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GI Flashcards

1
Q

Disease producing asymptomatic unconj bilirubinemia

A

Gilbert syndrome

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2
Q

Child vomited a large, long cylindrical white worm, what’s its route of infection?

A

Ascaris lumbricoides

Ingestion of eggs from human feces

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3
Q

What would be seen in mucosa bx of gastric in Menetrier disease

A

Mucous cell hyperplasia -> losing protein

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4
Q

Meningitis, see lymphocytes, plasma cells, macrophages, fibroblasts in CSF with elevated protein and depressed glucose. Emigrated from Ecuador. What infection?

A

TB

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5
Q

What 2 orgs cause HIV-assc esophagitis w/ ulcers?

A

CMV (linear ulcers)

HSV-1 (punched out ulcers)

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6
Q

Fever, confusion, nausea, elevated LFTs and bilirubin 4 days after laparotomy. What will be seen on liver bx?

A

Massive hepatic necrosis

Most likely from the use of halothane as anesthetics

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7
Q

Kid w/ bilious vomiting and cecum fixed to RU abd wall. What’s the problem?

A

Failure of midgut to rotate around SMA

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8
Q

2 day old w/ bilious vomiting. No large segment of small bowel but see distal ileum winding around a thin vascular stalk. What’s the intrauterine process affected?

A

Vascular occlusion (responsible for apple peel atresia, which is predominant when atresia happens distal to 2nd segment of duodenum. Before that segment, it’s failure to recanalize)

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9
Q

Pt w/ pruritus, rash, flushing, abd cramps, and nests of mast cells in mucosa. What do you expect to see in stomach?

A

Gastric hypersecretion

This is systemic mastocytosis, and all the histamine secretions by mast cells will result in acid secretion

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10
Q

What structure receives blood supply from the foregut even though it’s not a foregut derivative?

A

Spleen (mesodermal origin)

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11
Q

Another term for ectopy?

A

Heterotopy

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12
Q

Bx of eyelid shows cells with clear droplets in them. What are the disease associations?

A

That’s xanthelasma -> lipid accumulates in macrophages (foam cells)
It’s assc. w/ primary or secondary hyperlipidemia, so things like PBC and obstructive biliary lesions can cause this

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13
Q

What do you need a life-long supplement of after total gastrectomy?

A

B12 (“water soluble vitamin”) bc no longer making IF -> give B12 parenterally

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14
Q

How does HBV increase the risk of HCC?

A

Integration into genome (DNA virus) -> continues to produce HBx protein even after infection clears -> disrupts cell cycle control by activating multiple growth-promoting proteins and inactivating p53

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15
Q

3 characteristics histological findings of GERD

A 
Lamina propria papillae elongation
Basal zone hyperplasia
Inflammatory cells (lymphocytes, eosinophils, neutrophils)
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16
Q

Disease associations of imperforate anus

A

Most common: GU anomalies -> fistulas (urorectal, urovesical, urovaginal), renal agenesis, hypospadias, dpispadias, bladder extrophy
Less common: VACTERL -> Vetebral defects, Anal atresia, Cardiac anomalies, TE fistula, Esophageal atresia, Renal anomalies, Limb anomalies

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17
Q

Distended macrophages in the intestinal lamina propria. What’s the disease? What does macrophage contain?

A

Whipple

Macrophages contain PAS-positive and diastase-resistant granules and rod-shaped bac

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18
Q

Neutrophils w/in crypt lumina (intestine). What’s the disease?

A

UC

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19
Q

Inflammation w/ scattered noncaseating granulomas (intestine). What’s the disease?

A

Crohn

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20
Q

Massive infiltration of lamina propria w/ atypical lymphocytes. What’s the disease?

A

GI lymphomas

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21
Q

Jaundice + dyspnea w/ hyperlucency lung fields and flattened diaphragm in nonsmoker. Hx of neonatal hepatitis. What’s the disease?

A

a1-antitrypsin deficiency

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22
Q

What’s a Courvoisier sign?

A

Palpable but nontender bladder

See this sign in adenocarcinoma at the head of pancreas compressing common bile duct

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23
Q

Palpable but nontender gallbladder + weight loss + dark urine + pale stools

A

Adenocarcinoma at the head of pancreas compressing common bile duct
Palpable but nontender gallbladder = Courvoisier sign
Dark urine + pale stool + pruritis = obstructive jaundice

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24
Q

5 risk factors for pancreatic cancer

A 
Smoking!!! -> most important
DM
Age > 50
Chronic pancreatitis
Genetics: hereditary pancreatitis, MEN, HNPCC, FAP

Moderate alcohol use in the absence of chronic pancreatitis doesn’t confer risk

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25
Q

Pancreatic juice ion conc w/ respect to plasma?

A 
Isotonic secretion overall
Same conc of Na+, K+ as plasma
Higher HCO3- than plasma
Lower Cl- than plasma
Cl- decreases in proportion to HCO3- increase (this is opposite of sweat glands, which secrete more Cl- compared to HCO3-)
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26
Q

What kind of diarrhea do you see in Crohn and carcinoid syndrome? What is the characteristics of that type of diarrhea?

A

Secretory diarrhea

High electrolyte content from poor absorption and increased losses from inflamed mucosa

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27
Q

What’s an important cause of rectal prolapse in children?

A

CF

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28
Q

Dx for severe upper abd pain + vomiting + fever w/ necrotic gallbladder? Give 5 steps of pathogenesis.

A

Acute calculous cholecystitis
Steps: gallbladder outflow obstruction (cholelithiasis) -> protective mucus layer disrupted by stones, so epithelium exposed to detergent action of bile salts -> PGs released and further aggravate inflammation -> gallbladder hypomotility -> ischemia from distention and internal pressure -> bacteria invasion of necrotic tissue

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29
Q

What is “ramified, tubular glands in submucosa w/ pH secretions close to 9.0”

A

Brunner’s glands -> unique to duodenum

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30
Q

Pathogenesis of hepatic encephalopathy?

A

Increased inhibitory neurotransmission (GABA) and impaired excitatory neurotransmission (glutamate and catecholamines)
NH4+ increases activity of of 2 enzymes:
1. glutamine synthetase w/in astrocytes -> converting glutamate released from neurons to glutamine, which accumulates and causes hyperosmality and mitochondrial dysfx -> astrocyte dysfx
2. glutamate DH w/in neurons -> depletes alpha-glutamate in an attempt to detoxify
Might also have elevated oxindole during this condition -> tryptophan derivative formed by bacteria in the gut and is normally cleared by liver -> oxindole causes sedation, muscle weakness, hypotension, and coma

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31
Q

Finely eosinophilic granules in cytoplasm + portal inflammation + hepatocyte ballooning + necrosis

A

HBV

Eosinophilic granules are aggregates of HBsAg -> “ground glass”

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32
Q

Lymphoid aggregates w/in portal tracts + focal areas of macrovesicular steatosis

A

HCV

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33
Q

Confirmatory test in Dubin-Johnson? Why is liver black?

A

High coproporphyrin I in urine

Liver is black from dense pigment composed of epinephrine metabolites w/in lysosomes

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34
Q

What condition do you see smooth muscle cell Ab?

A

Autoimmune hepatitis

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35
Q

Steps of acute pancreatitis?

A

Damage to pancreatic acinar cells (direct insult or ischemia) -> activation of TRYPSIN inside acinar cells by lysosomal enzyme (MAIN EVENT) -> autodigestion (fat necrosis by lipase and everything else comes later)
In severe cases get acute necrotizing pancreatitis -> see diffuse enlargement w/ area of necrosis)

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36
Q

What do you see in liver bx in Reye syndrome? Brain? How about labs?

A

Liver bx: microvesicular steatosis WITHOUT inflammation; EM see decreased mito and glycogen depletion
Brain: cerebral edema
Labs: prolonged PT/PTT, high ammonia, bilirubin, AST, ALT

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37
Q

5 ways to inactivate hep A?

A 
Boiling 85C for 1 min
UV
Water chlorination
Bleach (1:100 dilution)
Formalin
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38
Q

What is D-xylose?

A

Monosaccharide that can be absorbed directly w/out the action of pancreatic enzyme
So it’s used to distinguish malabsorption of pancreatic from GI mucosa defects

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39
Q

Common sx of PBC? Histologic features?

A

Pruritus (first sx!), xanthelasma, pale stool
Florid duct lesion: interlobular bile duct destruction by granulomatous inflammation & lymphocyte-predominant portal tract infiltrate -> so features similar to GVHD
End-stage findings can’t be distinguished from secondary biliary cirrhosis or chronic hepatitis
Prolonged pruritus + fatigue is also assc. w/ PSC

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40
Q

“green-brown plugs in dilated bile canaliculi, yellowish-green deposition w/in hepatic parenchyma” describes?

A

Cholestasis in general (can be obstructive or nonobstructive) -> so find the etiology

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41
Q

What does prolonged cholestasis predispose you to?

A

Fat malabsorption -> so think about conditions resulting from fat-sol vitamins deficiency (for example, osteomalacia from vit D deficiency)

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42
Q

Psoas sign?

A

Pain w/ hip extension (causes psoas major to be stretched out)
Psoas major inserts on lesser trochanter of femur via tendon shared w/ iliacus m. -> they both are major flexor of hip

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43
Q

Another name for pancreatic cholera or WDHA syndrome?

A

VIPoma (pancreatic non-beta islet cell tumor) -> VIP also secreted by neurons in GI mucosa
WDHA = Watery Diarrhea, Hypokalemia, Achlorhydia (b/c VIP inhibits gastric H+ secretion)
Fixed w/ somatostatin

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44
Q

2 complications of glucagonoma?

A

DM

Necrolytic migratory erythema of skin

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45
Q

Example of pulsion diverticulum? Traction diverticulum?

A

Pulsion (false diverticula): colonic diverticula
Traction (true diverticula due to inflammation and subsequent scarring): midesophageal diverticula (from mediastinal lymphadenitis like TB and fungal infections, and periesophageal scarring)

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46
Q

Sx of carcinoid syndrome? What’s the cardiac finding? Do you get hypertension or hypotension?

A

Facial flushing, bronchospasm, diarrhea
Cardiac finding: fibrous intimal thickening w/ endocardial plaques limited to right heart -> eventually get pulmonic stenosis and restrictive cardiomyopathy
Get hyPOtension

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47
Q

Marker of HBV that’s worrisome for vertical transmission?

A

HBeAg -> viral replication and increased infectivity
So if mom is infected w/ HBV, always give newborn passive immunization w/ HBIG, followed by active immunization w/ recombinan HBV vaccine

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48
Q

What does anti-HBc IgM signify?

A

Window period (HBsAg has cleared but anti-HBs has not yet appeared) -> most specific marker for dx of acute hep B

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49
Q

What does HBsAg signify?

A

Infectivity

But NOT the most worrisome marker in pregnant women, HBeAg is

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50
Q

What molecule is present after either successful vaccination against HBV or clearance of HBV?

A

Anti-HBsAg IgG -> indicator of noninfectivity and immunity

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51
Q

What are ppl on TPN (total parenteral nutrition) susceptible to and why?

A

Gallstone formation
B/c there’s no stimulation of CCK release -> so now bile duct movement -> biliary stasis
If this involves ileal resection, condition is further made worse by the fact that bile acid circulation is disturbed -> supersaturation of hepatic bile w/ cholesterol

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52
Q

What 3 Ab do you find in ppl w/ celiac disease?

A

Anti-gliadin IgA
Anti-endomysial
Anti-reticulin

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53
Q

Are spleen, pancreas, and adrenal glands retroperitoneal?

A

Spleen = intraperitoneal -> injury creates hemoperitoneum
Pancreas = retroperitoneal except tail (intraperitoneal) -> so if car collision w/ retroperitoneal hematoma -> choose trauma to pancreas
Adrenal glands = retroperitoneal

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54
Q

What does secretin do besides stimulating HCO3- release and inhibiting H+ release?

A

Stimulates pyloric sphincter contraction

so pancreas can start secreting juice to digest stuff in intestine

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55
Q

1st step in screening for malabsorption?

A

Sudan III stool stain -> quantify fat content

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56
Q

Labs to check if wanna know about liver/bile duct damage? Labs to check if wanna know about prognosis?

A

Liver damage markers: AST, ALT, Alk Phos, GGT (differentiate bet. biliary from other causes when alk phos is elevated)
PROGNOSIS MARKER: PT time (elevated first b/c factor VII has the shortest HL), serum albumin, bilirubin

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57
Q

2 histologic presentations of acute viral hepatitis?

A

Hepatocyte INJURY: ballooning degeneration
Hepatocyte DEATH: bridging necrosis, mononuclear inflammation -> might present w/ fever and dark urine (from increased serum bilirubin)

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58
Q

Acute portal HTN w/ normal liver bx. What’s the cause?

A

Portal vein thrombosis (key is normal liver bx -> indicates that presinusoidal process is responsible)
Ascites is UNCOMMON b/c don’t normally develop sinusoidal HTN -> will just get esophageal varices

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59
Q

What do you see on liver bx in Budd Chiari?

A

Centrilobular congestion (“dilation of sinusoids + perivenular hemorrhage” esp w/ acute obstruction) and fibrosis

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60
Q

What’s a lymphoid polyp?

A

Intestinal mucosa infiltrated w/ lymphocytes

Benign, common in children

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61
Q

Where is portal vein in relation to IVC and liver on X-section scan?

A

Ant. to IVC

Medial/just within right lobe of liver

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62
Q

What do you see on barium swallow in DES (diffuse esophageal spasm)? What are prestening sx?

A

“corkscrew” esophagus from periodic, non-peristaltic esophageal muscle contraction
Present w/ dysphagia and chest pain

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63
Q

What creates an umbilical hernia?

A

Weakness in the abdominal wall around umbilicus -> covered by skin and usually closes spontaneously by 2 yo

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64
Q

What’s the main defect in Zenker diverticulum?

A

Cricopharyngeal muscle dysfx (from diminished relaxation of pharyngeal muscles during swallowing) -> pulsion diverticulum (false) -> might be able to palpate as lateral neck mass

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65
Q

What’s the pathogenesis in achalasia?

A

Degenerative changes in MYENTERIC PLEXUS

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66
Q

Gastric ulcers vs. erosions?

A

Erosions: don’t extend thru muscularis mucosa (so limited to mucosal layer) -> but acute erosive gastropathy can cause upper GI bleed that leads to melena
Ulcers: extend into submucosal layer

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67
Q

Why can’t you generate protective immune responses against HCV?

A

ENVELOPE GLYCOPROTEIN that’s prone to frequent mutation

No proofreading 3’->5’ exonuclease activity

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68
Q

Locations of carcinoid tumor? What’s the cell of origin?

A

Ileum, appendix, rectum -> these gotta met to liver to produce sx
If bronchial or extraintestinal -> produce sx w/out having to metastasize first
Enterochromaffin cells of intestine mucosa

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69
Q

Where is the majority of painful anal fissures? What might you find on PE w/ chronic anal fissures?

A

Single post. midline of anal verge distal to dentate line -> poorly perfused area
Might see anal skin tag w/ chronic fissure

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70
Q

What kind of filaments makes up microvilli?

A

Actin

71
Q

Air in gallbladder and biliary tree. Where’s the gallstone?

A

Ileum at ileocecal valve
This is from gallstone ileus -> get cholecystenteric fistula bet. gallbladder and adjoining gut tissue -> gallstone passed to small intestine and gets all the way thru to ileocecal valve and gets trapped there
Won’t have air in gallbladder/biliary tree if stone is just in cystic duct or common bile duct (“choledocolithiasis”)

72
Q

What kind of channel does PPI inhibit?

A

H+/K+ ATPase -> so primary active transport! (unlike other drugs that affect voltage-gated ion transports, which are usually passive)

73
Q

What molecule do you use to screen for carcinoid tumors?

A

5-hydroxyindoleacetic acid (breakdown product of serotonin)

74
Q

What encodes heat labile (LT) and heat stable (ST) enterotoxins by ETEC (enterotoxigenic E. coli)?

A

Plasmid

75
Q

What org causes “stacked-brick” intestinal adhesion?

A

EAEC (enteroaggressive E. coli) -> don’t invade, implicated in persistent diarrhea in infants in developing countries

76
Q

What does hep D virus need HBV for?

A

Coating -> needs HBsAg to coat its viral particles (circular ss RNA molecules)

77
Q

2 phases of HBV infection?

A

Proliferative phase: HBsAg and HBcAg bound to MHC I on host cell surface -> activates CD8+ T cells which destroy infected hepatocytes (MAIN MECHANISM OF LIVER INJURY)
Integrative phase: infectivity ceases and liver damage tapers off when Abs appear, risk of HCC remains elevated
Host’s Abs only have a role in neutralizing ABV infectivity BEFORE virus enter hepatocytes (so Ab not assc. w/ hepatocellular damage)

78
Q

Layers of stomach from top to muscularis mucosae and the cell composition

A

Top = simple columnar epithelium -> mucus
Upper glandular layer = parietal cells (oxyntic/pink, round, plate-like)
Deeper aspect of gastric glands = chief cells (small, basophilic, granular)
Muscularis mucosae

79
Q

What do each of 3 HBV Ags do?

A 
HBcAg = nucleocapsid core protein -> stays in hepatocytes and assembles virion
HBeAg = nucleocapsid core (stays in hepatocytes and assembles virion) and precore protein (directs secretion into blood)
HBsAg = noninfective envelope glycoprotein that forms spheres and tubules 22nm in diameter -> hepatocytes secrete a lot of this (out of proportion to amont of HBcAg produced -> so it's a "product of viral synthesis that poorly correlates w/ viral replication")
80
Q

What kind of grains contain gluten?

A

Wheat, rye, barley contain gluten

Oats and rice don’t

81
Q

Why do you get pancytopenia in chronic liver disease/cirrhosis?

A

Hypersplenism

82
Q

What is Cooper’s ligament and where is it?

A

Cooper’s ligament = pectineal ligament = thickened part of pectineal fascia
Overlies pectineal ridge of pubic bone, posterior to femoral canal

83
Q

What is transversalis fascia in relation to inguinal canal?

A

It forms posterior wall of inguinal canal

Deep inguinal ring is an opening in transversalis fascia

84
Q

Liver bx in extrahepatic biliary atresia? When does it present w/ total obstruction?

A

Bx: intrahepatic bile ductule proliferation, portal tract edema and fibrosis, parenchymal cholestasis
Obstruction by 3rd week of life -> biliary cirrhosis by 6 months of life

85
Q

What distinguishes pancreatic pseudocysts from true cysts?

A

Pseudocysts are lined by granulation tissue and no epithelial lining -> gets fibrosis and thickening over time

86
Q

What kind of pancreatic neoplasm do you see glycogen-rich cuboidal epithelium in?

A

Serous pancreatic neoplasms (as opposed to mucinous cystic kind which is lined by columnar mucinous epithelium)

87
Q

When is pica most common and what’s the usual thing ppl eat?

A

Common in pregnancy

Ice is the most common ingested substance

88
Q

2 ways to get hereditary pancreatitis?

A
  1. SPINK1 gene mutated (secreted by pancreatic acinar to fx as trypsin inhibitor)
  2. production of abnormal trypin that’s not susceptible to inactivating cleavage by other trypsin
89
Q

4 parts of duodenum and their structural relations?

A 
1st part (horizontal): only one not retroperitoneal
2nd part (vertical): head of pancreas
3rd part (horizontal): SMA (right in front of it), pancreas uncinate process
4th part (vertical): ends at ligament of Treitz
90
Q

How is urease breath test performed?

A

Pt consumes C-13 labeled urea and then monitor BREATH for precence of that C-13
For H pylori testing

91
Q

Who is at high risk of getting trypanosoma cruzi and how does it manifest?

A

Central & S. America

Neurotoxin destroys myenteric plexi in eso (get 2ndary achalasia), intestines (megacolon), ureters (megaureter)

92
Q

Dx of “intrahepatic hydatid cysts w/ surrounding fibrous rxn”?

A

Echinococcus

93
Q

Pancreatic finding in CF?

A

Exocrine gland fibrotic atrophy

94
Q

What structures could be bleeding if using Pringle maneuver doesn’t stop the bleeding?

A

Pringle maneuver = occludes portal triad

So think about IV or hepatic veins if this doesn’t stop the bleeding

95
Q

In neonate whose mother is + for HBeAg, what are the risk of chronic infection, viral replication rate, and level of liver enzymes?

A

Risk of chronic infection: high
Viral replication rate: high
Level of liver enzymes: mildly elevated

96
Q

What causes direct hernia?

A

Breakdown of transversalis fascia

97
Q

Diff bet. coverings of direct and indirect hernias?

A

Indirect hernia: covered by all 3 spermatic fascial layers

Direct hernia: covered only by external spermatic fascia

98
Q

Cephalic vs. gastric vs. intestinal phases?

A

Cephalic: cholinergic mediates
Gastric: gastrin mediates
Intestinal: ileum & colon releases peptide YY -> binds ECL to inhibits gastrin-stimulated histamine release -> so effectively downregulates gastric secretion

99
Q

What is anti-HAV IgM a marker of?

A

Acute infection

100
Q

What’s another name for migratory thrombophlebitis? And what conditions is this assc. w/?

A

Trousseau’s syndrome: adenocarcinomas produce thromboplastin-like substance that causes chronic intravascular coagulation
Assc. w/ adenocarcinomas of pancreas, colon, lung

101
Q

What is hemorrhagic diathesis assc. w/?

A

Celiac sprue (malabsorption of vit K)

102
Q

What should you do when you discover porcelain gallbladders?

A

Cholecystectomy -> risk of gallbladder carcinoma even if asymptomatic!

103
Q

How does glucagonoma present?

A

DM, normocytic normochromic anemia
Necrolytic migratory erythema (raised rash typically affecting groin area) -> coalesce to form large lesion w/ CENTRAL CLEARING of BRONZE-colored induration -> can also affect mucus membrane so might see glossitis, cheilitis, blephritis

104
Q

Diarrheal drugs affecting motility? Absorption? Secretion?

A

Motility: diphenoxylate (opiate that slows motility -> combined w/ atropine to get adverse sx at higher dose -> discourage abuse)
Absorption: kaolin-pectin, attapulgite (adsorb things to make stools less watery)
Secretion: bismuth subsalicylate, probiotics, octreotide

105
Q

How does hepatic adenoma usually present?

A

Sudden collapse from rupture and intraabdominal bleeding; or just RUQ pain
Seen in women on long-term OCP
Don’t see AFP elevation like HCC

106
Q

What colon tumor manifests as secretory diarrhea (diarrhea containing a lot of mucoid material) and hypokalemia?

A

Villous adenomas

107
Q

Diff in presentation of left sided colon cancers and right sided? What about rectal?

A

Left sided: obstruction + abd pain, distention, n/v
Right sided: iron deficiency anemia, anorexia, malaise, weight loss
Rectal: tenesmus and thin stool

108
Q

“moldy” grains that cause specific G-to-T mutation in p53. What’s the cancer risk?

A

Liver cancer

It’s referring to aflatoxin -> produced by Aspergillus and grows on food like corn, soybean, peanuts

109
Q

How does H. pylori lead to duodenal ulceration?

A

H. pylori infection -> decreased in delta cells (produce somatostatin) -> increased H+ secretion by parietal cells -> gastric fluid w/ very low pH that’s not adequately neutralized by duodenal bicarb production -> duodenal ulcers and duodenal gastric metaplasia

110
Q

What deficiencies should you worry about w/ gastrojejunostomy?

A 
Iron (absorption in duodenum and proximal jejunum)
B12
Folate
Fat-sol vitamines (esp vit D)
Ca2+
111
Q

Where is vit C absorbed?

A

Distal small bowel thru active transport process

112
Q

Where is B6 absorbed?

A

Jejunum and ileum by passive diffusion

113
Q

Where are B7 and B5 absorbed?

A

Small and large intestine via Na+-dependent multivitamin transporter

114
Q

What organs does whipple disease involved besides bowel?

A

Joint: arthropathy, polyarthritis

Psychiatric and cardiac abnormalities

115
Q

What kind of pts is parenteral nutrition appropriate for?

A

Pts in need of prolonged bowel rest -> like those suffering from acute pancreatitis

116
Q

What is cavernous hemangioma and what does it look like under the scope?

A

Most common benign liver tumor -> congenital malformations that enlarge by ectasia, NOT hyperplasia or hypertrophy
See well-circumscribed masses of spongy consistency, blood-filled vascular spaces lined by single epithelial layer -> can surgically remove, but DONT bx (fatal hemorrhage)

117
Q

What is ulcerative anal mass assc. w/?

A

SCC assc. w/ HPV 16 and 18 -> immunocompromised state (HIV) makes it more likely, esp if homosexuals

118
Q

Hard mass obstructing ileocecal valve w/ cholesterol content of 85%. What is this?

A

Gallstone ileus!

119
Q

What does coffee ground emesis mean?

A

Blood exposed to gastric acid & oxidation of heme iron -> sign of upper GI bleed

120
Q

How does opioid lead to severe RUQ pain?

A

Opioid stimulates SMC in sphincter of Oddi -> constriction and spasm -> biliary colic
So use NSAIDs for pain control instead if this happens

121
Q

How does opioid cause constipation?

A

By binding to mu receptors on gut ENTEROCYTES -> slowing motility

122
Q

What is acute acalculous cholescystitis and when should you suspect it? What are the complications?

A

Acute inflammation of gallbladder in absence of gallstones
Suspect in hospitalized pts who are very ill & complain of RUQ pain and fever. Jaundice + palpable RUQ mass might be present (won’t see this in acute calculouus cholecystitis)
Complications: gangrene, perforation, emphysematous cholecystitis

123
Q

What is choledochal cyst?

A

Congenital dilations of common bile duct

124
Q

Diff bet. 2 kinds of pigment gallstones?

A

Black: 2ndary to intravascular hemolysis
Brown: 2ndary to biliary infection like fluke infection

125
Q

What does 99mmTc-pertechnetate scan detect?

A

Gastric mucosa

126
Q

What happens in failure of proper hindgut descent

A

Diff degrees of anal agenesis or imperforate anus

127
Q

How do you dx intussusception?

A

PE (might feel tubular mass in RLQ) & barium enema (might be therapeutic too)

128
Q

What kind of virus is HEV?

A

Naked, ss RNA

129
Q

What artery supplies pylorus?

A

Gastroduodenal (also gives rise to right gastroepiploic)

130
Q

What is right gastric artery a branch of?

A

Proper hepatic artery

131
Q

Veins draining rectum?

A

Sup. rectal veins -> portal circulation
Middle rectal veins -> int. iliac -> systemic circulation
Inf. rectal veins -> int. pudendal -> systemic circulation

132
Q

What are Councilman bodies?

A

Apoptotic hepatocyte bodies - round acidophilic -> see this in anything that kill hepatocytes like acute viral hepatitis

133
Q

What does cryptosporidiosis look like? How does it present?

A

Endoscopy shows inflammation w/ NO ulcers -> bx shows basophilic clusters on surface of intestinal mucosal cells
Profuse, watery diarrhea in pts w/ advanced AIDS (CD4+ < 180)

134
Q

Flask-shaped colonic ulcers?

A

Entamoeba histolytica (might see trophozoites w/ phagocytosed RBCs)

135
Q

How is colorectal carcinoma that is colitis-assc. different from sporadic one?

A

More likely to arise from flat/non-polypoid dysplasia, have signet ring morphology or be mucinous, be multifocal, and develop early p53 mutations and late APC mutations (opposite sequence of sporadic form)

136
Q

Signs suggestive of chronic mesenteric ischemia? Most often cause?

A

Signs: epigastric/periumbilical pain that occurs 30-60 min after food intake -> pain severe enough (even tho PE normal) that pts avoid eating and lose weight
Don’t confuse w/ gallbladder pain!
Most often cause is atherosclerosis of celiac, SMA, IMA

137
Q

Most common causes of acute pancreatitis?

A

Gallstones and alcoholism
But if rule those out and no obv things going on (like post-surgery, hypercalcemia, infection, etc), consider hyperTG -> over 1000 mg/dL is directly toxic to tissue and will cause acute pancreatitis

138
Q

What is increased conc of oxalate in urine assc. w/?

A

Intestinal malabsorption syndromes (like Crohn’s) -> this is b/c you get calcium binding to lipids (lots floating around from fat malabsorption since you lose bile acids in feces) instead of oxalate -> so lots of free oxalate to form kidney stones
So Crohn = oxalate kidney stones!

139
Q

Where are Paneth cells and what do they secrete?

A

At base of intestinal crypts

Secrete lysozymes and defensins -> so antibacterial

140
Q

Parasite that causes biliary tract disease and cholangiocarcinoma? How do you get it and how do you tx it?

A

Clonorchis sinensis (chinese liver fluke)
From undercooked fish
Tx w/ praziquantel

141
Q

Parasite that causes liver (hydatid cyst)? How do you get it and how do you tx it?

A

Echinococcus granulosus
From dogs, sheep, ppl from endemic area (Mediterranean, ME, S. America, Iceland, Australia, New Zealand, Southern Africa)
Tx w/ albendazole, if resection don’t forget to inject ethanol first (risk of anaphylaxis otherwise)

142
Q

How do you tell which structure is eso on CT?

A

It’s bet. trachea and vertebral body -> just identify trachea based on the fact that it is radiolucent (air)
Eso has no visible lumen on CT

143
Q

Types of transporters involved in bile conjugation and what happens if they’re inhibited?

A

PASSIVE organic anion transporters (OATP): uptake of unconjugated bilirubn -> so get increased unconj bilirubin in blood if inhibited
ACTIVE organic anion transporter (MRP2): spits conjugated bile into biliary system -> so selective inhibition will result in isolated conj hyperbilirubinemia -> get increased conj bilirubin in plasma and urine (NOT feces)

144
Q

What’s the pathogenesis of alcohol-induced hepatic steatosis?

A

Decreased in FFA oxidation secondary to excess NADH production (from the 2 enzymes that metabolize alcohol)

145
Q

Where is fat digested? And where is it mostly absorbed (along w/ fat-sol vitamins) if there’s no bile?

A

Duodenum: main site of digestion
Jejunum: main site of absorptin
If bile is there, lipid will just diffuse thru brush border membrane w/out needing transport protein

146
Q

Where is bile absorbed?

A

Ileum

147
Q

Why are pt who had cholecystectomy less tolerant of large fatty meals?

A

They don’t have storage place for bile so can’t release large amount at once in coordinated fashion w/ meals
Problem is NOT w/ secretion or absorption of bile acid, which happens on a constant basis (have increased rate of enterohepatic circulation b/c of this actually)

148
Q

Slow and incomplete gallbladder emptying. Pt is likely to develop?

A

Biliary sludge (from bile precipitation) -> precursor to stone formation

149
Q

What lab do you follow elevated alk phos w/?

A

Get GGT

Alk phos elevated from bone or hepatic cause, GGT will help determine which one

150
Q

Curling vs. Cushing ulcers?

A

Curling ulcers: prox duodenum; in pts w/ severe trauma or burn
Cushing ulcers: eso, stomach, duodenum; in pts w/ high ICP -> very prone to perforation

151
Q

What is granulomatous gastritis?

A

Idiopathic & benign condition -> intramucosal epitheloid granulomas that cause narrowing of antrum secondary to transmural inflammation

152
Q

What 3 things happen in lactase-deficient pp when put on lactose challengel?

A

Increased stool osmotic gap
Increased breath H+ content
Decreased stool pH

153
Q

What kind of B12 deficiency does Diphyllobothrium latum cause?

A

Malabsorption type -> so impaired B12 absorption on Schilling test can’t be corrected by oral IF

154
Q

Most dangerous complication of UC? How do you dx it?

A

Toxic megacolon -> can lead to perforation

Dx w/ plain abdominal X-ray -> don’t do barium contrast or colonoscopy b/c risk of perforation

155
Q

What is the most common liver neoplasm in children? What’s the conditions assc. w/ it?

A

Hepatoblastoma -> fatal if not resected

Assc. w/ FAP and Beckwith-Wiedemann syndromes

156
Q

Most common site of gastric ulcers?

A

Lesser curvature of stomach at the border bet. acid-secreting (fundic) and gatrin secreting (antrum) mucosa

157
Q

Most useful dx feature in acute calculus cholecystitis?

A

NOT US and seeing stones -> lots of ppl have stones that doesn’t mean they have acute cholecystitis (features that are more suggestive are distended gallbladder, wall thickening, pericholecystic fluid, + sonographic Murphy sign)
Most useful tool is actually HIDA scan -> see no gallbladder filling (failed visualization) on radionuclide biliary scan

158
Q

The increase in activity of what enzyme is implicated in colon adenoma?

A

COX-2 (overexpression bet. APC and K-ras step)

159
Q

What gets crushed in SMA syndrome? What conditions predispose to this?

A

Crush transverse portion of duodenum -(SBO sx) and left renal vein
Risk factors: anything that causes diminished mesenteric fat (less cushion), lordosis, surgical correction of scoliosis (decreased SMA mobility)

160
Q

Diff in cells involved in pathogenesis of UC vs. Crohn’s?

A

Crohn: TH1 (granulomas)
UC: TH2

161
Q

Precipitating factors of hepatic encephalopathy?

A

Anything that alters ammonia balance
Drugs
Hypovolemia
Excessive nitrogen load: GI bleeding (Hb converted to ammonia), constipation
Metabolic: incl increased dietary protein
Infections
Portosystemic shunting

162
Q

What’s globus hystericus?

A

Sensation of lump in throat w/out any structural abnormalities

163
Q

Saliva composition as related to fluid flow rate?

A

If fluid flow rate is slow enough, salivary ducts will be able to reabsorb Na+ and Cl- and secrete more HCO3- and K+ out
If fluid flow rate is high, secretions approximate plasma conc

164
Q

What receptor does gastrin stimulate in parietal cells?

A

CCK receptors

165
Q

What’s the structure w/ increased pressure in portal HTN?

A

Don’t think of anastomosis, think of blood that now isn’t able to drain into portal vein b/c of increased pressure
So it’ll be splenic vein HTN -> blood backs up and get splenomegaly in cirrhosis -> this is from expansion of red pulp

166
Q

Favorite site for Crohn vs. UC?

A

Crohn: terminal ileum (rectal sparing)
UC: rectum

167
Q

Signs and sx of B12 deficiency. What GI hormone is overproduced?

A

Gastrin
B12 deficiency -> think pernicious anemia (this chronic atrophic gastritis causes loss of parietal cells over time -> so now less acid and IF are made, less secretin will be made as well -> gastrin increases b/c there’s no acid to inhibit antral G cells)

168
Q

Lactase deficiency results from defect on what level exactly?

A

Decreased GENE EXPRESSION

NOT at the protein level, posttranslational, etc.

169
Q

What are incretins and what do they do?

A

GLP-1 and GIP (gastric inhibitory peptide)
Stimulates insulin release after sugar consumption independent of insulin release from blood glucose rise -> why you get more insulin release w/ oral sugar consumption than IV sugar

170
Q

Signs of estrogen excess in cirrhotic pts besides the obvious stuff?

A

Obv stuff: gynecomastia, testes atrophy, decreased bony hair

Others are spider angioma, palmar erythema, Dupuytren’s contractures

171
Q

4 orgs causing diarrhea in HIV pts and how to distinguish bet. them?

A

CMV: most common -> ULCERS and inflammation, see large cells w/ basophilic inclusions in cyto AND nucleus
Cryptosporidum: inflammation but NO ulcers, see basophilic cells (protozoan) attached to brush border
MAC: chronic NOT acute, see necrotizing and nonnecrotizing granulomas, acid-fast bacili
Microsporidum: distortion of villus but NO inflammation, see small spores w/ diagonal or equatorial belt-like structures

172
Q

Levels where eso, aorta, and IVC passes thru diaphragm?

A

“I 8 (ate) 10 Eggs At 12”
IVC at T8
Eso (and vagus trunks) at T10
Aorta at T12

173
Q

Mass at head of pancreas. What would relieve jaundice?

A

Place stent into common bile duct

Question Bank (10 decks)

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