Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

80 Cards in this Set

  • Front
  • Back
GERD def + etiology
XII. Gastroesophageal Reflux Disease
A. reflux of gastric contents into esophagus
B. etiology
1. incompetence of lower esophageal sphincter
2. hiatus hernia (cardia of ST pushes up thru diaphragm)
3. increased abdominal pressure
a. obesity, pg, eating too much or too quickly
Most post to most ant as move from throat to abdomen (gradient)
LES = lower esophageal sphincter / circular layer muscles in diaphgrqgm closing jx of stomach + esophagus
GERD sxs + sns
C. sxs & sns
1. heartburn
a. burning in epigastrium, substernal area
b. can radiate to back, neck, both arms
c. worse bending over or lying down
2. regurgitation of gastric contents into mouth
GERD diag + complications
D. complications
1. esophagitis
2. stricture
3. dysphagia
E. diagnosis
1. history
2. assess gastric acidity
3. x-ray
4. endoscopy
5. esophageal manometry
a. measures pressure at lower esophageal sphincter
Hiatus hernia Def + etiology
XIII. Hiatus Hernia
A. protrusion of the stomach above the diaphragm
B. etiology
1. unknown, but see esophageal reflux
2. 40% of population
a. less than 50% symptomatic
b. most with GERD
Hiatus hernia sxs + sns
Like esophageal reflux
1. heartburn
a. burning in epigastrium, substernal area
b. can radiate to back, neck, both arms
c. worse bending over or lying down
2. regurgitation of gastric contents into mouth
Gastritis def + etiology
XIV. Gastritis
A. inflammation of the gastric mucosa
B. many different types
1. histological, endoscopic, radiological, clinical
C. etiology
1. idiopathic
2. stress
3. trauma
4. drugs (NSAID’s)
5. alcohol
6. viruses
7. Helicobacter pylori
a. 50% of all people by age 60
Gastritis sxs + sns + diagnosis
D. sxs & sns
1. dyspepsia
a. vague GI sx
b. epigastric or substernal burning or pain
c. belching, borborygmus
E. diagnosis
1. x-ray, endoscopy, biopsy, histology
2. antibody detection for H. pylori
3. H. pylori breath test
Pics of GI tract
Esophagitis leads to
Barretts esophagus - why ppi's are prescribed so much (no longer than 6 wks)
Peptic ulcer def
XV. Peptic Ulcer
A. ulceration of the mucous membrane of areas exposed to gastric acid and pepsin
B. types
1. duodenal
a. most common
b. 5x more than gastric
c. 5x more in males
d. 1/2 - 2/3 secrete more acid than normal
e. males aged 20-30
f. females aged 40-50
2. gastric
a. lesser curvature of stomach
b. 80% have decreased acid
c. aged 50-60
Peptic ulcer etiology
C. etiology
1. Helicobacter pylori
a. 50 – 70% of duodenal ulcers
b. 30 – 50% of gastric ulcers
2. drugs
a. NSAID’s
Aa. 50% of all ulcers
b. cigarettes
c. corticosteroids
d. aspirin
e. caffeine
f. alcohol
3. decreased mucous production
4. food allergens
5. stress
Peptic ulcer sxs + sns
D. sxs & sns
1. burning, gnawing, aching pain
a. often radiates through to back
2. empty feeling, *hunger (but peptic ulcer wrse w food)
3. steady, *well-circumscribed
4. epigastric pain
5. duodenal
a. consistent pain pattern
b. absent on waking but appears mid-morning
c. *better with food (alkaline in SI while acid in ST)
d. recurs 2-3 hours after eating
e. nocturnal pain
6. gastric
a. rarely follow a pattern
b. often worse with food
Peptic ulcer complications + diagnosis
E. complications
1. hemorrhage
2. perforation
3. obstruction
F. diagnosis
1. endoscopy
2. upper GI series
3. anti-H. pylori antibodies
a. serum 85% sensitivity and specificity
i. quantitative remain positive 6 – 12 months after tx
ii. qualitative remain positive up to 3 years after tx
4. H. pylori breath test
a. sensitivity and specificity greater than 90%
5. stool antigens
a. sensitivity and specificity like breath test
XVI. Diarrhea
A. increased volume, fluidity, or frequency of bowel movements
1. more than 300gm/d (average in US is 100-300gm/d)
B. a symptom, not a disease
C. etiology
1. osmotic
a. non-absorbable, water-soluble solutes in bowel
i. lactose, simple CHO
2. secretory
a. secrete electrolytes and water
i. bacterial toxins, viruses
3. exudative
a. mucosal inflammation and ulceration
4. decreased intestinal transit time
a. not enough exposure to absorptive surface for a sufficient amount of time
D. parasitic infections
1. Entameba histolytica
2. Giardia lamblia
3. Enterobius vermicularis
4. dx by O & P
a. stool antigens for Giardia infections
Fecal oral contamination (most ppl get during childhood)
Hpylori cause 70% of ulcers
Tx w 2 antibiotics + ppi
XVII. Constipation
A. difficult or infrequent bowel movements
B. a symptom not a disease
1. stools too hard, too small, infrequent, difficult to expel, feeling of incomplete evacuation
C. sns
1. 3-5 stools per week
2. more than 3 days without stool
3. weight less than 35gm
D. etiology
1. obstruction
2. drugs
3. tumors
4. functional disorders
a. IBS, hypothyroidism
5. psychological
E. complications
1. hemorrhoids
2. diverticulosis
3. colon CA
Gastroenteritis def + etiology
XVIII. Gastroenteritis
A. inflammation of mucous membrane of ST + intestine
B. etiology
1. bacteria
a. most common to invade mucosa: Salmonella, Campylobacter, Shigella, E. coli b.most common to produce exotoxin in food: Staphylococcus aureus, Bacillus cereus, Clostridium perfringens
c. Vibrio cholerae
d. Clostridium botulinum
i. botulism
ii. home-canned foods
iii. vegetables, fruit, fish, condiments
iv. abrupt onset 18-36 hrs after toxin ingestion
v. bilateral symm neurologic sx
vi. begins in cranial nerves with descending weakness or paralysis
vii. nausea, vomiting, diarrhea
viii. no fever
ix. no sensory disturbances
x. clear sensorium
2. viruses (most common cause)
3. parasites
a. Giardia
b. Cryptosporidium
c. Entamoeba
4. toxic
a. nonbacterial food poisoning
b. drugs
5. food allergies
Gastroenteritis sxs + sns
C. sxs & sns
1. usually sudden onset
2. malaise, anorexia
3. nausea, vomiting
4. cramps, diarrhea with or without blood and mucous
5. borborygmus
6. distended, tender abdomen
D. diagnosis
1. history
2. stool analysis
3. stool culture
Mucus membrane problems
Vit a (careful of LV)
Malabsorption definition
XIX. Malabsorption
A. impaired absorption of nutrients from the SI
B. etiology
1. food allergy
2. insufficient digestive agents
a. HCl, bile salts, pancreatic enzymes, lactase
3. bacterial overgrowth
4. celiac disease
5. Crohn’s disease
Malabsorption sxs + sns
C. sxs & sns
1. weight loss, malaise
2. flatulence, abdominal distention, bloating
3. carpopedal spasms
a. Ca deficiency
4. bruising
5. diarrhea, steatorrhea
a. pale, bulky, soft, sticky, malodorous stools
6. anemia
7. glossitis
a. B vitamin deficiencies
8. CHO intolerance - lactase deficiency
a. inability to digest lactose
b. 75% of all adults of all ethnicities
i. 20% of adults of NW European origin
c. bloating, flatulence, nausea, diarrhea, cramps after ingestion of dairy products
Malabsorption diagnosis + tx
D. diagnosis
1. clinical
2. fecal fat
3. comprehensive stool examination
4. d-xylose absorption
a. normal test in the presence of sxs indicates pancreatic insufficiency and not SI absorptive problem
5. lactose absorption
6. SI biopsy
E. treatment
1. remove offending substance
2. HCl
3. pancreatic enzymes
4. multiple vitamin and mineral supplementation
5. mixed carotenoids
Celiac disease Def + etiology
XX. Celiac Disease
A. gluten sensitive enteropathy (GSE)
1. intolerance to gluten creating malabsorption
B. epidemiology
1. 1 out of 133 people in US
2. up to 15% of siblings and children of person with celiac
C. etiology
1. genetic
2. autoimmune
Celiac disease (associatd diseases)
D. associated diseases
1. dermatitis herpetiformis
a. papulovesicular, pruritic rash
b. symmetric distribution
i. face, elbows, knees, buttocks
2. type I DM, Hashimoto’s thyroiditis, chronic active hepatitis, SLE, PSS, RA, Addison’s Disease, Raynaud’s Disease, CFS, fibromyalgia
Celiac disease sxs + sns
E. sxs & sns
1. malabsorptive sx after eating gluten containing foods (wheat, barley, rye, spelt, kamut)
2. abdominal cramping
3. flatulence
4. abdominal distention and bloating
5. diarrhea or constipation
6. glossitis, angular stomatitis, aphthous ulcers
7. anorexia
8. osteopenia or osteoporosis
9. arthralgias
10. fatigue
11. paresthesias
12. migraines
13. infertility
14. steatorrhea
15. anemia
16. weight loss
Celiac dx + tx
F. dx
1. clinical suspicion
2. anti-tissue transglutaminase antibody – tTG
3. anti-endomysial antibody – EMA
a. both have 90% sensitivity and specificity
4. anti-deaminated gliadin peptide – DGP
5. total serum IgA
6. anti-gliadin antibody – AgA
a. only in children less than 2 years of age
7. SI biopsy
a. confirms dx
G. tx
1. gluten avoidance
Inflammatory Bowel Disease (IBD)
XXI. Inflammatory Bowel Disease (IBD)
A. Crohn’s Disease and Ulcerative Colitis (UC)
B. relapsing, remitting
C. chronic inflammation at various places in GI tract
Crohns disease def + etiology
XXII. Crohn’s Disease
A. regional enteritis
B. transmural inflammatory bowel disease
1. usually affects distal ileum and proximal colon but can affect any part of GI tract
C. etiology
1. autoimmune
2. genetics
4. infectious agents
5. food sensitivities
6. lack of fiber in diet
7. stress
8. cigarette smoking
Crohns disease epidemiology + pathology
D. epidemiology
1. equal among both genders
2. more in Jews
3. familial tendency
4. peaks between 15 and 35
E. pathology
1. diseased bowel sharply demarcated from normal bowel
a. segmental lesions may be separated by norml bowel
2. ulceration and inflammation of all layers of intestinal wall
a. cobblestone appearance
3. edema - lymphocytic infiltration - fibrosis
4. ulceration, fibrosis, obstruction, fistulas, abscesses
5. malabsorption
Crohns disease sxs + sns
F. sxs & sns
1. chronic, possibly intermittent, diarrhea
2. fever
3. anorexia, weight loss, malaise
4. RLQ pain and fullness or mass
5. extraintestinal manifestations
a. immunologic or infectious aspects
i. peripheral arthritis
ii. episcleritis
iii. erythema nodosum
iv. aphthous stomatitis
b. 2x as common if disease also in colon
Crohns disease diagnosis, prognosis
G. diagnosis
1. clinical
2. lab
a. anemia, leukocytosis, increased ESR
b. O&P, stool cultures
3. imaging
a. x-ray
i. barium enema
ii. UGI with SI follow-through
b. abdominal CT scan
4. colonoscopy
H. prognosis
1. lifelong exacerbations
2. CA
Ulcative colitis Etiology, epidemiology, pathology
XXIII. Ulcerative Colitis
A. inflammatory ulcerative bowel disease
1. only in colonic mucosa
B. etiology
1. see CD
C. epidemiology
1. familial tendency less than CD
2. peaks at ages 15-30 and 50-70
D. pathology
1. usually begins in rectosigmoid area
a. extends proximally
2. degeneration - infiltration with leukocytes - ulceration
(tends to get better with cigarette smoking!)
Ulcative colitis sxs + sns
E. sxs & sns
1. intermittent bloody diarrhea
2. abdominal cramps
3. commonly insidious onset of increasing urge to defecate, mild cramps, blood and mucous in stools
4. may have sudden onset of fulminant disease
a. violent diarrhea, high fever, toxemia
5. often have rectal involvement
a. ulcerative proctitis
6. hemorrhage
7. extraintestinal manifestations
a. peripheral arthritis, episcleritis, erythema nodosum
i. fluctuate with disease
b. ankylosing spondylitis, sacroiliitis, uveitis
i. independent course from disease
c. spondylitis and uveitis may have genetic overlap with UC
d. primary sclerosing cholangitis (PSC)
Ulcative colitis Diagnosis + prognosis
F. diagnosis
1. history
2. stool examination
3. sigmoidoscopy
4. colonoscopy
5. plain films of abdomen to show extent
6. barium enema usually not done due to risk of perforation
G. prognosis
1. chronic with repeated exacerbations and remissions
2. fulminating disease with complications in 10% of those with rapid initial attack
3. 10% recover completely from a single attack
4. increased risk of colon CA (way more than chrones)
4. highest CA risk if entire colon involved and disease present for greater than 10 years
5. CA risk significantly increased if colitis proximal to sigmoid colon
Complications of constipation
Diverticuli (bulge in intestines/ pressure against mucosa + toxic material damaging cells)
Irritable Bowel Syndrome def + etiology
XXIV. Irritable Bowel Syndrome
A. spastic colon
B. functional bowel disorder
C. motility disorder involving entire GI tract
D. women 3: men 1
E. 50% of all GI referrals
F. etiology
1. no anatomic cause
2. emotional factors
3. stress
4. diet
5. drugs
6. hormones
Irritable Bowel Syndrome pathology + sxs + sns
G. pathology
1. proximal SI hypersensitive to food
2. LI hypersensitive to pressure and hormones
H. sxs & sns
1. abdominal discomfort or pain
a. accompanied by two of the following
i. defecation
ii. change in frequency of bm
iii. change in consistency of bm
2. almost always in waking state
3. triggered by stress, food
4. postprandial distention
5. sense of incomplete evacuation after bm
6. two types
a. spastic colon
i. variable bm
ii. alternating constipation and diarrhea
iii. mucorrhea
iv. lower abdominal pain, usually in LLQ
v. colicky or dull ache
vi. fatigue, depression, anxiety, difficulty concentrating, headache, nausea, bloating, flatulence
b. painless diarrhea
i. urgent, watery diarrhea immediately upon rising in morning or during or after a meal
Irritable Bowel Syndrome diagnosis
I. diagnosis
1. Rome criteria
a. abdominal pain or discomfort for at least 3 days/month in the last 3 months with two or more of the following symptoms
i. improvement with defecation
ii. onset of discomfort associated with change in frequency of bm
iii. change in stool consistency
2. rule out all other GI disorders with similar sx
a. UC, malabsorption, lactose intolerance, celiac disease, duodenal ulcers, gastroenteritis
b. bleeding, weight loss, fever
3. CBC, CMP, thyroid testing
4. hydrogen breath test
5. comprehensive stool examination
6. ultrasound
7. barium enema
8. sigmoidoscopy
9. colonoscopy
Diverticular disease definition + etiology
XXV. Diverticular Disease
A. diverticulosis
1. the presence of sac-like mucosal projections through the muscular layer of the colorectum
B. diverticulitis
1. inflammation of diverticuli
C. usually in sigmoid colon
D. rare before 40 yrs old
E. etiology
1. muscular spasm and increased intraluminal pressure
2. constipation
3. low fiber diet
Diverticular disease sxs + sns/complications
F. sxs & sns
1. 70% asx
2. 15% bleed
3. 25% become inflamed (diverticulitis) - pain, local abdominal tenderness especially in LLQ, fever
G. complications
1. obstruction
2. fistula
3. hemorrhage
4. perforation
5. abscess
6. peritonitis
Hemorrhoids Def + Etiology
XXVI. Hemorrhoids
A. varicosities of veins of hemorrhoidal plexus
B. often with inflammation, thrombosis, bleeding
1. may be internal or external (int tx LV - drain back thru portal v)
a. above or below anorectal line
b. internal from superior hemorrhoidal plexus
c. external from inferior hemorrhoidal plexus
C. etiology
1. weakness of veins
2. increased intra-abdominal pressure
a. constipation, pg, heavy lifting
3. liver disease
a. drainage superior to anorectal line through portal system
b. drainage inferior to anorectal line through portal or caval systems
Hemorrhoids sxs + sns + diagnosis
D. sxs & sns
1. itching, burning, pain, swelling, bleeding
2. often protrude
a. manually replaced
3. thrombosis
a. painful, hard swelling
E. diagnosis
1. inspection
2. rectal exam
3. anoscopy
Tx/ fiber (water soluble / psyllium seeds)
Keasy tech/ galvanic current : positive galvanism (pushes fluid out of tissues, shrinks hemorrhoids)
A. inflammation of the rectal mucosa
B. etiology
1. IBD
2. STI’s
3. infectious agents/parasites
4. antibiotic use
5. immunocompromised patients
C. sxs & sns
1. rectal pain, itching
2. rectal bleeding
3. passage of mucous by rectum
D. diagnosis
1. proctoscopy
2. sigmoidoscopy
3. biopsy, smear, culture
Lv disease: jaundice/ definition
Liver Disease
A. many different manifestations of liver dysfunction
B. jaundice
1. yellowing of skin, sclera, and other tissues due to excess circulating bilirubin
2. bilirubin from breakdown of erythrocytes
3. unconjugated (indirect) bilirubin transported in plasma bound to albumin and taken to liver
4. conjugated with glucuronic acid in liver to form conjugated (direct) bilirubin
5. then secreted into bile canaliculi to form bile
6. this then excreted in feces and urine
7. much reabsorbed and used again
Lv disease: jaundice pathology + sxs
8. pathology
a. increased bilirubin formation, impaired hepatic uptake, or decreased conjugation cause unconjugated hyperbilirubinemia
b. impaired biliary excretion causes conjugated hyperbilirubinemia
c. clinically often see mixed hyperbilirubinemia
d. try to find where it is coming from
9. hemolysis, hepatocellular dysfunction, biliary obstruction
10. sxs & sns
a. mild jaundice without dark urine is usually unconjugated hyperbilirubinemia due to hemolysis or Gilbert’s syndrome
b. deep jaundice or dark urine often hepatic or biliary disorder
For parasites / herb
Mo Yao / myrrh
LV disease: cholestasis
C. cholestasis
1. impairment of bile flow
2. intrahepatic
a. hepatitis, alcoholic liver disease, drug use
3. extrahepatic
a. common bile duct stone, pancreatic carcinoma
4. sxs & sns
a. jaundice, dark urine, pale stools, pruritis
LV disease-hepatomegaly
D. hepatomegaly
1. liver enlargement
LV disease: portal hypertension
E. portal hypertension
1. increased portal vein pressure
2. cirrhosis most common cause
3. shunting of portal blood into systemic circulation
a. high systemic concentrations of hormones and other substances usually extracted by liver
i. portal encephalopathy
b. esophageal varices, caput medusae
LV disease: ascites
F. ascites
1. fluid in the peritoneal cavity
2. chronic disorders usually cirrhosis
3. pathology
a. low serum osmotic pressure from hypoalbuminemia
b. high portal venous pressure
4. sxs & sns
a. abdominal discomfort
b. shifting dullness on abdominal percussion
c. fluid waves in advanced disease
LV disease: Portal systemic encephalopathy
G. portal systemic encephalopathy
1. chronic liver disease
2. shunting of portal venous blood
3. sxs & sns
a. personality changes
b. impaired consciousness
c. constructional apraxia
d. musty sweet odor to breath
e. asterixis
i. arms outstretched, wrists dorsiflexed
ii. flapping tremor
4. hyperreflexia, positive Babinski
LV disease: fatty liver
Fatty Liver
A. excess accumulation of lipid in hepatocytes
1. most common response of liver to injury
B. etiology
1. CF, inborn errors of metabolism, Wilson’s disease, hemochromatosis, vitamin A toxicity, obesity, DM, malnutrition, chemicals, drugs
C. sxs & sns
1. often non-tender, asx hepatomegaly
2. can present with RUQ pain, tenderness, jaundice
D. treatment
1. eliminate cause
LV disease: non alcoholic fatty liver disease
Non-Alcoholic Fatty Liver Disease
A. most common liver disease in US
1. 25% of all people
2. up to 75% of obese individuals
B. etiology
1. obesity
2. type II DM
3. insulin resistance
4. hypertriglyceridemia
5. alcohol abuse
6. hepatitis
C. sxs & sns
1. asx
D. dx
1. serum ferritin
3. US
E. complications
1. Non-Alcoholic SteatoHepatitis
2. cirrhosis
A. accumulation of fibrous tissue in liver
1. imbalance between production and degradation of extracellular matrix
B. etiology
1. common response to hepatocellular injury
2. inflammation, toxins, altered hepatic blood flow, inborn errors of metabolism, hemochromatosis, Wilson’s disease, chemicals, drugs, CHF
C. sxs & sns
1. portal hypertension
D. diagnosis
1. percutaneous liver biopsy
E. treatment
1. find underlying cause
Cirrhosis Def + etiology
A. diffuse disorganization of hepatic tissue
1. regenerative nodules surrounded by fibrous tissue
B. etiology
1. a leading cause of death worldwide
2. chronic alcohol abuse
3. hepatitis C and B
4. autoimmune
Cirrhosis Pathology + sxs + sns
C. pathology
1. progression of fibrosis to cirrhosis depends on extent of injury, continuing damage, liver’s reaction
D. sxs & sns
1. asx
2. weakness, anorexia, malaise, weight loss
3. jaundice, pruritis, telangiectasias, xanthelasma
4. malnutrition, fat malabsorption
5. esophageal varices
6. palpable firm liver
Cirrhosis tx + complications
E. complications
1. portal hypertension a. esophageal varices
2. hypoxemia
3. jaundice, ascites, renal failure, hepatic encephalopathy
F. diagnosis
1. liver function tests
2. albumin, PT time
3. US
4. biopsy
G. treatment
1. withdrawal of toxic agents
2. nutrition
Hepatitis etiology + epidemiotlogy
A. liver inflammation with hepatocellular necrosis
B. etiology of acute viral hepatitis
1. HAV
2. HBV
3. HCV
C. epidemiology
1. HAV
a. incubation 2-6 weeks
b. fecal-oral spread
i. virus shed during incubation period
c. often subclinical or unrecognized infections
2. HBV
a. incubation 6-25 weeks
b. parenteral spread
i. usually contaminated blood products
ii. shared needles of IV drug users
iii. sexual contact
iv. hospital personnel
c. sexual contact
d. closed institutions
e. chronic HBV carriers are reservoir
i. less than 0.5% population in North America
ii. greater than 10% population in Far East
3. HCV
a. incubation 3-16 weeks
b. blood-borne
c. chronic, idiopathic, acute
Hepatitis sxs + sns
sxs & sns
1. prodromal phase
a. anorexia, malaise, nausea, vomiting, fever
b. distaste for cigarettes if smokes
2. icteric phase
a. 3-10 days after prodrome
b. dark urine
c. followed closely by jaundice
d. systemic sx regress and patient feels better
e. jaundice peaks within 1-2 weeks
3. recovery phase
a. lasts 2-4 weeks
4. hepatomegaly and jaundice
Hepatitis laboratory
E. laboratory
1. very high liver enzymes
a. high in prodrome, peak before maximal jaundice, fall slowly in recovery phase
2. HAV
a. IgM Ab early in disease and decreases in several weeks
b. IgG anti-HA in several weeks and persists for life
3. HBV
a. HBsAg
i. during incubation period
ii. 1-6 weeks before clinical sxs
iii. disappears during recovery
b. anti-HBs
i. weeks or months later, after clinical recovery and persists for life
c. HBcAg
i. in liver cells, usually not looked for in serum
ii. anti-HBc at onset of clinical illness and persists for years or life
4. HCV
a. blood-borne
b. anti-HCV
i. several weeks after acute infection
d. genotyping
Hepatitis diagnosis + prognosis
F. diagnosis
1. clinical
2. liver enzymes
3. antigen/antibody testing
4. difficult to diagnose in prodromal phase
G. prognosis
1. HAV rarely becomes chronic
2. HBV chronic in 5-10% of cases
a. mild persistent hepatitis
b. chronic active hepatitis with eventual cirrhosis
c. subclinical chronic carrier state
i. hepatocellular CA
3. HCV most likely to become chronic
a. up to 80% of cases
b. benign, mild chronic hepatitis
c. 20% develop cirrhosis
i. hepatocellular CA usually only with cirrhosis
1. isolation not important
2. HAV
a. hygiene
b. immune globulin
i. household contacts
ii. travelers to endemic areas
3. HBV
i. accidental exposure
ii. given within 24 hours and again 1 month later
iii. regular sexual contacts of positive individuals
iv. given within 2 weeks of last contact
b. HBV vaccination
i. safe with no side effects
ii. postexposure vaccine after accidental exposure
iii. sexual contact with positive individuals
iv. preexposure vaccine
I. treatment
1. licorice
2. selenium 200-1000 mcg/day
3. silymarin 150 mg TID
4. interferon with ribavirin
Cholelithiasis def + etiology
A. biliary (GB) calculi (stones)
B. etiology
1. female, obesity, family hx, Western diet
2. supersaturation of cholesterol in bile solution
Cholelithiasis sxs + sns
sxs & sns
1. asx
2. cystic duct obstruction
a. transient colicky pain in epigastrium or RUQ
b. radiation to right lower scapula
c. constant pain, rising to a crescendo and falling gradually
d. nausea, vomiting
3. biliary or pancreatic duct obstruction
a. pain, jaundice, pancreatitis, cholangitis
4. dyspepsia, fatty food intolerance with RUQ pain
a. nausea, belching, bloating, fullness
i. R/O peptic ulcer, functional dyspepsia
Cholelithiasis tx + diagnosis
1. US
E. treatment
1. cholecystectomy
2. bile acids
3. lithotripsy
4. elimination diet
5. increase fiber, avoid refined CHO
Cholecystitis def + etiology / diag + tx
A. acute inflammation of GB
B. etiology
1. cholelithiasis in 95%
C. sxs & sns
1. RUQ colicky pain radiating to right lower scapula
2. nausea, vomiting, fever
3. positive Murphy’s sign
4. usually improves in 2-3 days and resolves in 1 week
D. diagnosis
1. ultrasound
E. treatment
1. as for cholelithiasis
Esophageal cancer def + etiology
Esophageal Cancer
A. squamous cell carcinoma in proximal 2/3
B. adenocarcinoma in distal 1/3
C. etiology
1. alcohol
2. tobacco use
3. HPV
a. Barrett’s esophagus
Esophageal cancer sxs + sns / diag + tx
D. sxs & sns
1. dysphagia
2. chest pain
3. weight loss
4. hoarseness
5. lymphatic spread to neck
6. lung and liver metastasis
E. dx
1. endoscopy
2. biopsy
3. CT scan
4. endoscopic US
F. prognosis
1. depends on stage (depth of tumor)
2. 5 year survival less than 5%
G. tx
1. surgery
2. chemotherapy
3. radiation
Stomach Cancer incidence + etiology
Stomach Cancer
A. incidence
1. 2nd most common CA in world
a. high in Japan, Chile, Iceland
2. 7th most common CA death in US
3. 75% of patients are over age 50
B. etiology
1. H. pylori
2. associated with gastritis
3. salted, smoked, cured foods
4. adenomatous polyps
Stomach Cancer sxs + sns / tx + prognosis
C. sxs & sns
1. like dyspepsia or peptic ulcer
2. early satiety
3. dysphagia
D. dx
1. endoscopy
2. biopsy
3. CT scan
4. endoscopic US
E. prognosis
1. 5 year survival 5-15%
2. depends on stage (depth of tumor)
F. treatment
1. surgery
2. chemotherapy
3. radiation
Pancreatic Cancer def + incidence
Pancreatic Cancer
A. ductal adenocarcinoma
1. 80% in head of pancreas
2. endocrine tumors much less common
B. incidence
1. average age 55
2. 1.5-2x more in men
3. family hx
4. cigarette smoking
5. DM
Pancreatic Cancer sxs + sns / diag + tx
sxs & sns
1. sx occur late in disease
2. weight loss in 90% of patients at dx
3. severe upper abdominal pain radiating to back
4. by dx, in 90% of pts, tumor has spread to lymph, liver, lung
D. diagnosis
1. lab tests often normal
2. US
3. CT
E. treatment
1. 5 yr survival less than 2%
2. surgery
3. chemotherapy
Colorectal cancer def + incidence
Colorectal Cancer
A. polyps
1. any mass of tissue arising from bowel wall and protruding into lumen
2. 50% of people have them
3. adenomas may become malignant
4. most in rectum and sigmoid colon
5. most asx but rectal bleeding is common complaint
6. surgically removed
7. 2 annual inspections of entire colon with colonoscopy
8. if negative, then colonoscopy q2-3 yrs
B. incidence
1. 2nd after lung CA
2. over age 50
a. increased risk after age 40 with peak after 60
3. colon CA more in women; rectal CA more in men
Colorectal cancer Etiology
1. chronic UC
2. familial polyposis
3. low fiber, high fat, high refined CHO diet
4. intake of processed meats
5. intake of charred meats
6. low vegetable, fruit, fiber intake
7. physical inactivity
8. overweight
9. alcohol
10. tobacco
11. calcium and aspirin may be protective
Colorectal cancer sxs + sns / diag + tx
sxs & sns
1. early dx depends on routine examination
a. stool occult blood
2. blood in the stool
a. occult if in right colon; frank if in left
b. rectal CA presents often as bleeding
c. always R/O CA with rectal bleeding
3. anemia
4. grows slowly before it is large enough to produce sx
5. colicky abdominal pain if obstruction especially in left colon
6. alternating constipation and frequency of stools
E. diagnosis
1. FOB
2. 65% within reach of sigmoidoscope
3. colonoscopy
4. biopsy
5. CT colonography
F. treatment
1. surgery
2. chemotherapy
Liver Cancer
Liver Cancer
A. metastasis most common hepatic tumor
1. lung, breast, colon, pancreas, stomach
2. can be from anywhere
3. often the 1st manifestation of CA elsewhere
B. primary hepatocellular carcinoma much less common than metastasis
1. most common malignancy in parts of Africa and SE Asia
a. chronic HBV
2. cirrhosis
a. chronic HCV
Liver Cancer sxs + sns / diag + tx
Sxs & sns
1. weight loss, anorexia, fever
2. hard, enlarged, tender liver
3. many different metabolic derangements possible
D. diagnosis
1. alpha-fetoprotein for primary hepatocellular carcinoma
2. US
3. CT scan
4. liver biopsy
E. treatment
1. very poor results with any tx
Erythrocytes/ liver/ bilirubin
As age - get fragile membranes / SP breaks them down
As hemoglobin released from erythro becomes bilirubin --- taken back to liver and is changed
B4 LV- uncongugated bilirubin
In LV - complexes it with glucoronic acid to become conjugated bilirubin
Uncong/ indirect bilirubin test
Conjugated / direct bilirubin test
-SP to active- hypersplenism (autoimmune) sequesters and breaks down too many erythrocytes
-LV uptake problem / hepatic uptake of bilirubin off (still uncongugated)
- or uptake ok... Conjugation problem (once in LV)
- excess hemolysis of red blood cells / other enzyme problems
- LV prob itself / obstruction/ can't get rid after conjugated (direct hyperbilirubinemia)
- or blocked after leaves LV (same as above)
*Enterohepatic circulation of bile (80%bile produced by liver goes bak to liver) oat bran- water soluble fiber binds to bile acids and increases absorption rate / less sent back to liver (lowers cholesterol) ? Controversial idea
Jaundice mild/severe
Light jaundice/ mild / no urine or stool color changes : usu uncongugated
*Gilbert syndrome- mild uncong hyperbilirubinemia (stress/fatigue) mediteranean origin (yellowish)
Darker jaundice/ usu congugated hyperbilirubinemia
*liver panel - look at enzymes