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STEP 1 > 07b: GI 2 > Flashcards

07b: GI 2 Flashcards

1
Q

List the mechanism behind which fatty alcohol liver changes occur

A

High alcohol = high acetaldehyde and low NAD+ so decreased gluconeogenesis, FA oxidation, and lipoprotein assembly and increased FA synthesis/buildup

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2
Q

Alcoholic hepatitis can be distinguished from fatty liver by which histological findings?

A

Swollen, NECROTIC hepatocytes with PMN infiltration and mallory bodies (eosinophilic inclusions of damaged keratin)

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3
Q

Viral hepatitis, apoptosis and cell shrinkage, nuclear fragmentation, and intensely eosinophilic remnants called (X).

A

X = councilman (“acidophilic”) bodies

Note: different from mallory bodies, which are intracytoplasmic inclusions seen in alcoholic hepatitis

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4
Q

List some triggers for hepatic encephalopathy that work by increasing (X) substance

A

X = NH3

  1. Dietary intake
  2. GI bleed (Hgb breakdown increases nitrogen products in gut and bac synthesis of NH3)
  3. Infection
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5
Q

List some triggers for hepatic encephalopathy that work by decreasing (X) substance removal

A

X = NH3

  1. Renal failure, diuretics
  2. Bypassed hepatic blood flow (post-TIPS procedure)
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6
Q

Rx of hepatic encephalopathy

A
  1. Lactulose

2. Rifaximin or neomycin

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7
Q

Lactulose mechanism of action

A

Catabolized by gut flora, increased short chain FA, decrease colon pH, and increase NH3 conversion to NH4+

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8
Q

Universal vaccination against (X) would likely cause steep decline in hepatocellular carcinoma.

A

X = HBV (countries with high rates of HBV have over 85% of all HCC cases!)

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9
Q

T/F: Chronic HBV infection can lead to HCC with our without cirrhosis.

A

True (integration of viral genome into host DNA triggers neoplastic change)

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10
Q

Aflatoxin ingestion causes (X) change in (Y) gene.

A 
X = G:T to T:A transversion
Y = p53
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11
Q

Most common benign liver tumor

A

Cavernous hemangioma

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12
Q

35 yo patient with RUQ fullness/pain and liver mass presents with recent-onset seizures and neuro deficits. Diagnosis?

A

Cavernous hemangioma (frequently involves brain; may cause intracerebral hemorrhage)

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13
Q

Malignant liver tumor associated with CD31 positive cells and (X) exposure.

A

Angiosarcoma

X = arsenic, vinyl chloride

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14
Q

Budd-Chiari syndrome:

A

Thrombosis/compression of hepatic veins (centrilobular congestion/necrosis)

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15
Q

Alpha1 antitrypsin deficiency: liver histology

A

PAS positive, diastase-resistant globules

Diastase normally breaks down glycogen, but globules in AAT deficiency are resistant

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16
Q

Causes of unconjugated hyperbilirubinemia

A
  1. Hemolysis
  2. Physiologic (newborn)
  3. Crigler-Najjar
  4. Gilbert syndrome
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17
Q

Abetalipoproteinemia: (AD/AR/X-linked) mutation of (Y). What’s the typical clinical presentation?

A

AR
Y = MTP (microsomal TG transfer protein; necessary for proper apo-B folding and lipid transfer to chilomicrons/VLDL)

Child (under 1 yo) presenting with malabsorption

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18
Q

Abetalipoproteinemia: expected biopsy findings of small intestine

A

Normal villi/mucosal architecture, but enterocytes at tips of villi contain clear/foamy cytoplasm (lipid accumulation)

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19
Q

2 month old boy born at term via uncomplicated vaginal delivery presents with jaundice, dark urine, pale stool, and firm hepatomegaly. Diagnosis? Rx?

A

Biliary atresia (obstruction of extrahepatic bile ducts; conjugated hyper-bilirubinemia)

Urgent surgical intervention

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20
Q

All hereditary causes of hyper-bilirubinemia are inherited in (X) fashion

A

X = AR

Gilbert, Crigler-Najjar, Dubin-Johnson, Rotor

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21
Q

Relatively common, benign cause of (conjugated/unconjugated) hyperbilirubinemia that comes about during stress, illness, fasting.

A

Gilbert

Unconjugated (mildly decreased UDP-glucuronosyltransferase conjugation and impaired BR uptake)

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22
Q

Crigler-Najjar pathogenesis:

A

Absent UDP-glucuronosyltransferase (type I) or low enzyme levels (type II), leading to high levels of unconjugated BR

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23
Q

Crigler-Najjar Type II Rx:

A

Phenobarbital (increases liver enzyme synthesis)

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24
Q

Patient with jaundice and grossly black liver

A

Dubin-Johnson (conjugated hyper-BRemia due to defective liver excretion of BRDG into bile)

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25
(X) is a milder version of Dubin-Johnson
X = Rotor (impaired hepatic excretion of BRDG into bile)
26
Wilson's disease: (AD/AR/X-linked) mutation in (X) causing (increase/decrease) in (production/excretion) of (Y).
AR X = hepatocyte copper-transporting ATPase Decreased excretion Y = copper (into bile via incorporation into apoceruloplasmin)
27
Hemochromatosis: (AD/AR/X-linked) mutation in (X) causing (increase/decrease) in:
AR X = HFE Increased intestinal Fe absorption (due to impaired iron sensing)
28
Common cause of death in hemochromatosis
HCC
29
T/F: Both hemochromatosis and Wilson's present before age 40
False - hemochromatosis presents after age 40
30
Classic hemochromatosis triad:
1. Cirrhosis 2. DM 3. Skin pigmentation ("bronze diabetes")
31
Hemochromatosis: aside from liver/skin, what are other organs susceptible to Fe deposition?
1. Pancreas (DM) 2. Heart (restrictive/dilated cardiomyopathy) 3. Pituitary (hypogonadism) 4. Joints (arthropathy)
32
48 yo M presents with pruritis, jaundice, dark urine and "beading" of bile ducts on ERCP. Diagnosis?
Primary sclerosing cholangitis
33
Concentric onion skin fibrosis of bile duct occurs in (X) disease and is associated with (Y) patient population.
X = Primary sclerosing cholangitis Y = IBD patients (esp UC)
34
p-ANCA positive biliary tract disease
Primary sclerosing cholangitis
35
Primary sclerosing cholangitis: increased risk for which malignancies?
Cholangiocarcinoma and gallbladder cancer
36
Biliary tract disease associated with plane xanthomas
Primary biliary cholangitis
37
51 yo F with Hx of Hashimoto thyroiditis presents with extreme generalized pruritis (esp at night) and light-colored stools. Running diagnosis? What labs/tests would you order?
Primary biliary cholangitis 1. Serum alk phos and gamma-glutamyl transpeptidase 2. BR, cholesterol 3. Anti-mitochondrial Ab
38
What's the pathogenesis of Primary sclerosing cholangitis?
Autoimmune; lymphocytic infiltrate and granuloma formation; destruction of intra-lobular bile ducts
39
Black, spiculated, friable gallstone is (radiopaque/radiolucent), composed of (X), and seen in (Y).
Radiopaque X = Ca-bilirubinate Y = hemolysis (ex: SCD)
40
Brown gallstone is (radiopaque/radiolucent), composed of (X), and seen in (Y).
Radiolucent X = bacterial infection of obstructed bile? Y = biliary infection
41
Patient receiving total parenteral nutrition is at risk for which biliary tract complication? Why?
Gallstone formation; low CCK release causes biliary stasis and increase risk of stone formation
42
Acute cholecystitis: most specific method of diagnosis
Radionuclide biliary scan (obstructed gallbladder won't take up radiotracer)
43
Patient with Hx of gallstones presents with colicky pain, N/V, abdominal distension, and high-pitched bowel sounds. Diagnosis? Which imaging finding can help confirm?
Gallstone ileus (fistula between gallbladder and intestine allows gallstone to pass in and obstruct ileocecal valve) Air in biliary tree on imaging
44
Burn patient admitted to hospital and stabilized, but develops severe RUQ pain, radiating to back, along with N/V. What's the likely diagnosis?
Acalculous cholecystitis (likely due to hypoperfusion)
45
Patients with chronic cholecystitis can develop (X) gallbladder, usually found incidentally on imaging. What's the next step in management?
X = porcelain (calcified; dystrophic intramural Ca deposition) Prophylactic cholecystectomy (high rates of gallbladder adenocarcinoma)
46
Charcot triad for ascending cholangitis:
Jaundice, Fever, RUQ pain
47
Reynold's pentad for ascending cholangitis
``` Charcot triad (Jaundice, fever, RUQ pain) Plus altered mental status, shock/hypotension ```
48
List the causes of acute pancreatitis. Star the two most common.
"I GET SMASHED" 1. Idiopathic 2. Gallstones* (#1) 3. EtOH* (#2) 4. Trauma 5. Steroids 6. Mumps 7. Autoimmune 8. Scorpion sting 9. Hypertriglyceridemia, hypercalcemia 10. ERCP 11. Drugs (sulfa, NRTIs, PIs)
49
Acute pancreatitis diagnosed by 2/3 of which criteria?
1. Acute epigastric pain (radiates to back) 2. Serum amylase/lipase 3x normal 3. Imaging findings
50
(Amylase/lipase) more specific for pancreatic pathology
Lipase
51
Pancreatic pseudocyst is lined by which type of tissue?
Fibrous, granulation tissue (not epithelium)
52
(Hyper/hypo)-calcemia is a cause of acute pancreatitis and (hyper/hypo)-calcemia is a complication of aute pancretitis.
Hypercalcemia; hypocalcemia (Ca soaps precipitate)
53
T/F: Amylase/lipase are always elevated in acute and chronic pancreatitis.
False - may not be elevated in chronic disease, but always in acute
54
Hereditary pancreatitis: (X) gene is mutated, leading to abnormal (Y)
``` X = SPINK1 or trypsinogen Y = trypsin (not susceptible to inactivation/cleavage) ```
55
Pancreatic adenocarcinoma arise from (X) pancreatic structure and are associated with which tumor marker?
X = ducts (disorganized glandular structures) CA 19-9 (and CEA, but less specific)
56
Risk factors for pancreatic adenocarcinoma
1. Smoking (2x) 2. Chronic pancreatitis 3. Diabetes 4. Age over 50 5. Jewish/AA males
57
Courvoisier sign:
Obstructive jaundice (dark urine, pale stools) with palpable, non-tender gallbladder Seen in pancreatic adenocarcinoma
58
Nodular regeneration of hepatocytes is typically found in which patients?
Those with cirrhosis (due to chronic HBV/HCV infection)
59
Confirming fat malabsorption can be done using (X) stain for stool.
X = Sudan III (most sensitive screen for malabsorptive disorders)
60
Stool microscopy in watery diarrhea (ex: vibrio cholerae) will show (leukocytes/erythrocytes/mucus)
Mucus (and some sloughed off epithelial cell) = "rice water stool"
61
(X) and (Y) bind directly on parietal cell and decrease acid production via which common pathway?
``` X = somatostatin Y = prostaglandins ``` Gi (decrease cAMP)
62
(X) and (Y) bind directly on parietal cell and increase acid production via which common pathway?
``` X = ACh Y = Gastrin ``` Gq (increase IP3/Ca)
63
"Alkaline tide" occurs as a result of (X). Describe this phenomenon.
X = meal/vomiting (high gastric acid secretion) H+ secretion from parietal cell into lumen means increased HCO3- excretion from cell into blood (since carbonic anhydrase generates H+ and HCO3- from H2O and CO2); this leads to high blood pH
64
T/F: The actions of both Cimetidine and Lansoprazole are irreversible.
False - H2 blockers (cimetidine) are reversible, PPIs inhibit irreversibly
65
All antacids can cause which electrolyte abnormality?
Hypokalemia
66
(X) antacid can cause constipation and (Y) antacid can cause diarrhea.
``` X = aluminum hydroxide (aluMINIMUM amount of feces) Y = Mg hydroxide (Mg2 = Must Go2 bathroom) ```
67
(X) drug inhibits gastric and pancreatic lipase, thus decreasing fat breakdown/absorption. Clinically used for (Y).
``` X = orlistat Y = weight loss ```
68
Psyllum and methylcellulose are in (X) class of drugs
X = bulk-forming laxatives Draw water into gut lumen
69
List examples of osmotic laxatives
1. PEG (Polyethylene glycol) 2. Lactulose 3. Mg hydroxide, Mg citrate (questionable efficacy)
70
Senna belongs in (X) class of drugs and works by:
X = Stimulant laxatives Stimulates enteric nerve and colonic contraction
71
Docusate belongs in (X) class of drugs and works by:
X = emollient laxatives Promoting water and fat incorporation into stool
72
Aprepitant belongs in (X) class of drugs and works by:
X = anti-emetic (substance P antagonist) blocks NK1 (neurokinin 1) receptors in brain
73
Patient with Roux-en-Y gastric bypass experiences diarrhea, nausea, sweating, palpitations and flushing after meals. What's the diagnosis/mechanism and treatment?
Dumping syndrome (eating high levels of simple CHO causes hyperosmotic fluid shift since food enters jejunum directly; diarrhea and volume contraction increases release of vasoactive substances like bradykinin/VIP) Eat small, more frequent meals that are low in simple CHO and high in protein

STEP 1 (21 decks)

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