GI_UW Flashcards
What is Zollinger-Ellison syndrome? What is it a/w?
Most common cause of ZES is usually a gastrinoma - non-beta islet cell tumors of the pancreas that secrete high levels of gastrin. Usually sporadic but sometimes A/w MEN I.
What age does Zollinger Ellison usually present? What are the initital sx? What does endoscopy show?
Age 20-50 with initital sx of heartburn, abdominal pain and diarrhea. Frank GI bleeding can also occur. Endoscopy shows thickened gastric folds, multiple peptic ulcers, refractory ulcers despite PP use, ulcers in duodenum and even in the jejunum (suggesting extra gastric acid that cannot be fully neutralized in the duodenum).
Multiple duodenal ulcers with a single jejunal ulcer is almost pathognomic for what disease?
Gastrinoma
MEN Type 1 is caused by?
Single mutation of the MEN I tumor suppressor gene on chromosome 11
What is found in MEN 1?
Primary hyerparathyroidism (>90%), Enterohepatic tumors (60-70%) - gastrinomas are the most common type of pancreatic endocrine tumor seen in MEN I, pituitary tumors (10-20%)
What is found in MEN 2A?
Medullary thyroid cancer (>90%), pheochromocytoma (40-50%), parathyroid hyperplasia (!0-20%)
What is found in MEN 2B?
Medullary thyroid cancer, pheochromocytoma, Other things like mucosal and intestinal neuromas and marfaoid habitus.
What is Whipple disease caused by?
Rare multi-systemic illness cause - infectious disease caused by Tropheryma whippelii.
What is the ppt of Whipple disease?
GI sx of abdominal pain, diarrhea, malabsorption with flatulence, stomach distention, steattorrhea etc. Can also have migratory polyarthropathy, chronic cough and mycoardial or valvular involvement leading to CHF/valvular regurtigation. Pigmentation, low grade dever anad lymphadenopathy can also be seen.
What finding is a classical biopsy finding?
PAS positive material in the lamina propria of the SI.
What drugs commonly caused drug-induced esophagitis? How does it cause esophagitis?
Antibiotics - tetracyclines, anti-inflammatory agents - Aspirin and NSAIDS, Biphosphonates - alendronate, Others - potassium chloride (first one discovered to cause this), quinidine and iron. Direct mucosal injury and esophagitis through mechanisms like local acid burn.
How to treat drug induced esophagitis?
Stop offending drug.
What is the underlying mechanism for developmnt of cholesterol gallstones during pregnancy and women taking OCPs?
Estrogen induced increase in cholesterol secretion. Progesterone also causes reduction in bile acid secretion => increased cholesteroal saturation fo bile. Progesterone also slows down gallbladder emptying and facilitates the formation fo cholestoral gallstones during pregnancy.
How does PTN lead to possible cholecystitis?
Causes gallbladder stasis and predisposes to gallstone formation and bile sludging.
What is a hyperplastic polyp? Benign or Malignant?
Arise from hyperplastic mucosal proliferation. Most common non-neoplastic polyps found. No work-up needed. Benign.
What is a hamartomatous polyp? Benign or Malignant?
Juvenile polyp (non-malignant), generally removed due to bleeding risk and Peutz Jeghers polyp (Generally non-malignant)
What is an adenoama? Benign or Malignant?
Most common type of polyp found in the colon. Found in 30-50% of elderly people. They are potentially premalignant although less than 1% of such polyps become malignant. Less than 5% of patients have positive occult stool tests.
What are the risk factors for an adenoma progressing into malignancy?
Sessile (they can be either sessile or pedunculated but sessile has greater chance of becoming malignant), villous and greater than 2.5cm.
Adenoma can be divided histologically into?
1) Tubular 2)tubulovillous 3) and villous (most likely of all the histological subtypes to become malignant). As villous component increases, the chance of malignant icreases.
What is characteristic for abdominal angina? What other evidence is usually present?
Chronic mesenteric ischemia - Chronic occlusion of visceral arteries leads to worsening postprandial pain that leads to avoidance of food. Many disorders will cause dyspeptic symptoms and weight loss but very few present with severe abdominal pain. Evidence of associated atherosclerotic disease is usually present.
Cocaine and opiates intoxication can predispose to what?
Seizures. Cocaine can also lead to rhabodmyolysis.
What drug can increase digoxin serum levels and cause toxicity in a patient on a stable digoxin regimen?
Amiodarone
What is the presentation of acute digoxin toxicity?
GI symptoms like anorexia, nausea, vomiting, abdominal pain.
What is the presentation of chronic digoxin toxicity?
Less pronounced GI symptoms but more significant neurologic and visual symptoms (changes in color vision, scotomas, blindness).
For patients on digoxin, what is recommended when starting amiodarone therapy?
Decrease digoxin dose by 25-50% and closely monitor digoxin levels once weekly for the next several weeks.
What are esophageal varices?
Enlarged veins in the lower esophagus
In patients with small non-bleeding varices, what is prophylactic tx to reduce likelihood of progression to large varices and risk of variceal hemorrhage? What is the mechanism for this?
Non-selective beta blockers like propannolol, nadolol. Decreases adrenergic tone so that there is unopposed alpha-mediated vasoconstriction => decreases portal blood flow. Endoscopic variceal ligation is the altnernate preventive therapy in patients with contraindications to beta blocker therapy.
What lab tests are usually positive in patients with primary biliary cirrhosis (PBC)
Anti-mitochondrial antibodies.
PBC is more common in what sex and what do the LFTs usually show?
More common in women and presents with elevated alk phosphatose out of proportion to AST and ALT levels.
All patients with cirrhosis, regardless of etiology should undergo surveillance for what and how often?
Hepatocellular carcinoma. Every 6 months.
What is the typical presentation for achalasia?
Dysphagia for solids and liquids, heartburn, regurgitation of food, and weight loss.
What does barium swallow show for achalasia and what does manometry show? Which test is diagnostic?
Dilated esophagus with distal narrowing (barium swallow - birds beak). Manometry shows elevated LES pressures, incomplete LES relaxation after swalling and or absence of peristalsis in the esophageal body. Manometry id diagnostic.
What can mimic achalasia and what test should be done to rule out the disease that mimics it?
Esophageal malignancy at esophageal-gastric junction can have similar sx (dysphagia), radiographic and manometric (pseudoachalasia) findings. Endoscopy should be done to rule out cancer. Usually clues that favor malignancy are excessive weight loss, symptom onset of less than6 months and presentation at age > 60.
What is the presentation of small bowel obstruction? What do you see on radiograph?
Colicky abdominal pain, obstipation, vomiting, abdominal distention, diffuse tenderness. N/V may be more frequent with SBO than LBO. Depending on level of obstruction, radiographs can show dilated bowel loops with multiple air fluid levels.
When is immediate surgical intervention indicated for patients with small bowel obstruction?
1) Increased risk/signs of strangulation 2) Those who develop clinical or hemodynamic stability and 3) fail to improve after conservative measures such as bowel rest, nasogastric tube placement, pain control, fluid resuscitation.
What are the causes of steatorrhea?
Pancreatic Insufficiency, impaired bile salt absorption, impaired intestinal epithelium, and other rare causes. Examples of each - Pancreatic insufficiency (chronic pancreatitis due to alcohol abuse, cystic fibrosis or autoimmune/hereditary pancreatitis), pancreatic cancer. Bile salt related - small-bowel Crohn’s disease, bacterial overgrowth, primary biliary cirrhosis, primary sclerosing cholangitist, surgical resection of ileum (at least 60-100 cm). Impaired intestinal epithelium - celiac disease, AIDS enteropathy, Giardiasis. Rare caues - Whipple disease, Zollinger-Ellison syndrome, Medicaton-induced.
What are the sx of steatorrhea
Fatty, maladorous stools that float. Possibly abdominal distension, borborygmi (rumbling/gurgling sound made by gas).
What are the sx of chronic pancreatitis? How is it dxed?
After 90% of pancreatic function loss, patients develop fat and protein malabsorption. Develop postprandial epigastric pain (15-30 minutes) that is intermitten but then becomes persistent with disease progression. Dxed by measuring pancreatic function tests to document exocrine pancreatic insufficiency.
Can retroperitoneal hemorrhage occur without a supratherapeutic INR?
Yes
What should raise suspicious for retroperitoneal hematoma?
Back pain, hemodynamic compromise, evidence of anemia, hx of anticoagulation, dizzyness weakness etc.
What is the rome diagnostic criteria for IBS?
Recurrent abdominal pain/discomfort >= 3 days/month for the past 3 months and >=2 of the following: 1) symptom improvement with bowel movement 2) change in frequency of stool 3) change in the form of stool.
Do ppl with IBS require extensive workup for diagnosis?
Ppl with sx consistent with the Rome diagnositc criteria and no alarm features such as weight loss, nocturnal or worsening abdominal pain, rectal bleeding and abnormal labs do not require extensive workup.
What are the manometry findings for achalasia?
Decreased esophageal body peristalsis and poor relxation of the lower esophageal sphincter are typical.
How do achalasia patients present?
Progressive dysphageia, chest pain, food regurgitation and aspiration.
Helicobacter pylori infection is a significant risk factor for what cancers?
Gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma.Eradication of infection may cause remission in some MALT lymphoma patients but is not curative for gastric adenocarcinoma.
In gastric adenocarcinoma, what determines prognosis and tx options. What is the initial test for this?
Tumor staging at time of dx. CT scan is the initial staging modality.
What does octeotride do?
Reduces splanchnic blood flow, inhibits gastric acid secretion, and exerts gastric cytoprotective effects.
Acute pancreatitis is most often due to? What else is it due to?
Alcohol use, gallstones (2 together account for 75%) or medications. Hyperlipidemia types 1, IV and V, infections (CMV, legionella, aspergillus, trauma, iatrogenic like post ERCP)
What are the commonly implicated drugs that cause acute pancreatitis?
Diuretics, anti-seizure drugs (like valproic acid, azathioprine), and antibiotics (metronidazole)
What does CT show for acute pancreatitis?
Diffuse or focal parenchymal changes, edema, necrosis or liquefaction.
What are the PE findings for acute pancreatitis?
Typically - sudden onset of persistent, severe epigastric pain that radiates to the bac, may get partial relief from sitting up and leaning forward. May have mild epigastric tenderness to palpation or severe tenderness.
Wht are complications of acute pancreatitis?
Ileus, ARDS, pleural effusion, renal failure, pancreatic pseudocyst/abcesses/necrosis,
What is the ppt of drug induced pancreatitis?
Usually mild form of pancreatitis. Nausea, vomiting, abdominal pain radiating to back. Lab results show elevated serum amylas and lipase.
Wht is the classic presentation of biliary colic? How is it different from cholecystitis?
Ingestion of large (usually fatty mea) => epigastric pain, could have right shoulder pain => resolves in a few hours. Patients abdomen is soft/non-tender. Paitents may have recurrent symptoms. This presentation is different from cholecystitis in that the pain usually resolves in 4-6 hours and there is no abdominal tenderness to palpation (Murphy’s sign), fever, leukocytosis.
What is the pathophysiology of biliary colic?
Ingestion of meal => gallbladder contraction => increased intra-bladder pressure against an obstructed cystic duct causing pain => gallbladder relxation then allows stone to fall back from duct => pain resolution.
What is angiodysplasia?
Dilated, thin-walled vessels lined by endothelium and prone to recurrent, occult and chronic painless bleeding.
Angiodysplasia is usually seen in patients aged ? And can occur where?What diseases do patients with angiodysplasia usually have?
Age greater than 60. Can occur anywhere in the GI tract including colon, SI and stomach. Often discovered in patients with underlying aortic stenosis (Heye’s syndrome) or end-stage renal disease.
What is the presentation of angiodysplasia (AVM)?
Anemia, painless GI bleeding, murmur of aortic stenosis.
How does aortic stenosis / end stage renal disease contribute to angiodysplasia?
Turbulent flow through the valve causes disruption of Von Willenbrand multimers and increaes risk of bleeding => leads in indetification of angiodysplasia. Uremic platelet dysfunction in ESRD also increases bleeding risk.
Gastrinoma diagnosis is strongly suggested by what lab result?
> 1000pg/mL
Patients wit non-diagnostic serum gastrin levels when suspected for gastrinoma should be evaluated with what test?
Secretin stimulation test.
Hyperbilirubinemia with normal transaminases and alk pho suggested what kind of bilirubin disorder?
Inherited metabolism disrodes - dubin-johnson, for example.
Hyperbilirubinemia with elevated transaminases with normal alkaline phosphtase suggest what kind of etiology?
Intrisnsic liver disease (viral hepatitis, hemochromatsosis)
Hyperbilirubinemia with elevated alk phos out of proprotion to transaminaseds suggests what kind of etiology?
Intrahepatic cholestasis or biliary obstruction.
What is the clinical presentation of malignant biliary obstruction? Exam findings and lab findings?
Painless (KEY) jaundice, pruritus, weight loss, acholic stools with dark urine. Exam: normal or show RUQ mass, tenderness or hepatomegaly. Lab: increased direct bilirubin, elevated alk pho and GGPT, and normal to elevated AST/ALT
What are some causes of biliary obstruction?
Pancreatic or biliary cancer. Benign causes = choledocolithiasis, benign bliiary strictures.
What is the pathophysiology of acute severe pancreatitis accompanied by hypotnesion?
Severe pancreatitis => release of activated pancreatic enzymes that enter the vascular system => increases vascular system permeability wtihin and around pancreas => fluid migration from vascular system to surrounding retroperitoneum => inflammatory mediators enter vascular system and systemic inflammation ensures => widespread vasodilation, sysemic hypotension, capillary leak, shock, and associatd end-organ damange.
What factors are a/w with increased risk of severe pancreatitis?
Age>75, obesity, alcoholism, CRP>150mg/dL at 48 hours after ppt, rising BUN and creatinine in first 48 hrs, chest x-ray with pulmonary infiltrates or pleural effusion, CT scan/MRCP with pancreatic necrosis and extrapancreatic inflammation.
Complications of severe pancreatitis
pseudocyst formation (contains pancreatic enzymes, blood, fluid and tissue debris surrounded by necrotic or fibros capsue) and take 3-4 weeks to develop after acute pancraetitis, acute renal failure, ARDS, necrotizing pancreatitis, peripancreatic fluid collection, GI bleeding.
Episodes of dysphagia, regurgitation and or chest pain precipiated by emotional stress raises suspicion for ?
Esophagela motility disorder such as diffuse esophageal spasms.
What test estabilishes dx of diffuse esophageal spassm?
Manometry.
Patients with Zollinger Ellison syndrome may have malapbsorption due to?
Inactivation of pancreatic enzymes by the increased production of stomach acid (as a result of the increased gastrin secretion).
What are the sx/clinical ppt of patients with tumors of the head of the pancreas?
Nagging epigastric pain that is worse at night, food intolerance, weight loss, jaundice, enlarged non-tender distended gallbladder, scleral icterus sometimes.
How does pancreatic cancer lead to jaundice / steatorrhea?
Most pancreatic cancers are located in the head of the pancreas => leads to obstruction of pancreatic duct (resulting in steatorrhea due to difficulty secreting fat digesting enzymes) and obstruction of common bile duct (resulting in jaundice/scleral icterus).
What are characteristic imaging findings with regards to biliary tracts for patients with pancreatic cancer
Intra and extra-hepatic biliary tract dilatation due to back up caused by obstruction that results from pancreatic (usually head) tumors.
What conditions can cause increased BUN/Creatinine ratio
GI bleeding (like chronic duodenal ulcer) which leads to hemoglobin braekdown by bacteria in the GI tract with resultant urea reabsorption, patient receiving systemic steroids, prerenal azotemia (dehydration).
What is the presentation of esophageal performation?
Acute-onset, severe, substernal neck/abdominal, neck pain.
Sometimes, there is present subcutaneous emphysema in the neck or characteristic crunching sound on chest auscultation(Hamman Sign) due to mediastinal emphysema..indicating what etiology?
Esophageal performation
What is the diagnostic study of choice for esophageal performation?
gastrografin-constract esophagography or CT esophagography (water-soluble) do not do barium contrast because it may cause granulomatous inflammatory response in the mediastinum and pleura.
Positive urine bilirubin is typically indicative of?
Buildup of conjugated bilirubin. Could be due to defective hepatic storage and uptake of bilirubin.
Ulcerative colitis affects what layers vs Crohns
Crohns: transmural. Ulcerative colitis: mucosal layer.
What findings on colonoscopy and biopsy confirm dx of ulcerative colitis?
Biopsy: mucosal inflammation. Colonoscopy: friable mucosa.
What complication of UC requires regular surveillance?
Colorectal/colon cancer risk is increased in patients with UC. Advise routine surveillance with yearly colonoscopies for patients with UC beginning 8-10 years after dx.
What are potential extraintestinal manifestation of UC?
Sclerosing cholangitis, uveitis, erythema nodusum, spondylarthropathy. Severe complications = toxic megacolon and colon cancer.
Factitious diarrhea from laxative abuse diagnosis can be confirmed by what findings on biopsy?
Dark brown discoloration of the colon with lymph follicles shining through as pale patches (melanosis coli).
What risk factors/considerations call for an upper GI endoscopy in patients with sx of GERD?
Men age >50 with chronic (>5 years) symptoms or CANCER risk factors or alarm symptoms (melena, persistent vomiting, hematemesis, weight loss, anemia, dysphagia/odynophagia)
Wht are the manometry findings of esophageal dysmotility a/w scleroderma
Absence of persitatltic waves in the lower 2/3rds of the esophagus and significant decrease in LES tone.
Wht are the important clinical clues of esophageal dysmotility a/w scleroderma
“sticking sensation in the throat” or heartburn a/w dysphagia.
What is primary sclerosing cholangitis? What is it a/w?
Chronic, progressive disorder with unknown etiology with inflammation, fibrosis, stricturing of medium and large sized intra and extra-hepatic bile ducts. Continued bile duct destruction leads to end stage liver disease and portal hypertension. 90% of patients have underlying inflammatory bowel disease, mostly ulcerative colitis. It is a progressive condition and without liver transplanation patients typically die after 12 years.
What is the 1) clinical ppt of primary sclerosing cholangitis 2) lab pattern 3) Other serologic findings 4) ERCP/MRCP
1) fatigue and pruritus. Depending on stage (since it’s progressive - steatorrhea, fat-soluble vitamin deficiencies, metabolic bone disease) 2) cholestatic pattern - higher alk phos levels compared to elevated ASTs/ALTs 3) + p-ANCA, increased serum IgM, hypergammaglobulinemia 4) beading - multifocal narrowing with intra and extra hepatic duct dilation.
What are the complications of PSC?
1) Intra and extrahepatic biliary stricture 2) cholangitis and cholelithiasis (cholesterol and or pigment stones) 3) cholangiocarcinoma 4) cholestasis (decrease in fat soluble vitamins and osteoporosis) 5) colon cancer.
Primary biliary cirrhosis is more common in men or women? By what ratio. Does it usualy have an a/w IBD?
More common in women by a ratio of 9:1. Usually no association with IBD
What does the D-xylose test try to measure?
It’s a simple sugar (monosaccharide) that doesn’t need to be broken down. Absorption requires intact mucosa in small intestine and used to assess absorptive capacity of the proximal small intestin.
Patients with proximal smal lintestine disease have what kind of D-xylose test results?
Decreased urinary excretion and decreased serum D-xylose concentration. Most of it is fecally excreted since there is poor intestinal absorption.
What is the typical presentation of toxic megacolon?
Total or segmental nonobstructive colonic dilation, severe bloody diarrhea, systemic findings (fever, tachyardia, elevated WBC count, hypotension).
What kind of patients are at higher risk for developing toxic megacolon?
Patients with inflammatory bowel disease.
How is toxic megacolon diagnosed?
Abdominal xrays and >=3 of the following: fever>38C (100.4), pulse>120/min, WBC>10,500 and anemia. Abdominal x-rays (dilated right or transverse colon >6cm), possible multipe air-fluid levels, and thick haustral markings that do not extend across the etire lumen.
What is the immediate tx regimen for toxic megacolon?
Prompt IV steroids, nasogastric decompression, antibiotics and fluid management.
What is the “succession splash” and what can it indicate.
Place stethoscope over the upper abdomen - rock patient at hip back and forth to hear abodminal succession splash which is essentially the present of a hollow viscious filled with fluid and gas. It can indicated gastric outlet obstruction.
Patient from developing country with sx of malapsorption should be considered for tx with what for suspected ?
Empiric metronidazole for suspected giardiasis
What is the pathophysiology for diarrhea from giardiasis?
Trophozoties adhere to mucosal surface by adhesive disks and produce malabsoprtion, which can sometimes be severe and lead to weight loss.
What are th sx of giardiasis?
Foul smelling stools, fatty stools, bloating, flatulence, nausea, malaise and abdominal cramps.
What are the most common underlyign cuases of cirrhosis in the US
1) Chronic alcohol abuse 2) viral hepatitis.
What are clinical ppt / sx of chornic liver disease?
New-onset ascites, pedal edema, spider angiomata, palmar erythema, caput medusae, nail changes, gynecomastia, splenomegaly, testicular atrophy.
What are clinical clues for the cirrhosis etiology of hemochromatosis
Family hx of cirrhosis, hx of diabetes, “bronze” skin appearance, high transferrin saturation
What are clinical clues for the cirrhosis etiology of alpha 1 antitrypsin deficiency.
co-existing lung involvement, family hx of cirrhosis.
What are clinical clues for the cirrhosis etiology of cardiac cirrhosis
Co-existing right sided heart failure
What are clinical clues for the cirrhosis etiology of medications
MTX, isoniazid
What are clinical clues for the cirrhosis etiology of Wilson disease
Family hx of cirrhosis at young age, Kayser-Fleischer rings in eyes
Chronic pancreatitis presentation
Recurrent bouts of upper abdominal pain, diarrhea/steatorrhea, weight loss, Type 2 diabetes
What is the diagnostic test/finding for chronic pancreatitis?
Calcifications on CT or plain film.
What is cryoprecipiate used as replaement therapy for?
Patents with fibrinogen, vWF, or Factor VIII deficiency.
What does fresh frozen plasma contain? What is it indicated for?
All clotting factors and plasma proteins from one unit of blood. Indicated for active bleeding with severe coagulopathy (liver disease, DIC, supratherapeutic warfarin anticoagulation). Note that fresh frozen plasma is generally not needed to corect minimally abnormal prothrombin time (INR
Platelet transfusions are typically given for?
1) Patients with platelet count
Packed red bleed cell (PRBC) transfusions are not recommended in acute GI bleeds (otherwise stable) unless ?
Hb is less than
What Hb threshold is considered for unstable patients with sx related to anemia or ACS with active ischemia.
Dysphagia inititally with solids and then to liquids is likely due to what kind of obstruction?
Mechanical
Dysphagia with both solids and liquids from the beginning is likely due to what ?
Motility disorders
For suspected motility disroders, what studies are recommended?
Barium swallow followed by manometry to confirm the diagnosis.
Modified acid fast specimen of stool showing oocysts in patient with low CD4 counts 80 cells/mm^3 and severe diarrhea likely contracted which microorganism?
Cryptosporidium parvum.
What is a pneumoperitoneum?
Free air under the diaphragm.
Sudden onsest of severe epigastric pain that spreads over the entire abdomen should raise suspicion for? What can you see on chest/abdominal radiographs
Chemical peritonitis due to perforated ulcer. Radiographs show free air under the diaphragm.
What is the definition of acute liver failure (fulminant hepatitis)
Acute onset of severe livery injury with encephalopathy and impaired synthetic function (INR>=1.5) in a patient without cirrhosis or underlying known disease.
What are the characteristic findings of acute liver failure?
Acute onset of markedly elevated transaminases (often in thousands), reduced hepatic synthetic function, encephalopathy,RUQ pain, pruritus, jaundice.
What are etiologies of acute liver failure
1) drug induced hepatotoxicity (eg acetominophen) 2) viral hepatitis (Hep A and B) 3) alcoholic of autoimmune hepatitis 3) wilson, budd-chiari syndrome 4) ischemia (ex. Hypovolemic or cardiogenic shock with poor perfusion to liver), malignant infiltration of the liver.
What are the lab findings for acute liver failure
Increased prothrombin time, increased INR>=1.5, transaminases (AST, ALT 10x normal), increased biliribuin. Worsening INR/PT and bilirubin indicate progressive liver failure. Patients with progressive liver failure can present with decreasing transaminase levels.
What is obstipation
Inability to pass flatus or stool
What is small-intestine bacterial overgrowth? How does it typically present?
Malabsorption syndrome due to anatomic or dysmotility disorders. Presents with abdominal bloating, flatulence, diarrhea. Weight loss and nutritional deficines may occur in severe cases
What is the gold standard for small intestine bowel obstruction dx?
Endoscopy with jejunal aspirate containing >10^5 organisms.
What are the common organisms that cause small intestinal bacterial overgrowth?
Streptococci, bacteroides, Escheria, lactobacillus.
Non-caseating granulomas are characteristic/pathognomic for which IBD?
Crohn’s disease as compared to ulcerative colitis. However, note that it is present in only 60% of patients with Crohn’s.
What are characteristic features of Crohn’s disease
Transmural involvement of colon, skip lesions, cobblestone appearance of the colon, creeping fatty appearance of mesentery, fistulas, fissues and periannal disease.
What is thrombocytosis
Body produces too many platelets.
Chronic inflammatory diarrhea is a/w with what blood lab values/findings?
anemia, elevated ESR, acute phase reactants, reactive thrombocytosis. Blood/leukocyte positive stool is an important finding.
Acute erosive gastritis is characterized by the development of what?
Severe hemorrhagic erosive lesions after the exposure of gasric mucosa to various injurious agents (such as massive doses of aspirin and NSAIDS) or after a substantial decrease in blood flow.
What is postcholecystectomy syndrome?
Persistent abdominal pain or dyspepsia either post-operatively or months to years after cholectystectomy.
What are the common etiologies of postcholecystectomy syndrome?
Biliary (retained common bile duct, cystic duct stone) or extra-biliary (pancreatic, PUD) causes.
What should be considered/suspected in a patient with cirrhosis and ascities accompanied by a fever or a mental status change?
Spontaneous bacterial peritonitis. It can have a sublet presentation.
What is the test of choice for spontaneous bacterial peritonitis?
Paracentesis is the test of choice, with + ascites fluid culture and PMN level greater than 250/mm^3 being the main criteria for making the dx. Note that paracentesis should be done before antibiotic cultures.
How do you calculate the osmotic gap
290 - [2(stool Na + stool K)]. It is greater than >50 mOsm/kg in all forms of osmotic diarrhea.
What test results characterize lactose intolerance?
Low stool pH (due to fermentation products), positive hydrogen breath test (due to increased hydrogen levels from bacterial metabolism), increased stool osmotic gap, postive stool test for reducing substances (not sure why for this last one).
Variety of neoplasms, particularly which ones, can be a/w hypercoagulability?
Visceral adenocarciomas - gastric, pancreatic and ovarian.
What is the most common cause of iron deficiency anemia in an elderly patient?
GI blood loss.
What are findings typical of microcytic anemia?
Low serum iron and ferritin with an elevated TIBC.
In evaluating ascites, what helps distinguish between etiologies?
Serum to ascites albumin gradient. Serum albumin concentration - periotneal fluid albumin concentration. If greater than 1.1g/dL, then etiology is portal hypertnesive (budd-chiari, cardiac, cirrhosis). If less than 1.1g/dl, absence of portal htn and etiologies such as TB, pancreatic ascities, nephrotic syndrome. etc.
What are Mallory-Weiss tears and what do they cause?
Tears in the mucosa of the distal esophagus and proximal stomach due to increased intragastric pressure during vomiting. They cause upper GI bleeds (10% of them)
What are causes of peptic strictures (esophageal)? How do they appear on barium swallow?
GERD (!), radiation, systemic sclerosis, and caustic ingestions. Symmetric, circumferential narrowing on barium swallow.
Diagnosis of acute bowel ischemia is based on?
High clinical suspicion in patients with abdominal pain that is out of proportion to exam findings, associated metabolic acidosis, and patients with risk factors for thromboembolic disease (like afib, peripheral vascular disease).
Why do patients with acute bowel ischemia have metabolic acidosis?
High serum lactate levels
What is the most common site of metastasis for the colon?
Liver
What are the common findings of liver malignancy/metastases?
Firm hepatomegaly, RUQ, mildly elevated liver enzymes.
What is a VIPoma
Rare tumor affecting the cells that produce the vasoactive intestinal peptide.
What is the role of VIP?
Binds to intestinal epithelial cells to increase fluid and electrolyte secretion into the intestinal lumen.
What is the clinical presentation of VIPoma?
VIPoma syndrome (pancreatic cholera). Watery diarrhea, hypo or achlorydia (decreased gastric acid secretion), a/w flushing, lethargy, nausea, vomiting, muscle weakness/cramps (due to hypokalemia)
What are the lab findings for VIPoma
Hypokalemia (increased intestinal potassium secretion), hypercalcemia (increased bone resoprtion), hyperglycemia (due to increased glycogenolysis) and stool studies that show secretory diarrhea with increased sodium and osmolal gap (
How do you diagnose VIPoma?
1) VIP levels of >75 pg/mL with watery diarrhea 2) abodminal CT or MRI to localize tumor in pancreas
Unexplained leukocytosis in hospitalized patients should raise suspicioun for?
C difficile, even without diarrhea. C difficile colities can range from mild watery diarrhea to fulminant colitis with toxic megacolon.
C difficile colitis diagnosis is made by?
Stool studies for C difficile toxin (PCR)
Diffuse esophageal spasm is usually seen in what patient population and presents with?
Usually seen in young females and can present with intermittent episodes of chest pain and dysphagia. Barium swallow may reveal “corkscrew” esophagus.
What are the manometry findings for diffuse esophageal spasm?
High amplitude peristaltic contractions with normal relaxation response in lower esophageal sphincter.
What is Zenker’s diverticulum? What patient population is it found in?
Disorder of the proximal esopahgus. Upper esophageal sphincter dysfunction and esophageal motility are believed to cause ZD. Develops immediately above the UES sphincter wih posterior herniation between fibers of cricopharyngeal muscles. generally seen in males. Diverticulum varies in size
What is the ppt of Zenker’s diverticulum? Treatment?
Usually in patients 60 years old and up. Generally asymptomatic, however occasionally patient will complaint of food sticking in throat, halitosis, dyphagia and regurgitation/aspiration, variable neck mass. No pain. Tx is open/endoscopic surgery, cricopharyngeal myotomy.
What is the preferred imaging modality to confirm dx?
Barium esophagram.
Zenker’s patients are at risk for?
Aspiration pneumonia.
Scleroderma / esophageal issues.
Collagen vascular disorder which can present with loss of peristalsis of distal esophagus. There is fibrosis and complete atrophy of the esophageal smooth muscle. LES sphincter becomes incompetnent with time => reflux esophagitis and a stricture.
Infectious esophagitis is generally caused by? And occurs in which patient population? What tests reveals the cause?
Candida, herpes or cytomegalovirus. Generally occurs in immunocompromised invidiuals presents with dysphagia, oral thrush or odynophagia.
What is hepatorenal syndrome.
When patients with severe liver disease develop systemic hypoperfusion and subsequent renal failure.
What lab findings point to a diagnosis of hepatorenal syndrome?
Elevated creatnine and very low urine sodium level (typically less than 10mEq/L)
What is the pathophysiology of hepatorenal syndrome.
Patients with severe level disease => can develop generalized systemic vasodilation due to generation of nitric oxide in splanchnic circulation due to portal hypernension => systemic vasodilation => reduces periphera vascular resistence => leads to renal hypoperfusion and pre-renal renal failure.
What are carcinoids? what do they typically secrete?
Well-differentiated, rare neuroendocrine tumors. They can secrete several products such as histamine, serotonin (from trypophan which is also needed for niacin synthesis), vasoactive intestinal peptide, that are metabolized in the liver.
Where are carcinoids most commonly found?
They are most commonly found in distal small intestine, proximal colon and the lung and often metastasize to the liver.
When carcinoids metastasize to the liver what happens?
When they metastastize to the liver, they secrete their products before the liver can metabolize them, thus leading to carcinoid syndrome.
What are the clinical manifestations of carcinoid syndrome? What is the most charcteristic?
Skin: Episodic Flushing!!!!, telangiectasias, cyanosis. GI: secretory Diarrhea, cramping. Cardiac: valvular lesions (right > left side) Pulmonary: bronchospasm Miscellaneous (niacin deficiency = dermatitis, diarrhea and dementia).
How do you dx of carcinoid syndrome?
5 HIAA levels, ct/mri of abdomen/pelvis to localize tumore, octeotride scan to detect mets, Echo if there are cardiac manifestations
What is BRBPR (bright red blood per rectum)
Scant hematochezia - minimal rectal bleeding - small amounts of blood on toilet paper, few drops of blood in toilet bowl after defecation, small amounts of blood on surface of stool. Red blood intermixed with stool is NOT included in this category.
What should be the initial procedure of patients less than 50 years old with BRBPR?
Anoscopy
What are the major hereditary risk factors for pancreatic cancer?
First-degree relative with pancreatic cancer, hereditary pancreatitis, germline mutations (BRCA1, 2, Peutz-Jeghers syndrome).
What are the sx of Zn deficiency
Alopecia, skin lesions (bullous pustular lesions around body orifices and or extremities), abnormal taste, impaired wound healing
Zn deficiency can result from?
Chronic parenteral nutrition (some formulations don’t have Zn) and malabsorption. It is digested primarily in the jejunum.
What is the most common complication of peptic ulder disease?
Hemorrhage. (Blood or coffee-ground like material on nasogastric tube lavage can confirm this dx)
Hereditary hemochromatosis is a/w ? fold increased risk of hepatocellular carcinoma?
20-200x risk
What is the most sensitive and specific imaging study to detect gallstones?
Abdominal ultrasound
What is the tx of actively bleeding esophageal varices
1) hemodynamic support (volume resuscitation - ideally through 3 large bore peripheral IV lines) 2) prophylactic antibiotics (should be given to cirrhotic patients with GI bleeding to decrease infectious complications) 3) somatostatin analogues (octeotrides) inhibit the release of vasodilator hormones which leads indirectly to splancnic vasoconstriction and decreased portal blood flow.
NSAIDS commonly cause iron deficiency anemia how?
NSAIDs and asprin can cause gastritis and/or gastric ulcers leading to chronic GI blood loss from the GI tract and depletion of iron stores.
What test is the initially preferred test for patients with hx of chronic pancreatitis that present with abdominal pain but have jaundice?
Abdominal ultrasound to exclude biliary obstruction and dilation. U/S is not sensitive for identifying pancreatic necrosis, assessing acute pancreatitis or detecting small tumors less than 3cm.
What test is the initial preferred test for patients with hx of chronic pancreatitis that present with abdominal pain without jaundice?
CT with contrast, more sensitive for diagnosing pancreatic cancer, delineating tumor extent and staging the tumor.
In patients with a hx of IBD and worsening symptoms accompanied by signs of sepsis, what dx should be considered and what test should be ordered?
Dx: Toxic megacolon, Test: Abdominal radiograph (to confirm presence of dilated colon greater than 6cm)
What is the most widely used criteria to clinically diagnose toxic megacolon?
Must have radiograph evidence of colonic distension plus 3 of the following: 1) Fever >38 degrees C 2) Heart Rate >120 beats/min 3) Neutrophilic leukocytosis > 10,500/mL 4) Anemia PLUS at least one of the following: 1) Volume depletion 2) altered sensorium 3) Electrolyte disturbances 4) hypotension.
What age does IBD present at?
Usually in 20s but there is a bimodal distribution with a second peak around age 60.
IBD
Note that Crohns and UC can sometimes be hard to distinguish and that neutrophilic cryptitis can be seen in both.
What are the sx of Celiac disease?
bulky, foul smelling stools, loss of muscle mass/subctuaneous fat and fatigue (From poor fat and protein absorption), pallor (anemia)/fatigue (from low iron), bone pain/osteomalacia and osteoporosis (from low calcium and vitamin D), easy bruising (low vit K) and hyperkeratosis (low vit A)
What positive serology results is Celiac disease highly correlated with?
Positive IgA anti-tissue transglutaminase and IgA anti-endomysial antiobodies. However, many patients with biopsy proven celiac will have negative results on IgA antibody testing due to an associated selective IgA deficiency.If this comes back negative and suspicion for celiac is stil lhigh, should do total IgA (of IgG serologic testing should be done).
What is the diagnostic criteria for acute pancreatitis?
2 of the 3 following criteria: 1) acute onset of severe epigastric pain that radiates to the back 2) elevated amylase and lipase levels >3 times the upper limit of normal and 3) CT scan abnormal findings (focal or diffuse pancreatic enlargement). CT scan is not needed if first two criteria are met. May be performed if patients have unclear dx or fail to improve with conservative management.
Wht is the first line therapy for H pylori associated PUD
Amoxicillin + clarithromycin + PPI
What is the physiology behind pain improving with eating / being worse on empty stomach for duodenal ulcer?
Empty stomach = acid secretion into duodenum and pain is worse. After eating, there is alkali secretion into the duodenum that relieves the pain.
Tea and toast type of diet is a/w what nutritional deficiency.
Folic Acid
Folic acid deficiency causes what kind of anemia
Macrocytic anemia and decreased RBC production
What is the best test for diagnosing and evaluating the abdomen of patients during an acute episode of diverticulitis?
CT scan. Avoid things like colonoscopy, sigmoidoscopy and barium enema for risk of perforation.
What is the best tx for acute uncomplicated diverticulitis?
IV antibiotics.
What happens when a patient doesn’t respond to IV antibiotics for suspected acute diverticulitis? What do you suspect/do?
Suspect a complication such as formation of an abscess, fistula or a frank perforation.
what is the pathophysiology of the shifting pain from the peri-umbilical area of the RLQ in acute appendicitis?
Initially is visceral and referred, and then becomes somatic. In the initial stages, on the viscera are inflammed => dull, poorly localized (peri-umbilical) and constant. Afferent visceral never fibers from the appendix accompany the sympathetic nerves and enter spinal cord at T10 level, leading to periumbilical pain (referred pain at this level). As the disease progresses, subsequent inflammation of the parietal periotneum and skeletal muscles causes somtaic pain => well localized (RLQ) and more severe in intensity.
What is pellagra. What is it characterized by?
Condition that occurs due to niacin deficiency. Triad of 3Ds: diarrhea (watery), dementia, dermatitis and eventually, if left untreated leads to death. Initially, there is generalized weakness, irritability, vomiting, abdominal pain, loss of appetitie. Skin rash - in sun-exposed areas.
Who gets pellagra?
People from India, Africa, and China who eat corn based diet and people also with carcinoid syndrome, Hartnup’s disease and alcoholics.
What is the stepwise approach to the tx of ascites?
- Sodum and water restriction (2L/day) 2) Spironolactone 3) Loop diuretic (furosemide) - not more than 1L/day of diuresis) 4) Frequient abdominal paracentesis (2-4 L/day, as long as the renal function is OK).
Tropical sprue is characterized by malabsorption of nutrients, especially which ones?
Vitamin B12 and folic acid, causing megaloblastic anemia.
Typical biopsy of small intestine affected by Tropical sprue shows what?
Blunting of villi with infiltration of chronic inflammatory cells, including lymphocytes, plasma cells and eosinophils.
What is spontaneous bacterial peritonitis (SBP)?
Ascitic fluid infection without an obvious intra-abdominal surgical etiology. Most likely due to intestinal bacterial translocation directly into ascitic fluid or hematogenous spread to the liver and ascitic fluid (due to other bacterial infections).
What tests/results confirm the dx of Spontaneous bacterial peritonitis?
Ascitic fluid with PMNs of >=250/microL and positive peritoneal fluid culture.
SBP is commonly caused by which organisms and how should SBP be treated?
Usually due to gram-negatives. Tx includes broad spectrum antibiotics such as 3rd generation cephalosporins (cefotaxime).
Chronic GERD and Barrett’s esophagus are risk factors which what kind of esophageal cancer?
Adenocarcinoma of the esophagus.Patients with Barrett’s esophagus have 1% per year risk of developing adenocarcinoma of the esophagus.
What are the major risk factors for squamous cell cancer of the esophagus?
Smoking, alcohol (2 major ones), hot food/beverages, picked vegetables, food rich in N-nitroso compounds
