jdlevenson's version from 2015-06-20 04:06


Question Answer
Periodic non peristaltic contractions of the esophagusDiffuse Esophageal Spasm. Recall, normally contractions of esophagus are coordinated. Stimulated by esophageal distension by a food bolus. Contractions originate above site of distension and propel bolus downwards. DES several portions contract at same time preventing propagation of food bolus towards the stomach. They can be painful.
Corkscrew esophagus on bariumDiffuse esophageal spasm from simultaneous non coordinated contractions of esophagus.
Diffuse esophageal spasms – intermittent dysphagia and occasional chest pain that is or is not relieved by rest?Is NOT relieved by rest or associated with exertion
Diffuse esophageal spasm can mimicUnstable angina in intensity and location.
DES is crampy or burning or bothCRAMPY.
Duodenal ulcers cause pain when1-3 hours after a meal or at night. Pain is relieved by intake of food or antacids.
Gastric atrophychronic gastritis; may be due to H. Pylori, pernicious anemia, radiation or granulomatous conditions
Chronic gastritis with antral sparing = vs chronic gastritis that is antral predominant = ?Autoimmune; H. Pylori.
Pernicious anemia affects parietal cells which are locatedIn UPPER GLANDULAR LAYER; secretes gastric acid and IF. Whereas CHIEF CELL are located in DEEPER ASPECT of gastric glands.
Dysphagia for liquids and solids in association with dilated esophagus and absent peristalsis in the smooth muscle portion of the esophagus is diagnostic forAchalasia
Achalasia is from dysfunction of ganglion cells of/ degenerative to myenteric plexus. It can be congenital orT. Cruzi.
Zenker diverticulum pathogenesisCricopharyngeal dysfunction -> diminished relaxation during swallowing -> more force required for peristalsis -> intense contractions -> increase oropharyngeal intraluminal pressure -> hernation of muscle in zones of weakness/ posterior hypopharynx -> Zenker -> FALSE/ pulsion
True diverticulum known as vs False known asTrue – traction and False –pulsion
Zenker symptomsdifficulty in swallowing felt at troat, coughing, choking and sometimes nasal regurgitation; may lead to food retention and pneumonia
Lateral neck mass and dysphagiaZenker
True diverticula in the esophagus happens at mid-portion and fromMediastinal lymphadenitis as seen in TB and fungal infections.
Mallory-Weiss syndrome, longitudinal mucosal tears around esophagogastric.. caused byINTRALUMINAL PRESSURE IN THE STOMACH during retching or vomiting; presents with painFUL hematemesis
Lymph node spread in esophagus, upper vs middle vs lower? Relevant for cancerUpper – cervical; middle – mediastinal or tracheobronchial; lower- celiac and gastric
Barrett’s increases the risk of adenocarcinoma by how much30-40 times. Adenocarcinomas develop from metaplasia -> dysplasia -> malignancy.


Question Answer
Pancreatic juice contentsISOTONIC but more HC03- and lower Cl- than plasma (and then also Na and K to balance; equal to levels in serum). Stimulated by secretin.
If pancreatic secretions have more Bicarbonate then they have lessCl.
Trypsinogen can be activated byTrypsin and first by enterokinase (intestinal brush border enzyme)
Secretin is released in response toH+ concentrations. Duodenal S cells.
Leptin produced byAdipocytes in proportion to quantity of fat stored.
Leptin acts onArcuate nucleus of HT to inhibit production of neuropeptide Y (decreases appetite since NPY is normally a potent appetite stimulant) and stimulates POMC -> alpha MSH (increases satiety).
Serum leptin is correlated withbody fat content. Produced most in large fat cells.
Most obese people do or do not have mutation in leptin receptor?Do NOT. Rather, probably leptin desensitization akin to insulin resistance.
Prolonged starvation, what happens to leptin levelsLOW.
Dumping syndromewithout stomach as reservoir for ingested food, dumping syndrome with colicky abdominal pain, n/ diarrhea. Avoid large meals and simple sugars.
Protein digestion in stomach depends onacid from parietal cells (-> denatures dietary protein improving proteolysis and converts pepsinogen to pepsin) and pepsinogen (from chief cells). Pepsin cleaves denatured polypeptides at aromatic amino acid locations and then pancreatic and intestinal proteases do the rest to get them into basic amino acids in IS.




Question Answer
Cholestasis characterized byDeposition of bile pigment within the hepatic parenchyma and presence of green-brown plugs in dilated bile canaculi, regardless of whether it is obstructive or nonobstructive
Cholestasis isWhen bile cannot flow from bile ducts to duodenum.
Cholestasis causesHepatocellular dysfunction or intrahepatic or extrahepatic dysfunction
Cholestasis intrahepatic causesPBC, PSC (which is also commonly extrahepatic), cholestasis of pregnancy, drug-induced (erythromycin, contraceptives)
Cholestasis extrahepatic causesCholedocholithiasis; malignancy (pancreatic; gallbladder)
Prolonged cholestasis would lead to what kind of malabsorptionFat malabsorption and so things like osteomalacia (from too little Ca/ Vit D) and its resulting decreased bone density
Cholelithiasis (cholesterol or bilirubin) arises from three scenariosa. supersaturation of cholesterol or bilirubin; b. decreased phospholipids (lecithin) or bile acids (normally increase solubility) or c. stasis (leading to increased growth of bacteria and bilirubin gallstones)
Recall bile acids in bile have what key functionSolubilize cholesterol; higher risk of cholesterol precipitate
Cholesterol removed from body in 2 ways1. Conversion into bile acids from cholesterol, 2. Excretion of free cholesterol into the bile
Liver, conversion of cholesterol to bile acids and salts1. Free cholesterol converted into cholic and chenodeoxycholic acids through a series of chemical reactions beginning with cholesterol 7-alphahydroxylase (rate limiting step!). 2. Bile acids then conjugated with glycine or taurine (improving solubility and emulsifying ability) to create bile salts. 3. Actively secreted into bile canaculi. Along with phosphatidylcholine, a PLipid, they act as detergent for free cholesterol.
Air in gallbladder and biliary tree?Cholecystenteric fistula between gallbladder and adjoining gut tissue due to persistent pressure on these tissues. Allows gall stone into small bowel and resulting communication between gallbladder and small bowel allows intestinal gas to enter the gb and biliary tree. Gall bladder passes through without problem until it hits the ileocecal valve, which is used to seeing fluids and so the gallbladder gets stuck*! Small bowel obstruction symptoms (pain and distension, vomiting, tenderness and tinkling bowel sounds)
Treatment of gallstone ileusSurgical removal of offending stone; cholecystectomy and repair of the fistula are rarely necessary.
Obstruction of cystic duct or common bile duct by a gallstone is referred to asCholedocolithiasis. Can lead to biliary colic, jaundice and cholangitis.
Cholangitis triad (Charcot)Jaundice, fever, RUQ pain. Also murphy’s sign – inspiratory pause during RUQ palpation.
Cholecystectomy, what effect on lipid digestionNone really except increased uptake of bile via enterohepatic circulation and maybe some difficulty tolerating fatty meals at one sitting because lack ability to release a large amount of stored bile into the gut in a coordinated fashion.
Lipids digested in? absorbed in?Digested in duodenum, absorbed in jejunum, passively once as micelles and then reform chylomicrons via triglycerides and cholesterol esters.



Question Answer
When don’t you see ascites with portal HTNportal vein thromboses since ascites results from sinusoidal hypertension*; instead, splenomegaly, varicosities at portocaval anastomoses, esophageal varices
Portal HTN with intact liver means likelyPortal vein thrombosis
Primary biliary cirrhosisautoimmune reaction; lymphocytic infiltrate with granulomas**; destruction of INTRAlobular bile ducts; middle aged women; like other biliary tract diseases, pruritus, jaundice, dark urine, light colored stool, hepatosplenomegaly and increased bili, cholesterol and ALP.
PBC micro and macroscopicallyPortal inflammation; eventual fibrosis and destruction of bile ducts with granulomas and bile duct proliferation, portal tracts and liver parenchyma
Pyogenic hepatic abscessResult of local spread of infection within the biliary tere or peritoneal cavity or from hematogenous seeding from the liver. Fever abdominal pain chills anorexia weight loss nausea or vomiting.
Hepatic adenomaYong and middle aged women with long history of OCP most commonly (also anabolic steroid use); rare, benign; may regress spontaneously or rupture (leading to abdominal pain and shock); clinical presentationabdominal pain in epigastric or RUQ and imaging is done OR sudden collapse because of the rupture and bleeding
Ascites pathogenesisFibrosis of portal vein causing mechanical compromise (such as due to alcohol cirrhosis -> micronodular cirrhosis a/w hepatocyte death) + dilation of splanchnic arterial vasculature and intrahepatic vasoconstriction = increased portal vein hydrostatic pressure = ascites + renal sensing underperfusion takes in more Na and water
Treatment for ascitesFurosemide and spironolactone
Small intestinal mucosa with enlarged foamy macrophages with rod-shaped bacilli and PAS-positive diastase resistant granules (lysosomes and partially digested bacteria)T. Whippelii/ Whipple disease
Since PAS can stain glycoproteins brilliant magenta, effective forPolysac of fungal cell wall, mucosubstance secreted by epithelia, and BMs. Also glycogen when used with diastase. Diastase digests glycogen to form maltaose and glucose.
Whipple disease, about the bug?Gram positive, actinomycete, rod-shaped; has PAS positive diastase resistant granules
Whipple disease commonly seen inMiddle aged Caucasian males presenting as malabsorption with diarrhea and weight loss
AST and ALThepatocellular damage/ liver injury
Gamma glutamyl transpeptidase and alk phosbiliary injury. Gamma glutamyl important to differentiate from bone disease.
Albumin, bilirubin, PTLiver function, most important prognostic indicators for patients with cirrhosis
Cirrhosis histologyfibrosis and noular parenchymal regeneration; dilation of sinusoids and perivenular hemorrhages happens from budd-chiari syndrome
Intrahepatic hydatid cystsEchinococcus (whereas amoeba -> liver abscess)
Granulomatous destruction of bile ductsPBC
Lactate is or is not elevatedYes elevated since liver is typically the place where lactate is metabolized so without as many hepatocytes, there will be less lactate disposal.
Cirrhosis causesChronic viral hep, alcohol, hemochromatosis, nonalcoholic fatty liver disease