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208 Cards in this Set
- Front
- Back
Source of salivary secretions
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Parotid (most serous), submandibular, submaxillary, and sublingual glands (most mucinous)
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Products contained in saliva (fct)
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(1) alpha amylase (begins starch digestion); inactivated by low pH in stomach
(2) bicarbonate (neutralizes oral bacterial acids, maintains dental health) (3) mucins (glycoproteins) lubricate food (4) antibacterial secretory products (5) growth factors promote epithelial renewal |
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Salivary glands secretion innervations
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Sympathetic (T1-T3) and parasympathetic (facial, glossopharyngeal n)
Slow flow (hypotonic) High flow (isotonic) |
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Gastrin
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) G cells (antrum of stomach)
(b) incr H+ secr, growth of gastric mucosa, gastric motility Also incr pepsinogen (chief) and histamine (ECL) (c) Incr by stomach distension, aa;s, peptides, vagal stim (d) Decr by stomach pH<1.5 (e) incr in Zollinger Ellison syndrome. Phenylalanine and tryptophan potent stimulators |
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Cholecystokinin
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) I cells (duodenum and jejunum)
(b) incr pancreatic secr, incr gallbladder contr Decr gastric emptyin (c) incr by fatty acids, amino acids (d) n/a (e) in cholelithiasis, pain worsens after fatty food ingestion due to incr CCK |
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Secretin
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) S cells (duodenum)
(b) incr pancreatic HCO3, bile secretion Decr gastric acid secretion (c) incr by FA in duodenum (d) n/a (f) incr HCO3 neutralizes fastric acid in duodenum, allowing pancreatic enzymes to fct |
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Somatostatin
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) D cells (pancreatic islets, GI mucosa)
(b) decr gastric acid and pepsinogen secretion, pancreatic and small int fluid secretion, GB contraction, insulin and glucagon release (c) incr by acid (d) decr by vagal stimulation (e) inhibitory hormone; antigrowth effects (digestion and absorption of substances needed for growth); used to treat VIPoma and carcinoid tumors |
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Glucose-dependent insulinotropic peptide (GIP)
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) K cells (duodenum, jejunum)
(b) exocrine: decr H+ secretion Endocrine: incr insulin release (c) incr by FA, aa, oral glucose (d) n/a (e) an oral glucose load is used more rapidly than the equivalent give by IV |
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Vasoactive intestinal peptide
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) parasympathetic ganglia in sphincters, GB, small intestine
(b) incr intestinal water and electrolyte secretion, incr relaxation of intestinal smooth muscle and sphincters (c) incr by distention and vagal stim Decr by adrenergic output (d) VIPoma-non alpha or beta islet cell pancreatic tumor that secretes VIP and causes copius diarrhea |
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Nitric oxide
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) n/a
(b) incr smooth muscle relaxation, including LES (c) n/a (d)n/a (e) loss of NO secretion implicated in incr LES tone in achalasia |
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Motilin
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) small intestine
(b) produces MMC's (c) incr in fasting state (d) n/a (e) n/a |
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Histamine
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) enterochromaffin cells
(b) incr gastric acid secretion (directly and potentiates gastrin and vagal stimulation) (c) gastrin, ach (d) n/a (e) n/a |
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GRP
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) vagal nerve endings
(b) stimulates gastrin release from G cells (c) cephalic stimulation, gastric distension (d) n/a (e) n/a |
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Pancreatic polypeptide
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) F cells of pancreas, small intestine
(b) protein, fat, glucose in lumen (c) n/a (d) decr pancreatic secretion (e) n/a |
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Enteroglucagon
(a) source (b) action (c) stimulus (d) inhibition (e) notes |
(a) L cells of intestine
(b) decr gastric/pancreatic secretions Incr insulin release (c) n/a (d) n/a (e) n/a |
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Intrinsic factor
(a) source (b) action (c) regulation (d) notes |
(a) parietal cells (stomach-body/fundus)
(b) vitB12 binding protein (required fro B12 uptake in terminal ileum) (c) n/a (d) autoimmune destruction of parietal cells causing chronic gastritis and pernicious anemia |
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Gastric acid
(a) source (b) action (c) regulation (d) Notes |
(a) parietal cells (stomach)
(b) decr stomach pH (c) incr by histamine, Ach, gastrin Decr by stomatostatin, Gip, prostaglandin secretion (d) gastrinoma: gastrin secreting tumor that causes continuous high levels of acid secretion and ulcers |
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Pepsinogen
(a) source (b) action (c) regulation (d) notes |
(a) chief cells (stomach-body/fundus)
(b) protein digestion (c) incr by vagal stimulation, local acid (d) inactive pepsinogen (goes to active by H+) |
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Bicarbonate
(a) source (b) action (c) regulation (d) notes |
(a) mucosal cells (stomach, duodenum, Brunner's glands)
(b) neutralizes acid, prevents autodigestion (c) incr by secretin (d) bicarb trapped in mucus that covers gastric epithelium |
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Leukoplakia
(a) description (b) complictions (c) predisposing factors |
(a) white plaques on oral mucosa (hyperkeratosis)
(b) 10% have epithelial dysplasia (precancerous) (c) smoking, tobacco, alcohol abuse, chronic friction, irritants |
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Erythroplakia
(a) description (b) complications |
(a) flat, smooth, red lesion in oral cavity
(b) high risk of malignant transformation (atypical epithelial cells) |
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Hair leukoplakia description
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Wrinkled surface, patched on side rather than middle of tongue; no malignant transformation
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Lichen planus
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White reticular lesions on buccal mucosa/tongue
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Benign tumors of oral cavity
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Hemaniogoma, hamartoma, fibroma, lipoma, adenoma, papilloma, neurofibroma, nevi
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SCC of oral cavity
(a) peak age (b) risk factors (c) common site |
(a) 40-70
(b) tobacco, alcohol, esp together (c) lower lip (but floor and tongue also) |
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Achalasia
(a) pathophys (b) symptoms (c) etiology (d) diagnosis (e) increase risk for? |
(a) failure of Les to relax due to loss of myenteric (Auerbach's) plexus; high LES opening pressure
(b) dysphagia, regurg, aspiration, chest pain (c) idiopathic; secondary to Chagas or malignancy (d) barium sloww: bird's beak (e) esophageal carcinoma |
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Esophageal varices
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Related to portal HTN; painless bleeding of submucosal veins in lower 1/3 of esophagus
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Mallory-Weiss syndrome
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Painful mucosal lacerations at GE jct due to severe vomiting; found in alcoholics/bulimics
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Boerhaave syndrome
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Transmural esophageal rupture due to violent retching
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Sliding hernia
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GE jct above diaphragm (assoc w/reflux); 90% of stomach hernias
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Paraesoageal hernia
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Gastic cardia above diaphragm; at risk for strangulation and infarction
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Schatszki rings
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Mucosal rings at squamocolumnar jct below aortic arch
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Tracheoesophageal fistula
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-usually esoph blind pouch w/fistula b/w lower eso and trachea
-assoc w/other congenital malformations |
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Esophageal strictures assoc w/?
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Lye ingestion
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Esophagitis associated w?
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Reflux, infection (HSV-1, CMV, Candida, chemical ingestion
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Plummer Vinson Syndrome
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Triad: dysphagia (esophageal web), glossitis, iron deficiency anemia
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Zenker diverticula
(a) location (b) symptoms |
(a) jct of pharynx and esophagus in elderly men
(b) dysphagia, regurg of undigested food soon after ingestion |
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Esophageal Diverticula
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Protrusion of 1+ layer of pharyngeal or esophageal wall
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Traction diverticula
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True diverticula in mid esophagus; usually asypmtomatic
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Barrett's esophagus
(a) describe (b) cause (c) incr risk for? |
(a) glandular metaplasia; replacement of nonkeratinized stratified squamous w/intestinal epithelium
(b) GERD (c) esophageal adenocarcinoma |
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Risk factors for esophageal cancer
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Alcohol/achalasia
Barrett's Cigarettes Diverticuli Esophageal web Esophagitis Familial |
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Portion of esophagus mainly affected by squamous cell? Adenocarcinoma?
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Upper/middle 1/3: squamous
Lower 1/3: SCC |
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Celiac sprue
(a) pathophys (b) pathology (c) incr risk of? (d) screening |
(a) Abs to gluten (gliadin) in wheat and grains
(b) atrophy of villi in jejunum (small bowel only; mainly jejunum); lymphocytes in lamina propria (c) neoplasm esp lymphoma (d) tissue transflutaminase |
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Tropical sprue
(a) etiology (b) pathology |
(a) unknown; prob infectious (resopnds to antibiotics)
(b) smilar to celiac but can affect whole bowel |
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Whipple's disease
(a) etiology (b) pathology (c) symptoms (d) epidemiology |
(a) infx w/Tropheryma whippelii (G+ bacilli)
(b) PAS positive macs in lamina propria, mesenteric nodes (c) malabsorption, arthralgias, cardiac and neuro sx (d) older men |
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Disaccharidase deficiency
(a) most common (b) path (c) symptoms (d) etiology |
(a) lactase deficiency
(b) normal appearing villi (c) osmotic diarrhea (d) can be self limited if following villi injury (viral diarrhea) |
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Pancreatic insufficiency
(a) etiologies (b) effect |
(a) CF, obstructing cancer, chronic pancreatitis
(b) malabsorption of fat and fatsoluble vitamins |
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Dermititis herpetiformis (associated with what GI disease)?
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Celiac sprue
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Acute gastritis
(a) describe (b) etiologies (c) symptoms |
(a) disruption of mucosal barrier; inflammation
(b) stress, NSAIDs, uremia, alcohol, burns, brain injury |
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Cushing's ulcers
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Caused by CNS trauma (incr vagal stimulation, incr Ach, incr acid)
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Curling's ulcer
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Caused by burns (incr plasma volume, sloughing of fastric mucosa)
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Chronic gastritis Type A
(a) location (b) associations |
(a) fundus/body of stomach
(b) autoimmune disorder characterized by autoabs to parietal cells, pernicious anemia, or achlorhydria |
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Chronic gastritis Type B
(a) location (b) etiology (c) incr risk for? |
(a) antrum
(b) H pylori (c) incr risk of MALTomas |
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Menetrier's disease
(a) describe (b) sx (c) incr risk for? (d) pathology |
(a) gastric hypertrophy
(b) protein loss, incr mucous cells (c) precancerous (d) rugae so hypertrophied they look like gyri |
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Stomach cancer
(a) type (b) behavior (c) risk factors (d) histology (e) presentation |
(a) almost always adenocarcinoma
(b) aggressive; spread to LN/Liver (c) nitroasmines (smoked foods), pernicious anemia/achlorhydria, type A blood, chronic gastritis, genetic predisposition (d) 50% in antrum and pylorus; (e) usually asymptomatic until late; mayy have acanthosis nigricans; Virchow's node |
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Virchow's node
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Involvement of left supraclavicular node by mets from stomach (most common site of met)
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Linitis plastica
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Infiltrating gastric carcinoma (fibrous response)
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Krukenberg's tumor
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Bilateral mets to ovaries (abundent signet rings)
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Gastric ulcer
(a) symptoms (b) epidemiology (c) etiologies (d) risk for future malignancy |
(a) epigastric pain can be greater w/meals (wt loss)
(b) often in older pts (c) H pylori infx in 70%; chronic NSAIDs also implicated; due to decr mucosal protection against gastric acid (d) rarely do become malignant |
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Duodenal ulcer
(a) etiology/sx (b) associations (c) appearance (d) complications |
(a) incr acid secretion or decr protection; pain decr w/meals-wt gain
(b) 100% have H pylori infx (c) clean, "punched out" margins; hypertrophy of Brunner's glands (d) bleeding, penetration into pancreas, perforation, obstruction (not intrinsically cancerous) |
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Pyloric stenosis
(a) describe (b) classic case (c) treatment |
(a) congenital hypertrophy of pyloric muscle
(b) firstborn boy, projectile vomiting 3-4wks after birth; assoc w/olive mass in epigastric region (c) surgical |
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Ischemic bowel disease
(a) etiology/most common artery (b) epidemiology (c) symptoms |
(a) thrombosis/embolism of SMA (50%); venous thrombosis for 25%; commonly occurs at splenic flexture
(b) >60YO (c) abdominal pain, n/v |
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Duodenal atresia
(a) describe (b) presentation (c) associations |
(a) congenital absence of region of bowel
(b) polyhydramnios, obstruction, bile stained vomiting in neonate; "double bubble" due to failure of recanalization (c) down's syndrome |
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Intussusception
(a) epidemiology (b) cause (c) complications |
(a) usually infants
(b) telescoping of 1 bowel segment into distal segment;; often due to mass (c) can compromise blood supply |
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Volvulus
(a) describe (b) complications (c) common location (d) peak age |
(a) twisting of bnowel around it's mesentery
(b) obstruction, infarction (c) sigmoid colon common; redundant mesentery (d) elderly |
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GI lymphoma
(a) most common type (b) at risk population? |
(a) usually NHL, large cell, diffuse
(b) immunosuppressed |
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MALToma
(a) histo (b) outcome (c) associations? (d) treatment |
(a) often follicular
(b) follow a more benign course than other GI lymphomas (c) h pylori (d) may regress after Ab therapy |
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Appendicitis
(a) epidemiology (b) presentation (c) complications (d) differential |
(a) all age groups
(b) diffuse periumbilical pain; n/v/f (c) perforation (peritonitis) (d) diverticulitis (elderly), ectopic pregnancy (use beta hCG to rule out) |
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Chron's disease
(a) possible etiology (b) distribution (c) gross morphology (d) microscopic morphology (e) complications (f) intestinal manifestation (g) extraintestinal manifestation (h) genetic history (i) cancer risk |
Chron's disease
(a) possible etiology: postinfectious (b) distribution: anywhere in Gi; typically terminal ileum; skip lesions common (c) gross morphology; transmural inflammation; creeping fat, "string sign" on barium swallow; cobblestone (d) microscopic morphology: noncaseating granulmonas and lymphoid aggregates (e) complications: linear ulcers, strictures, fistulas, perianal dz, malabsorption, nutritional depletion (f) intestinal manifestation; diarrhea that may or may not be bloody (g) extraintestinal manifestation: immunologic disorders, migratory polyarthritis, erythema nodosum; ankylosing spondylitis; uveitis; immunological disorders (h) genetic history; fam hx of any type of IBD assoc w/incr risk (i) cancer risk: slight |
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Ulcerative colitis
Chron's disease (a) possible etiology (b) distribution (c) gross morphology (d) microscopic morphology (e) complications (f) intestinal manifestation (g) extraintestinal manifestation (h) genetic history (i) cancer risk |
Ulcerative colitis
(a) possible etiology: autoimmune (b) distribution: continuous always w/rectal involvement (c) gross morphology: mucosal/submucosal inflammation onlyl pseudopolyps; "lead pipe" appearance on imaging (d) microscopic morphology: crypt abscesses and ulcers, bleeding (e) complications; severe stenosis, toxic megacolon, colorectal carcinoma (f) intestinal manifestation; bloody diarrhea (g) extraintestinal manifestation; pyoderma gangrenosum, primary sclerosing cholangitis (h) genetic history; fam hx of any type of IBD incr risk (i) cancer risk; 5-25% |
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Treatment for Chron's
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Corticosteroids, infliximab
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Treatment for UC
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Sulfasalazine, inflixamab, colectomy
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Diverticulum
(a) describe (b) most common location |
(a) blind pouch popping out of alimentary tract communicates w/lumen of gut; most acquired
(b) sigmoid colon |
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True diverticulum
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All 3 gut layers outpouch
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False diverticulum
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Only mucosa and submucosa outpouch; usually acquired. Occur esp where vasa recta perforate muscularis externa
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Diverticulosis
(a) describe (b) cause (c) associated with? (d) common location (e) epidemiology/presentation |
(a) many diverticula
(b) incr intraluminal pressure w/focal weakness in wall (c) low fiber diet (d) sigmoid colon (e) ~50% >60YO; usually asymptomatic or vague disconfort and/or painless rectal bleeding |
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Diverticulitis
(a) describe (b) presentation (c) complications (d) treatment |
(a) inflammation of diverticula
(b) LLQ pain, fever, leukocytosis (c) perforation (peritonitis, abscess, bowel stenosis; fsitula w/bladder) (d) antibiotics |
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Meckel's diverticulum
(a) cause (b) complication (c) five 2's |
(a) persistance of vitelline duct or yolk stalk; most common congenital anomaly of GI tract
(b) may contain ectopic acid secreting gastric mucosa; can cause bleedingk, instussusception, volvulus, obstruction near terminal ileum (c) 2in; 2ft from ileocoecal valve; 2% of population; commonly prsents in first 2yr of life; may have 2 types of epithlia (gastric/panc) |
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Hirschprung's disease
(a) etiology (b) presentation (c) risk incr w/what genetic condition? |
(a) congenital megacolon; failure of neural crest cell migration (lack of both plexi)
(b) chronic constipation early; usually failure to pass meconium (c) risk incr w/Down syndrome |
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Meconium ileus
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Meconium plug obstructs intestine preventing stool passage at birth; CF
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Necrotizing enterocolitis
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Necrosis of intestinal mucosa and possible perforation; neonates; can involve entire Gi
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Intestinal adhesion
(a) describe (b) cause |
(a) acute bowel obstruction; have well demarcated necrotic zones
(b) commonly from recent surgery |
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Angiodysplasia
(a) describe (b) location (c) epidemiology/presentation |
(a) tortuous dilation of vessels leading to bleeding
(b) usually cecum and asc colon (c) older patients/lowe rintestinal bleeding |
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Imperforate anus
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Failure of perforation of the membrane that separates endodermal hindgut from ectodermal anal dimple
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Majority of colonic polyps; usually location
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90% benign hyperplastic hamartomas; often rectosigmoid
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Significance of villous morphology of polyp
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More likely to be malignant
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Tubular adenoma
(a) gross (b) epidemiology |
(a) pedunculated; 75% of adenomatous polyps
(b) sporadic or familial; avg age of onset 60; usually in left colon |
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Villous adenoma
(a) gross (b) risk of malignancy |
(a) largest, least common; usually sessile
(b) 1/3 cancerous |
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Peutz Jehger's syndrome
(a) inheritence (b) presentation (c) incr risk of? |
(a) audosomal dominant benign polyposis syndrome
(b) hamartomatous polyps in colon and small intestine; hyperpigmented buccal mucosa, lips, hands, genitalia (c) incr risk of CRC and other visceral malignancies |
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Turcot syndrome
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Colonic polyps assoc w/brain tumors
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Gardner Syndrome
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Colon polyps assoc w/desmoid tumors risk of colon cancer nearly 100%
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Difference in left sided vs right sided colorectal cancer?
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Left (obstruction
Right (bleed) |
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Risk factors for colorectal cancer
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Villous adenomas
Chronic IBD (espUC) Incr age FAP HNPCC Past medical Hx or Fam Hx |
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Tumor marker for CRC
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CEA
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Majority of CRC (type)
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Adenocarcinoma (98%)
Squamous in anal region and assoc w/papilloma viruses |
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Family Adenomatous polyposis
(a) inheritence (b) gene/chromosome (c) presentation (d) risk for cancer |
(a) AD
(b) APC c5q (c) thousands of polyps; pancolonic; always involve rectum (d) virtually 100% |
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HNPCC/Lynch syndrome
(a) mutation (b) site of Gi tract involvement (c) risk for cancer |
(a) DNA mismatch repair genes
(b) proximal colon always involved (c) 80% |
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Carcinoid tumor
(a) most common site (b) EM (c) classic symptoms |
(a) small intestinal tumor of endocrine cells
(b) dense core bodies (c) wheezing; right sided heart murmurs; diarrhea; flushing (due to serotonin) Only if met outside of GI due to serotonin inactivation by liver 1st pass metabolism |
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Micronodular cirrhosis most often due to?
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Metabolic insult (alcohol, hemochromatosis, wilson's)
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Macronodular (>3cm) cirrhosis most often to? Incr risk for?
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Significant liver injury leading to hepatic necrosis (post infection, drug induced).
Incr risk for HCC |
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Major diagnostic use of aminotransferases (AST/ALT)?
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Viral hepatitis (ALT>AST)
Alcoholic hepatitis (AST>ALT) MI (AST) |
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Major diagnostic use of GGT (gamma glutamyl transpeptidase)
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Various liver diseases (incr w/heavy alcohol consumption)
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Major diagnostic use of alkaline phosphatase
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Obstructive liver disease (HCC)
Bone disease Bile duct disease |
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Major diagnostic use of amylase
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Acute pancreatitis, mumps
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Major diagnostic use of lipase
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Actue pancreatitis
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Major diagnostic use of ceruplasmin
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Wilson's disease (decr)
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Reye's syndrome
(a) epidemiology (b) findings (c) etiology |
(a) fatal childhood hepatoencephalopathy
(b) fatty liver (microvescicular change); hypoglycemia; coma (c) assoc w/viral infx (esp VZV influenza B) treated w/salicylates |
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3 major stages of alcoholic liver disease
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Hepatic steatosis
Alcoholic hepatitis Alcoholic cirrhosis |
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Hepatic steatosis
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Short term change assoc w/minor alcohol intake; macrovesicular fatty change
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Alcholic hepatitis histology
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Sustained long term consumption
Swollen necrotic hepatocytes w/neutrophilic infiltration Mallory bodies present AST>ALT (>1,5) |
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Alcoholic cirhossis
(a) appearance (b) location of damage (b) symptoms |
(a) micronodular, irregularly shrunken liver w/hobnail appearance
(b) sclerosis around central vein (Zone III) (c) manifestations of chronic liver disease |
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Leading etiologies of cirrhosis
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hepC and alcohoism
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Leading causes of intrahepatic portal HTN
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Most common cause usually secondary to cirrhosis; also schistosomiasis; sarcoid
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Leading causes posthepatic portal HTN
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Right sided heart failure, Budd Chiari syndrome
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Leading cause of prehepatic portal HTN
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Portal vein obstruction
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Clinical manifestations of portal HTN
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Ascites
Varices (hrmorrhoids, esophageal, caput medusae) Encephalopathy Splenomegaly Gynecomastia (impaired estrogen metabolism) Gonadal atrophy Amenorrhea Spider angiomata Palmar erythema Atelectasis |
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Nutmeg liver
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Backup of blood into liver; usually right sided heart failure or Budd chiari
Mottled like nutmeg Centrolobular congestion and necrosis can result in cardiac cirrhosis |
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Primary Sclerosing cholangitis
(a) presentation (b) associated w? (c) predisposition for? (d) imaging appearance (e) diagnosis (LFT) |
Concentric "onion skin" bile duct fibrosis
(a) chronic fibrosing inflammatory disease of extrahepatic and larger intrahepatic bile ducts (b) IBD (c) predisposition for cholangiocarcinoma; can lead to secondary biliary cirrhosis (d) "beading" on ERCP; alternating strictures and dilation (e) incr ALP |
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Budd chiari syndrome
(a) describe (b) presentation (c) associated with? |
(a) occlusion of IVC or hepatic veins w/centrilobular congestion and necrosis leading to congestive liver disease
(b) HSM, ascites, abd pain, liver failure; NO JVD! (c) pvera-pregnancy-HCC |
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Hepatocellular jaundice
(a) composition of hyperbilirubinemia (b) urine bilirubin (c) urine urobilinogen |
(a) composition of hyperbilirubinemia: conjugated/unconjugated
(b) urine bilirubin: high (c) urine urobilinogen: normal or low |
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Obstructive jaundice
(a) composition of hyperbilirubinemia (b) urine bilirubin (c) urine urobilinogen |
(a) composition of hyperbilirubinemia: conjugated
(b) urine bilirubin: incr (c) urine urobilinogen: decr |
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Hemolytic jaundice
(a) composition of hyperbilirubinemia (b) urine bilirubin (c) urine urobilinogen |
(a) composition of hyperbilirubinemia: unconjugated
(b) urine bilirubin: absent (no color) (c) urine urobilinogen: incr |
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Hemochromatosis
(a) classic triad; other sx (b) cause (c) blood chemistry (ferritin, iron, TIBC, transferrin) (d) MHC association (e) treatment |
Hemosiderin/iron deposition in tissues
(a) triad: cirrhosis, diabetes mellitus, skin pigmentation CHF, incr risk of HCC, arrythmias, gonadal insuff, arthropathy (b) primary (autosomal recessive) or due to multiple blood transfusions (c) incr ferritin, incr iron, decr TIBC, incr transferrin sat (d) HLA A3 (e) repeated phlebotomy, deferoxime |
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Wilson's disease
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AR inherited disease; inability to excrete copper and failure of copper to enter circulation as ceruloplasmin (copper accumulation)
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Wilson's disease presentation
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Rarely before 6
Asterixis Basal ganglia defeneration (Parkinsonism) Ceruploplasmin low, cirrhosis, corneal deposits, copper accumulation, carcinoma, choreiform movements Dementia Hemolytic anemia Weakness, fevers, angiomas, eventually portal HTN |
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Labs for wilson's disease
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Low serum ceruloplasmin, incr urinary copper excretion
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Liver cell adenoma
(a) incr risk w? |
Benign mass
May rupture Incr risk with anabolic steroid/oral contraceptive use |
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Nodular hyperplasia
(a) appearance (b) histology |
(a) solitary nodule w/fibrous capsule and bile ductules
(b) stellate fibrous core present; nodular regenerative hyperplasia (normal hepatocytes w/loss of architecture) |
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Cholangiocarcinoma
(a) associations? (b) clinical (c) spread |
(a) assoc w/primary sclerosing cholangitis
(b) wt loss, jaundice, pruritis (c) metastatsize via hematogenous/lymphatic spread |
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Hepatoblastoma
(a) epidemiology (b) presentation |
(a) rare, malignant neoplasm of children
(b) hepatomegaly, n/v/d, wt loss, elevated AFP |
|
Hepatocellular carcinoma
(a) epidemiology (b) associations (c) clinical (d) markers |
(a) 90% of primary liver neoplasms
(b) cirrhosis, HCV, HBV (c) tender hepatomegaly, ascites, wt loss, fever, polycythemia, hypoglycemia (d) AFP present in 50-90% of cases |
|
Acute viral hepatitis
(a) clinical (b) labs |
(a) malaise, anorexia, fever, nausea, upper abd pain, hepatomegaly
(b) elevated liver enzymes |
|
Chronic hepatitis
(a) etiologies (b) histology |
(a) HBV, HCV, drug toxicity, Wilson's, alcohol, alpha 1 antitrypsin deficiency, autoimmune hep (b) chronic inflammation w/hepatocyte destruction, cirrhosis, liver failure
|
|
Fulminant hep
(a) presentation (b) etiology (c) pathology |
(a) massive hepatic necrosis and progressive hepatic dysfct
(b) HBV, HCV, HDV, HEV, chloroform, carbon tetrachloride, certain mushrooms, aceaminophen overdose (c) progressive shrinkage of liver |
|
Pyogenic liver abscesses (main cause and route of infx)
|
E coli
Klebs Strep Staph Ascending cholangitis most common cause |
|
Parasitic liver abscesses (presentation)
|
Entamoeba (thick, brown abscess fluid)
Ascaris lumbricoides (can block bile ducts, eosinophilia, verminous abscesses) |
|
Parasitic infx
|
Schistosomiasis; splenomegaly, portal HTN, ascites
Amebias; Entamoeba histolytica, bloody diarrhea, pain, fever, jaundice, hepatomegaly |
|
Extrahepatic biliary atresia
(a) etiology (b) presentation |
(a) incomplete recanalization
(b) within first weekso f life: jaundice, dark urine, light stools, HSM |
|
Intrahepatic biliary atresia
(a) etiology (b) association (c) presentation |
(a) diminished number of bile ducts
(b) sometimes assoc w/alpha 1 antitrypsin def (c) infancy; cholestasis, pruritis, growth retardation, incr serum lipids, icterus |
|
Gilbert's syndrome
(a) labs (b) clinical presentation (c) precipitating factor |
(a) elevated unconjugated bilirubin w/out overt hemolysis; decr UDP glucuronyl transferase or decr bilirubin uptake
(b) asymptomatic (c) stress |
|
Crigler Najjar syndrome type I
(a) cause (b) presentation (c) treatment |
(a) AR; completely absence of glucuronyl transferase
(b) present early; incr unconjugated bilirubin; kernicterus (brain deposition), jaundice (c) plasmapheresis and phototherapy; death within a few years |
|
Crigler Najjar syndrome type II
(a) cause (b) presentation (c) treatment |
(a) AD w/mild deficiency of glucuronyl transferase
(b) no kerniecterus but incr unconjugated bilirubin (c) phenobarbital (incr liver enzyme synth) |
|
Dubin Johnson Syndrome
(a) cause (b) presentation |
(a) defective liver excretion of biirubin due to impaired transport
(b) liver is black; benign |
|
Rotor's syndrome
|
Asymptomatic similar to Dubin Johnson but no pigmented liver
|
|
Problem/result
(a) Gilbert's (b) Crigler Najjar (c) dubin johnson |
(a) Gilbert's: impaired bilirubin uptake; increased unconjugated bilirubin
(b) Crigler Najjar: problem with bilirubin conjugation; increased unconjugated bilirubinemia (c) dubin johnson; problem with excretion of conjugated bilirubin; incr conjugated bilirubinemia |
|
Cholestasis
(a) general presentation (b) intrahepatic causes (c) extrahepatic causes |
(a) impaired excretion of bilirubin; chalky stool
(b) viral hep, cirrhosis, drug tox (c) gallstones, carcinoma of bile duct, ampulla of vater or head of pancreas |
|
Primary biliary sclerosis
(a) describe (b) presentation (c) serum markers (d) associations |
(a) intrahepatic autoimmune disorder
(b) severe obstructive jaundice; steatorrhea, pruritis, hypercholesterolemia (xanthoma); fatigue and pruritis (c) incr ALP, incr AMA (d) scleroderma, CREST |
|
Secondary biliary sclerosis
(a) cause/presentation (b) complications (c) serum markers |
(a) extrahepatic biliary obstruction; incr pressure in intrahepatic ducts causing injury/fibrosis; often presents w/jaundice
(b) ascending cholangitis, bile, stasis (c) incr ALP, incr conjugated bilirubin |
|
General cause of gallstones
|
Solubilizing bile acids and lecithin are overwhelmed by incr cholesterol and/or bilirubin
|
|
2 types of stones
|
Cholesterol
Pigmented |
|
Cholesterol stones
(a) appearance on imaging (b) risk factors |
(a) radiolucent w/calcifications-accounts for 80% of stones
(b) obesity, chron's, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, native american origin |
|
Pigment stones
(a) appearance on imaging (b) cause |
(a) radioopaque
(b) chronic RBC hemolysis, alcoholic cirrhosis, advanced age, biliary infx |
|
Complications of gallstones
|
Ascending cholangitis, acute pancreatitis, bile stasis, cholecystitis, biliary colic, fistula b/w GB abd small intestine
|
|
Biliary colic
|
Gallstones interfere with bile flow causing bile duct contraction
|
|
Charcot's traid of cholangitis
|
Jaundice, fever, RUQ pain
|
|
If gallstone obstructs ileocecal valve, what can be seen on imaging?
|
Air
|
|
Diagnosis of gallstones?
|
Ultrasound
|
|
Treatment of gallstones
|
Cholecystectomy
|
|
Cholelithiasis in a young person; think?
|
Hereditary spherocytosis, sickle cell, or other chronic hemolytic process
|
|
Carcinoma of gallbladder
(a) symptoms/epidemiology (b) pathology (c) prognosis (d) risk factors |
(a) primarily in elderly; dull abdominal pain, mass, wt loss, anorexia (present late)
(b) typically involves fundus and neck; 90% adenocarcinomas (c) poor (d) cholelithiasis, cholecystitis, porcelain gallbladder |
|
Carcinoma of bile ducts (cholangiocarcinoma)
(a) associated with gallstones? (b) epidemiology (c) symptoms (d) risk factors |
(a) no
(b) M>F; elderly more frequent (c) obstructive jaundice (d) chronic inflammation, infections, ulcerative cholitis |
|
Define acute pancreatitis
|
Autodigestion of pancreas by enzymes
|
|
Causes of acute pancreatitis
|
Gallstones, ethanol, trauma, steroids, mumps, autoimmune disease/biliary tract diseases, scorpion sting, hypercalcemia/hyperlipidemia, drugs (sulfas)
|
|
Clinical presentation of acute pancreatitis
|
Epigastric abdominal pain radiating to back, anorexia, nausea,
|
|
Labs in acute pancreatitis
|
Elevated amylase, lipase (higher specificity), leukocytosis
|
|
Complications of acute pancreatitis
|
DIC
ARDS (pancreatic enzymes on lung tissue) Diffuse fat necrosis Hypocalcemia (Ca collects in pancreatic calcium soap deposits) Pseudocyst formation Hemorrhage Infection |
|
Gross description of acute pancreatitis
|
Gray areas of destruction, white areas of fat necrosis, red areas of hemorrhage
|
|
Chronic pancreatitis complications/presentation
|
Repeated episodes of mild pancreatitis can lead to damage; may lead to pancreatic insufficiency (steatorrhea, fat soluble vitamin deficiency, DM, pseudocyst formation)
|
|
Pancreatic pseudocyst
|
Possible sequelae of pancreatitis or trauma; fibrous capsule; no epithelial lining or direct communication with ducts
|
|
Cystic fibrosis
(a) inheritance (b) gene defect (c) presentation (d) outcome |
(a) AR
(b) CFTR chloride transport defective; thick mucus secretion and high sodium and chloride levels in sweat (c) present with meconium ileus, steatorrhea, pulmonary infx (usually pseudomonas) (d) mean survivial 20YO; usually due to pulmonary infx |
|
Pancreatic adenocarcinoma: risk factors
|
Smoking, high fat diet, chemical exposure
|
|
Presentation of pancreatic adenocarcinoma
|
(1) abdominal pain radiating to back
(2) wt loss due to malabsorption and anorexia (3) migratory thrombophlebitis (redness and tenderness on palpation of extremities-Trousseau's syndrome) (4) obstructive jaundice w/palpable gallbladder (Courcoisier's sign) |
|
Tumor markers for pancreatic adenocarcinoma
|
CEA and CA199
|
|
Most common place for pancreatic adenocarcinoma
|
Pancreatic head (may compress bile duct and cause obstructive jaundice)
|
|
Dysentery; poultry/domestic animals, water
MCC/pathogenesis/treatment |
-Campy/invades epithelium/only treat severe cases (erythromycin)
-Salmonella/penetrates lamina propria causing PMN response and prostaglanding synthe which stim cAMP/severe cases only |
|
Dysentery: no animal reservoir; fecal/oral transmission; musocal ulcerations
MCC/treatment |
Shigella/fluoros TMPSMX for severe cases
|
|
Dysentery: pseudoappendicitis; arthritis; milk/domestic animals/fecal oral
|
Yersinia, heat stable enterotoxin; treat only severe cases (aminoglycosides, TMPSMX)
|
|
Dysentery: antibiotic use: MCC/treatment
|
C diff, metronidazole
|
|
Dysentery: food/water, fecal oral (G- rod, lactose fermenter
|
E coli
|
|
Dysentery; flask like lesions, extraintestinal abscesses (liver): MCC/treatment
|
Entameoba histolytica (mebendizol)
|
|
Watery diarrhea: day care, water, fecal oral, microvilli blunted: mCC/treatment
|
Rotavirus/supportive
|
|
Watery diarrhea: older kids/adults; blunting of microvilli
|
Norwalk virus/supportive
|
|
Watery diarrhea: nosocomial (young kids, IC)
|
Adenovirus 40/41
|
|
Watery diarrhea: rice water stools: MCC, treatment
|
Vibrio cholerae; oral rehydration, tetracycline shortens symptoms
|
|
Watery diarrhea: raw or undercooked fish
|
Vibrio parahaeomolyticus (treatment not indicated)
|
|
Watery diarrhea: undercooked fruits/veggies
|
ETEC
|
|
Watery diarrhea, children, AIDS
|
Crypsosporidium (intracellular brush border)
|
|
Watery diarrhea: day care, camping, beavers, dogs
|
Giardia (metronidazole)
|
|
Diarrhea: ham, potato salad, cream pastries: MCC, pathogenesis
Diarrhea and vomiting |
Staph aureus
Heat stabile enterotoxin in food Recovery without treatment |
|
Vomiting followed by diarrhea: fried rice
|
B cereus
Recovery without treatment |
|
Cimetidine
(a) mechanism (b) clinical use (c) toxicity |
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux (c) Potently inhibits P450 Antiandrogen effects (prolactin release, gynocomastia, impotence, decr libido in males) Decr renal excretion of creatinine Can cross BBB (confusion, dizziness, HA) |
|
Ranitidine
(a) mechanism (b) clinical use (c) toxicity |
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux (c) decr renal excretion of creatinine |
|
Famotidine
(a) mechanism (b) clinical use |
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux |
|
Nizatidine
(a) mechanism (b) clinical use |
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux |
|
Omeprazole, Lansoprazole
(a) mnechanism (b) clinical use |
(a) irreversibly inhibit H/K ATPase in stomach parietal cells
(b) Peptic ulcer, gastritis, esophageal reflux, ZE syndrome |
|
Bismuth, sucralfate
(a) mechanism (b) clinical use |
(a) bind ulcer base providing physical protection, allow HCo3- secretion to reestablish pH gradient in mucous layer
(b) incr ulcer healing, traveler's diarrhea |
|
Misoprostol
(a) mechanism (b) clinical use (c) toxicity |
(a) PGE1 analogue. Incr production and secretion of gastric mucous barrier; decr acid production
(b) prevention of NSAID induced peptic ulcers; maintenance of patent ductus arteriosus; also used to induce labor (c) diarrhea; contraindicated in childbearing potential (abrotifacient) |
|
Triple therapy of H pylori
|
Metronidazole
Amoxicillin Bismuth |
|
Pirenzepine
(a) mechanism (b) clinical use (c) toxicity |
(a) block M1 receptors on ECL1 cells (decr histamine secretion) and M3 receptors on parietal cells (decr H+ secretion)
(b) peptic ulcer (rarely used) (c) tachycardia, dry mouth, difficulty focusing eyes |
|
Propantheline
(a) mechanism (b) clinical use (c) toxicity |
(a) block M1 receptors on ECL1 cells (decr histamine secretion) and M3 receptors on parietal cells (decr H+ secretion)
(b) peptic ulcer (rarely used) (c) tachycardia, dry mouth, difficulty focusing eyes |
|
Major antacids
|
Aluminum hydroxide
Magnesium hydroxide Calcium carbonate |
|
Overuse of aluminum hydroxide side effects:
|
Constipation and hypophopshatemia
Proximal muscle weakness Osteodystrophy Seizures |
|
Overuse of magnesium hydroxide side effects:
|
Diarrhea
Hyporeflexia Hypotension Cardiac arrest |
|
Overuse of calcium carbonate side effects:
|
Hypercalcemia, rebound acid incr
|
|
Infliximab
(a) mechanism (b) clinical use (c) toxicity |
(a) a monoclonal antibody to TNF, proinflammatory cytokine
(b) chronic's disease, rheumatoid arthritis (c) respiratory infection (incl reactivation of latent TB), fever, hypotension |
|
Sulfazalazine
(a) mechanism (b) clinical use (c) toxicity |
(a) a combo of sulfapyridine (antibacterial) and mesalaine (anti inflammatory); activated by colonic bacteria
(b) ulcerative colitis; Chron's disease (c) malaise, nausea, sulfonamide toxicity, reversbile oligospermia |
|
Ondansetron
(a) mechanism (b) clinical use (c) toxicity |
(a) 5-HT3 antagonist; powerful central acting antiemetic
(b) control of vomiting postop and in patients undergoing cancer chemotherapy |
|
Metoclopramide
(a) mechanism (b) clinical use (c) toxicity |
(a) D2 receptor antagonist. Incr resting tone, contractility, LES tone; does not influence colon transport time.
(b) diabetic and post surgery gastroparesis (c) incr parkinsonian effects; drug interaction w/digoxin and diabetic agents; contraindicated in patients with small bowel obstruction |