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.
