Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
252 Cards in this Set
- Front
- Back
|
From what portion of the gut is the pancreas formed embyologically speaking?
|
Foregut (portion of duodenum)
|
|
|
Embryologic failure of neural crest cell migration into the bowel wall leads to what?
|
Hirschprungs
|
|
|
Failure of obliteration of the omphalomesenteric (viteline) duct leads to what?
|
Meckels!
|
|
|
Intestinal atresia distal to the duodenum ('apple peel" atresia) occurs due to what?
|
Vascular occlusion. Apple peel is distal ileum spiraling around ileocolic vessel.
|
|
|
Failure of recannalization during gut development leads to what?
|
Duodenal atresia
|
|
|
What 3 things does the ventral pancreatic bud give rise to?
|
Portion of pancreatic head, uncinate process, main pancreatic duct
|
|
|
What is pancreatic divisum?
|
Ventral and dorsal pancreatic buds fail to fuse. Accessory duct (from dorsal bud) drains most of pancreatic juices.
|
|
|
Is Meckel's a true or false diverticulum? What does each kind involve?
|
True! Mucosa, submucosa and muscle. False does not contain muscluar layer.
|
|
|
In Hirschsprung, what parts of the bowel are most frequently invovled.
|
Rectum and anus are always involved - neural crest cells migrate caudally, so more caudal structure are always invovled first! (since due to a failure of migration)
|
|
|
What other congenital anomalies are most associated wtih imperforate anus?
|
Other urogenital anomalies. VACTERL also, but less commonly.
|
|
|
What GI condition is associated with dermatitis herpitiformis (pruritic papulovesicular rash on extensor surfaces)?
|
Celiac!
|
|
|
What two derm conditions are associated with Crohns?
|
Erythema nodosum (painful nodules under skin) and pyoderma gangrenosum (deep ulcer wtih violaceous border)
|
|
|
What does trypsin do?
|
Activates all propancreatic enzymes, including itself
|
|
|
What converts trypsinogen to trypsen?
|
Pancreatic enterokinase/enteropeptidase
|
|
|
What happens if trypsinogen is prematurely activated?
|
Pancreatic autodigestion!
|
|
|
A gene mutation that renders trypsinogen insensitive to inactivation would cause what?
|
Pancreatitis!
|
|
|
GI distress with garlic odor on breath - what intoxication?
|
Arsenic!
|
|
|
Tx of arsenic poisening?
|
Dimercaprol. Displaces arsenic from enzymes that it is inhibiting.
|
|
|
Tx of choice for acute lead or mercury poisening?
|
CaNa2EDTA. Dimercaprol also works for lead.
|
|
|
Tx of cyanide poisening?
|
Amyl nitrite
|
|
|
Tx of iron poisening?
|
Deferoxamine
|
|
|
What is methylene blue used to treat?
|
Metheomoglobinemia
|
|
|
What organ is supplied by the celiac trunk though it is not foregut derived? Where is it actually derived from?
|
Spleen. Derived from medoermal dorsal mesentery
|
|
|
Is the liver derived from the foregut?
|
Yes!
|
|
|
What hormone stimulates release of pancreatic bicarb? Secreted from what cell type, where?
|
Secretin! Secreted from S cells in duodenum
|
|
|
What is the most potent stimulator of secretin secretion?
|
Acid!
|
|
|
Where are partietal cells located?
|
Fundus and body of stomach
|
|
|
What 2 hormones are secreted by gastric parietal cells?
|
Gastric acid and IF
|
|
|
What 3 things stimulate parietal cells to release acid?
|
Histamine, Ach, Gastrin.
|
|
|
What 2 thigns inhibit gastric acid secretion from parietal cells?
|
PGE2 (and misoprostol) and somatostatin
|
|
|
Besides stimulating acid production, what effect does gastrin have on parietal cells?
|
Causes proliferation and hyperplasia!
|
|
|
D-xylose absorption helps differentiate between absorption difficulties of what two etiologies?
|
Pancreatic enzyme vs gut mucosal etiology. D-xylose is a monosaccaride, so no pancreatic enzymes are necessary to absorb it, just gut mucosa.
|
|
|
Why are fistulats common in crohns and not UC?
|
Crohn's involves full thickeness of bowel wall!
|
|
|
GI condition with rheumatological, CNS, ocular and constitutional sx. What d/o?
|
Whipple's disease!
|
|
|
Ruptured gastric ulcer on lesser curvature of the stomach causes bleeding from what artery?
|
Left gastric
|
|
|
Ruptured duadenal ulcer on posterior wall of duodenum causes bleeding from what artery?
|
gastroduodenal
|
|
|
Do duodenal ulcers perforate more if they are anterior or posterior? Hemorrhage more?
|
Perforate - anterior! Bleed - posterior
|
|
|
Which extends deeper, erosions or ulcers? How deep (in terms of layers)
|
Ulcers are deeper, and can penetrate into the muscularis layer. Erosions DO NOT involve the muscularis, only mucosa and submucosa
|
|
|
Why does crohns predispose you to kidney stones? What kind?
|
Oxalate stones. XS fat that is not-absorbed binds Ca in gut lumen, keeping oxalate from binding it, so more oxalate is absorbed. Oh no!
|
|
|
Where are Peyer's patches found?
|
Illeum!
|
|
|
Which portion of the small intestine has the largest number of goblet cells?
|
Illeum!
|
|
|
Does the colon have crypts (of Lieberkuhn)? Villi?
|
Crypts yes, but no villi
|
|
|
What do the chief cells produce?
|
Pepsinogen!
|
|
|
In order, 3 most common sites of colon cancer?
|
Rectosignmoid>ascending>descending
|
|
|
What does the PAS stain highlight well?
|
Glycoproteins of fungi cell walls (Whipple's dz), basement membranes
|
|
|
What is diphenoxylate?
|
Lomotil - mu opiod agonist that slows motility, helps with diarrhea (similar to meperidine).
|
|
|
What kind of diarrhea is octreotide helpful for?
|
Secretory diarrhea
|
|
|
What are bismuth and sucralfate used for?
|
Increased ulcer healing (bind to base of ulcer and protect), Traveler's diarrhea
|
|
|
Esophageal mass showing histology with "keratin nests and pearls". What is it?
|
SCC
|
|
|
What is associated with betal nut chewing and eating N-nitroso containing compounds?
|
Esophageal SCC
|
|
|
Is achalasia associated with esophageal cancer? Which kind?
|
Yes, both!
|
|
|
How many calories come from 1g of protein, fat and carbs?
|
4cals from protein and carbs, 9 cal from fat
|
|
|
What is the progression of colon cancer from normal colon to carcinoma, including genetic events?
|
Normal colon - loss of APC gene -> colon at risk - K-RAS mutation -> adenoma - loss of p53 -> carcinoma
|
|
|
What property of a drug makes it more likely to undergo hepatic vs renal clearance?
|
High lipophillicity (can cross cellular barriers more easily and enter hepatocytes)
|
|
|
The 3rd part of the duodenum is close to what 2 blood vessels?
|
SMA and IVC
|
|
|
Where do most (90%) anal fissure occur relative to the anus?
|
Posterior midline of anal verge (relatively poorly perfused)
|
|
|
What solid organs are retroperitoneal?
|
Pancreas (except tail), adrenals, kidneys
|
|
|
Are the abdominal aorta and IVC retroperitoneal?
|
Yes!
|
|
|
What parts of the GI tract are retroperitoneal?
|
Parts 2, 3 and part of 4 of the duodenum, ascending and descending colon, rectum
|
|
|
What parts of the GU system are retroperitoneal?
|
Bladder, ureters
|
|
|
What happens to levels of SHBG in cirrhosis? What does this result in?
|
They INCREASE. This means more testosterone is bound, so the fraction of free is less, resulting in an estrogen state!
|
|
|
What are the 3 phases of the stimuation of acid secretion in the stomach?
|
Cephalic, gastric (both pro acid) intestinal (anti acid)
|
|
|
How does gastric acid secretion get downregulated after a meal?
|
Intestinal influences (peptide YY secreted from ileum and colon, binds to ECL cells to turn off). Also somatostatin and PGs.
|
|
|
Inhaled anesthetics (particularly halothane) have what potential toxicity? Presentation?
|
Hepatotoxicity. Presents like acute viral hepatitis. Elevated liver enzymes, long PT, eosinophilia.
|
|
|
dysphagia and chest pain, think what?
|
Diffuse esophageal spasm! (DES)
|
|
|
Treatment of copper xs in wilsons?
|
Penicillamine
|
|
|
Is ceruloplasmin low or high in Wilson's?
|
Low!
|
|
|
Gallbladder hypomotility results in the formation of what?
|
Biliary sludge!
|
|
|
What color gallstone is seen in biliary tract infection?
|
Brown!
|
|
|
Black pigment gallstones are indicative of what?
|
Hemolysis
|
|
|
How does the mutation in hemochomatosis work?
|
Protein on basolateral surface of intestinal cells is mutated (HFE gene), so serum iron levels can't be sensed (by binding with transferin receptor), and unregulated iron absorption from GI tract occurs.
|
|
|
What effect does homechromatosis have on the liver?
|
Cirrhosis and HCC
|
|
|
What % of a cholesterol stone is cholesterol? What % of a pigment stone is cholesterol?
|
80% or greater for cholesterol stones, <20% for pigment stones
|
|
|
What does B-glucuronidase do?
|
Converts conjugated bilirubin back to unconjugated for reuptake in the gut. (glucuronyltransferase works the other way)
|
|
|
MoA of infection producing brown pigment stones?
|
B-glucuronidase is released from injured hepatocytes and bacteria, which results in reconjugation of bilirubin into unconjugated, and results in brown pigment.
|
|
|
How does estrogen increase risk of gallstones?
|
Upregulates cholesterol synthesis (by stimulating HMG-CoA reductase) -> bile supersaturated with cholesterol.
|
|
|
How does progesterone increase risk of gallstones?
|
Reduces bile acid secretion and causes gallbladder hypomotility.
|
|
|
Who gets acute acalculous cholecystitis?
|
Hospitalized pts
|
|
|
What 2 colon cancer promoting steps happen between the loss of APC and the K-RAS mutation?
|
1) methylation abnormalities 2) COX-2 overexpression
|
|
|
What colon cancer promoting step happens between the K-RAS mutation and the loss of p53?
|
DCC inactivation
|
|
|
Is COX-2 overexpressed or underexpressed in colon cancer? What tx could this suggest?
|
Overexpressed - aspirin!
|
|
|
What % of duodenal ulcers have H pylori?
|
Almost 100%
|
|
|
Most effective means of long term relief of duodenal ulcers?
|
Abx! Eradicate h pylori!
|
|
|
MoA metoclopramide? Uses (2)?
|
D2 antagonist. Increases motility, anti-emetic
|
|
|
MoA misoprostol?
|
PGE1 analog. Increases production and secretion of gastric mucosa, decreases acid production.
|
|
|
GI wise, what is misoprostol used for?
|
Protection from NSAID induced ulcers
|
|
|
Which is better for treating peptic ulcer disease - PPIs and H2 blockers?
|
PPIs!
|
|
|
Bilateral ovarian tumors, abundant mucus, signet ring cells. What primary? What are these tumors called?
|
Stomach cancer. Krunkenberg tumors.
|
|
|
Virchow's node and Sister Mary Joseph's nodule make you think of what primary?
|
Stomach! Or pancreas
|
|
|
Stomach cancer is usually of what type?
|
Adenocarcinoma
|
|
|
Stomach cancer is associated with what skin finding?
|
Acanthosis nigricans
|
|
|
Which type of stomach cancer is associated with H pylori, intestinal or diffuse type?
|
Intestinal
|
|
|
Intestinal type stomach cancer is usually located where in the stomach? Appearance?
|
Lesser curvature, looks like ulcer with raised margins.
|
|
|
Where is H pylori typically found in greatest concentration?
|
Prepyloric area of the gastric antrum.
|
|
|
Can H pylori colonize normal duadenal mucosa?
|
No! Only gastric mucos or areas of gastric metaplasia in the duodenum
|
|
|
Hepatocytes filled with protein granules that takes on a "ground glass" appearance, also eosinophillic. What infection, what are the granules made of?
|
Hep B. Granules are made of spheres and tubules of HBsAg.
|
|
|
Hepatitis showing liver with lymphoid aggregates in portal tracts and focal areas of macrovesicular steatosis - what bug?
|
Hep C!
|
|
|
What branches (2 main) does the splenic artery give off before reaching the spleen? Which of these is most subjec to ischemia if the splenic is blocked?
|
Left gastroepiploic, short gastrics. Short gastrics most subject to ischemia since have poor anastamoses.
|
|
|
Where is a-1-antitrypsin produced?
|
Primarily in the liver
|
|
|
In what parts of the gut are lipids digested and absorbed?
|
Digested in duodenum, absorbed in jejunum
|
|
|
Where in the gut is Fe absorbed?
|
Duodenum
|
|
|
Where in the gut is folate absorbed?
|
Jejunum
|
|
|
Where in the gut is B12 absorbed?
|
Terminal ileum (with If)
|
|
|
What 2 things can the stomach absorb?
|
Water and EtOH
|
|
|
Where are the vitamin ADEK absorbed?
|
Jejunum, along with fat!
|
|
|
Pt with UC presents w/ poss toxic megacolon. What study should you do, and what 2 studies should you NOT do.
|
Plain abd xray do d/x. AVOID colonoscopy and barium enema for risk of rupture.
|
|
|
Mechanism of enterococcus becoming VRE?
|
Substitution of D-lactate for D-alanine in cell wall
|
|
|
MoA systemic mastocytosis. Clinical presentation?
|
Bone marrow produces too many mast cells, which release histamine! Increased gastric acid production, pruritis, flushing, syncope, flushing, tachycardia.
|
|
|
Whcih is more common after Hep C infection: stable chronic hepatitis or chronic hepatitis progressing to cirrhosis?
|
Stable chronic, followed closely by chronic progressing to cirrhosis
|
|
|
Is the rectum always invovled in UC?
|
YES
|
|
|
Pts at increased risk of HCC shoudl be regularly monitored with serum levels of what?
|
AFP!
|
|
|
How does L sided colon cancer typically present?
|
Obstruction
|
|
|
Tenesmus and thin stool are a typical presentation of what?
|
Rectal mass, concern for rectal adenocarcinoma
|
|
|
MoA of HBV infection triggering HCC?
|
Viral DNA integration into host genome
|
|
|
Mechanism of esophageal fail in CREST?
|
Fibrous replacement of the muscularis
|
|
|
"Corkscrew esophagus"?
|
DES
|
|
|
MoA atropine?
|
Block muscarinic Ach receptors (parasympathetic antagonist)
|
|
|
Lactose challenge in someone with lactose intolerance does what to stool ostmotic gap, breath H+ and stool pH?
|
Increases osmotic gap, increases breath H+, and decreases pH
|
|
|
What are the walls of a pancreatic psuedocyst made of? What is the cyst fluid made of?
|
Walls: granulation tissue and fibrosis. Fluid: enzymes and inflammatory debris
|
|
|
As pancreatic juice secretion rate increases, what happens to the concentrations of HCO3 and Cl-?
|
HCO3 increases and Cl decreases.
|
|
|
If a sample of gastric mucosa turns a solution of urea pink (increases pH), what does this imply?
|
H pylori infection! H pylor have urease to break down urea!
|
|
|
What is the primary means of copper excretion?
|
Hepatic excretion into bile (5-15% is excreted renally)
|
|
|
What does the mutation in HNPCC mess with?
|
DNA mismatch repair
|
|
|
Is ti common in HNPCC to have other cancers occuring simultaneously or after colon cancer resection?
|
Yes.
|
|
|
In HNPCC, is there a primary adenomatous polyp?
|
No. Cancer develops from macroscopically normal colon mucosa
|
|
|
How can staph aureus cause a hepatic abcess?
|
Hematogenous spread.
|
|
|
What cell type allows Shigella to enter the body? Where are these cells found?
|
M-cells in Peyer's patches of ileal mucosa
|
|
|
A bimodal distribution in a population of speed of metabolism of a drug is due to differences in what process?
|
Acetylation!
|
|
|
Is increased gastric acid secretion necessary for gastric ulcer formation 2/2 h pylori? Duodenal?
|
Increased acid is only necessary for duodenal, because duodenum doesnt' produce it's own acid. Acid is necessary for ulcer formation once H pylori degrades mucosa.
|
|
|
Can you get carcinoid syndrome from just a primary GI tumor?
|
No! Must have metastasized to get symptoms (to avoid first pass)
|
|
|
How does gallstone illeus form?
|
Large gallstone makes fistula with small bowel, goes into intestine, jams at ileocecal valve -> illeus! Can also get air in biliary system from connecting to gut.
|
|
|
Difference in diverticula formed during adults vs fetal life?
|
Adult - usually false, due to pulsion. Fetal - usually true.
|
|
|
Prolonged cholestasis, think what conditions?
|
Malabsorptive (ADEK vitamins)
|
|
|
In what 2 ways does N-acetyl cystein help acetopminophen toxicity?
|
Providing a sulfhydryl group and acting as a glutathione substitute
|
|
|
What is Crigker-Najjar?
|
Lack of UGD leads to unconjugated hyperbili. Unconjugated bili cant be removed by kidneys, so builds up in tissue like brain -> kernicterus
|
|
|
MoA Dubin Johnson. Clinical presentation?
|
Failure of excretion of conjugated bilirubin into bili canniliculi -> goes into blood -> urine instead. Black liver, but clinically silent
|
|
|
What 2 things increase CCK secretion?
|
Fatty acids and amino acids
|
|
|
What are the 2 main cell types in the gastric body? What do they produce?
|
Parietal cells (HCl, IF) and Chief cells (pepsinogen).
|
|
|
What are the 3 main cell types in the gastric antrum? What do they produce?
|
G cells (gastrin), mucus cells (mucus) and D cells (somatostatin)
|
|
|
What are the 3 main cell types in the first part of the duodenum? What do they produce?
|
I cells (CCK) S cells (secretin) K cells (GIP)
|
|
|
Nest or sheets of uniform cells with eosinophillic cytoplasm and oval to round stippled nuclei - in appendix. What is it?
|
Carcinoid tumor!
|
|
|
Most common sites of carcinoid tumors?
|
Illeum! Also appendix and rectum.
|
|
|
Can Kaposi's sarcoma be in the gut?
|
Yes!
|
|
|
AIDs pt with bloody diarrhea, histology shows spindle shaped tumor cells with small vessel proliferation?
|
Kaposi's sarcoma. HHV-8
|
|
|
Numerous discrete, flask shaped ulcerative lesions on colonoscopy, what agent?
|
Entamoeba histolytica
|
|
|
Is alcohol use a risk factor for pancreatic cancer?
|
Nope!
|
|
|
Is diabetes a risk factor for pancreatic cancer?
|
Yes!
|
|
|
Are duodenal ulcers associated with an increased risk of malignancy?
|
Nope!
|
|
|
How do you treat Whipple's disease?
|
Abx!
|
|
|
"Distended macrophages in the lamina propria" What conditions?
|
Whipple's disease! Lives in macrophages.
|
|
|
What is seen on microscopic examination of the intestines of people with lactose intolerance?
|
Normal bowel mucosa!
|
|
|
"Collections of neutrophils within the crypt lumina" is seen in what condition?
|
UC!
|
|
|
Do inflammatory polyps have neoplastic potential?
|
Nope!
|
|
|
Which is more likely to progress to malignancy - villous or tubular adenomatous polyps?
|
Villous!
|
|
|
Cirrhosis and basal ganlgia atrophy, think what?
|
Wilson's disease
|
|
|
What med can be used to control symptoms in carcinoid?
|
Octreotide
|
|
|
What is the main determinant of bioavailability after oral intake?
|
Liver blood flow (first pass metabolism)
|
|
|
What levels of cholesterol, bile acids, and phosphatidyl choline DECREASE risk of gallstones?
|
LOW cholesterol, HIGH bile acids and phosphatidylcholine (make cholesterol soluble)
|
|
|
How does AZT (Zidovudine) work?
|
NRTI - integrates into viral genome and messes up 3'-5' phospodiester bond formation.
|
|
|
"Fibrosis and nodular parenchymal regeneration" describes what?
|
End stage cirrhosis
|
|
|
Crichopharyngeal muscle dysfunction causes what condition?
|
Zenkers (diminished relaxation during swallowing causes increased luminal pressure)
|
|
|
Black liver with lysosomes containing pigment composed of epinephrine metabolities - what d/o?
|
Dubin-Johnson. No clinical problems.
|
|
|
After gastrectomy, pts require lifelong supplmementation of what?
|
B12! (A WATER soluble vitamin)
|
|
|
How does ribavirin work in treating hep C?
|
Interferes with duplication of viral material.
|
|
|
Opiod administration is followed by RUQ pain. What's going on?
|
Opiod induced smooth muscle contractino of sphincter of oddi -> increased pressure leads to biliary colic
|
|
|
What is acute clinical illness with hep C like?
|
Very mild - malaise, nausea, RUQ pain.
|
|
|
What is acute Hep B infection like?
|
Malaise, fever, skin rash, pruritis, joint pain, lymphadenopathy
|
|
|
Can gilbert's make you jaundiced?
|
Yes! Common triggers: excersize, stress, etc
|
|
|
Grossly edematous pancreatic with surrounding focal areas of fat necrosis, calcium deposition and interstitial edema - what kind of pancreatitis?
|
Interstitial (vs necrotizing)
|
|
|
Pancreatitis with chaky white areas of fat necrosis interspersed with hemorrhage - what kind of pancreatitis?
|
Necrotizing (hemorrhagic)
|
|
|
What layer of the bowel wall should be bx'ed to ***** for Hirschsprugns?
|
Submucosa (Meissners). Also missing Auerbach's (in muscularis) but only want to biopsy as deep as you have to
|
|
|
Parietal cells are found in what layer of the gastric wall?
|
Upper part of submucosa (where the glands are)
|
|
|
How do you definitively dx celiac dz?
|
Small intestine biopsy
|
|
|
"Epigastric calcifications" think what?
|
Acute/chornic pancreatitis
|
|
|
Red-pink PAS staining granules in periportal hepatocytes with emphysema. What is it?
|
A1AT (granules are unsecreted A1AT)
|
|
|
The lesser omentum is made up of what 2 ligaments?
|
Hepatogastric and hepatoduodenal
|
|
|
HIV esophagitis: white pseudomembranes vs linear ulceration vs "punched out" ulcers, what bugs?
|
White = candida, linear = CMV, punched out = HSV
|
|
|
HIV esophagitis: intranuclear inclusions alone vs intranuclear and intracytoplasmic - which bugs?
|
Intranuclear alone = HSV (also eosinophillic, in squamous cells at border of ulcer). Both = CMV
|
|
|
What enzyme is most responsible for acute necrotizing pancreatitis?
|
Trypsin!
|
|
|
Coloinc mass that is cauliflower shaped and secretes tons of mucus. What is it?
|
Villous adenoma (one possible presentation)
|
|
|
What does 7-a-hydroxylase do? What does it's suppression increase risk of?
|
Converts cholesterol into bile salts. Suppression increases risk of gallstones.
|
|
|
Frequent first initial symptoms of PBC? What conditions is it associated with?
|
Pruritis (especially at night)! Sjogrens, Raynauds, scleroderma, etc
|
|
|
Which type of stomach cancer has a signet ring pattern? Growth pattern?
|
Diffuse! Infiltrates gastric wall.
|
|
|
What is the growth pattern of intestinal type gastric cancer?
|
Grows into stomach lumen, can reach large size
|
|
|
What about vomitting causes Mallory-weiss tears?
|
Increased intra abdominal/gastric pressure
|
|
|
Liver "microvesicular steatosis without inflammation". Also mitochondiral abnormalities. What condition?
|
Reye's syndrome
|
|
|
"Granulomatous bile duct destruction" what condition? What immunologic disorder is it similar to?
|
PBC. Similar to Graft-vs-host
|
|
|
Duodenal ulcer is distal duodenum - think what?
|
ZES
|
|
|
Spilling of the contents of a hyaditid cyst could cause what?
|
Anaphylaxis!
|
|
|
Which has more prognostic implication in alcoholic cirrhosis - liver enzyme levels or PT?
|
PT! Enzyme just show damage, PT and serum albumin show function.
|
|
|
Portal/systemic veins involved in: esophageal varices?
|
Portal: left gastric systemic: esophageal veins
|
|
|
Portal/systemic veins involved in: hemorrhoids?
|
Portal: superior rectal vein systemic: middle and inferior rectal veins
|
|
|
Portal/ssytemic veins involved in: caput medusae?
|
Portal: paraumbilical veins systemic: superficial and inferior epigastric veins
|
|
|
What is the mneumonic to remember VIPoma?
|
WDHA syndrome. Watery Diarrhea, hypokalemia, achlorhydria (gastric acid secretion inhibited by VIP)
|
|
|
How do you treat VIPoma?
|
Somatostatin (blocks effect of VIP)
|
|
|
What is the effect of VIP on gastric acid secretion? On intestinal smooth muscle and sphincters?
|
Decreases gastric acid secretion. Relaxes intestinal smooth muscle and sphincters
|
|
|
What are Curling ulcers? Associated with what (2)?
|
Ulcers in the proximal duodenum is association with severe trauma or burns (2/2 decreased plasma volume)
|
|
|
What are Cushing ulcers? MoA?
|
Esophageal, gastric or duadenal ulcers arising in pt with elevated ICP (as in after head trauma). 2/2 vagus stimulation from incr ICP increasing gastric acid secretion
|
|
|
How does the histological grade of UC associated CRC compare to sporadic? What about gene mutations? Which is multifocal?
|
Histologic grade is HIGHER in UC associated. p53 mutations occur EARLIER and APC mutations LATER in Uc associated. UC associated is multifocal, not from polyp.
|
|
|
Colicky abdominal pain and bluish line at tooth/gum border. What toxicity?
|
Lead! "Lead colic" and "lead line"
|
|
|
What kinds of neuro symtpoms do you see with lead poisening?
|
Wrist/foot drop from peripheral neuropathy, impaired concentration, deficits in short term memory
|
|
|
What does NF-kB stimulate?
|
Cytokines!!!!!!!!!!!!!
|
|
|
What is the initial test to confirm malabsorptive diarrhea?
|
Sudan III stool test! Looks for fecal fat (>7g/day is diagnostic)
|
|
|
An alk phos is elevated. How do you clarify if it's billiary or bone?
|
GGT!
|
|
|
What is the most common hepatic neoplasm?
|
Mets!
|
|
|
Uniformly light pink cells interspersed in a tumory looking mess - what is it?
|
Keratin! Implies SCC (as opposed to adenocarcinoma, in the esophagus for example)
|
|
|
Postprandial epigastric/periumbilical pain not relieved by food or antacids, in a pt with known atherosclerosis. Weight loss. What is it?
|
Chornic mesenteric ischemia.
|
|
|
Who does PBC usually happen in?
|
Middle aged women
|
|
|
Liver bx showing extensive lymphocyte infiltration and granulomatous destruction of bile ducts. What is it?
|
PBC!
|
|
|
What is going on pathologically in PSC?
|
Inflammation of intra and extrahepatic biliary ducts! CholANGITIS
|
|
|
Why do women with hemochromatosis sometimes present later than men?
|
Blood loss from menstruation/pregnancy
|
|
|
In acute cholecystitis, does the galbladder get inflammed and necrotic?
|
Yes!
|
|
|
A decrease in what biochemical process leads to alcoholic hepatic steatosis?
|
Decrease in FFA oxidation (from icnreased NADH/NAD+ ratio) (gluconeogenesis is also decreased)
|
|
|
Is isoniazid directly hepatotoxic?
|
Yes!
|
|
|
2 methods of TPN induced gallstone formation?
|
1) Lack of enteral stimulation leads to decreased CCK release and decr gallbladder contraction 2) disrupted enterohepatic circulation of bile salts.
|
|
|
What is the most common longterm outcome after HBV infection?
|
Complete resolution (unlike hep C) in which stable chronic/or chronic->cirrhosis is most common
|
|
|
HIv protease inhibitors (like indinavir) has what 3 main side effects?
|
1) Central fat w/ peripheral wasting (lipodystrophy) 2) Hyperglycemia (insulin resistence) 3) inhibition of P450
|
|
|
What immune cell is increased in Crohns? Why?
|
TH1 - granulomatous inflammation!
|
|
|
3 week old child with clinical sign of cholestasis, marked bile duct prolferation, intrahepatic cholestasis and poral tract edema and fibrosis, dx?
|
Biliary atresia
|
|
|
Chronic gastritis related to H pylori vs autoimmune - what part of stomach affected?
|
Antrum - h pylori (type B). Body = autoimmune (type A, parietal cells)
|
|
|
Does portal vein thrombosis cause liver hepatocyte changes histologically?
|
Nope! Since is before liver in cirulcation
|
|
|
What does HAV do histologically to hepatocytes?
|
Causes balooning degeneration, Councilman bodies (eosinophillic apoptotic hepatocytes) and mononuclear cell infiltrates
|
|
|
What is the most common benign hepatic lesion?
|
Cavernous hemangioma.
|
|
|
Do you biopsy a liver cavernous hemangioma to dx?
|
No! These are just pools of blood, so could cause serious hemorrhage!
|
|
|
"Fever and dark urine" is a typical presentation for what GI disease?
|
Acute hepatitis (HAV, commonly)
|
|
|
Moldy grains, corn, soybeans and peanuts in humid conditions grow what? What does this bug predispose to?
|
Aspergillus (aflatoxin) -> p53 mutations and HCC
|
|
|
Which is through umbilicus and covered by peritoneum, omphalocoele or gastroschisis?
|
Omphalocoele!
|
|
|
What is the most common type of TEF?
|
Blind pouch esophagus with tracheoesophageal fistula
|
|
|
What is carried in the hepatoduodenal ligament?
|
Portal triad: hepatic artery, portal vein, common bile duct
|
|
|
The frequency of basal electrical rhythm of the stomach, duodenum and illeum is in what order?
|
duodenum (12 waves/min)>ileum (8-9w/m)>stomach (3w/m)
|
|
|
The middle colic (MSA) has a strong anastomoses with what artery, from where?
|
Left colic (IMA)
|
|
|
The superior epigastric (internal thoracic/mammary) has a strong anastomoses with what artery, from where?
|
Inferior epigastric (external iliac)
|
|
|
The superior pancreaticoduodenal (celiac) has a strong anastomoses with what artery, from where?
|
Inferior pancraticoduodenal (SMA)
|
|
|
The superior rectal (IMA) has a strong anastomoses with what artery, from where?
|
middle and inferior rectal (internal iliac)
|
|
|
Why are internal hemorrhoids not painful and external ones are?
|
internal = visceral innervation, external = somatic innervation
|
|
|
What happens at the pectinate line?
|
endoderm (might form adenocarcinoma) meets ectoderm (might form SCC)
|
|
|
What liver zone is affected first by alcohol? viral hepatitis?
|
Alcohol = zone 3. Viral hepatitis = zone 1
|
|
|
What liver zone is affected first by ischemia?
|
Zone 3
|
|
|
A direct and indirect hernia both go through two things: what are they?
|
Indirect: deep and superficial rings. Direct: Hesselbach's triangle and superficial ring.
|
|
|
Who gets femoral hernias?
|
Women!
|
|
|
What makes Hesselbach's triangle?
|
Inferior epigastric vessels, lateral border of rectus abdominus, inguinal ligament
|
|
|
Who gets direct vs indiret hernias?
|
Indirect commonly babies, direct commonly older men
|
|
|
What is a direct hernia covered by, layer wise?
|
Just the external spermatic fascia (indirect has 3 layers of spermatic fascia)
|
|
|
What does GIP do (2)?
|
1) Dedr gastric acid secretion 2) increase insulin release
|
|
|
What hormone produces migratory motor complexes? Where is it found?
|
Motilin. Found in small intestine.
|
|
|
What salivary gland tumor is malignant and commonly involves the facial nerve?
|
Mucoepidermoid carcinoma
|
|
|
What is Plummer-Vinson syndrome?
|
Dysphagia 2/2 esophageal webs, glossitis, iron deficiency anemia. Risk factor for esophageal SCC
|
|
|
Gastric hypertrophy with protein loss, parietal cell atrophy, and incr mucous cells - stomach rugae look like brain gyri - what d/o?
|
Menetrier's disease.
|
|
|
Familial adenomatous polyposis + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium -> what d/o?
|
Gardner's syndrome
|
|
|
Familial adenomatous polyposis + malignant CNS tumor - what d/o?
|
Turcot's syndrome
|
|
|
"onion skin" bile duct fibrosis with "beading" or intra and extrahepatic bile ducts?
|
PSC
|
|
|
Anti mitochondrial abs, what d/o?
|
PBC
|
