hepatobil: 3/6 Flashcards
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
Mnemonic for Rotor syndrome
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
What gives urine a dark color?
conjugated bilirubin or excess urobilin.
27
Physiologic neonatal jaundice
- causes?
- what type of hyperbili?
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
Tx for physiologic neonatal jaundice
- 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
Mild icterus w/stress or fasting.
Gilbert syndrome
| -Mildly dec. UDP-glucuronosyltransferase conjugation activity.
30
Type 2 Crigler Najjar
| -Tx:
- Phenobarbital, which inc. liver enzyme synthesis.
| - type 2 = less severe.
31
What gives bruises their green color?
Heme =heme oxidase=> biliverdin ==> bilirubin
-heme oxidase is what gives bruises their greenish color
b/c biliverdin = green pigment.
32
What are the greatest prognostic factors in cirrhosis?
- degree of hypoalbuminemia.
- increased prothrombin time (extrinsic, factor 7)
- bilirubin levels
33
What leads to excess estrogen state in liver failure?
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
Urea (BUN) levels in liver failure?
LOW
- urea cycle happens in liver.
- blood ammonia levels will be high!
35
Neuro probs & inc. transaminase levels but no signs of liver failure.
-think of what disease?
Wilson's disease
36
Slit lamp exam
| -used to Dx which GI disease?
Wilsons
| -Kayser-Fleischer rings.
37
What is primary excretion method for copper?
- Bile => stool.
| - renal loss = ~10%
38
Hepatic abscess usually due to:
- developed countries:
- third world:
- bacterial (ie. staph aureus)
| - parasite (ie. entamoeba histolytica)
39
Common complicatino of prolonged TPN?
| -w/regards to gallbladder
- gallstones
- due to dec. CCK due to lack of enteral stimulation.
- you can give these pts exogenous CCK to prevent this.
40
Acalculous cholecystitis
- inflamed and enlarged gallbladder.
- seen in hostpitalized/ER pts.
- mortality can range btwn 10-90%
41
- Brown pigment gallstones:
| - Black pigment gallstones:
- brown = biliary infection (ie. clonorchis sinensis)
| - black = intravasc. hemolysis
42
Echinococcus granulosus
| -can do what to liver?
-forms big cyst in the liver.
43
What happens if cyst in liver due to echinococcus granulosus bursts?
- risk of anaphylactic shock.
| - surgeons pre-inject cyst w/ethanol to kill cysts/denature antigens before removal.
44
What is estrogen's influence on cholesterol levels?
- estrogen stimulated HMG-CoA reductase.
- inc. cholesterol
- inc risk of cholesterol gallstones.
45
Unexplained chronic hepatitis in pt younger than 30
-Wilsons disease
46
Serum sickness
| -type what HSR?
-type 3
47
hepatic encephalopathy
| -inc. ammonia: what effect does it have on inhibitory & excitatory NTs?
- inc. GABA
| - dec. glutamate & dec. catecholamines.
48
How does a GI bleed lead to inc. blood ammonia?
| -how can you prevent this?
- 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
Acholic stool
-pale stool
50
Serum copper levels in wilsons disease
- total copper =
- free copper =
- urine copper =
- total copper = dec.
- free copper = inc.
- urine copper = inc.
51
Tx for wilsons
Treat with penicillamine or trientine.
52
Can wilson's diseaes cause hemolytic anemia?
yes
53
Wilsons disease
- inheritance pattern
- which chromosome?
- which gene?
- auto recessive
- chrom 13
- ATP7B gene = codes for hepatocyte copper transporting ATPase that pumps copper into bile.
54
hemochromatosis
| -effect on testicles?
-testicular atrophy via deposition of iron. Causes gonadal dysfunction.
55
Common cause of secondary hemochromatosis?
transfusion therapy
| -beta-thalassemia major.
56
Hemochromatosis
- ferritin =
- TIBC =
- iron =
- transferrin sat =
- hepcidin =
- ferritin = inc
- TIBC = dec
- iron = inc
- transferrin sat = inc
- hepcidin = reduced
57
How much total body iron is enough to set off metal detectors at airports?
50g
58
Primary hemochromatosis
- what mutation on what gene?
- HLA association?
- due to C282Y or H63D mutation on HFE gene.
| - Associated with HLA-A3.
59
Secondary biliary cirrhosis
| -what does this refer to?
Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head).
60
Primary biliary cirrhosis
- what kind of inflammation?
- which abs?
- Tx?
- granulomatous
- anti-mitochondrial (including IgM).
- Ursodeoxycholic acid
61
Primary sclerosing cholangitis
- how is the fibrosis described?
- cause?
-concentric "onion skin" fibrosis of bile duct.
-alternating strictures and dilation with “beading” of
intra- and extrahepatic bile ducts on ERCP.
*unknown cause.
62
Primary sclerosing cholangitis
- associated w/what disease?
- what other findings?
- ulcerative colitis
- P-ANCA positive (like UC)
- Hypergammaglobulinemia (IgM).
- Can lead to 2° biliary cirrhosis and cholangiocarcinoma.
63
Cholesterol stones
| -radiolucent or opaque?
- radiolucent.
| - 10-20% opaque due to calcifications.
64
cholesterol gallstones
| -not obvious risk factors
- Crohn disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss, and Native American.
- estrogen up regs HMG-CoA reductase
65
Pigment stones
- black =
- brown =
*due to what & radio-opaque or lucent?
- black = hemolysis = radiopaque
| - brown = infection = radiolucent
66
Which are the only type of gallstones that are radio-opaque & what causes them?
-black pigment stones caused by hemolysis.
67
Which is part of bile
| -conjugated or non conjugated bili?
conjugated
68
cholelithiasis
| -aka?
gallstones
69
In what pt would biliary colic present w/o pain?
diabetic
70
Most common primary infection of gallbladder
| -which bug?
-CMV
71
HIDA
| -used to Dx what disease?
Cholecystitis
72
Typical pain in cholecystitis
RUQ pain radiating to right scapula.
73
Rokitansky-aschoff sinus formation:
- gallbladder mucosa diving down into smooth muscle.
| - in cholecystitis
74
Porcelain gallbladder
- what is it?
- inc risk for what?
- Calcified gallbladder due to chronic cholecystitis.
- gallbladder carcinoma.
* dystrophic calcification
* remove it
75
Can acute pancreatitis lead to hypocalcemia?
yes
76
Rupture of post. duodenal ulcer
| -can risk damaging which organ?
- pancreas
| - can cause acute pancreatitis.
77
Scorpion sting can lead to what organ problem?
- acute pancreatitis
| * steroid use can also lead to acute pancreatitis
78
Lipase & amylase
- are they always elevated in chronic pancreatitis?
- how about acute?
- not always in chronic (b/c lots of pancreas may be destroyed and not making these anymore).
- always in acute.
79
Pancreatic adenocarcinoma
| -arises from which cells?
- pancreatic duct
| - disorganized glandular structure with cellular infiltration
80
Pancreatic adenocarcinoma
| -most common location?
- pancreatic head
| - can lead to obstructive jaundice
81
Is alcohol a direct risk factor for pancreatic adenocarcinoma?
-no, its indirect risk factor
82
Trousseau syndrome
- what is it?
- found in which diseases?
- 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
Courvoisier sign
- what is it?
- seen in what disease?
- Obstructive jaundice with palpable, nontender gallbladder.
| - pancreatic adenocarcinoma at head of pancreas.
84
whipple procedure =
-removing head/neck pancreas, prox duodenum, gallbladder.
85
What mutations often seen in pancreatic adenocarcinoma?
- K-RAS
| - SPINK1 and PRSS1
86
Histamine receptor on parietal cell
- H1 or H2?
- suffix for H2 blockers?
- H2
| - "dine"
87
Cimetidine
| -side effects?
- 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
PPIs
| -reversible or irreversible?
- irreversible
| - so it def. efficacy.
89
PPI
| -side effects
- 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
sucralfate
| -prodrug. what does it need to be activated?
-Needs acidic pH before it becomes a gel. Don't use antacid w/this drug.
91
Misoprostol
| -uses?
- Prevention of NSAID-induced peptic ulcers.
- maintenance of a PDA.
- induce labor (ripens cervix).
92
Side effects of misoprostol
- diarrhea, abortifacent.
- Anything w/"prost" is contraindicated in pregnancy. B/c PG analogs induce contraction and result in abortion by triggering labor.
93
Antacids
| -can cause hypo or hyperkalemia?
hypokalemia
94
Aluminum hydroxide
| -side effects
-Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures.
95
Calcium carbonate
| -side effects
- Hypercalcemia, rebound acid inc.
| - Can chelate other drugs (ie. tetracyclines).
96
Magnesium hydroxide
| -side effects
-Diarrhea, hyporeflexia, hypotension, cardiac arrest.
| -
97
antacids increase pH of stomach
| -effects of this?
- 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
Sulfasalazine
- combo of which drugs?
- side effects?
- sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory).
- Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
99
receptors in the central vomit trigger zone.
| -aka chemoreceptor trigger zone
- 5-HT3 = pro-vomit
- D2 = pro-vomit
- CB1 receptors = anti-vomit
100
- 5-HT3 = pro or anti vomit?
- D2 = pro or anti vomit?
- CB1 receptors = pro or anti vomit?
- 5-HT3 = pro-vomit
- D2 = pro-vomit
- CB1 receptors = anti-vomit
101
Ondansetron
| -side effects
-headache, constipation
102
Aprepitant
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
Metoclopramide
| -mech
- D2 receptor antagonist.
- increases: resting tone, contractility, LES tone, motility.
- Does not influence colon transport time.
104
Metoclopramide
- use:
- tox:
-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
Digoxin has drug interactino w/which GI med?
metoclopramide
106
- Ach + serotonin = inc. gut motility
| - D2 = dec. gut motility.
So blocking D2 receptors will inc. gut motility.
| -thats what metoclopramide does.
107
In which organelle does bilirubin conjugation happen?
ER
108
Is unconjugated or conjugated bilirubin involved w/kernicterus?
- unconjugated
| - seen in Crigler Najjar.
