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80 Cards in this Set
- Front
- Back
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GERD def + etiology
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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 |
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Esophagus
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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 |
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GERD sxs + sns
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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 |
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GERD diag + complications
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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 |
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Hiatus hernia Def + etiology
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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 |
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Hiatus hernia sxs + sns
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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 |
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Gastritis def + etiology
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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 |
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Gastritis sxs + sns + diagnosis
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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 |
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Endoatlas.com
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Pics of GI tract
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Esophagitis leads to
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Barretts esophagus - why ppi's are prescribed so much (no longer than 6 wks)
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Peptic ulcer def
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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 |
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Peptic ulcer etiology
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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 |
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Peptic ulcer sxs + sns
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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 |
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Peptic ulcer complications + diagnosis
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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 |
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Diarrhea
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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 |
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Helicobacter
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Fecal oral contamination (most ppl get during childhood)
Hpylori cause 70% of ulcers Tx w 2 antibiotics + ppi |
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Constipation
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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 |
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Gastroenteritis def + etiology
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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 |
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Gastroenteritis sxs + sns
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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 |
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Mucus membrane problems
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Vit a (careful of LV)
Zinc |
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Malabsorption definition
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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 |
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Malabsorption sxs + sns
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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 |
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Malabsorption diagnosis + tx
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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 |
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Celiac disease Def + etiology
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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 |
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Celiac disease (associatd diseases)
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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 |
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Celiac disease sxs + sns
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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 |
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Celiac dx + tx
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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 |
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Inflammatory Bowel Disease (IBD)
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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 |
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Crohns disease def + etiology
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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 |
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Crohns disease epidemiology + pathology
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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 |
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Crohns disease sxs + sns
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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 |
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Crohns disease diagnosis, prognosis
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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 |
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Ulcative colitis Etiology, epidemiology, pathology
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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!) |
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Ulcative colitis sxs + sns
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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) |
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Ulcative colitis Diagnosis + prognosis
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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 |
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Complications of constipation
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Diverticuli (bulge in intestines/ pressure against mucosa + toxic material damaging cells)
Hemorrhoids |
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Irritable Bowel Syndrome def + etiology
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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 |
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Irritable Bowel Syndrome pathology + sxs + sns
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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 |
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Irritable Bowel Syndrome diagnosis
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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 |
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Diverticular disease definition + etiology
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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 |
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Diverticular disease sxs + sns/complications
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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 |
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Hemorrhoids Def + Etiology
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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 |
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Hemorrhoids sxs + sns + diagnosis
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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) |
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Proctitis
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Proctitis
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 |
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Lv disease: jaundice/ definition
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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 |
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Lv disease: jaundice pathology + sxs
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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 |
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For parasites / herb
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Mo Yao / myrrh
Artemesia- |
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LV disease: cholestasis
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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 |
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LV disease-hepatomegaly
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D. hepatomegaly
1. liver enlargement |
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LV disease: portal hypertension
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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 |
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LV disease: ascites
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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 |
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LV disease: Portal systemic encephalopathy
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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 |
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LV disease: fatty liver
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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 |
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LV disease: non alcoholic fatty liver disease
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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 2. ALT, AST 3. US E. complications 1. Non-Alcoholic SteatoHepatitis 2. cirrhosis |
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Fibrosis
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Fibrosis
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 |
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Cirrhosis Def + etiology
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Cirrhosis
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 5. PSC, PBC 6. NASH |
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Cirrhosis Pathology + sxs + sns
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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 |
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Cirrhosis tx + complications
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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 |
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Hepatitis etiology + epidemiotlogy
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Hepatitis
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 |
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Hepatitis sxs + sns
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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 |
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Hepatitis laboratory
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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 c. HCV-RNA d. genotyping |
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Hepatitis diagnosis + prognosis
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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 |
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prophylaxis
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prophylaxis
1. isolation not important 2. HAV a. hygiene b. immune globulin i. household contacts ii. travelers to endemic areas 3. HBV a. HBIG 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 |
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Cholelithiasis def + etiology
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Cholelithiasis
A. biliary (GB) calculi (stones) B. etiology 1. female, obesity, family hx, Western diet 2. supersaturation of cholesterol in bile solution |
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Cholelithiasis sxs + sns
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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 |
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Cholelithiasis tx + diagnosis
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diagnosis
1. US E. treatment 1. cholecystectomy 2. bile acids 3. lithotripsy 4. elimination diet 5. increase fiber, avoid refined CHO |
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Cholecystitis def + etiology / diag + tx
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Cholecystitis
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 |
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Esophageal cancer def + etiology
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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 4. GERD a. Barrett’s esophagus |
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Esophageal cancer sxs + sns / diag + tx
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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 |
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Stomach Cancer incidence + etiology
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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 |
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Stomach Cancer sxs + sns / tx + prognosis
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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 |
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Pancreatic Cancer def + incidence
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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 |
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Pancreatic Cancer sxs + sns / diag + tx
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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 4. MRCP 5. ERCP E. treatment 1. 5 yr survival less than 2% 2. surgery 3. chemotherapy |
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Colorectal cancer def + incidence
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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 |
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Colorectal cancer Etiology
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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 |
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Colorectal cancer sxs + sns / diag + tx
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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 |
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Liver Cancer
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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 |
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Liver Cancer sxs + sns / diag + tx
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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 |
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Erythrocytes/ liver/ bilirubin
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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 |
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Jaundice mild/severe
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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 |
