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Flashcards in hepatobil: 3/6 Deck (108)
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1
Q
Histological features of cirrhosis
A
-Portal bridging fibrosis and nodular hepatocyte
regeneration.
2
Q
Fetor hepaticus
-what is it?
-what disease is it found in?
A
-breath smells musty.
-cirrhosis. Due to hepatocyte failure.
3
Q
Inc or dec estrogen in cirrhosis?
A
increased estrogen
-liver plays role in removing estrogen.
4
Q
Name some sxs of inc. estrogen in cirrhosis
A
-spider nevi
-gynecomstia
-testicular atophy
-palmar erythema
5
Q
How does cirrhosis cause anemia?
A
-Cytopenias along with the splenomegaly suggest hypersplenism as a cause for this patient’s anemia, leukopenia, and thrombocytopenia.
-The circulating blood cells are sequestered within the large spleen.
-One of the most common causes is congestive splenomegaly from portal hypertension resulting from cirrhosis.
6
Q
Cirrhosis
-is PTT, PTT, or bleeding time changed?
A
-PT time is increased.
-factor 7 = shortest half life of pro-coag factors, its made in the liver.
7
Q
Is ALT or AST specific for liver?
A
ALT
-L for Liver.
8
Q
GGT
-where is it found?
-what causes increase?
A
-SER of hepatocytes
-P450 induction b/c leads to SER hyperplasia.
*ie. chronic alcoholism.
9
Q
Reye syndrome
-Sxs
-mechanism
-associated w/which bugs most commonly?
A
-hepatoencephalopathy. mitochondrial abnormalities, fatty
liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma.

-aspirin metabolites dec. β-oxidation by reversible inhibition of mitochondrial enzyme.

-VZV and influenza B.
*okay to give kawasaki disease kids aspirin!
10
Q
alcoholic hepatitis
-mechanism of damage to hepatocytes?
-is there any WBC infiltration?
-intracytoplasmic findings?
A
-ethanol does direct chemical damage to hepatocytes.
*mediator = acetaldehyde.
-neutrophil infiltration
-mallory bodies (damaged IFs).
11
Q
Mallory bodies found in which diseases?
A
-alcoholic hepatitis.
12
Q
Micronodular, irregularly shrunken liver with “hobnail”
appearance.
A
-alcoholic cirrhosis
13
Q
alcoholic cirrhosis
-sclerosis seen predominantly where?
A
-Sclerosis around central vein (zone III).
14
Q
2 contributing factors to hyperammonemia in cirrhosis.
A
1-urea cycle happens in the liver.

2- w/portal HTN, you get more portosystemic shunts so things bypass your liver. This leads to less ammonia being brought to the liver for urea cycle in the first place.
15
Q
hepatic encephalopathy
-hyper or hyporeflexia?
A
-hyperreflexia
16
Q
gaurding and rebound tenderness in HCC pt?
-why?
A
-tumor can rupture and leak stuff & cause bloody ascites & peritonitis.
17
Q
Tumor marker for HCC?
A
-AFP
-levels do not correlate w/size, stage, or prognosis. Just let you know its there.
18
Q
Cavernous hemangioma
-do you biopsy these?
A
-no, risk of hemorrhage.
19
Q
Hepatic adenoma
-associated w/use of what?
A
Oral contraceptives & anabolic steroids.
20
Q
Budd chiari
-JVD present?
A
-no.
-associated w/absence of JVD.
21
Q
α 1-antitrypsin deficiency
-where does it accumulate?
-how do you stain for it?
A
-ER of hepatocytes
-PAS (+)
*remember, its a co-dominant trait.
22
Q
Crigler Najjar
-what is it?
-leads to what?
-whats the milder version called?

A
-Absent UDP-glucuronosyltransferase
-indirect hyperbili
-Gilbert = Mild dec. of UDP-glucuronosyltransferase
23
Q
Dubin-Johnson syndrome
-what is it?
-leads to what?
-whats liver look like?
-whats the milder version called?
A
-Defective liver excretion of bile. Defect in canalicular transport. So instead the conjugated bili spills into blood.
-direct hyperbili
-grossly black liver.
-Rotor syndrome
24
Q
Too much cholesterol in bile can lead to gallstones.
-too much of what else can lead to gallstones?
A
-billirubin.
-pigmented gallstones.
25
Q
Mnemonic for Rotor syndrome
A
Rotor rooter = getting stuff out (of toilet). Like getting
stuff out of liver. Defect in canalicular transport of bile, spills into blood stream instead.
-conjugated hyperbili.
26
Q
What gives urine a dark color?
A
conjugated bilirubin or excess urobilin.
27
Q
Physiologic neonatal jaundice
-causes?
-what type of hyperbili?
A
1-immature UDP-glucuronosyltransferase
2-lots of RBC destruction at birth b/c newborns have Hb-F - so these cells destroyed and replaced w/Hb-A (Hb-F not resposive to 2,3-DPG, Hb-A is).

-unconjugated hyperbilirubinemia
28
Q
Tx for physiologic neonatal jaundice
A
-we use BLUE light.
-bilirubin absorbs light and fragments into water soluble fragments, and baby can pee it out.
-it does NOT conjugate the bilirubin! it just makes it more water soluble!
29
Q
Mild icterus w/stress or fasting.
A
Gilbert syndrome
-Mildly dec. UDP-glucuronosyltransferase conjugation activity.
30
Q
Type 2 Crigler Najjar
-Tx:
A
-Phenobarbital, which inc. liver enzyme synthesis.
-type 2 = less severe.
31
Q
What gives bruises their green color?
A
Heme =heme oxidase=> biliverdin ==> bilirubin
-heme oxidase is what gives bruises their greenish color
b/c biliverdin = green pigment.
32
Q
What are the greatest prognostic factors in cirrhosis?
A
-degree of hypoalbuminemia.
-increased prothrombin time (extrinsic, factor 7)
-bilirubin levels
33
Q
What leads to excess estrogen state in liver failure?
A
1-dec. catabolism of androstenedione which will be converted to estrogen.
2-inc conc. of sex hormone-binding protein. This binds free T and thus dec ratio of freeT:free estrogen.
34
Q
Urea (BUN) levels in liver failure?
A
LOW
-urea cycle happens in liver.
-blood ammonia levels will be high!
35
Q
Neuro probs & inc. transaminase levels but no signs of liver failure.
-think of what disease?
A
Wilson's disease
36
Q
Slit lamp exam
-used to Dx which GI disease?
A
Wilsons
-Kayser-Fleischer rings.
37
Q
What is primary excretion method for copper?
A
-Bile => stool.
-renal loss = ~10%
38
Q
Hepatic abscess usually due to:
-developed countries:
-third world:
A
-bacterial (ie. staph aureus)
-parasite (ie. entamoeba histolytica)
39
Q
Common complicatino of prolonged TPN?
-w/regards to gallbladder
A
-gallstones
-due to dec. CCK due to lack of enteral stimulation.
-you can give these pts exogenous CCK to prevent this.
40
Q
Acalculous cholecystitis
A
-inflamed and enlarged gallbladder.
-seen in hostpitalized/ER pts.
-mortality can range btwn 10-90%
41
Q
-Brown pigment gallstones:
-Black pigment gallstones:
A
-brown = biliary infection (ie. clonorchis sinensis)

-black = intravasc. hemolysis
42
Q
Echinococcus granulosus
-can do what to liver?
A
-forms big cyst in the liver.
43
Q
What happens if cyst in liver due to echinococcus granulosus bursts?
A
-risk of anaphylactic shock.
-surgeons pre-inject cyst w/ethanol to kill cysts/denature antigens before removal.
44
Q
What is estrogen's influence on cholesterol levels?
A
-estrogen stimulated HMG-CoA reductase.
-inc. cholesterol
-inc risk of cholesterol gallstones.
45
Q
Unexplained chronic hepatitis in pt younger than 30
A
-Wilsons disease
46
Q
Serum sickness
-type what HSR?
A
-type 3
47
Q
hepatic encephalopathy
-inc. ammonia: what effect does it have on inhibitory & excitatory NTs?
A
-inc. GABA
-dec. glutamate & dec. catecholamines.
48
Q
How does a GI bleed lead to inc. blood ammonia?
-how can you prevent this?
A
-Hb gets into gut, broken down into ammonia (globin chains = protein, protein = broken down to ammonia).
-give lactulose: bacterial action on lactulose will acidify the colon contents, turn ammonia into ammonium, and trap it in the colon.
*lactulose converted to acetic acid & lactic acid
49
Q
Acholic stool
A
-pale stool
50
Q
Serum copper levels in wilsons disease
-total copper =
-free copper =
-urine copper =
A
-total copper = dec.
-free copper = inc.
-urine copper = inc.
51
Q
Tx for wilsons
A
Treat with penicillamine or trientine.
52
Q
Can wilson's diseaes cause hemolytic anemia?
A
yes
53
Q
Wilsons disease
-inheritance pattern
-which chromosome?
-which gene?
A
-auto recessive
-chrom 13
-ATP7B gene = codes for hepatocyte copper transporting ATPase that pumps copper into bile.
54
Q
hemochromatosis
-effect on testicles?
A
-testicular atrophy via deposition of iron. Causes gonadal dysfunction.
55
Q
Common cause of secondary hemochromatosis?
A
transfusion therapy
-beta-thalassemia major.
56
Q
Hemochromatosis
-ferritin =
-TIBC =
-iron =
-transferrin sat =
-hepcidin =
A
-ferritin = inc
-TIBC = dec
-iron = inc
-transferrin sat = inc
-hepcidin = reduced
57
Q
How much total body iron is enough to set off metal detectors at airports?
A
50g
58
Q
Primary hemochromatosis
-what mutation on what gene?
-HLA association?
A
-due to C282Y or H63D mutation on HFE gene.
-Associated with HLA-A3.
59
Q
Secondary biliary cirrhosis
-what does this refer to?
A
Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head).
60
Q
Primary biliary cirrhosis
-what kind of inflammation?
-which abs?
-Tx?
A
-granulomatous
-anti-mitochondrial (including IgM).
-Ursodeoxycholic acid
61
Q
Primary sclerosing cholangitis
-how is the fibrosis described?
-cause?
A
-concentric "onion skin" fibrosis of bile duct.
-alternating strictures and dilation with “beading” of
intra- and extrahepatic bile ducts on ERCP.

*unknown cause.
62
Q
Primary sclerosing cholangitis
-associated w/what disease?
-what other findings?
A
-ulcerative colitis
-P-ANCA positive (like UC)
-Hypergammaglobulinemia (IgM).
-Can lead to 2° biliary cirrhosis and cholangiocarcinoma.
63
Q
Cholesterol stones
-radiolucent or opaque?
A
-radiolucent.
-10-20% opaque due to calcifications.
64
Q
cholesterol gallstones
-not obvious risk factors
A
-Crohn disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss, and Native American.
-estrogen up regs HMG-CoA reductase
65
Q
Pigment stones
-black =
-brown =

*due to what & radio-opaque or lucent?
A
-black = hemolysis = radiopaque

-brown = infection = radiolucent
66
Q
Which are the only type of gallstones that are radio-opaque & what causes them?
A
-black pigment stones caused by hemolysis.
67
Q
Which is part of bile
-conjugated or non conjugated bili?
A
conjugated
68
Q
cholelithiasis
-aka?
A
gallstones
69
Q
In what pt would biliary colic present w/o pain?
A
diabetic
70
Q
Most common primary infection of gallbladder
-which bug?
A
-CMV
71
Q
HIDA
-used to Dx what disease?
A
Cholecystitis
72
Q
Typical pain in cholecystitis
A
RUQ pain radiating to right scapula.
73
Q
Rokitansky-aschoff sinus formation:
A
-gallbladder mucosa diving down into smooth muscle.
-in cholecystitis
74
Q
Porcelain gallbladder
-what is it?
-inc risk for what?
A
-Calcified gallbladder due to chronic cholecystitis.
-gallbladder carcinoma.
*dystrophic calcification
*remove it
75
Q
Can acute pancreatitis lead to hypocalcemia?
A
yes
76
Q
Rupture of post. duodenal ulcer
-can risk damaging which organ?
A
-pancreas
-can cause acute pancreatitis.
77
Q
Scorpion sting can lead to what organ problem?
A
-acute pancreatitis
*steroid use can also lead to acute pancreatitis
78
Q
Lipase & amylase
-are they always elevated in chronic pancreatitis?
-how about acute?
A
-not always in chronic (b/c lots of pancreas may be destroyed and not making these anymore).
-always in acute.
79
Q
Pancreatic adenocarcinoma
-arises from which cells?
A
-pancreatic duct
-disorganized glandular structure with cellular infiltration
80
Q
Pancreatic adenocarcinoma
-most common location?
A
-pancreatic head
-can lead to obstructive jaundice
81
Q
Is alcohol a direct risk factor for pancreatic adenocarcinoma?
A
-no, its indirect risk factor
82
Q
Trousseau syndrome
-what is it?
-found in which diseases?
A
-Migratory thrombophlebitis—redness and tenderness on palpation of extremities.
-due to hypercoaguability which is a common paraneoplastic syndrome seen in adenocarcinomas (most common of pancreas, lung, colon).
-adenocarcinomas make a thromboplastin type molecule that causes coag.
83
Q
Courvoisier sign
-what is it?
-seen in what disease?
A
-Obstructive jaundice with palpable, nontender gallbladder.
-pancreatic adenocarcinoma at head of pancreas.
84
Q
whipple procedure =
A
-removing head/neck pancreas, prox duodenum, gallbladder.
85
Q
What mutations often seen in pancreatic adenocarcinoma?
A
-K-RAS
-SPINK1 and PRSS1
86
Q
Histamine receptor on parietal cell
-H1 or H2?
-suffix for H2 blockers?
A
-H2
-"dine"
87
Q
Cimetidine
-side effects?
A
-potent inhibitor of P450
-antiandrogenic effects (prolactin release, gynecomastia, impotence, dec. libido in males).
-cross blood-brain barrier (confusion, dizziness, headaches) and placenta.
-dec. renal excretion of creatinine (so does ranitidine).
88
Q
PPIs
-reversible or irreversible?
A
-irreversible
-so it def. efficacy.
89
Q
PPI
-side effects
A
-Increased risk of C. difficile infection, pneumonia. Hip fractures,  serum Mg2+ with long-term use.
-hypergastrinemia (b/c low pH = neg. feedback on gastrin, and PPIs are inc. pH by dec. acid secretion).
90
Q
sucralfate
-prodrug. what does it need to be activated?
A
-Needs acidic pH before it becomes a gel. Don't use antacid w/this drug.
91
Q
Misoprostol
-uses?
A
-Prevention of NSAID-induced peptic ulcers.
-maintenance of a PDA.
-induce labor (ripens cervix).
92
Q
Side effects of misoprostol
A
-diarrhea, abortifacent.
-Anything w/"prost" is contraindicated in pregnancy. B/c PG analogs induce contraction and result in abortion by triggering labor.
93
Q
Antacids
-can cause hypo or hyperkalemia?
A
hypokalemia
94
Q
Aluminum hydroxide
-side effects
A
-Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures.
95
Q
Calcium carbonate
-side effects
A
-Hypercalcemia, rebound acid inc.
-Can chelate other drugs (ie. tetracyclines).
96
Q
Magnesium hydroxide
-side effects
A
-Diarrhea, hyporeflexia, hypotension, cardiac arrest.
-
97
Q
antacids increase pH of stomach
-effects of this?
A
-By alkalinizing the stomach, they will un-ionize weak bases and make them more lipid soluble. Therefore, weak bases will be more readily absorbed.
-Alkalinizing the stomach will also ionize weak acids and make them less lipid soluble, so they will NOT be as readily absorbed.
98
Q
Sulfasalazine
-combo of which drugs?
-side effects?
A
-sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory).
-Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
99
Q
receptors in the central vomit trigger zone.
-aka chemoreceptor trigger zone
A
-5-HT3 = pro-vomit
-D2 = pro-vomit
-CB1 receptors = anti-vomit
100
Q
-5-HT3 = pro or anti vomit?
-D2 = pro or anti vomit?
-CB1 receptors = pro or anti vomit?
A
-5-HT3 = pro-vomit
-D2 = pro-vomit
-CB1 receptors = anti-vomit
101
Q
Ondansetron
-side effects
A
-headache, constipation
102
Q
Aprepitant
A
first NK-1 receptor blocker. NK = neurokinin (ie. substance P or bradykinin = these are inflammatory mediators that also transmit pain). This will block nausea coming from pain.
103
Q
Metoclopramide
-mech
A
-D2 receptor antagonist.
-increases: resting tone, contractility, LES tone, motility.
-Does not influence colon transport time.
104
Q
Metoclopramide
-use:
-tox:
A
-Diabetic and post-surgery gastroparesis, antiemetic.

- parkinsonian effects.
-Restlessness, drowsiness, fatigue, depression, nausea, diarrhea.
-Drug interaction with digoxin and diabetic agents.
-Contraindicated in patients with small bowel obstruction or Parkinson disease (D1-receptor blockade).
105
Q
Digoxin has drug interactino w/which GI med?
A
metoclopramide
106
Q
-Ach + serotonin = inc. gut motility
-D2 = dec. gut motility.
A
So blocking D2 receptors will inc. gut motility.
-thats what metoclopramide does.
107
Q
In which organelle does bilirubin conjugation happen?
A
ER
108
Q
Is unconjugated or conjugated bilirubin involved w/kernicterus?
A
-unconjugated
-seen in Crigler Najjar.