PNP 401
Pathophysiology
for the Practical Nurse II
FINAL REVIEW
FINAL EXAM (35%):
April 20, 2023
Lecturer: Dr. Lisa Caputo
FINAL: APRIL 20 – 35%
90 questions – 2 hours
u Test will begin at 7:00pm SHARP and end at
9:00pm
u IN PERSON EXAM – Room K2241
u ALL multiple choice – options A, B, C, D, E
u Questions equally weighted and distributed
amongst class time
u If you have academic accommodations, a test
will be arranged for you in the Test Center
u
u Case-based
MC (50 Questions)
u Non-case MC (40 Questions)
REVIEW: Overview
u
Introduction to Cancer
u
Reproductive Disorders
u
Renal Disorders
u
**Gastrointestinal Disorders
u
**Skin Disorders
u
**Approximately 70% of Final Exam (Units 4 & 5)
UNIT 1
ONCOLOGY
CANCER
u Second
leading cause of death worldwide
u Disorder of altered cell differentiation and
growth
u Aka Neoplasia – “new growth” neoplasm
u Neoplastic cells lack normal regulatory controls
over cell growth and differentiation
u Result of both hereditary and environmental
causes
u Classified by type of cell the tumor resembles
(location of origin)
BENIGN vs. MALIGNANT
n
Tumors that stay in one spot and demonstrate limited
growth are generally considered to be benign.
n
They can be dangerous if they press on vital organs,
such as the brain.
n
More dangerous, or malignant tumors form when two
things occur:
na
cancerous cell manages to move throughout the
body using the blood or lymph systems, destroying
healthy tissue in a process called invasion
n that
cell manages to divide and grow, making new
blood vessels to feed itself in a process called
angiogenesis
METASTASIS
n
When a tumor successfully spreads to other parts of the
body and grows, invading and destroying other healthy
tissues, it is said to have metastasized. This process
itself is called metastasis, and the result is a serious
condition that is very difficult to treat.
n
The most common sites of cancer metastasis are the
lungs, bones, and liver. Although most cancers have the
ability to spread to many different parts of the body,
they usually spread to one site more often than others.
Cancer Type
Main Location of Metastasis
Breast
Lungs, Liver, Bones
Colon
Liver, peritoneum, lungs
Kidney
Lungs, Liver, Bones
Lungs
Adrenal Glands, liver, lungs
CANCER: Causes
n
Familial inheritance: Genes and a genetic predisposition
inherited from family members. It is possible to be born with
certain genetic mutations or a fault in a gene that makes one
statistically more likely to develop cancer later in life.
n
Aging: The most important risk factor for cancer is growing older*
n
Most cancers occur in people over the age of 65. As we age, there
is an increase in the number of possible cancer-causing mutations
in our DNA. This makes age an important risk factor for cancer.
n
Viruses: Several viruses have also been linked to cancer such as:
human papillomavirus (a cause of cervical cancer), hepatitis B
and C (causes of liver cancer), HIV, and Epstein-Barr virus
Cancer Staging:
Stage
Stage
Stage
Stage
Stage
0: Carcinoma in situ (aka Severe Dysplasia)
1: Localized to one part of body
II: Advanced but still local – may have lymph involvement
III: Locally advanced but with much more lymph involvement
IV: Metastasis
CHEMOTHERAPY
§ Use of anti-neoplastic drugs, often in
combination
§ Include: antimitotics, antibiotics, alkylating
agents, and antimetabolites
§ Acts by killing cells that are over proliferative
(thereby preventing further cell division of
cancerous cells)
§ In the process, also harms those cells that divide
rapidly under normal circumstances – ie. cells in
bone marrow, digestive tract, and hair follicles
à lead to side effects
RADIATION THERAPY
§
§
§
§
§
§
§
Ability to control cell growth
Ionizing Radiation – damages DNA of exposed tissue
Cancerous cells more susceptible to this process since most
cancerous cells have inhibited their own DNA repair ability –
ie. damage to these cells often goes unnoticed
In order to avoid exposure of the radiation to normal tissues
(eg. skin or organs), shaped radiation beams are used at
different angles in order to intersect at point of interest (ie.
tumor site)
Radiation fields may also target the surrounding draining
lymph nodes if they are involved with the tumor, or if there is
believed to be metastatic spread
Different cancers respond differently to radiation therapy
The response of a cancer is based on its radiosensitivity (ie.
dose-dependent response)
METAPLASIA & DYSPLASIA
u
Metaplasia: refers to changing of one cell type to another.
This is one-way cells can adapt to a persistent stressor. In
the presence of a persistent stressor, cells may develop
changes that lead to cancer
u
Dysplasia: refers to the actual change in cell size, shape,
uniformity, arrangement and structure. Dysplasia is often
a cellʼs response to a chronic or persistent stressor
u Caused
u Cells
by abnormal differentiation of dividing cells
are not cancerous but may appear as early
changes that can progress to cancer
METAPLASIA & DYSPLASIA:
The Cervix
Disorders of Uterine Cervix
n
The outside of the cervix (exocervix) and the vagina are
covered by a layer of flat cells called squamous cells. These
are visible on physical exam when the cervix is visualized.
n
The canal of the cervix (endocervix) is lined by tall columnlike cells columnar cells.
CERVICAL CANCER:
Presentation
n
The majority of women are screened routinely, the most
common finding is an abnormal Papanicolaou test result
n
Clinically, the first symptom is abnormal vaginal bleeding,
usually post-coital
n
Vaginal discomfort, malodorous discharge, and dysuria are
not uncommon
n
The tumor grows by extending upward to the endometrial
cavity, downward to the vagina, and laterally to the pelvic
wall. It can invade the bladder and rectum directly.
n
Symptoms that can evolve, such as constipation,
hematuria, fistula, and ureteral obstruction with or without
hydroureter or hydronephrosis, reflect local organ
involvement
CERVICAL CANCER:
Etiology
n
Carcinoma of the cervix is considered a
sexually transmitted disease
n
Evidence of the link with HPV infection (high
risk, types 16 and 18)
n
Other risk factors: smoking, nutrition, family
history, multiple sexual partners, sexually
active before 18 years of age, weakened
immune system
CERVICAL CANCER:
Prevention
n HPV
vaccine: A newly developed vaccine
targets 4 viral subtypes (HPV 6, 11, 16, and
18) most commonly associated with cervical
intraepithelial lesions, genital warts, and
cervical cancer
n The vaccine aims to prevent cervical cancer
but does not treat it
n Three doses are given. The vaccine is best
given before sexual activity begins, but
women who are sexually active may be
vaccinated
CERVICAL CANCER:
Prevention
n
GARDASIL is a vaccine indicated in girls and women
between the ages 9-26 (now approved for use up to
age 45) for the prevention of cervical, and vaginal
cancers; precancerous or dysplastic lesions; and
genital warts caused by human papillomavirus (HPV)
Types 6, 11, 16, and 18. (Note: also administered to
boys and young men 9-26 to prevent anal cancer).
n
GARDASIL should be administered in 3 separate
intramuscular injections in the deltoid region of the
upper arm or in the higher anterolateral area of the
thigh over a 6-month period with the first dose at an
elected date, the second dose 2 months after the first
dose, and the third dose 6 months after the first dose
(ie. day 1, 2 months, 6 months)
BREAST CANCER:
Risk Factors
n
No single known cause
n
Being older is the primary risk factor. Most
women who develop breast cancer have no
risk factors other than simply being a woman
and getting older (especially being over 50)
n
Family history, history of previous cancer:
Having a 1st-degree relative (mother, sister,
daughter) with breast cancer doubles or
triples risk of developing the cancer, but
breast cancer in more distant relatives
increases risk only slightly.
n
Positive BRCA-1/BRCA-2 mutation
n
ESTROGEN!! (Increases risk of Breast,
Ovarian & Endometrial Cancers)
n
Gynecologic history: Early menarche, late
menopause, or late first pregnancy increases
risk. Women who have a first pregnancy
after age 30 are at higher risk than those
who are nulliparous
n
Oral contraceptive use: Only very slightly
increases risk
n
Hormone replacement therapy
n
Obesity
n
Alcohol
n
Diet: Diet may contribute to development or
growth of breast cancers, but conclusive
evidence about the effect of a particular diet
is lacking
n
High socioeconomic status
BREAST CANCER:
Pathology
u Most
breast cancers are epithelial tumors that
develop from cells lining ducts or lobules; less
common are non-epithelial cancers of the
supporting stroma
u Breast
cancer invades locally and spreads
initially through the regional lymph nodes,
bloodstream, or both
u Metastatic
breast cancer (Stage IV) may affect
almost any organ in the body—most commonly,
lungs, liver, bone, brain, and skin
BREAST CANCER:
PAGETʼS DISEASE OF THE NIPPLE
n
Paget's disease of the nipple (not to be confused with
the metabolic bone disease also called Paget's
disease) is a form of ductal carcinoma in situ (DCIS)
that extends into the overlying skin of the nipple and
areola, manifesting with an inflammatory skin lesion
n
Paget's disease of the nipple presents with skin
changes, including erythema, crusting, scaling, and
discharge; these usually appear so benign that the
patient ignores them, delaying diagnosis for a year or
more.
n
About 50% of patients with Paget's disease of the nipple have a palpable mass at
presentation
BREAST CANCER: S/S
n
Remember, lumps in the breast are very common,
especially just before your period. Most lumps are
often not breast cancer
n
Less commonly, the presenting symptom is breast
pain or enlargement or a thickening in the breast.
n
Most often breast cancer is first noticed as a
painless lump in the breast or armpit
n
Other signs might include: lump or swelling in the
armpit, changes in breast size or shape, dimpling
or puckering of the skin (orange peel), redness,
swelling and increased warmth in the affected
breast, inverted nipple
BRONCHOGENIC CARCINOMA:
Risk Factors
§
Cigarette Smoking – increases risk by 4-120 times; in some
patients, may return risk to normal after 15 years of smoking
cessation
§
§
§
Asbestos exposure
§
§
§
§
Exposure to uranium or radon
History of Interstitial lung disease
Exposure to toxic agents – arsenic, nickel, chromium, chloromethyl
ether
Prior lung cancer
Lung disease (eg. COPD)
HIV infection
SMALL CELL CARCINOMA
§ 15-20% of all lung cancers
§ Bronchial origin – centrally located
§ Grows and metastasizes rapidly
§ 95% of cases have metastasis at time of diagnosis
§ S/S include cough, sputum (hemoptysis uncommon),
§
§
§
wheezing, atelectasis, infection with fever, pleural
effusion, superior vena cava syndrome, dyspnea with
intrapulmonary spread, metastasis
More CENTRAL
Treatment primarily limited to chemotherapy d/t early
and rapid spread
Poor survival rate – 10-15% 5-year survival rate
NON-SMALL CELL CARCINOMA:
ADENOCARCINOMA
§
§
§
§
Most common type of non-small cell carcinoma (50%)
§
Expansile growth pattern that destroys and displaces the
adjacent lung parenchyma
§
§
§
§
Arises in the mucous gland
Most common type seen in **women and non-smokers
Develops in peripheral nodules as silent, solitary, coin
lesions (versus extensive involvement seen in small-cell)
Glandular tumour that produces mucin
More PERIPHERAL
S/S: cough, bloody purulent sputum, stridor/wheezing,
atelectasis, tracheal shift, fever, weight loss
Treatment with surgery to resect solitary nodules
SQUAMOUS CELL CARCINOMA
§
§
§
§
§
35% of all non-small cell lung cancers
§
§
More vascular symptoms d/t location
§
Surgery not an option if SVC affected, otherwise resected
Originates in the central bronchi
Metastasizes to lymph nodes
May affect superior vena cava à backflow
S/S include swollen jugular veins, unilateral arm swelling,
facial swelling, dizziness, headache, stupor, visual
disturbances
May produce an apical lung tumour – Pancoast tumour
à pain in shoulders and along ulnar distribution of arm
and hand
SQUAMOUS CELL CARCINOMA:
PANCOAST TUMOUR
COLON & COLORECTAL CANCER:
Manifestations
n
Many rectal cancers produce no symptoms and are
discovered during digital or proctoscopic screening
examinations
n
Change in bowel habits is present in 43% of patients
n
*Bleeding is the most common symptom of rectal
cancer, occurring in 60% of patients. Bleeding often
is attributed to other causes (eg, hemorrhoids),
especially if the patient has a history of other rectal
problems. Profuse bleeding and anemia are rare.
Bleeding may be accompanied by the passage of
mucus, which warrants further investigation.
COLON CANCER:
Metastasis
n
When colon or rectal cancer
spreads, it most often spreads to
the liver. Sometimes it spreads
to the lungs, peritoneum, bones,
or brain.
n
This may go unnoticed, but large
deposits in the liver may cause
jaundice and abdominal pain
(due to stretching of the
capsule).
n If the tumor deposit obstructs
the bile duct, the jaundice may
be accompanied by other
features of biliary obstruction,
such as pale stools.
LEUKEMIA
n
Leukemia is a type of cancer that causes the blood or bone
marrow to make too many white blood cells, causing a
breakdown of the body's immune system
n
This uncontrolled production doesn't give these cells a chance to
properly mature. The immature cells either won't function well or
will interfere with the production of other white blood cells.
n
Cancer of the blood or bone marrow
n
Abnormal increase in white blood cells (WBC)
n
Ie. Leukocytosis
n
Most occur in adulthood (90%)
n
Acute vs. Chronic Leukemia
n
Lymphocytic vs. Myelocytic (Myelogenous) Leukemia
ACUTE vs. CHRONIC LEUKEMIA
ACUTE LEUKEMIA:
n
n
n
n
n
CHRONIC LEUKEMIA:
Rapid increase in the number of n Excessive accumulation of
immature blood cells
relatively mature, but still
abnormal WBCs
Leads to crowding of blood cells
which prevents bone marrow n Takes months to years to
from producing healthy blood
progress
cells (all types)
n Cells are produced at a much
Get rapid progression and
higher rate than normal cells à
accumulation of the malignant
many abnormal WBCs in blood
cells which go into bloodstream
n Monitored for long time before
and spread to other organs
treatment
Requires immediate and
n Most common in older people,
aggressive treatment
but can occur at any age
Most common in children
LYMPHOCYTIC LEUKEMIA
n
Involve B-cell lymphocytes (WBCs)
n
Malignant change takes place in a specific marrow cell
that is responsible for the formation of B-cell
lymphocytes
n
B-cell lymphocytes are part of the infection-fighting
immune system cells
Acute Lymphocytic Leukemia (ALL)
n
Most common leukemia in children; 85% five-year
survival in children, 50% in adults
Chronic Lymphocytic Leukemia (CLL)
n
Most common in adults > 65 y.o; 75% five-year survival
MYELOCYTIC LEUKEMIA
n
Involves Red Blood Cells (erythrocytes) and platelets
n
Malignant changes take place in specific marrow cell
responsible for the formation of RBCs and platelets
Acute Myelocytic Leukemia (AML)
n
More common in young adult males; *only 40% fiveyear survival
Chronic Myelocytic Leukemia (CML)
n
Occurs mainly in adults; 90% five-year survival
LEUKEMIA: S/S
§
Leads to damage of the bone marrow by displacing normal marrow cells
with immature WBCs
§
Since bone marrow is damaged (where all hematopoiesis occurs) à will
lead to decrease in all functional blood cells (WBCs, platelets, RBCs) pancytopenia
§
Lack of blood platelets à easily bruised, excessive bleeding, petechiae,
bleeding gums
§
Lack of functional WBCʼs à weakened immune system à frequent
infection, opportunistic infections
§
Lack of RBCs à Anemia à dyspnea, pallor
§
§
§
Other s/s include: malaise, fevers, chills, night sweats, fatigue
Nausea or bloating d/t hepatosplenomegaly à unintentional weight loss
headaches
UNIT 2
REPRODUCTIVE
DISORDERS
ENDOMETRIOSIS
n
A non-malignant disorder in which functioning
endometrial tissue is present outside the uterine cavity
n
Reported incidence varies, about 10 to 15% in actively
menstruating women aged 25 to 44
n
Average age at diagnosis is 27, but endometriosis also
occurs among adolescents
n
Up to 25 to 50% of infertile women have endometriosis
n
In patients with severe endometriosis and distorted
pelvic anatomy, incidence of infertility is high.
n
Thirty to forty percent of women with endometriosis will
be subfertile
ENDOMETRIOSIS: S/S
n
Patients with endometriosis present with a variety of symptoms
including the following:
n
Dysmenorrhea
n
Heavy or irregular bleeding (Menorrhagia)
n
Pelvic pain
n
Lower abdominal or back pain
n
Dyspareunia
n
Dyschezia (pain on defecation) often with cycles of diarrhea and
constipation
n
Bloating, nausea, and vomiting
n
Inguinal pain
n
Pain on micturition (urination) and/or urinary frequency
n
Pain during exercise
ENDOMETRIOSIS: Location
n
Most endometriosis is found on these structures in the pelvic
cavity where it can produce pain felt in the pelvis and/or lower
back areas. The pain is often more severe before, during, and/or
after the menstrual period:
n
Ovaries (the most common site)
n
Fallopian Tubes
n
The back of the uterus and the posterior cul-de-sac
n
The front of the uterus
n
Uterine ligaments such as the broad or round ligament of
the uterus
n
Pelvic and back wall
n
Intestines, most commonly the rectosigmoid
n
Urinary bladder and ureters
PELVIC INFLAMMATORY
DISEASE (PID)
§ Acute or Chronic infection of the
reproductive tract – most commonly, in the
fallopian tubes and/or ovaries
§ Cervicitis
§ Endometritis
§ Salpingitis
§ Oophoritis
§ Common cause of infertility & ectopic
pregnancy
PID: Etiology
§ Most commonly caused by STD (gonorrhea,
chlamydia), sometimes Group B strep or H.
Influenza
§ Often preceded by an episode of vaginitis or
cervicitis
§ Insertion of contaminated IUD or other
instrumentation (organisms from urinary tract)
§ Infection associated with abortion or childbirth
§ Hematogenous spread (often from peritoneal
cavity)
PID: Pathophysiology
§ Infection typically occurs immediately following
§
§
§
§
menses d/t vulnerability of the endometrium
Polymicrobial – after vaginitis or cervicitis
Infection ascends uterus into fallopian tubes, filling
and obstructing tubes with purulent exudate
Exudate drips out of fimbriae onto ovaries and
surrounding pelvic cavity à abscesses à life
threatening (need immediate drainage) à
septicemia à septic shock à death
Adhesions and strictures of ovaries and tubes are a
common complication à infertility, ectopic
pregnancies
UTERINE FIBROIDS: Anatomy
n
Uterine fibroids usually develop in the corpus (body) of the
uterus
n
Some fibroids grow on stalks that grow out from the surface of
the uterus or into the cavity of the uterus. These are called
pedunculated.
n
Divided into three groups based on where they grow:
n
SUBMUCOSAL/SUBENDOMETRIAL FIBROIDS: grow into the
uterine cavity. Just under the surface of the uterine lining
n
INTRAMURAL/MYOMETRIAL FIBROIDS: grow within the wall
of the uterus
n
SUBSEROSAL FIBROIDS: grow on the outside of the uterus,
just under the outside covering of the uterus
UTERINE FIBROIDS: Types
n
SUBMUCOSAL: These fibroids develop within the uterine cavity
and can cause excessive menstrual bleeding along with
prolonged menstrual cycles. They can also cause difficulties
and/or complications with conception, pregnancy, and/or vaginal
delivery.
n
INTRAMURAL: develop in the uterine wall and expand. These
fibroids can cause the uterus to appear larger in size which can
be mistaken for weight gain or pregnancy. Associated symptoms
include heavy menstrual bleeding, pelvic and back pain, frequent
urination and pressure.
n
SUBSEROSAL: Develop in the outer portion of the uterus and
continue to grow outward. These fibroids typically do not affect a
woman's menstrual flow, or cause excessive menstrual bleeding,
but can cause pain due to their size and the added pressure on
other organs.
STDs
§ Sexually Transmitted Diseases, formerly,
Venereal Diseases
§ Any infection spread by sexual contact
§ Bacterial, Viral, Protozoan
§ Bacterial à Chlamydia, Gonorrhea,
Syphilis
§ Viral à Genital Herpes (HSV-2), Genital
warts (HPV)
§ Protozoan à Trichomoniasis
STDs: Bacterial
Chlamydia:
n
Cause: C. trachomatis
n
S/S: mild dysuria and discharge;
asymptomatic
Gonorrhea:
n
Cause: N. gonorrhea
n
S/S: dysuria, discharge (yellow-green in
men; white-clear in women); often
asymptomatic in women
STDs: Bacterial
§ Syphilis:
§ Cause: T. pallidum
§ S/S: Primary syphilis – painless ulcer at
site of entry; Secondary – rash, fever,
headache
STDs: Viral
Genital Herpes:
n
Cause: Herpes Simplex 2
n
S/S: vesicles, ulcers
Genital Warts:
n
Cause: Human Papillomavirus (6, 11)
n
S/S: soft, gray mass or polyp
STDs: Protozoan
Trichomoniasis:
n
Cause: T. vaginalis
n
S/S: asymptomatic; women may
have discharge and dysuria
UNIT 3
RENAL DISORDERS
FLUID IMBALANCE
§
§
§
§
§
Fluid balance is maintained by the following:
Thirst – hypothalamus promotes fluid intake when
needed
ADH (Antidiuretic Hormone) – promotes
reabsorption of water in kidneys (to prevent
dehydration)
Aldosterone – promotes water and sodium
reabsorption in kidneys
ANP (Atrial Natriuretic Peptide) – regulates fluid,
sodium, and potassium levels to decrease
workload on the heart; increases GFR (glomerular
filtration rate); inhibits ADH to increase fluid loss
HYPONATREMIA: Cause
§
§
Excessive sweating, vomiting, or diarrhea
§
Endocrine disorders à adrenal insufficiency or Addison’s
disease (decreased aldosterone); increased ADH
§
Early Chronic Renal Failure (will later turn into
Hypernatremia)
§
Excessive water intake
§
Ie. Too much fluid
Use of specific diuretic medications in combination with
low-sodium diets
HYPERNATREMIA: Cause
§ Diabetes Insipidus = insufficient ADH (not to be
confused with Diabetes Mellitus)
§ Loss of thirst mechanism (in hypothalamus)
§ Watery diarrhea
§ Prolonged hyperventilation
§ Increased sodium intake
§ Ie. Too much fluid loss
CALCIUM IMBALANCE
§ Ingested in food (mainly dairy products), stored in
bone, and excreted in urine and stool
§ Regulated by Parathyroid hormone (PTH) and
Calcitonin
§ Also influenced by Vitamin D and Phosphate levels
§ Calcium provides structural strength needed for
bones and teeth
§ Calcium is also needed for cardiac nerve
conduction impulses, and muscular contraction
§ Also plays a role in blood clotting
CALCIUM IMBALANCE: S/S
§ Hypocalcemia:
§ Tetany = involuntary
skeletal muscle spasm
(Chvostek’s sign à
face tap)
§ Tingling fingers
§ Confusion, Irritability
§ Arrhythmias à weak
contractions
§ Hypercalcemia:
§ Lethargy
§ Anorexia, nausea
§ Constipation
§ Polyuria, thirst
§ Renal calculi
§ Arrhythmias à
strong contractions
with hypertension
ACID-BASE IMBALANCE
There are 4 basic types of acid-base imbalance:
1.
Respiratory Acidosis (increased carbon dioxide)
2.
Metabolic Acidosis (decreased bicarbonate ions)
3.
Respiratory Alkalosis (decreased carbon dioxide)
4.
Metabolic Alkalosis (increased bicarbonate ions)
RENAL FUNCTION
n
Kidneys regulate water
n
Kidneys remove wastes
n
Kidneys regulate electrolytes
n
Normal Blood Value Ranges
n
n
Wastes, such as urea and creatinine, must also be
removed from the body
n
Urea and other wastes are made when the body
breaks down protein, such as meat
n
Creatinine is a waste product of the muscles
n
*As kidney function decreases, the levels of urea and
creatinine in the blood increase
Normal urine output = 1-2L/day
Terminology
§
Incontinence: the inability to control the flow of urine, leading to either constant or
intermittent accidental leakage
§
Dysuria: pain or burning sensation during or immediately following urination. This
may be a sign of a urinary tract infection.
§
Hematuria: Blood in the urine can be small amounts, clots, or very bloody. This will
usually cause the urine to appear darker in color.
§
Urgency: the uncomfortable feeling of pressure in the bladder that makes you feel you
have to go "right now”
§
Hesitancy: incomplete evacuation of the bladder during each episode of urination.
There may be a sudden stoppage of the urine flow due to spasms in the bladder or
urethra or there may be difficulty starting the flow of urine.
§
Frequency: urinating more than eight times during the day or more than once overnight
ACUTE RENAL FAILURE
n
Rapid decline in renal function
n
Glomerulus filtration rate (GFR) is decreased
n
Excretion of nitrogen wastes is reduced, and fluid and electrolyte balance
cannot be maintained
n
In all cases of acute renal failure (ARF), creatinine and urea build up in the
blood over several days, and fluid and electrolyte disorders develop. The
most serious of these disorders are hyperkalemia (increase K+) and fluid
overload
n
Phosphate retention leads to hyperphosphatemia
n
Hypocalcemia is thought to occur because the impaired kidney no longer
produces calcitriol and because hyperphosphatemia causes calcium
phosphate precipitation in the tissues
n
Acidosis develops because hydrogen ions cannot be excreted
n
With significant uremia, coagulation (clotting) may be impaired, and
pericarditis may develop
ACUTE RENAL FAILURE: S/S
Initially, weight gain and peripheral edema
may be the only findings. Often, predominant
symptoms are those of the underlying illness
n Later, as nitrogenous products accumulate,
symptoms of uremia may develop, including
anorexia, nausea and vomiting, weakness,
myoclonic jerks, seizures, confusion, and
coma
n Asterixis (An abnormal tremor consisting of
involuntary jerking movements, especially in
the hands) and hyperreflexia may be present
on examination.
n
ACUTE RENAL FAILURE:
Manifestations
Initial signs/symptoms include:
1) Elevated BUN and creatinine (ie. azotemia) because of decreased GFR.
2) Oliguria caused by decreased GFR and/or tubule obstruction.
3) Hyperkalemia occurs if GFR is greatly reduced and there is significant
acidosis. Typical *ECG changes can occur and predispose to
arrhythmias.
4) Fatigue and malaise likely due to water intoxication (ie. Hyponatremia),
hyperkalemia, acidosis, and elevated metabolic wastes (ie. Toxicity).
Later symptoms include:
1) Dyspnea, orthopnea, and third heart sound caused by fluid overload.
2) Edema caused by fluid overload.
3) Altered mental status occurs when metabolic wastes become
increasingly elevated in the blood.
4) Uninalysis may show hematuria, proteinuria, and pyuria.
CHRONIC RENAL FAILURE
n
Progressive and irreversible destruction of kidney structures
n
Inability of the kidney to perform its normal functions in terms of
regulating fluid, electrolyte balance, controlling blood pressure,
eliminating wastes etc.
n
Decreased renal function interferes with the kidneys' ability to maintain
fluid and electrolyte homeostasis
n
The ability to concentrate urine declines early and is followed by
decreases in ability to excrete phosphate, acid, and potassium
n
Plasma concentrations of creatinine and urea rise as GFR diminishes
n
Renal osteodystrophy (abnormal bone mineralization resulting from
hyperparathyroidism, calcitriol deficiency, elevated serum phosphate, or
low serum Ca) usually takes the form of increased bone turnover due to
hyperparathyroid bone disease à osteopenia, osteomalacia,
osteoporosis
n
Progression occurs in 4 stages: diminished renal reserve, renal
insufficiency, renal failure and end stage renal disease
CHRONIC RENAL FAILURE:
Stages
Diminished Renal Reserve (Stage 1 & 2)
n
Normal GFR is between 120-130mL/min
n
Diminished renal reserve is when GFR drops to
50% of normal (ie. 60mL/min)
n
Serum creatinine and BUN are still normal, and
no signs and symptoms present
n
Patients with mildly diminished renal reserve
are asymptomatic
n
Examples: survival with only one kidney
CHRONIC RENAL FAILURE:
Stages
§
Renal Insufficiency (Stage 3)
§
Reduction in GFR to 20%-50% of normal (ie. 2460mL/min)
§
During compensation by nephrons, each remaining
nephron must filter more solute particles from blood.
Additional water may be lost in the urine.
§
Early sign of renal insufficiency: isosthenuria
(excretion of unconcentrated urine), aka. polyuria
with urine that is almost isotonic with plasma –
cannot concentrate or dilute urine
§
Will see azotemia, anemia, hypertension develop
CHRONIC RENAL FAILURE:
Stages
Renal Failure and End-Stage Renal Disease (Stage 4 &5)
n
Renal failure develops when GFR is <20% (ie. <24mL/min)
n
Kidney can no longer regulate the volume and solute composition
of extracellular fluids
n
Edema, metabolic acidosis, and hyperkalemia begin to appear
n
*Stage when Dialysis usually begins
n
End-stage renal disease occurs when GFR is <5% of normal (ie.
<6mL/min)
n
Without renal replacement therapy, fatal complications are likely
CHRONIC RENAL FAILURE: S/S
n
With more severe renal insufficiency, neuromuscular
symptoms may be present, including coarse muscular
twitches, peripheral sensory and motor neuropathies,
muscle cramps, hyperreflexia, and seizures
n
Anorexia, nausea, vomiting, weight loss, stomatitis, and an
unpleasant taste in the mouth (dysgeusia) are almost
uniformly present. The skin may be yellow-brown.
n
Occasionally, urea forms sweat crystallizes on the skin
(uremic frost).
n
Pruritus may be especially uncomfortable.
n
Undernutrition leading to generalized tissue wasting is a
prominent feature of chronic uremia.
CHRONIC RENAL FAILURE:
Summary of Clinical Manifestations
1)
Fluid (water), sodium and potassium: Sodium and
volume overload are common in uremia. Excess
ingestion of sodium and water contributes to
circulatory congestion, hypertension, ascites,
edema, and weight gain
2)
Metabolic Acidosis: As more nephrons are lost, acid
excretion is reduced and metabolic acidosis results.
Kidneys are unable to excrete excessive H+ ions.
CHRONIC RENAL FAILURE:
Summary of Clinical Manifestations
3)
Bone and Mineral: Decreased activation of
Vitamin D results in decreased absorption of
calcium from the gut, and a fall in serum calcium
levels. Increased plasma phosphate levels cause
bone resorption à osteopenia and osteomalacia
4)
Cardiovascular and Pulmonary: Symptoms of
circulatory congestion, hypertension, and
pulmonary edema occur because of sodium and
volume overload.
CHRONIC RENAL FAILURE:
Summary of Clinical Manifestations
5)
Hematological: Decreased production of erythropoietin
(hormone released by kidneys to stimulate RBC
production in bone marrow) causes anemia. Decreased
RBC production.
6)
Neurological: Symptoms include sleep disorders, poor
concentration, loss of memory, seizures, hiccups,
twitching, and coma. Sensory peripheral neuropathy can
also occur.
7)
GI: Common findings include anorexia, nausea, and
vomiting.
GLOMERULONEPHRITIS:
Clinical Presentation
The common clinical presentation of nephritic syndrome involves hematuria,
proteinuria, reduced GFR, and hypertension. However, Nephritic Syndrome
generally follows one of three paths:
1.
Acute glomerulonephritis: An abrupt onset of symptoms, often resulting in
acute renal failure, followed by full recovery of renal function; typically
preceded by an acute infection (strep)
à most common cause of renal failure in kids (post-strep)**
2.
Rapidly progressive glomerulonephritis: An abrupt onset of symptoms, in
which recovery from acute renal failure does not occur. Over weeks to
months this disorder progresses to chronic renal failure.
3.
Chronic glomerulonephritis: Acute glomerulonephritis which progresses
slowly over a period of years (ie. 5-20) to chronic renal failure.
URINARY OBSTRUCTIONS
n
The two most damaging effects of obstruction are stasis of
urine, which predisposes to infection and calculi, and
increased backpressure, which can impair renal blood flow
and damage renal tissue
n
Obstruction can be either partial or complete
n
Impedance to urinary flow increases the pressure within the
renal pelvis and calices. This can obstruct blood flow to the
renal medulla and cause ischemic damage and necrosis
n
Irreversible nephron damage can occur within a few days of
complete obstruction; whereas recovery can take weeks
after the obstruction is removed
n
Dilation of the ureters (ie. Hydroureter) and renal pelvis (i.e.
Hydronephrosis) occurs with prolonged obstruction
RENAL CALCULI: Types
n
There are four basic types of stones:
n Calcium
(oxalate or phosphate) account for
70-80% of stones
n Magnesium
ammonium phosphate (Struvite),
15%
n Uric
acid (urate), 8%
n Cystine,
n Calcium
3%
oxalate = most common!
RENAL CALCULI: Types
n
Calcium stones are usually associated with hypercalcemia and
hypercalciuria
n
Excessive bone resorption caused by immobilization, bone
diseases, hyperparathyroidism and renal tubular acidosis are
contributing factors
n
Struvite (aka. Magnesium ammonium phosphate) stones form
only in alkaline urine, and in the presence of bacteria that possess
an enzyme called urease
n
Uric acid stones develop in conditions of gout and high
concentrations of uric acid in the urine
n
Cystine stones are rare. Seen in cystinuria, results from a genetic
defect in renal transport of cystine
UTI: Etiology
n
Most uncomplicated UTIs are caused by
Escherichia coli
n
Obstruction: incomplete bladder emptying creates
a continuous pool of urine in which bacteria can
grow, prevents flushing of bacteria, and allows
bacteria to ascend easily to higher structures
n
Stones (calculi): Large stones can obstruct urine
flow (urinary stasis). Rough surface of the stones
irritates the mucosa. Bacteria can live within a
stone and cause infection.
UTI: Etiological Factors
n
Vesicoureteral reflux: Bacteria-laden urine is forced
backward from the bladder up into the ureters and kidneys,
where pyelonephritis can develop
n
Diabetes Mellitus: excess glucose in the urine provides a
rich medium for bacterial growth
n
Characteristics of urine: alkalotic urine promotes bacterial
growth (vegetarians, vegans)
n
Concentrated urine promotes growth (not enough fluids)
n
Gender: Women are susceptible to periurethral colonization
with coliform bacteria. Use of diaphragms, frequency of
intercourse, new sexual partners, increase risk
UTI: Etiological Factors
§
Age: Urinary stasis may be caused by incomplete
bladder emptying as a result of enlarged prostate.
Neuromuscular conditions can cause incomplete
emptying, Parkinsonʼs disease
§
Sexual activity: irritation of the perineum and
urethra during intercourse can promote migration of
bacteria. Spermicides can alter vaginal pH
§
Recent use of antibiotics: change the normal flora,
providing opportunity for pathogenic bacteria growth
and colonization
UTI: Classifications
n
Urethritis: Inflammation from infection of the urethra
with bacteria (or with protozoa, viruses, or fungi) occurs
when organisms that gain access to it acutely or
chronically colonize the periurethral glands
n
Cystitis: Urinary bladder inflammation. In women,
sexual intercourse usually precedes uncomplicated
cystitis (honeymoon cystitis)
n
Acute pyelonephritis: Pyelonephritis is inflammation
from bacterial infection of the kidney parenchyma
UTI: DIAGNOSIS
Laboratory Assessment:
•
•
•
Urinalysis testing for leukocyte esterase and nitrate
Presence of pyuria and hematuria
Use clean-catch, midstream specimen
UTI: PYELONEPHRITIS
n
Refers to inflammation affecting the tubules, interstitium
and renal pelvis
n
Bacterial Infection of the upper urinary tract
n
Although obstruction (strictures, calculi, tumors, prostatic
hyperplasia, neurogenic bladder, VUR) predisposes to
pyelonephritis, most women with pyelonephritis have no
demonstrable functional or anatomical defects
n
Two forms: Acute and Chronic Pyelonephritis
n
Acute pyelonephritis is active bacterial infection
n
Chronic pyelonephritis results from repeated or continued
upper urinary tract infections
UNIT 4
GASTROINTESTINAL
DISORDERS
DYSPHAGIA: Causes
Neurological Disorders:
§ Infection
§ Stroke
§ Brain damage
§ Achalasia à failure of the
lower esophageal sphincter
to relax d/t lack of
innervation
§
§
Muscular Disorders:
Muscular dystrophy
Achalasia
DYSPHAGIA: Causes
§
Mechanical Obstruction:
§
Congenital Atresia –
developmental defect where
upper and lower esophageal
segments are separated;
may have connecting fistula
to trachea
§
Stenosis/Stricture –
secondary to fibrosis
(inflammation, ulceration,
radiation therapy, scar tissue
from ingestion of corrosive
chemicals)
DYSPHAGIA: Causes
Mechanical Obstruction:
uEsophageal
Diverticula – outpouchings of
esophageal wall à cause bad breath,
chronic cough, and hoarseness
uTumours
GASTROESOPHAGEAL
REFLUX DISEASE (GERD)
n
Gastroesophageal Reflux: refers to backwards movement of gastric
contents into the esophagus
n
Causes heart burn
n
The most common disorder originating in the GI tract
n
Gastroesophageal reflux is a normal physiologic phenomenon
experienced intermittently by most people, particularly after a meal.
n
Gastroesophageal reflux disease (GERD) occurs when the
amount of gastric juice that refluxes into the esophagus exceeds the
normal limit, causing symptoms with or without associated
esophageal mucosal injury (esophagitis)
n
Irritation can lead to complications such as narrowing of the
esophagus, ulcers and even a slightly increased risk of esophageal
cancer
HIATAL HERNIA: Etiology
n
Hiatal hernias are more common in women than in
men
n
Muscle weakening and loss of elasticity as people
age is thought to predispose to hiatus hernia,
based on the increasing prevalence in older people
n
Obesity predisposes to hiatus hernia because of
increased abdominal pressure
n
Conditions such as chronic esophagitis may cause
shortening of the esophagus by causing fibrosis of
the longitudinal muscles and, therefore, predispose
to hiatal hernia
HIATAL HERNIA: Types
n
Hiatal hernias are categorized as being either
(1) sliding or (2) para-esophageal
SLIDING HIATAL HERNIA
PARA-ESOPHAGEAL HH
ACUTE GASTRITIS:
Cause
§
Infection
§
Allergies – food (shellfish) or drugs
§
Ingestion of spicy food – eg. Hot peppers
§
Excessive alcohol intake
§
Aspirin – especially if taken on empty stomach
§
Ingestion of corrosive substances
§
Radiation therapy
§
Chemotherapy
CHRONIC GASTRITIS
§
Seen in those with chronic peptic ulcers,
alcoholics, and the elderly
§
Often, idiopathic
S/S:
§
Often vague
§
Mild epigastric pain, anorexia, intolerance for
spicy or fatty foods
PEPTIC ULCER DISEASE:
Gastric Ulcer
n
Gastric Ulcer: Normal or
decreased gastric acid
secretion and delayed
stomach emptying with
increased diffusion of gastric
acid back into the stomach
tissues
n
A break in the mucosal
barrier causes hydrochloric
acid to injure the epithelium.
n
Deep and penetrating.
PEPTIC ULCER DISEASE:
Duodenal Ulcer
n
Duodenal ulcers: normal
diffusion of acid back into
stomach tissues with
increased secretion of
gastric acid and faster
stomach emptying time.
n
This reduces the buffering
effect of food and delivers
large acid bolus to
duodenum
Without normal functioning of pyloric sphincter, bile refluxes into the stomach.
Reflux of bile acids may break the integrity of the mucosal barrier and
produce hydrogen-ion back-diffusion, leading to mucosal inflammation.
PEPTIC ULCER DISEASE:
Gastric vs. Duodenal Ulcers
Feature
Gastric Ulcer
Duodenal
Age
Usually 50 or older
Usually 50 or older
Stomach acid production
Normal or hyposecretion
Hypersecretion
Pain
30-60min after ingestion;
Worsens with ingestion of
food
1.5-3hr after ingestion, often
at night, awakens patient;
Relief with ingestion of food
Location of pain
Upper epigastrium
Right of epigastrium
Stomach emptying
Delayed
Faster
PERITONITIS
n
Peritonitis is most often caused by introduction of
an infection into the otherwise sterile peritoneal
environment through organ perforation, but it
may also result from other irritants, such as
foreign bodies, bile from a perforated gallbladder
or a lacerated liver, or gastric acid from a
perforated ulcer
n
Women also experience localized peritonitis from
an infected fallopian tube or a ruptured ovarian
cyst
PERITONITIS:
Frequency & Cause
n
The most common etiology of primary
peritonitis is Spontaneous Bacterial
Peritonitis (SBP) caused by chronic liver
disease
n
Up to 30% of all patients with liver cirrhosis with
ascites develop SBP
n
The common etiologic entities of secondary
peritonitis include perforated appendicitis;
perforated gastric or duodenal ulcer; perforated
(sigmoid) colon caused by diverticulitis or
cancer; and strangulation of the small bowel
PERITONITIS:
Presentation
§
The diagnosis of peritonitis is clinical
§
Abdominal pain, which may be acute or insidious, is the usual chief
complaint. Initially, the pain may be dull and poorly localized (visceral
peritoneum) and often progresses to steady, severe, and more localized
pain (parietal peritoneum).
§
Anorexia and nausea are frequent symptoms and may precede the
development of abdominal pain.
§
On physical examination, patients with peritonitis generally appear unwell
and in acute distress. Many of them have a temperature that exceeds
38°C
§
On abdominal examination, almost all patients demonstrate tenderness
to palpation.
§
Patients with severe peritonitis often avoid all motion and keep their hips
flexed to relieve the abdominal wall tension. The abdomen is often
distended, with hypoactive-to-absent bowel sounds
§
Abdomen is rigid
PARALYTIC ILEUS:
Causes
n Pre-existing
intestinal infection
(gastroenteritis)
n Electrolyte
or mineral imbalances (eg.
Decreased K+ levels)
n Complications
n Mesenteric
of abdominal surgery
ischemia
n Appendicitis
n Lung
or Kidney disease
n Certain
medications, narcotics
CHRONIC INFLAMMATORY
BOWEL DISEASE (IBD)
§
Genetic & immunologically based disease
§
2 types: Crohn’s Disease & Ulcerative Colitis
§
High clinical diversity in each disease – range
from mild to severe
§
Most common among Eastern Europeans and
Caucasians
§
Characterized by periods of remission and
exacerbation
§
Occurs in both males and females
CROHNʼS DISEASE
n
Crohn disease is an idiopathic, chronic,
transmural inflammatory process of the bowel
that often leads to fibrosis and obstructive
symptoms, which can affect any part of the
gastrointestinal (GI) tract from the mouth to
the anus
n
It most commonly affects the lower part of the
small intestine, called the ileum. The swelling
extends deep into the lining of the affected
organ. The swelling can cause pain and can
make the intestines empty frequently, resulting
in diarrhea
CROHNʼS DISEASE
§
Crohnʼs disease is an inflammatory bowel disease, the
general name for diseases that cause swelling in the
intestines
§
Because the symptoms of Crohnʼs disease are similar
to other intestinal disorders, such as irritable bowel
syndrome and ulcerative colitis, it can be difficult to
diagnose
§
NB. Unlike Crohn’s, Ulcerative Colitis causes
inflammation and ulcers in the top layer of the lining of
the large intestine only
§
In Crohnʼs disease, *all layers of the intestine may be
involved, and normal healthy bowel can be found
between sections of diseased bowel (skip lesions)
CROHNʼS DISEASE:
Features
§
§
§
§
§
§
Characteristic feature of Crohnʼs is sharply
demarcated, granulomatous lesions, surrounded by
normal-appearing mucosal tissue
Often referred to as, skip lesions
All the layers of the bowel are involved (transmural)
Submucosal layer affected to greatest extent
Surface of inflamed bowel usually has
“cobblestone” appearance, resulting from the
fissures and crevices that develop
There is usually sparing of smooth muscle layers of
the bowel, and marked inflammatory and fibrotic
changes to the submucosal layer
CROHNʼS DISEASE:
Fistula
n
A unique complication of Crohns disease is called a fistula
n
A fistula is an abnormal connection between organs in the
digestive tract, usually a connection between one piece of the
intestine and another. A fistula can be created after inflammation
becomes severe.
CROHNʼS DISEASE:
S/S
§
Patients with Crohnʼs disease may also present with complaints that are
suggestive of intestinal obstruction
§
Initially, the obstruction is secondary to inflammatory edema and spasm of
the bowel and manifests as postprandial bloating, cramping pains, and
loud borborygmi
§
Once the bowel lumen becomes chronically narrowed, patients may
complain of constipation and obstipation
§
Complete obstruction may sometimes be caused by impaction of
undigested foods
§
Perianal fissures or fistulae are common
§
Fistulas may develop between other sites including bladder, vagina,
urethra, and skin (eg. Fistula in ano)
§
Patients may have problems related to extraintestinal manifestations
of Crohnʼs disease, which may involve the skin, joints, mouth, eyes, liver,
and bile ducts
§
Young people with Crohnʼs disease commonly experience unexplained
growth failure and delayed puberty
ULCERATIVE COLITIS
n
Ulcerative colitis (UC) is an idiopathic, chronic,
inflammatory disorder limited to the colon
n
Ulcerative colitis is a lifelong illness that has a
profound emotional and social impact on patients
who are affected
ULCERATIVE COLITIS
§
Disease usually begins in the rectum and spreads
proximally, affecting primarily the mucosal layer
§
Inflammatory process tends to be confluent, and
continuous (instead of skipping areas like Crohnʼs
disease)
ULCERATIVE COLITIS:
Epidemiology
n
The rectum is involved in more than 95% of cases,
although some authorities believe that the rectum is
always involved in untreated patients. Ulcerative
colitis extends proximally from the anal verge in an
uninterrupted pattern to involve part or all of the
colon.
n
Ulcerative colitis seems to have a female
preponderance. Ulcerative colitis affects 30% more
females than males.
n
The incidence of ulcerative colitis peaks in people
aged 15-25 years and in people aged 55-65 years,
although it can occur in people of any age
ULCERATIVE COLITIS:
S/S
n
The clinical presentation of ulcerative colitis depends on the
extent of the disease process
n
Patients usually present with diarrhea mixed with blood
and mucus of gradual onset
n
They also may have signs of weight loss, and blood on rectal
examination
n
The disease is usually accompanied with different degrees of
abdominal pain, from mild discomfort to severely painful
cramps
n
Ulcerative colitis is associated with a general inflammatory
process that affects many parts of the body. Sometimes
these associated extra-intestinal symptoms are the initial
signs of the disease, such as painful, arthritic knees in a
teenager. The presence of the disease cannot be confirmed,
however, until the onset of intestinal manifestations
ULCERATIVE COLITIS:
Manifestations
n
Rectal bleeding: Ulceration is generally more continuous and rectal
bleeding is more common. Can result in blood loss anemia.
n
Diarrhea: Varies according to severity. May be up to 30-40 bowel
movements a day. Stools typically contain blood and mucus. Tissue
destruction interferes with absorption in the large intestine resulting in
a small volume diarrhea accompanied by tenesmus.
n
Colon obstruction and dilation: Inflammation impairs peristalsis
causing a functional obstruction and dilation (i.e. Toxic megacolon).
n
Colorectal carcinoma: Can create cell dysplasia and metaplasia.
Risk of developing cancer in persons who have had pancolitis for 10
years or more is 20-30 times that of general population
n
The risk of colon cancer is proportional to the duration of disease and
amount of colon affected, but not necessarily to the clinical severity of
the attacks
CROHN’S DISEASE
ULCERATIVE COLITIS
Terminal ileum involvement
commonly
seldom
Colon involvement
usually
always
Rectum involvement
common
usually
Distribution
Patchy areas of
inflammation, Skip lesions
Continuous area of
inflammation
Depth of inflammation
May be transmural, deep into
tissue
Shallow, mucosal
Type of inflammation
Granulomatous
Ulcerative and exudative
fistulae
common
seldom
Stenosis
common
Seldom
Smoking
Higher risk for smokers
Lower risk for smokers
Development of Cancer
Occasional
Relatively common
IRRITABLE BOWEL
SYNDROME (IBS)
§
GI disorder characterized by lower
abdominal pain, diarrhea and/or
constipation
§
Affects up to 20% of the population, worldwide
§
Most common among young and middleaged women
§
Many different types, diagnosed clinically
based on the presence of pain, diarrhea,
and constipation
IBS: Types/Etiology
Abnormal GI motility and secretion:
§
Caused by hypersensitivity or the effect of serotonin on the
enteric nervous system
§
Can lead to a diarrhea-type IBS (rapid transit time through
bowel) or a constipation-type IBS (delayed transit time)
Visceral Hypersensitivity:
§
Caused by immunological involvement or hypersensitivity
of autonomic NS
§
Leads to increased sensitivity to visceral pain à abdominal
pain
IBS: Types/Etiology
Post-infectious IBS:
§
Typically caused by bacterial enteritis
§
Leads to mild inflammation and abnormal immune
response in the gut
Overgrowth of flora:
§
Overgrowth of normal intestinal flora causes
increased production of methane gas
§
Leads to constipation and bloating
IBS: Types/Etiology
Food allergy or intolerance:
§
Immune response from food antigen in the mucosa
causes hypersensitivity reaction
Psychosocial Factors:
§
Emotional stress à autonomic NS, neuroendocrine
system à increased pain responses
DIVERTICULAR DISEASE
§
Diverticulum = outpouching or herniation of the
colonic mucosa through the muscular layer;
most common in the sigmoid colon
§
Diverticulosis = presence of multiple,
asymptomatic diverticula
§
Diverticulitis = inflammation of the diverticula;
most common in older population in North
America
§
May be congenital or acquired
DIVERTICULAR DISEASE:
S/S
§
§
§
Often, asymptomatic
Mild discomfort
Diarrhea, constipation and/or flatulence
Diverticulitis:
§ Inflammation à stasis of feces in pouches
§ Left lower quadrant pain/cramping (sigmoid m/c)
§ Steady pain with nausea and vomiting
§ Slight fever
§ Elevated WBC count
APPENDICITIS:
Pathophysiology
Appendicitis develops as follows:
Obstruction (gallstone, fecalith, spasm) of appendiceal
lumen occurs
1.
2.
Fluid builds up inside; microorganisms proliferate
3. Appendiceal
wall becomes inflamed; purulent exudate
forms à appendix swells à compression of vessels à
ischemia à necrosis of appendix wall à increased
permeability à escape of bacteria into surrounding area
APPENDICITIS:
Pathophysiology
4.
Abscess formation develops outside appendix à
Localized Bacterial Peritonitis (visceral peritoneum)
5.
Pressure builds inside appendix à increased
necrosis à gangrene in appendiceal wall à wall
appears blackish
6.
If the appendix ruptures à contents released into
peritoneal cavity à Generalized Peritonitis (parietal
peritoneum à life threatening)
APPENDICITIS: S/S
S/S typically develop as follows:
General periumbilical pain (as inflamed appendix becomes distended) à
nausea and vomiting
1.
Severe, localized Lower Right Quadrant pain = McBurney’s Point (as
visceral peritoneum over appendix becomes inflamed, ie. Localized Peritonitis)
2.
3.
Pain temporarily decreases (as appendix ruptures and contents spill out)
Steady, severe abdominal pain; fever; leukocytosis; rigid abdomen;
tachycardia; hypotension (as parietal peritoneum inflames, ie. Generalized
Peritonitis)
4.
APPENDICITIS:
Treatment
§
Appendectomy (surgical removal of
appendix)
§
Antimicrobial drugs
CHOLELITHIASIS:
Presentation
n
Gallstones are concretions that form in the biliary
tract, usually in the gallbladder
n
Migration of gallstones may lead to occlusion of the
biliary and pancreatic ducts, causing pain (biliary colic)
and producing acute complications, such as acute
cholecystitis (inflammation of gallbladder),
ascending cholangitis (inflammation of the bile
duct), or acute pancreatitis (life-threatening)
n
Chronic gallstone disease may lead to fibrosis and
loss of function of the gallbladder and predisposes to
gallbladder cancer
CHOLELITHIASIS:
Pathophysiology
n
The bile in which gallstones are formed usually is
supersaturated with cholesterol or billirubinate
n
Biliary sludge is often a precursor of gallstones.
It consists of Ca bilirubinate (a polymer of
bilirubin), cholesterol microcrystals, and mucin
n
80% of gallstones are composed of cholesterol
n
20% are brown or black pigment stones consisting of
calcium salts with bilirubin
n
3 factors contribute to formation: abnormalities in
composition of bile, stasis of bile, and inflammation of
gallbladder
ACUTE CHOLECYSTITIS
§ A complication of Gallbladder Stones
§ Acute cholecystitis occurs when persistent
stone impaction in the cystic duct causes the
gallbladder to become distended and
progressively inflamed
§ Patients experience the pain of biliary colic, but
instead of resolving spontaneously, the pain
persists and worsens
§ Pain may become pronounced in the right
upper quadrant
ACUTE CHOLECYSTITIS:
Presentation
n
Patients with the lithogenic state or asymptomatic gallstones have no
abnormal findings on physical examination
n
During attacks of biliary colic, and especially in acute cholecystitis,
patients may experience tenderness to palpation over the gallbladder
n
This can be elicited by having the patient inhale while the examiner
maintains steady pressure below the right costal margin (Murphy sign)
n
Localized rebound tenderness, guarding, or rigidity may occur with
pericholecystic inflammation
n
Patients with acute cholecystitis, ascending cholangitis, or acute
pancreatitis, in addition to abdominal pain, may exhibit fever and may
be tachycardic and hypotensive
n
In severe cases, bowel sounds are often absent
n
The *Charcot triad of severe right upper quadrant tenderness with
jaundice and fever is characteristic of ascending cholangitis
PANCREATITIS:
Causes
§ Biliary tract disease and alcoholism account for
≥ 80% of acute pancreatitis cases
§ The major causes are long-standing alcohol
consumption and biliary stone disease.
§ Gallstones are the most common cause of
Acute Pancreatitis
§ Alcoholism is the most common cause of
Chronic Pancreatitis
ACUTE PANCREATITIS:
S/S
n
The main presentation of acute pancreatitis is epigastric
pain or left upper quadrant pain radiating through to the
back
n
Often abrupt and dramatic, may follow a heavy meal or
alcoholic binge
n
Pain aggravated lying supine, less severe leaning forward
n
Nausea and/or vomiting is common
n
Fever, tachycardia, hypotension, cool clammy skin
n
Abdominal distention and hypoactive bowel sounds
n
Patients frequently have a history of previous biliary colic
and/or binge alcohol consumption, the major causes of
acute pancreatitis
ACUTE PANCREATITIS:
S/S
n
Pain usually develops suddenly in gallstone pancreatitis
n
In alcoholic pancreatitis, pain develops over a few days
n
The pain usually persists for several days. Sitting up
and leaning forward may reduce pain, but coughing,
vigorous movement, and deep breathing may
accentuate it
n
The patient appears acutely ill and sweaty
n
Pulse rate is usually 100 to 140 beats/min; respiration is
shallow and rapid
n
Blood pressure may be transiently high or low, with
significant postural hypotension
CHRONIC PANCREATITIS:
S/S
Chronic pancreatitis episodes are similar, but
lesser in severity to acute
n Patients have persistent, recurring attacks of
epigastric and left upper quadrant pain
n Precipitated by alcohol abuse or overeating
n
Anorexia, nausea, vomiting, constipation,
flatulence
n Disease progresses, causing pancreatic
functions to become deficient
n
n Leading
to signs of diabetes mellitus, malabsorption
syndromes (weight loss, fatty stools)
HEPATITIS: Phases
§ Phase 1 - Viral replication: Patients are asymptomatic during this phase.
Laboratory studies demonstrate serological and enzyme markers of
hepatitis.
§ Phase 2 - Prodromal phase: Patients experience anorexia, nausea,
vomiting, alterations in taste, arthralgias, malaise, fatigue, urticaria, and
pruritus. Some develop an aversion to cigarette smoke. When seen by a
health care provider during this phase, patients are often diagnosed as
having gastroenteritis or a viral syndrome.
§ Phase 3 - Icteric phase: Patients may note dark urine, followed by palecolored stools. In addition to the predominant gastrointestinal symptoms
and malaise, patients become icteric and may develop right upper
quadrant pain with hepatomegaly.
§ Phase 4 - Convalescent phase: Symptoms and icterus resolve. Liver
enzymes return to normal.
HEPATITIS A (HAV)
u Epidemiology:
HAV is a picornavirus that is resistant
to many environmental factors (e.g., temperature,
certain chemicals)
u It
is the most common cause of acute viral hepatitis
and is particularly common among children and
young adults
u Often,
the predominant etiologic agent of viral
hepatitis in the United States, HAV accounts for 2550% of new cases per year.
u Benign,
u It
self-limited disease
can cause acute fulminant hepatitis and death
from liver failure
HAV: Transmission
§ Hepatitis A virus exists in highest concentration in the
feces of infected individuals; the greatest fecal viral load
tends to occur near the end of the incubation period of
hepatitis A virus.
§ Most commonly, the virus spreads from person to person
via the fecal-oral route
§ Contaminated water and food, including shellfish
collected from sewage-contaminated water, have also
resulted in epidemics
§ May also be spread through sexual (anal-oral) contact
HEPATITIS B (HBV)
n A major
cause of infectious hepatitis worldwide,
hepatitis B virus belongs to the class of DNA
viruses
n Hepatitis
B virus is responsible for almost half of
the cases of acute viral hepatitis reported in the
United States. In 2016, the highest rates of acute
infection occurred in patients aged 25-45 years
n
Estimates suggest that 350 million people
worldwide are hepatitis B virus carriers
HBV: Transmission
§ The major reservoir of hepatitis B virus in the United
States consists of the 1.25 million carriers with
chronic hepatitis B virus infection
§ Hepatitis B virus is transmitted both parenterally (nonoral, i.e., intravenous) and sexually, most often by
mucous membrane exposure or percutaneous
exposure to infectious body fluids
§ Saliva, serum, and semen all have been determined
to be infectious
§ Percutaneous exposures leading to the transmission
of hepatitis B virus include transfusion of blood or
blood products, injection drug use with shared
needles, hemodialysis, and needlesticks
ALCOHOLIC LIVER
ALCOHOLIC LIVER
Pathologic changes observed in
patients with alcohol-induced
liver disease can be divided into
the following 3 groups:
alcoholic fatty liver (simple
steatosis), alcoholic hepatitis,
and alcohol-related cirrhosis.
FATTY LIVER
§ Accumulation of fat in hepatocytes; aka.
Steatosis
§ Liver becomes yellow, enlarges, owing to
excessive fat accumulation
§ Do not produce symptoms and is reversible
after alcohol intake has been discontinued
ALCOHOLIC HEPATITIS
§ Aka Liver Fibrosis
§ Intermediate stage
§ Often seen after an abrupt increase in alcohol
intake, common in “Binge” drinkers
§ Characterized by inflammation and necrosis of
liver cells, hepatic tenderness, pain, anorexia,
nausea, fever, jaundice, ascites, liver failure
May be asymptomatic
Always serious condition, may be fatal
Mortality rate in acute stages from 10-30%
§
§
§
§ Progresses to cirrhosis in 1-2 years
ALCOHOLIC CIRRHOSIS
§ End result of repeated bouts of drinking-related
injury
§ Onset of end-stage alcoholic liver disease
§ Gross appearance is fine, uniform nodules on its
surface
ALCOHOLIC CIRRHOSIS
n
Symptoms range from those of alcoholic hepatitis to the
complications of end-stage liver disease, such as Portal
Hypertension (often with esophageal varices and upper GI
bleeding, splenomegaly, ascites, and portal-systemic
encephalopathy)
n
Acute renal failure secondary to progressively decreasing
renal blood flow (hepatorenal syndrome) may develop
n
Hepatocellular carcinoma develops in 10 to 15% of patients
with alcoholic cirrhosis.
n
Once cirrhosis and its complications (e.g. ascites, bleeding)
develop, the 5-yr survival rate is about 50%; survival is
higher in patients who abstain and lower in patients who
continue drinking
CIRRHOSIS: Complications
§ Portal hypertension: is the most common serious complication in the
form of GI bleeding from esophageal, gastric, or rectal varices or portal
hypertensive gastropathy
§ Cirrhosis can cause other cardiovascular complications
§ Ascites can develop, with a risk of Spontaneous Bacterial Peritonitis
(SBP)
§ Progressive loss of hepatic architecture impairs function, leading to
hepatic insufficiency, manifest by coagulopathy, renal failure
§ Hepatocytes secrete less bile, contributing to cholestasis and jaundice
§ Malabsorption of vitamin D may contribute to osteoporosis
§ Blood disorders are common. Anemia results from hypersplenism,
chronic GI bleeding, folate deficiency
§ Coagulopathy results from impaired hepatic synthesis of the factors
necessary for clotting; malabsorption of vitamin K due to impaired bile
secretion into the duodenum
Jaundice:
Presentation & Cause
§
Results from abnormally high accumulation of bilirubin in the
blood
§
§
Gives a yellowish discoloration to the skin and deep tissues
§
Four major causes of jaundice:
§ excessive destruction of red blood cells ie. hemolysis (Pre-
Early signs of jaundice are often first seen in sclera of the
eye
hepatic)
§ impaired uptake of bilirubin by liver cells (Hepatic)
§ decreased conjugation of bilirubin (Hepatic)
§ obstruction of bile flow (Post-hepatic)
Jaundice: Causes
1.
§
Pre-hepatic Jaundice: Caused by excessive RBC destruction (hemolysis);
most often due to a hemolytic transfusion reaction, sickle cell anemia, and
hemolytic disease of the newborn (Rh Disease)
Characterized by indirect (free) hyperbilirubinemia, no bilirubin in the urine,
and decreased hematocrit.
Hyperbilirubinemia in the Neonate:
§
By the 2nd or 3rd day of life, 60% of infants become jaundiced due to
breakdown of fetal hemoglobin and an immature liver. This condition
usually resolves itself within a week. When jaundice occurs at birth or after 1
week it is more serious. This could lead to the neurological disorder called
kernicterus, as unconjugated bilirubin can pass the immature blood-brain
barrier. Treated by phototherapy or exchange transfusion.
Jaundice: Causes
2.
Hepatic (Hepatocellular) Jaundice: Caused by impaired
uptake of bilirubin or impaired conjugation of bilirubin.
•
Hepatitis (inflammation or infection) and cirrhosis are the most
common causes of this type of jaundice. During these
conditions there is cellular dysfunction that results in impaired
conjugation, and edema that interferes with bile secretion (ie.
Cholestasis).
Characterized by:
i.
Unconjugated and conjugated hyperbilirubinemia;
ii.
Increased amounts of water-soluble conjugated
bilirubin in the urine making it dark in colour; and
iii.
Elevated amounts of liver-specific enzymes in the blood
Jaundice: Causes
3.
Post-hepatic (Obstructive or Cholestatic) Jaundice: Occurs when
bile flow is obstructed at any point between the liver and the duodenum
•
Common causes include bile duct strictures, gallstones, and tumors
Characterized by:
i.
Elevated conjugated bilirubin in the blood
ii.
Elevated blood cholesterol
iii.
Dark coloured urine (increased conjugated bilirubin).
iv.
Pale coloured feces; steatorrhea (decreased urobilinogen)
v.
Accumulation of bile acids in the blood and depositing in the skin
(pruritus)
vi.
In time, obstructive jaundice can cause inflammation of the liver and
lead to hepatic jaundice
UNIT 5
SKIN DISORDERS
Functions of Skin
n
Protection: an anatomical barrier from pathogens and damage
between the internal and external environment in bodily defense;
Langerhans cells in the skin are part of the adaptive immune system.
n
Sensation: contains a variety of nerve endings that respond to
changes in heat and cold, touch, pressure, vibration, and tissue injury
(pain)
n
Heat regulation: increase perfusion and heat loss, while constricted
vessels greatly reduce cutaneous blood flow and conserve heat
n
Control of evaporation: the skin provides a relatively dry and semiimpermeable barrier to fluid loss
n
Storage and synthesis: acts as a storage center for lipids and water
n
Absorption: oxygen, nitrogen and carbon dioxide can diffuse into the
epidermis in small amounts
n
Water resistance: The skin acts as a water-resistant barrier so
essential nutrients aren't washed out of the body
Primary Skin Lesions
u
Macule - A macule is a change in surface color, without
elevation or depression and non-palpable, 5-10mm
diameter
u
Patch - A patch is a large macule (greater than 1cm)
u
Papule - A papule is a circumscribed, solid elevation of
skin with no visible fluid, varying in size from a pinhead to
either less than 5-10mm in diameter at the widest point
u
Plaque - A plaque has been described as a broad papule,
or confluence of papules equal to or greater than 1 cm
u
Nodule - A nodule is morphologically similar to a papule,
but, is greater than either 5 or 10mm in both width and
depth. The depth of involvement is what differentiates a
nodule from a papule.
Primary Skin Lesions
§ Vesicle - A vesicle is a circumscribed, fluid-containing, epidermal elevation
generally considered less than either 5-10mm in diameter at the widest point
§ Bulla - A bulla is a large vesicle described as a rounded or irregularly shaped
blister containing serous or seropurulent fluid, equal to or greater than either 5 10mm
§ Pustule - A pustule is a small elevation of the skin containing cloudy or purulent
material usually consisting of necrotic inflammatory cells (pus)
§ Cyst - A cyst is an epithelial-lined cavity containing liquid, semi-solid, or solid
material
§ Erosion - An erosion is a discontinuity of the skin exhibiting incomplete loss of the
epidermis, a lesion that is moist, circumscribed, and usually depressed
§ Ulcer - An ulcer is a discontinuity of the skin exhibiting complete loss of the
epidermis and often portions of the dermis and even subcutaneous fat
§ Fissure - A fissure is a crack in the skin that is usually narrow but deep
§ Wheal - A wheal is a rounded or flat-topped, pale red papule or plaque that is
characteristically evanescent, disappearing within 24 to 48 hours
SKIN INFECTIONS:
Cellulitis
§ Aka Erysipelas
§ Bacterial infection caused by
Streptococcus or
Staphlyococcus aureus
§ Most common in lower trunk
and legs
§ Red, swollen, painful
§ May get red streaks running
along lymphatic vessels
§ Systemic antibiotics required
SKIN INFECTIONS:
Furuncles
§ Aka Boil
§ Caused by S. aureus
§ Usually begins in hair follicle
and spreads to dermis
§ Face, neck, back
§ Initially – firm, red, painful
nodule à abscess à pus
drains
§ Squeezing them can spread
infection
§ Carbuncle = collection of
furuncles that coalesce
SKIN INFECTIONS:
Impetigo
u
Common in infants and
children; also, in adults
u
S. aureus or Group A strep
u
Easily spread by direct or
indirect contact
u Initially – small vesicles on face
à enlarge and rupture à
yellow-brown crusted mass;
lesion is red and moist under
crust with honey-colored liquid
u
Pruritis à further spread
u
Antibiotics required
SKIN INFECTIONS:
Herpes Simplex Virus 1 (HSV-1)
§ Aka Cold Sores or Fever Blisters
§ Viral infection on or near lips
§ HSV-2 can also cause oral lesions (or
genital)
§ Initially – asymptomatic
§ Virus remains latent in sensory nerve
ganglion or trigeminal nerve à
reactivated à cold sore
§ Triggered by common cold, sun, or
stress
§ Burning or tingling sensation along nerve à painful vesicles that
§
§
burst à crust
Spontaneous healing in 2-3 weeks; topical acyclovir used
Spread by direct contact with fluid from lesion
SKIN INFECTIONS:
Verrucae
§ Aka Warts
§ Caused by HPV
§ Common – plantar warts
(caused by HPV1-4)
§ Children and young adults
§ Common on soles, hands,
fingers, face
§ Initally – firm, raised papule à
rough surface
§ White or tan, often in multiples
§ Tx- laser, liquid nitrogen
freezing, topical ASA
SKIN INFECTIONS:
Tinea
§ Aka Ringworm
§ Fungal infection
§ Tinea Capitis – scalp; school-aged
children, transmitted by cats or humans;
circular bald patch with erythema or
scaling
§ Tinea Corporis – body; round red ring of
vesicles or papules with clear center;
pruritis or burning
§ Tinea pedis – aka. Athlete’s Foot;
affects toes, foul odor
§ Tinea unguinum – aka Onychomycosis;
toenails – white then brown; nails thicken
and cracks
SKIN INFECTIONS:
Scabies
§ Caused by mites that burrow
into the stratum corneum and
lay eggs à larvae migrate to
skin surface and mature to
adults à repeat cycle
§ Tiny, light brown lines with
small vesicles and erythema
§ Inflammation and pruritus
caused by mite feces
§ Spread by close contact
§ Tx – topical lindane
PSORIASIS
§ Psoriasis is a common and chronic skin
§
§
§
§
disorder
Plaque psoriasis is the most common type of
psoriasis and is characterized by red skin
covered with silvery scales and inflammation
Patches of circular to oval-shaped red plaques
that itch, or burn are typical of plaque psoriasis
The patches are usually found on the arms,
legs, trunk, or scalp but may be found on any
part of the skin
The most typical areas are the knees and
elbows
PSORIASIS: Cause
n
The patches of psoriasis occur because of an
abnormally high rate of growth of skin cells
n
The reason for the rapid cell growth is unknown, but
a problem with the immune system is thought to play
a role
n
The disorder is often hereditary
n
Psoriasis is common and affects about 1 to 5% of
the population worldwide
n
Light-skinned people are at greater risk, whereas
dark-skinned populations are less likely to get the
disease
PSORIASIS:
Frequency
§ Approximately 1-2% of people in the United
States, or about 5.5 million, have plaque psoriasis
§ Up to 30% of people with plaque psoriasis also
have psoriatic arthritis
§ Individuals with psoriatic arthritis have
inflammation in their joints and may have other
arthritis symptoms
§ Sometimes plaque psoriasis can evolve into more
severe disease, such as pustular psoriasis or
erythrodermic psoriasis (affects whole body). In
pustular psoriasis, the red areas on the skin
contain blisters with pus.
PSORIASIS: Onset
§ Psoriasis is a common, chronic, relapsing, inflammatory skin
disorder with a strong genetic basis
§
§
§
§
Psoriasis affects children and adults
Men and woman are affected equally
Females develop plaque psoriasis earlier than males
Plaque psoriasis first appears during 2 peak age ranges:
§ The first peak occurrence of plaque psoriasis is in people aged
16-22 years. The second peak is in people aged 57-60 years.
§ Average age of onset is the third decade, its prevalence
increases with age
§ Psoriasis can affect all races. Studies have shown that more
people in western European and Scandinavian populations have
psoriasis than those in other population groups.
PSORIASIS: S/S
§ The flare-ups can last for weeks or months. The
psoriasis goes away for a time and then
returns (chronic).
§ General characteristics of the scaly skin of the
most common type of psoriasis are as follows:
§ Plaques: Areas on the skin are elevated. The
plaque areas vary in size (1 to several
centimeters) and may range from a few to many at
any given time on the skin. The shape of the
plaque is usually oval but can be irregular in
shape. Smaller plaque areas may merge with
other areas and form a large affected area.
PSORIASIS: S/S
§ Red color: The color of the affected skin is very
distinctive. The rich, full red color is salmon colored.
Sometimes the skin can have a blue tint when the psoriasis
is on the legs.
§ Scales: The scales are dry, thin, and silvery-white. The
thickness of the scales may vary. When the scale is
removed, the skin underneath looks smooth, red, and
glossy. This shiny skin usually has small areas that
bleed (Auspitz sign).
§ Symmetry: Psoriatic plaques tend to appear on both sides
of the body in the same places. For example, the psoriasis is
usually on both knees or both elbows at the same time.
PSORIASIS: Other Forms
n
Some uncommon types of psoriasis can have more
serious effects
n
Psoriatic arthritis produces joint pain and swelling
n
Erythrodermic psoriasis causes all of the skin on
the body to become red and scaly. This form of
psoriasis is serious because, like a burn, it keeps the
skin from serving as a protective barrier against injury
and infection.
n
Pustular psoriasis will cause large and small pusfilled blisters (pustules) to form on the palms of the
hands and soles of the feet. Sometimes, these
pustules are scattered on the body.
Scalp: The scalp can have dry, scaly skin or
crusted plaque areas. Sometimes psoriasis
of the scalp is confused with seborrheic
dermatitis (aka. cradle cap in babies). In
seborrheic psoriasis, the scales are
greasy looking, not dry.
Droplets on skin: Sometimes, the skin is red
and looks like it has little drops on it. This
may be guttate psoriasis. Red drop-like
lesions are found on the skin. This type of
psoriasis usually occurs after a
streptococcal (bacterial) infection.
Pus on patches: Sometimes, the patches of
dry, scaly skin can crack and have pus on
top of them. This may be pustular
psoriasis. Usually limited to the palms of
hands and soles of feet.
PSORIASIS:
Environmental Triggers
§ Injury to the skin: Injury to the skin has been
associated with plaque psoriasis. For example,
a skin infection, skin inflammation, or even
excessive scratching can trigger psoriasis.
§ Sunlight: Most people generally consider
sunlight to be beneficial for their
psoriasis. However, a small minority find that
strong sunlight aggravates their symptoms. A
bad sunburn may worsen psoriasis.
PSORIASIS:
Environmental Triggers
u Streptococcal
infections: Some evidence suggests
that streptococcal infections may cause a type of
psoriasis. These bacterial infections have been
shown to cause guttate psoriasis, a type of
psoriasis that looks like small red drops (papules) on
the skin
u HIV:
Psoriasis typically worsens after an individual
has been infected with HIV. However, psoriasis often
becomes less active in advanced HIV infection.
CONTACT DERMATITIS
u
There are 2 types of contact dermatitis: allergic and irritant
u
Substances can cause skin inflammation by one of two mechanisms—
irritation (irritant contact dermatitis) or allergic reaction (allergic
contact dermatitis)
u
Like all allergic reactions, allergic contact dermatitis results from a
reaction of the immune system
u
u
The immune system overreacts to the foreign substance, usually an
animal or vegetable protein. The immune system is activated to
produce antibodies against this allergen. This overreaction is often
called a hypersensitivity reaction.
u
The antibody, called immunoglobulin E or IgE, is stored on special
cells called mast cells.
u
When they come in contact with the allergen, the antibodies promote
release of chemicals and hormones called "mediators." Histamine is
an example of a mediator.
It is the effects of the mediators that cause the symptoms of the allergic
reaction, in this case an itchy rash
CONTACT DERMATITIS:
Allergic Contact
n
In allergic contact dermatitis, you have a skin reaction to something that
has touched your skin at that site
n
Unlike most allergic reactions, the trigger is external rather than internal.
Your initial exposure does not cause a rash. However, it sensitizes your
skin so that you will react to the next exposure. If you seem to react the first
time you are exposed to an agent, you probably were exposed before
without knowing.
n
The initial sensitization typically takes 10-14 days from initial exposure
to a strong contact allergen such as poison ivy
n
Once an individual is sensitized to a chemical, allergic contact dermatitis
develops within hours to several days of exposure
n
Common plant allergens that cause dermatitis include poison ivy, poison
oak, and poison sumac
n
Many other substances can cause allergic reactions, including hair dyes or
straighteners; the metal nickel, which is found in jewelry and belt buckles;
tanning agents in leather; latex rubber; and citrus fruit, especially the peel.
The fragrances in soaps, shampoos, lotions, perfumes, and cosmetics can
cause a reaction.
SKIN CANCER
n
Skin cancer is the most common of all human
cancers
n
Some form of skin cancer is diagnosed in more
than 1 million people in the United States each
year
n
There has been an alarming increase in skin
cancers during the past several decades
n
Rising incidence of skin cancer has been
attributed primarily to increased sun exposure
SKIN CANCER
n
Skin cancers are of three major types: Basal Cell
Carcinoma (BCC), Squamous Cell Carcinoma (SCC),
and Melanoma
n
The vast majority of skin cancers are BCCs or SCCs.
While malignant, these are unlikely to spread to other
parts of the body. They may be locally disfiguring if not
treated early.
n
A small but significant number of skin cancers are
malignant melanomas
n
Malignant melanoma is a highly aggressive cancer that
tends to spread to other parts of the body. These
cancers may be fatal if not treated early.
SKIN CANCER:
Progression
n
Like many cancers, skin cancers start as
precancerous lesions. These precancerous
lesions are changes in skin that are not cancer but
could become cancer over time (i.e. Dysplasia)
n
Some specific dysplastic changes that occur in
skin are as follows:
n Actinic
keratosis is a patch of red or brown, scaly,
rough skin
n Dysplastic
nevi are abnormal moles. These can
develop into melanoma over time.
Actinic keratosis is a patch
of red or brown, scaly, rough
skin, which can develop into
squamous cell carcinoma.
Actinic keratosis is caused by
sun exposure. It is located on
the face, scalp, back of the
hands, chest, or other sunexposed areas.
A nevus is a mole, and
dysplastic nevi are abnormal
moles.
These can develop into
malignant melanoma over
time.
Normal moles (nevi) are
simply growths on the skin.
They are very common. Very
few moles become cancer.
BASAL CELL CARCINOMA
(BCC)
n
Most common skin cancer in humans, accounting for 75% of
all non-melanoma skin cancers
n
Basal cell carcinoma is the most common human cancer.
More than 800,000 people develop this type of cancer in the
United States each year.
n
Basal cell carcinoma usually develops on skin surfaces that
are exposed to sunlight, commonly on the head or neck
n
Usually occurs in persons who were exposed to great
amounts of sunlight
n
Incidence is twice as high among men as women, and
greatest in the 55-75 age group
n
Basal cell carcinoma is a cancer that originates in cells of
the outer layer of skin (epidermis)
BASAL CELL CARCINOMA
(BCC)
Because basal cell carcinoma spreads slowly, it occurs mostly in adults.
Basal cell tumors can take on many forms, including a pearly white or waxy
bump, often with visible blood vessels (cherry pie), on the ears, neck, or face.
Tumors can also appear as a flat, scaly, flesh-colored or brown patch on the
back or chest, or more rarely, a white, waxy scar.
BASAL CELL CARCINOMA
(BCC)
§ Non-metastasizing, malignant tumor that extends
wide and deep if left untreated
§ These tumors are most frequently on sunexposed areas of the body, such as the head and
neck, but can occur on other surfaces
§ All suspected basal cell carcinomas should
undergo biopsy for diagnosis
BASAL CELL CARCINOMA
(BCC)
§ A basal cell carcinoma (BCC) usually looks like
a raised, smooth, pearly bump on the sunexposed skin of the head, neck, or shoulders
§ Small blood vessels may be visible within the
tumor (telangiectasia)
§ A central depression with crusting and
bleeding (ulceration) frequently develops. Socalled "rodent ulcer“ or “cherry-pie” lesion
§ A BCC is often mistaken for a sore that does
not heal
SQUAMOUS CELL CARCINOMA
(SCC)
Squamous carcinoma is usually seen as an erythematous to skin-colored
scaling plaque or nodule, most typically on sun-exposed skin. Ulceration
may occur as the lesion enlarges.
SQUAMOUS CELL CARCINOMA
(SCC)
Squamous cell carcinoma is cancer that originates in the
squamous cells (keratinocytes)
n
Malignant tumors of the outer epidermis
n
They are commonly found on sun-exposed areas of the
skin of people with fair complexions. Metastasis is more
common with squamous cell carcinoma than with BCC
n
Squamous cell carcinoma is curable if caught and
treated early. If the skin cancer becomes more
advanced, treatment will depend on the stage of
cancer.
SQUAMOUS CELL CARCINOMA
(SCC)
n
Squamous cells (keratinocytes) are the main
structural cells of the epidermis (the outer layer of
skin)
n
Squamous cell carcinoma usually develops on sunexposed areas but may grow anywhere on the skin
or in the mouth, where sun exposure is minimal.
n
Squamous cell carcinoma is characterized by its
thick, scaly, irregular appearance
n
Fair-skinned people are much more susceptible to
squamous cell carcinoma than darker-skinned
people
MALIGNANT MELANOMA
Melanoma is a malignancy of pigment-producing cells
(melanocytes) located predominantly in the skin
MALIGNANT MELANOMA
§ Melanoma is a cancer that originates in the pigment-producing cells of the skin
(melanocytes)
§ Melanocytes are the pigmented cells in the skin that give skin its distinctive color.
Sunlight stimulates melanocytes to produce more melanin (the pigment that darkens
the skin) and increases the risk of melanoma
§ Rapidly progressing, metastatic form of cancer
§ Melanoma can begin as a new, small, pigmented skin growth on normal skin, most
often on sun-exposed areas, or it may develop from pre-existing pigmented moles
§ Increased incidence of melanoma has occurred during the past several decades and
has been attributed to increase in sun-exposure
§ Risk is greatest in fair-skinned people, those with blonde or red hair who sunburn
and freckle easily
§ The median age of melanoma diagnosis is 59 years old
§ Melanoma accounts for only 4% of all skin cancers; however, it causes the greatest
number of skin cancer–related deaths worldwide
§ Increased 5-year survival rate from approximately 40% in 1940s to 90% at present
MALIGNANT MELANOMA:
Clinical Picture
n
A new or changing mole or blemish is the most common warning sign for melanoma.
Variation in color and/or an increase in diameter, height, or asymmetry of borders of a
pigmented lesion are noted by more than 80% of patients with melanoma at the time of
diagnosis.
Primary risk factors and clinical warning signs for melanoma include the following:
n
Changing mole (most important clinical warning sign)
n
Clinical atypical/dysplastic nevi (particularly >5-10)
n
Large numbers of common nevi (>100)
n
Previous melanoma
n
Sun sensitivity/history of excessive sun exposure
n
Melanoma in first-degree relative(s)
n
Prior non-melanoma skin cancer (basal cell and squamous cell carcinoma)
n
Male sex
n
Age older than 50 years
n
A fair-skin phenotype (blue/green eyes, blond or red hair, light complexion, sun sensitivity)
and the occurrence of blistering sunburn(s) in childhood and adolescence are universal risk
factors for melanoma
Know your ABCDEʼs…
§ A: Asymmetry - means one half of a mole does not match the other
half. Normal moles are symmetrical.
§ B: Border irregularity- Margins may be notched or irregular
§ C: Color - A mole that does not have the same color throughout or
that has shades of tan, brown, black, blue, white, or red is suspicious.
Normal moles are usually a single shade of color.
§ D: Diameter - Benign moles are usually less than 6 millimeters in
diameter. >6mm is suspicious (>1/4 inch)
§ E: Elevation/Evolving - Melanoma lesions often grow in size or
change in height rapidly. A mole that is evolving—shrinking, growing
larger, changing color, begins to itch or bleed—should also be
checked.
THATʼS ALL!!!!!!!
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PNP401..DONE!
Donʼt fail J
Questions/Concerns:
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lisa.caputo@senecacollege.ca
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Next week (Apr 13) – Asynchronous – Self-study &
Practice Questions
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FINAL EXAM ON APRIL 20!!
IN-PERSON EXAM – Room K2241
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Good Luck!!!!!!!!!!!!!!!!!!!!