pleural layers glide
smoothly against each other when breathing
○ Three types of disorders:
■ Pleurisy
● Inflammation of the pleura
■ Pleural effusion
● Occur when infection or a medical condition or a chest injury
causes fluid plus blood, air , or other gasses to enter the pleural
space
■ Pneumothorax
● Occur when infection or a medical condition or a chest injury
causes fluid plus blood, air , or other gasses to enter the pleural
space
●
Pneumothorax
○ Collapsed lung
■ Rupture of visceral or parietal pleura leads to presence of air or gas in the
pleural space leading to the collapse of lung tissue
○ Can be complete or partial
○ Causes: blunt or penetrating chest injury, medical procedures, damage from
underlying disease, occur for no obvious reasons
○ Clinical manifestations: chest pain, shortness of breath
■
○
○
Also: tachycardia, decreased blood pressure, absent breath sounds on
the affected side
■ Can become life threatening if they become too large or compress other
structures
● Tension pneumothorax is an emergency medical condition that
requires immediate bedside treatment with a chest tube
○ Most commonly seen after traumatic chest injury or those
with mechanical ventilation
■ Symptoms are going to depend on how much of the lung is actually
collapsed
Treatment: inserting a needle or a chest tube between the ribs to remove the
excess air
■ Small pneumothoraxes might heal on their own
Two different types:
■ Spontaneous
● Primary (without underlying lung disease)
○ Collapsed lungs sometimes happen in people who don't
have other lung problems. It can occur due to abnormal air
sacs in the lungs that break apart and release air
● Secondary (with underlying lung disease)
○ Several lung diseases may cause a collapsed lung
■ Chronic obstructive pulmonary disease (COPD),
cystic fibrosis, and emphysema
■
Traumatic (from trauma, including medical procedures)
● Open- hole in chest wall; ie gunshot wound or knife wound
● Closed- blunt trauma hole in lung not chest wall
○ Visceral pleura damaged; parietal is not
○
Tension Pneumothorax
■ Injury created a one-way flap valve mechanism that allows air into the
pleural space with inspiration but then closes when you breathe out and
traps the air
● Can rapidly progress to cardiovascular collapse → cardiac arrest
■ Symptoms: severe hypoxemia and hypoxia, tracheal deviation and
hypotension
■ MEDICAL EMERGENCY!
●
Pleural Effusions
○ Presence of fluid in the pleural space “water on the lungs”
○ Severity depends on cause
■ Transudative effusion: watery and diffuses out of the capillaries
● Heart failure, pulmonary embolism
■ Exudative effusion: less watery; contains high concentrations of
white blood cells and plasma proteins
● Pneumonia, cancer
■ Hemothorax: body exudate
● Chest trauma
○ Clinical manifestations: may be asymptomatic ot cause dyspnea and
pleural pain
●
Restrive Lung Disease
○ Total decrease in volume or air that lungs can hold due to decreased lung
elasticity
○ Intrinsic
■ Pulmonary fibrosis
● Development of excess fibrous or connect tissue as a
result of acute or chronic inflammation or injury
○ Extrinsic
○
■ Multiple sclerosis, muscular dystrophy, and ALS
Treatment: medications and physical therapy
■ No cure
●
Acute Respiratory Distress Syndrome (ARDS)
○ Occurs when fluid builds up in the alveoli and the fluid keeps your lungs
from filling with enough air → less oxygen reached bloodstream →
deprives organs of oxygen
○ Typically happens to people who are already critically ill or have
significant injuries
○ Clinical Manifestations: Severe shortness of breath!
■ Develops from hours to days after trauma or infection
○ Causes:
■ Sepsis, pneumonia, COVID, inhalation of harmful substances
○ Survival rates low, if you do survive have long term lung damage
●
Obstructive Lung Disease
○ Conditions that make it hard to exhale all the air in the lungs
■ Exhaled air comes out slower than normal and abnormal amount
of air left in lungs
○ Causes: obstruction of bronchi
○ Two most common types: asthma and COPD
○ Asthma
■ Airways narrow and swell and may produce extra mucus
● Can cause coughing, wheezing, whistling sound when
exhaling and shortness of breath
■ Chronic inflammatory disorder of bronchial mucosa
■ Causes bronchial hyperresponsiveness and airway constriction
■ Asthma is reversible
■ Characterized by episodic attacks of bronchospasm, bronchial
inflammation, mucosal edema, and increased mucus production
■ Exposure to antigen leads to activation of innate and adaptive
immunity
● Early asthmatic response
○ Dendritic cells present antigen to helper T cells,
which release inflammatory cytokines/chemokines
that trigger bronchospasm and lead to airway
obstruction
○ Typically peaks within 30 minutes of exposure to
antigen and resolves within 1-3 hours
○ More common
● Late asthmatic response
○ Release of chemokines during early response
results in recruitments of other WBCs, leading to
■
■
●
inflammation and injury to pulmonary tissue if left
untreated
○ Begins 4-8 hours after early response and results in
bronchial hyperresponsiveness (increased
sensitivity to antigens)
○ Dominant cause of chronic asthma
Some people have symptoms everyday, some people may have
them just a couple times a year
● Uncontrolled asthma will cause damage to the lungs
Treatment: prevention and long term control are key!
● Short acting: primary treatment of acute attacks consists of
bronchodilators (beta-agonists) nebulizers or inhalers
○ Function to reverse symptoms of asthma by dilating
the previously constricted bronchi
● Long term: supportive treatments may include steroids and
anti-inflammatory medications
Chronic Obstructive Pulmonary Disease (COPD)
○ Also known as COPD
○ Risk Factors: smoking (cigarette, pipe, cigar, second hand smoke),
occupational hazards, air pollution, and genetic factors
■ Increased risk of developing heart disease and lung cancer
○ Symptoms: most common: dyspnea on exertion, difficulty breathing,
cough, mucus or sputum production and wheezing
○
○
Unlike asthma, COPD is not fully reversible
Two main types:
■ Emphysema- air sacs
● Inhalation of irritants lead to inflammation of alveoli
● Destruction of alveoli via breakdown of elastin within septa
and permanent enlargement of gas-exchange airways
■ Chronic bronchitis- airways
● Inhalation of irritants leads to inflammation of bronchi
goblet cells
●
■
●
Stimulates mucus secretion which becomes thickened and
impairs bronchial ciliary function
Usually occur together
Respiratory Infections
○ Common in US
○
○
○
○
Main function of upper respiratory system:
■ Filter, warm and humidify air
● Also clears patient airways for air to enter and exit the
lungs through the nose and mouth
● Larynx and above!
Main function of lower respiratory system:
■ Provide gas exchange for oxygen and carbon dioxide
■ Begins below the larynx!
Lower Respiratory Tract Infections
■ Acute bronchitis
● Acute infection of inflammation of large airways (bronchi)
● Self-limiting and typically caused by viral infections
● May also be due to bacteria but rare unless patient has
COPD
● Clinical manifestations are similar to pneumonia however
chest x-ray does not demonstrate infiltrates
● Treatment with supportive measures
● Coughing primary symptoms
■ Pneumonia, bronchitis, tuberculosis
■ Pneumonia
● Infection of the lower respiratory tract
● May be caused by bacteria, viruses or fungi (less likely
protozoa or parasites)
● Risk factors: advanced age, immunodeficiency, underlying
lung disease, alcohol use, aspiration, chest trauma,
endotracheal intubation, immobilization, etc.
○ MILD TO LIFE THREATENING
○ Normal life threatening to people older than 65,
young children, or people with health problems
●
●
Given the variety of causative agents, pneumonia is
typically categorized based on how it was obtained
○ Community acquired (CAP)
○ Hospital acquired (HAP)
○ Ventilator Associated (VAP)
○ All may have different antibiotic treatments
● Clinical manifestations
○ Differ based on cause
○ For the most part, patients with pneumonia will first
experience a viral upper respiratory tract infection
which then leads to viral or bacterial pneumonia
○ Symptoms: cough, pleuritic chest pain, fever, chills
and malaise
○ Severe pneumonia may progress to sepsis
■ Tuberculosis
● Caused by infection with Mycobacterium tuberculosis
● Leading cause of death from curable infectious diseases
● Highly contagious and spread by airborne droplets (aerosol
transmission)
● Typically affects the lungs but able to invade other organs
○ Hides inside macrophages and can become
dormant (latent tuberculosis)
○ Host cells may respond by creating caseating
granulomas
○ Disease may reactivate if patient becomes
immune-compromised
● Clinical manifestations
○ Fever, cough, hemoptysis, weight loss, chills, night
sweats
○ Latent tuberculosis is asymptomatic
■ But can develop symptoms weeks to years
later
■ Non contagious when nonactive
○ Active TB- actual disease
● Problem is patient with TB need may antibiotics as they
dont work well
○ Upper Respiratory Infections
■ Very common; typically self-limited and mild
■ Examples: viral colds, pharyngitis (sore throat), laryngitis
(inflammation fo voice box)
■ Symptoms: headache, sore throat, sneezing
Pulmonary Vascular Disease (PVD)
○
●
Any condition that affects the blood vessels in the lungs (these vessels
take the deoxygenated blood into the lungs and oxygenated them).
Problems can cause decreased quality of life and cardiac problems.
■ Pulmonary atrial hypertension
■ Pulmonary venous hypertension
■ Chronic thromboembolic disease
■ Pulmonary embolism
● Most commonly arise from the deep veins in the
thigh/calf (DVTs)
● Clinical Manifestations:
○ Sudden onset of pleuritic chest pain, dyspnea
(occurs suddenly and gets worse with exertion),
tachypnea, tachycardia, unexplained anxiety,
cardiac arrest and death
○ Depends on size of clot and if someone has
heart/lung problems
● Risk factors for pulmonary embolism include Virchow’s
Triad
○ Venous stasis (blood isn't moving),
hypercoagulability (pregnancy, increased estrogen,
sepsis, clotting disorders, etc) and injuries to the
endothelial cells that line the vessels (surgery,
atherosclerosis, etc)
● Pulmonary embolism will not appear on a x-ray or regular
CT scan (need to order CT scan angiogram)- have a high
index of suspicion in patients with risk factors or
concerning symptoms
○ But will be used to rule out other issues
● Treatment
○ Best treatment is prevention!
○ Oxygen and hemodynamic stabilization
○ Anticoagulation and or fibrinolytic agents
○ May need embolectomy
Lung Cancer
○ Most frequent cause of cancer in the US
○ Risk factors
■ Cigarette smoking (most common cause)
● However 10-20% of patients with lung cancer have never
smoked!
■ Air pollution (including second hand smoke), occupational
hazards, genetic factors, etc
○ Multiple different types of lung cancers; mostly divided into two main
classes
■
○
○
●
Small cell lung cancer
● Common in smokers
● Less common
■ Non-small cell lung cancer
● Umbrella term for several types (squamous cell,
adenocarcinoma, large cell)
Staging is based on the Tumor Nodes Metastasis (TNM) system
Treatment:
■ Chemotherapy, surgical resection, radiation and newer
immunotherapies
Pediatric Lung Disease
○ Croup
■ Also goes by laryngotracheobronchitis
■ Infection of the upper airway that leads to obstruction
■ Most commonly caused by viral infections
● Spread through direct contact/fluids with someone with the
disease
■ Common in children age 6 months to 5 years of life
■ Common manifestations:
● Harsh barking cough (or seal cough), hoarse voice, and
inspiratory stridor, sore throat, low grade fever
■ Most cases of croup are mild and self-limited some may require
hospitalization
○ Cystic Fibrosis
■ Autosomal recessive genetic disorder leading to multisystem
organ disease
● Type of gene mutation depends on gene mutation
● Must have to genes to have cystic fibrosis; one to be a
carrier
■ Gene mutation leads to abnormal chloride channel
● Cells are unable to transport chloride out of the cell
○ Salty sweat
● Normally, chloride outside the cell would attract a layer of
water molecules which helps moisturize and thin secretory
mucus
● Without water, the cells produce mucus that is dehydrated,
thickened, and prone to sticking together
■ Affects secretory tissues such as lungs, intestines, pancreas,
sweat ducts, and reproductive organs (vas deferens)
■ All newborns in the US are screened
● Can tell within first month without any symptoms
■ Especially injurious to lung tissue, as thick secretions can:
● Obstruct bronchioles (mucus plugging)
■
■
●
● Result in chronic inflammation
● Lead to increased risk of infections
Signs and symptoms:
● Persistent cough or wheeze, excess sputum production,
hemoptysis, recurrent and or severe pneumonia, and
symptoms of chronic hypoxia such as nail clubbing
● Salty sweat when you kiss your child
There is no cure!
● But symptoms can come and go
● Can manage and treat symptoms in attempt to help live a
longer life
● When diagnosed in adulthood, have less severe symptoms
Sudden Infant Death Syndrome (SIDS)
○ Sudden death of an infant <1 year
○ Most common cause on infant death in US
○ Most common at night when asleep
○ More common in 2-4 months of life and rare after 6 months
○ More common in winter months
○ More common in males
○ Risk factors:
■ Low birth weight, positive family history, environmental (cigarette
smoking, no fan, warm room/body)
■ Make sure baby sleeps on back
■ Think may be caused by brain dysfunction
○ Prevention:
■ AVOID prone sleeping
● Sleep on back
■ Avoid soft bedding, toys, ans blankets in the crib
■ AVOID bed sharing
■ Encourage breastfeeding and routine immunization
■ Cardiovascular home monitoring devices can be used in certain
cases but has not been proven to reduce the risk of SIDs
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