GI Medicine

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define odynophagia: painful swallowing
causes of esophageal chest pain: GER, dysmotility, increased visceral sensitivity
define dysphagia: difficulty swallowing, food sticking
what causes oropharyngeal dysphagia?: inability to protect nasopharynx or larynx during swallowing
what are symptoms of OP?: nasal regurgitation, coughing, aspiration
liquids or solids cuasing more problems in OP?: liquids
OP most commonly associated with which types of conditions?: cerebral or brainstem conditions (swallowing center), probs with striated muscle, imparment of UES opening
dysphagia for liquids alone suggests:: OP
dysphagia for solids alone suggests:: structural abnormality
dysphagia for solids and liquids suggests:: motility disorder
long history of intermittent dysphagia for solids suggests:: structural abnormality
worsening of solid food dysphagia suggests:: progressive narrowing due to stricture
significant weight loss in dysphagic patients over 50 suggests:: esophageal adenocarcinoma
significant weight loss in dysphagic childred suggests:: achalasia
combination of chest pain and dysphagia suggests:: diffuse esophageal spasm
raynaud's phenomenon and dysphagia suggests:: scleroderma
confirm esophageal motility disorder with: manometry
define reflux esophagitis: macroscopic damage to the esophagus visible at endoscopy as erosions or ulcerations
causes of GERD: abnormal LES (hypotonic LES, transient LES relaxations), hiatal hernia, defect in esophageal clearance mechanisms
atypical reflux symptoms: asthma, laryngitis, chronic cough, chest pain
Diagnostic tests for GERD: upper endoscopy, ambulatory pH monitoring
complications from GERD: stricture, Barrett's, ulcer
where do strictures tend to occur?: distal esophagus (greatest acid concentration)
what is barrett's esophagus?: when metaplastic columnar epithelium replaces normal squamous epithelium in distal esophagus
what does barrett's look like?: orange-red epithelium (vs. white/yellow for nl)
How do you confirm a dx of Barrett's?: mucus biopsies
What type of monitoring should you do for patients with Barrett's?: endoscopy/biopsy every 3 years
What to do if patient is unresponsive to GERD medical treatment?: laproscopic gastric fundoplication
List structural lesions of the esophagus: esophageal cancer, strictures, webs/rings, zenker's diverticulum
difference between a web and a ring?: ring is circumferential ring at squamocolumnar junction, web is semilunar and in mid to upper esophagus
what is a Zenker's diverticulum?: protrusion of the pharyngeal mucosa at pharyngoesophageal jxn through UES
how do you treat Zenkers Diverticulum?: surgical resection
Causes of esophagitis not due to GER (3): pill induced, caustic injury, infectious esophagitis (in immcomp: candida, HSV, CMV)
List esophageal motility disorders (3): Achalasia, Diffuse Esophageal Spasm, scleroderma esophagus
Pathophysio of Achalasia: denervation of esophagus from loss of ganglion cells in Auerbach's plexus, lose peristalsis in smooth muscle and impaired LES relaxation
Clinical findings in achalasia?: gradual onset of dysphagia for solid and liquid, regurgitation and vomiting
typical radiographic hallmark of Achalasia?: bird's beak
what is pseudo-achalasia?: a cancer that might resemble achalasia
clinical findings in Diffuse Esophageal Spasm?: intermittent, non-progressive dysphagia for solids and liquids, chest pain
pathophysio of scleroderma esophagus: atrophy and fibrosis of esophageal smooth muscle, hypotonic LES, severe reflux
Esophageal location of esophageal squamous cell carcinoma: throughout esophagus
esophageal location of esophageal adenocarcinoma: lower 1/3 of esophagus
symptoms of esophageal carcinoma: progressive solid food dysphagia, hoarseness, weight loss
list 5 causes of Dyspepsia: PUD, GERD, gastric cancer, non-ulcer dyspepsia, meds
what types of meds cause dyspepsia?: alcohol, caffeine, iron, NSAIDS, antibiotics
which symptoms suggest peptic ulcers?: pain between meals or at night and releived by food or antacids
four sources of afferent input into vomiting center: Vagal/splanchnic from GI (visceral distention, peritonitis), vestibular system, higher CNS, CTZ
where is the CTZ?: fourth ventricle
what stimulates the CTZ?: drugs, chemotherapeutics, toxins
some CNS related causes of vomiting: Increased ICP, Vestibular disorders, infections (encephalitis, meningitis)
Define gastroparesis: decreased gastric motility
define Ileus: decreased intestinal motility
causes of peritoneal irritation (4): cholecystitis, acute pancreatitis, appendicitis, perforations
what is the common cause of acute vomiting without abdominal pain?: food poisoning, infectious gastroenteritis, drugs
acute onset of vomiting with severe pain suggests:: intestinal obstruction or peritonitis
chronic or recurrent vomiting suggests: obstruction of pylorus or small intestine, gastroparesis, or CNS and systemic disorders
define hematemesis: bright red emesis
define melena: jet black tarry fould smelling stool
define hematochezia: bright red bloody bowel movements
list 4 causes of UGI bleeding: PUD, portal hypertension, gastric neoplasms, and erosive gastritis, Mallory Weiss tears
Is initial hematocrit a good indicator of acute blood loss?: not really, takes 24-72 hrs for equilibration
how much does one unit of blood raise hct?: 3-4%
define erosions: single or multiple, small (<3mm) white linear breaks that donâ€™t extend through the muscularis mucosa
define ulcers: mucosal breaks with obvous depth, white base, larger in size
most common sites of ulcers: duodenal bulb and gastric antrum
Causes of PUD: Hp, NSAIDs, Gastrinoma
How does Hp protect itself?: burrows into mucus layer by epithelial cells (pH 7) and uses urease to generate ammonia
how does Hp cause disease?: suppression of somatostatin
Mechanisms of NSAID induced injury: topical damage, PG inhibition thus loss of mucosal defense mechanisms, platelet inhibition so easier to bleed
clinical findings in peptic ulcer disease: dyspepsia
complications from PUD: penetration or perforation, extensive bleeding, edema/scarring leading to obstruction
Who gets stress gastritis?: ICU patients: severe burns/trauma/sepsis etc
Causes of gastroparesis (3): neuropathic (enteric or extrinsic nerves), myopathic process (involving gastric smooth muscle), post-surgical probs (vagotomy, gastric resection)
symptoms of gastroparesis: nausea, vomiting, early satiety, bloating
when does vomiting occur with gastroparesis?: after a meal
definition of constipation: two or less bowel movements per week or excessive difficulty or straining on defacation
which pelvic floor muscles are responsible for continence?: pubococcygeus and puborectalis
common causes of constipation: poor dietary (to little fiber/fluids) or toilet habits, structural abnormalities (malignancy), systemic disease (myopathy, neuropathy, endocrine disorder, lyte imbalance, medication use)
first line treatment for constipation?: dietary fiber supplement
constipation lab tests available?: colonic transit study, defecography, anal manemtry
Major causes of lower GI bleeding (6): diverticulosis, vascular ectasias, neoplasms, IBD, ischemic colitis, anorectal disease
describe lesions from Vascular Ectasias: small, multiple, painless, red flat submucosal blotch of vessels, looks like a fern
first thing to do w/ patient with acute GI bleed?: assess volume status and rescucitate if necessary
which acute GI bleed patients get colonoscopy?: anyone who is hospitalized due to bleeding
evaluation tests for acute GI bleed?: anoscopy, sigmoidoscopy, colonoscopy, angiography, nuclear bleeding scan (99Tc RBC scan)
what is damaged in Celiac Sprue?: diffuse damage to proximal small intestinal mucosa = malabsorption
which genes are associated with celiac sprue?: HLA-DQ2 and HLA-DQ8
describe celiac sprue pathogenesis:: gluten sensitive T cells respond, Th1 reaction leading to inflammation and damage of intestinal mucosa
what 3 nutrients are absorbed in the proximal small intestine?: calcium, iron, folate
impaired calcium absorption leads to:: osteoporosis
impaired iron absorption leads to:: iron deficiency anemia
impaired folate absorption leads to:: megaloblastic anemia
Sprue in jejunum and ileum leads to:: carb malabsorption: flatulence, steatorrhea, weight loss, cramps
clinical features of sprue in infancy:: failure to thrive, anorexia, irritability, abd pain, hypotnia, muscle wasting, abd distension, soft malodorous stool
clinical presentation of sprue in older children:: growth retardation, amenorrhea, rickets, osteoporosis, anemia
how to confirm diagnosis of sprue?: IgG and IgA against gliadin, foolow up + test with anti-tTG (tissue transglutaminase), if +, then sprue, confirm with bx
what disorder is associated with sprue?: dermatitis herpetiformis (pruritic papulovesicles over extremities and trunk), some px develop t-cell small bowel lymphoma (fatal)
treatment of sprue?: gluten free diet, celiac support group
3 main small bowel disorders: sprue, bacterial overgrowth, short bowel syndrome
causes of bacterial overgrowth (5): gastric achlorydia, anatomic abnormalities leading to stasis, motility disorder that slows transit, fistula b/w colon and sm intestine, misc (elderly, AIDS)
how does bacterial overgrowth lead dz?: bacteria deconjugate bile acids --> less micelle formation, direct damage to brush border, take up B12
resection of terminal ileum results in:: malabsorption of bile salts and B12
how much small bowel resection do you need to cause steatorrhea?: >100cm of ileum resected --> bile salts arent taken up, steatorrhea, malabsorption of fat soluble vitamins
four major bowel disorders: diverticulosis, polyps, neoplasms, appendicitis
what are colonic diverticula?: mucosal protrusions that go through the muscular wall
what causes diverticula?: low fiber diet, high bowel intraluminal pressure lead to muscular hypertrophy, vasa recta penetrate to nourish, weaken wall, and pseudo-diverticula form
which region of colon most involved in diverticula?: sigmoid: muscular contractions increase distally
does rectum get diverticula?: no, no tenia coli
complications of diverticula?: pain 2ndary to muscle spasm, perforation (diverticulosis), diverticular bleeding
describe diverticular bleeding?: abrupt onset, brisk output, red color, causes hemodynamic instability, 80% need transfusion
two types of colon polyps: adenomatous and non-adenomatous (hyperplastic, juvenile, hamartomas, inflammatory)
describe hyperplastic polyps: common, small (usu <5mm), in rectosigmoid region, elongated crypts w/ papillary fronds w/ lots of epithelial cells, not malignant
three types of adenomatous polyps: tubular adenomas (lowest risk), tubluvillous adenomas, villous adenomas (highest risk)
underlying pathophys of appendicitis?: obstruction of tiny appendiceal lumen (fecalith, inflammation, tumor, muscle hypertrophy)
presentation of appendicitis?: abd pain, cramps, vomiting, nausea, sense of constipation, RLQ pain, mild fever, leukocytosis
4 bowel motility disorders: acute intestinal obstruction, acute small bowel ileus, acute colonic pseudo obstruction ("colonic ileus"), IBS
who gets ileus?: commonly seen in hospitalized patients
when does IBS present?: early in life (first 2 decades)
IBS clinical presentation:: chronic lower abd pain, crampy, intermittent, not at night, worse 1-2h after meals, relieved by defacation
two causes of acute bowel ischemia: thrombotic SMA occlusion in px w/ atherosclerosis, embolic event in px w/ afib or LV thrombus
pathophys of ischemic colitis?: transient episodes of low blood flow, esp in watershed areas fed by both SMA/IMA
SMA-IMA watershed areas?: splenic flexure and distal sigmoid colon
clinical presentation of acute bowel ischemia?: bowel infarction, fever, tachy, hypoT, abd tenderness w/ guarding, leukocytosis, metabolic acidosis
clinical presentation of ischemic colitis?: usu elderly, mild LLQ cramps, tenesmus, blood in stool
diff b/w internal and external hemorrhoids?: internal: painless bleeding; external: no bleeding, but can get thromboses w/ pain/tenderness
define diarrhea: >2 loose stools/day or increased liquidity
define non-inflammatory diarrhea: leads to increased fecal fluid but does not disrupt the intestinal epithelium, characterized by watery, non-bloody and absence of fecal leukocytes
define inflammatory diarrhea: caused by infections, agents, or events which disrupt intestinal mucosa, most infectious causes usu affect colon so volume is less, frequent smaller volume bowel movements and lower abd cramps, dysentery, + fecal leukocytes
causes of acute diarrhea: infectious agents, bacterial toxins, medications, ingestion of non-absorbable osmotically active substances
how to distinguish inflammatory from non-inflammatory diarrhea?: presence of fecal leukocytes
signs of dehydration:: dry mouth, decreased urination, weakness, lethargy, dry mucus membranes
signs of severe inflammatory diarrhea: fever >38.5, dysentery >8x/day, severe abd pain/tenderness, elderly, imunocompromised
Oral rehydration solution:: 3.5g NaCl, 2.5g NaHCO3, 1.5g KCl, 20g Glucose in 1L of water
homemade oral rehydration solution: 1/2 tsp salt, 1 tsp baking soda, 8 tsp sugar, 8 oz OJ, in 1L water
six physological categories of diarrheas:: osmotic, secretory, inflammatory, motility, chronic infection, malabsorption
how big of an osmotic gap for osmotic diarrhea?: >50 mosm/Kg
when does osmotic diarrhea resolve?: when patients are fasting, because no longer ingesting osmotically active substance
common causes of osmotic diarrhea?: carb malabsorption (lactose, sorbitol), inorganic ion digestion (laxatives)
cause of fictitious diarrhea?: laxative abuse: consider in young women w/ eating disorder, px with psychiatric problems
pathophys of secretory diarrhea: increased intestinal secretion of lytes and water or decreased absorption, has normal osmotic gap
does secretory diarrhea resolve with fasting?: no, not due to an osmotically active substance
causes of secretory diarrhea: certain laxatives, endocrine tumors (VIPoma, calcitonin tumor), malabsorption of bile acids
causes of inflammatory diarrheas:: UC, Crohn's, infections
motility disorders causing diarrhea: rapid intestinal transit (irritable bowel syndrome), stasis leading to bacterial overgrowth (vagotomy, anatomic abnormalities)
causes of diarrhea due to malabsorption: impaired intraluminal digestion (pancreatic insufficiency, bile salt deficiency, gastrectomy), inadequate epithelial absorption (reduced surface area, small intestinal mucosal disorders), defective absorption via lymphatics
causes of pancreatic insufficiency: chronic pancreatitis, cystic fibrosis, surgical removal
causes of bile salt depletion:: bacterial overgrowth (bile salt deconjugation), disease or removal of terminal ileum, chronic liver disease, bile duct obstruction
causes of poor intestinal epithelial absorption: reduced surface area (resection), mucosal disorders (celiac sprue, tropical sprue, whipple's disease, crohn's disease)
malabsorbed nutrient in: megaloblastic anemia: B12
malabsorbed nutrient in: tetany, paresthesias: calcium, vitamin D
malabsorbed nutrient in: night blindness: vitamin A
uncomplicated diarrhea resolves with fasting suggests:: osmotic process
profuse water diarrhea with dehydration suggests:: secretory diarrhea
dysentery suggests:: inflammatory diarrhea
voluminous gas suggests:: carb malabsorption
useful stool analysis tests (6): fecal fat, fecal weight, stool osm and lytes, fecal leukocytes, lax screen, screen for ova/parasites
What does fecal fat quantity tell you?: >10g is significant, >20g suggest pancreatic insufficiency
describe d-xylose test: d-xylose is pentose sugar, passively absorbed across from lumen if normal intestinal mucosa and thus abnormality from pancreatic insufficiency
how to test for bacterial overgrowth in small bowel: aspirate small bowel fluid for culture, breath hydrogen analysis after oral carb administration
What does schilling test do?: tests if B12 deficiency due to pernicious anemia, terminal ileum disease, or bacterial overgrowth
Two types of gallstones: cholesterol stones and pigmented stones (calcium salts of bilirubin, carbonate, phosphate, palmitate)
three stages of cholesterol stone formation: formation of saturated bile, nucleation, growth of stone
two types of nucleation: homogenous and heterogenous
what is homogenous stone nucleation?: coalescence of cholesterol moolecules to precipitate
what is heterogenous stone nucleation?: some particle other than that of pure cholesterol acts as the nidus of nucleation
conditions associated with stone formation?: obesity, diet (high calorie, fasting), increased serum triglyceride, decreased serum HDL, clofibrate, cholestyramine, malabsorptive disorders, estrogen, pregnancy, Pima Indian
how does clofibrate predispose to stones?: raises cholesterol saturation of bile
how does cholestyramine predispose to gallstones?: prevents reabsorption of bile acids
list gallstone related diseases (5): asymptomatic gallstones, symptomatic cholelithiasis and chronic cholecystitis, acute calculous cholecystitis, choledocholithiasis, bacterial cholangitis
most common presentation of gallstone disease?: biliary colic, caused by transient gallstone obstruction of biliary tract
describe biliary colic pain: abrupt onset, gradually subsides, minutes to hours, RUQ and epigastrium, w/ nausea/vomiting
cause of cholecystitis: repeated minor episodes of cystic duct obstruction, leads to chronic inflammation and scarring
chronic cholecystitis predisposes to:: gallbladder adenocarcinoma
most sensitive test for gallstones?: US
treatment of cholelithiasis and cholecystitis?: cholecystectomy
what is acute calculous cholecystitis?: gallstone impacts and obstructs cystic duct
causes of gallbladder inflammation on acute calculous cholecystitis: release of phospholipase from gallbladder mucosal cells and its conversion to toxic substances
signs and symptoms of acute calculous cholecystitis?: RUQ pain, tender, fever, leukocytosis, murphy's sign
what is murphy's sign?: instruct patient to breath deeply during palpation in right subcostal area, sudden increase in pain and sudden termination of inspiration
complications of acute cholecystitis?: gallbladder empyema, sepsis, perforation
diagnosis of acute cholecystitis: US shows thickened wall, fluid surrounding wall
treatment of cholecystitis: IV hydration, IV abx, cholecystectomy
what is choledocholithiasis?: stones IN the bile duct
signs and symptoms of choledocholithiasis?: same as acute calculous cholecystitis
diagnosis of choledocholithiasis?: US shows dilated bile ducts, endoscopic ultrasound, cholangiography
treatment of choledocholithasis?: must be removed, even if asymptomatic
what is charcot's triad?: biliary colic, juandice, fever
symptoms of bacterial cholangitis: charcot's triad
treatment of bacterial cholangitis?: IV abx
who gets acalculous cholecystits?: patients hospitalized with serious illness
what is Primary sclerosing cholangitis?: idiopathic inflammaotry and fibrosing dz of biliary tree, immune mediated, progressive, cirrhosis and death
symptoms of PSC: often asyx, eventual elevation of alkaline phosphatase, pruritus, juandice, RUQ pain
Dx of PSC?: cholangiogram
Sphincter of Oddi Dysfunction and Papillary Stenosis causes?: biliary type pain
causes of acute pancreatitis: alcohol and gallstones most common, then drug induced and idiopathic
presentation of pancreatitis: begins abruptly, often after meal, severe epigastric pain, nausea, vomiting, more severe when supine, tachy, dehydration, leukocytosis, hemoconcentration
diagnosis of acute pancreatitis: elevated serum amylase, elevated serum pancreatic lipase, US and CT
serum amylase and gallstone or alcohol causes of acute pancreatitis?: in EtOH related, elevation persists for days and slowly drops, in gallstone related, amylase falls abruptly w/in 24-48 hrs
systemic complications of acute pancreatitis?: vascular instability, shock, DIC, renal insufficiency
local complications of acute pancreatitis?: pancreatic hemorrhage, hemosuccus pancreaticus, acute pancreatic fluid collections, pancreatic pseudocyst, necrosis
risk assessment of acute pancreatitis?: use Ranson's Criteria, the more criteria fulfilled, the worst outcome
treatment of acute pancreatitis?: supportive, limit systemic complications, prevent necrosis, prevent infection, lots of fluid resuscitation
leading cause of chronic pancreatitis?: alcohol, NOT gallstones
how does chronic pancreatitis manifest?: abd pain, impaired pancreatic excretions, chronic inflammation, fibrosis, atrophy, calicifications
complications of chronic pancreatitis: pancreatic pseudocyst, ascites, splenic vein thrombosis, biliary stricture
how to treat pancreatis pseudocyst?: surgical drainage
how to diagnose chronic pancreatitis?: fecal fat, CT, ERCP
treatment of chronic pancreatitis?: sx management
predisposing factors to pancreatic cancer?: cigs, EtOH, gallstones, animal rich diet, DM, chronic pancreatitis
sx of pancreatic cancer?: compression and invasion of adjacent structures, pruritus, enlarged liver
List 4 inflammatory bowel diseases: UC, Crohn's, microscopic colitis, collagenous colitis
central pathophys in IBD?: immune dysregulation, too much Th1, not enough Th2/3
CD genetic predisposition gene?: NOD2
what does NOD2 do?: activated NFkB in response to bacterial LPS, key in innate response to gut bacteria
typical initial lesion in Crohn's?: Apthous ulcer of mucosa (small shallow ulceration, white base)
Pathology of Crohn's: extending through all layers of intestinal wall, skip lesions, ulcers enlarge and deepen to form linear ulcerations, cobblestone appearance, perfs and abscesses, stricture and granulomas
List the three patterns of Crohn's: Inflammatory, Perforating, Fibrostenotic
highlight of inflammatory crohn's?: mucosal inflammation with erosion and ulceration predominating
highlight of perforating CD?: transmural inflammation, perf of bowel, formation of fistula and contained abscesses
sx of CD?: constitutional (fever, fatigue, weight loss), Diarrhea (multifactorial origin), abd pain, malnutrition, mild leukocytosis, anemia, fistula
rectal exam in CD reveals?: often, fistual-in-ano and anal fissures
Imaging studies for CD?: barium enema, CT, Colonoscopy
DDx of CD?: acute appendicitis, intestinal TB, fungal infxn, malignancy, vasculitis of intestinal vessels, UC
what is UC?: chronic inflammatory dz of colonic mucosa
do you get transmural inflammation in UC?: No, only in CD
UC progression?: from mild edema to ulcerations, fibrosis of colon, pseudopolyps (regenerating mucosa), crypts get messed up
Crypt damage in UC: crypt abscesses, distortion of crypts with shortening and branching
UC distribution: continuous, begins in columnar mucosa of anorecal junction, works proximally, no rectal sparing
what do you call UC if limited to rectum?: ulcerative proctitis
what do you call UC if limited to sigmoid?: limited UC
what do you call UC if extends throughout colon?: pancolitis
clinical presentation of UC: bloody diarrhea, tenesmus, cramps, fever, weight loss
dx of UC?: biopsy
DDx of UC?: infectious colitis, acute (shig, salm, campy, ecoli), radiation induced colitis, ischemic colitis
treatment of UC: surgical resection, but use Crohn's drugs too
extra-intestinal manifestations of IBD: joints, skin, eyes, liver
joint manifestations of IBD: peripheral arthritis, ankylosing spondylitis, sacroileitis
skin manifestations of IBD: erythema nodosum, pyoderma gangrenosum
ocular manifestations of IBD: conjuctivitis, scleritis, uveitis
liver manifestations of IBD: PSC
patients younger than 30 likely to have (liver dz)?: parenchymal disease
patients older than 65 likely to have (liver dz): gallstones and malignancies
patients between 30-50 likely to have (liver dz): chronic liver disease
children and young adults likely to have (liver dz): viral hepatitis
at what bilirubin level is juandice apparent?: > 3 mg/mL
stigmata of chronic liver disease: cachexia, muscle wasting, spider nevi, palmer erythema, dupuytren's contracture, leuconychia, parotid enlargement, skin pigmentation, gynecomastia, loss of secondary sexual hair
small nodular liver suggests:: cirrhosis
large nodular liver suggests:: malignancy
ascites in presence of juandice suggests:: cirrhosis
Define AST/SGOT: aspartate aminotransferase, from cytosol and mito and found in liver and lots of other cells

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