Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Final FA review > hepatobil: 3/6 > Flashcards

hepatobil: 3/6 Flashcards

1
Q

Histological features of cirrhosis

A

-Portal bridging fibrosis and nodular hepatocyte

regeneration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Fetor hepaticus

  • what is it?
  • what disease is it found in?
A
  • breath smells musty.

- cirrhosis. Due to hepatocyte failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Inc or dec estrogen in cirrhosis?

A

increased estrogen

-liver plays role in removing estrogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name some sxs of inc. estrogen in cirrhosis

A
  • spider nevi
  • gynecomstia
  • testicular atophy
  • palmar erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is ALT or AST specific for liver?

A

ALT

-L for Liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mallory bodies found in which diseases?

A

-alcoholic hepatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Micronodular, irregularly shrunken liver with “hobnail”

appearance.

A

-alcoholic cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

alcoholic cirrhosis

-sclerosis seen predominantly where?

A

-Sclerosis around central vein (zone III).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hepatic encephalopathy

-hyper or hyporeflexia?

A

-hyperreflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

gaurding and rebound tenderness in HCC pt?

-why?

A

-tumor can rupture and leak stuff & cause bloody ascites & peritonitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Tumor marker for HCC?

A
  • AFP

- levels do not correlate w/size, stage, or prognosis. Just let you know its there.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cavernous hemangioma

-do you biopsy these?

A

-no, risk of hemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hepatic adenoma

-associated w/use of what?

A

Oral contraceptives & anabolic steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Budd chiari

-JVD present?

A
  • no.

- associated w/absence of JVD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Too much cholesterol in bile can lead to gallstones.

-too much of what else can lead to gallstones?

A
  • billirubin.

- pigmented gallstones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What gives urine a dark color?

A

conjugated bilirubin or excess urobilin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mild icterus w/stress or fasting.

A

Gilbert syndrome

-Mildly dec. UDP-glucuronosyltransferase conjugation activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Type 2 Crigler Najjar

-Tx:

A
  • Phenobarbital, which inc. liver enzyme synthesis.

- type 2 = less severe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the greatest prognostic factors in cirrhosis?

A
  • degree of hypoalbuminemia.
  • increased prothrombin time (extrinsic, factor 7)
  • bilirubin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Urea (BUN) levels in liver failure?

A

LOW

  • urea cycle happens in liver.
  • blood ammonia levels will be high!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Neuro probs & inc. transaminase levels but no signs of liver failure.
-think of what disease?

A

Wilson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Slit lamp exam

-used to Dx which GI disease?

A

Wilsons

-Kayser-Fleischer rings.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is primary excretion method for copper?

A
  • Bile => stool.

- renal loss = ~10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hepatic abscess usually due to:

  • developed countries:
  • third world:
A
  • bacterial (ie. staph aureus)

- parasite (ie. entamoeba histolytica)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Acalculous cholecystitis

A
  • inflamed and enlarged gallbladder.
  • seen in hostpitalized/ER pts.
  • mortality can range btwn 10-90%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
  • Brown pigment gallstones:

- Black pigment gallstones:

A
  • brown = biliary infection (ie. clonorchis sinensis)

- black = intravasc. hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Echinococcus granulosus

-can do what to liver?

A

-forms big cyst in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

Final FA review (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions