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GI DRx > 05b: Cirrhosis > Flashcards

05b: Cirrhosis Flashcards

1
Q

Normal portal pressure is (X) mmHg. Clinical manifestations of portal HTN is seen at/over (Y) mmHg.

A 
X = 2-6
Y = 12
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2
Q

Two mechanisms that cause portal HTN.

A
  1. Increased resistance to portal flow (mechanical obstruction)
  2. Secondary increase in portal blood flow
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3
Q

Portal flow can be measured by which clinical tool?

A

Doppler ultrasound

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4
Q

About 60% of cirrhosis cases are caused by which two etiologies?

A

HCV and EtOH (either separately or in combo)

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5
Q

Most common cause of portal HTN worldwide is (X). And in the US is (Y).

A 
X = schistosomiasis
Y = cirrhosis
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6
Q

Portal HTN: Calculating the (X) gradient has been shown to have prognostic value in patients with cirrhosis. If below (Y) value, there’s significantly lower risk of bleeding from varices.

A

X = HVPG (Hepatic venous pressure gradient);

Y = 12 mmHg

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7
Q

Most forms of cirrhosis are (pre-hepatic/hepatic/post-hepatic).

A

Hepatic (sinusoidal)

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8
Q

Splenic/portal vein thrombosis is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.

A

Pre-hepatic

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9
Q

CHF can lead to (pre-hepatic/hepatic/post-hepatic) cirrhosis.

A

Post-hepatic

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10
Q

Schistosomiasis is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.

A

Hepatic (pre-sinusoidal)

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11
Q

Budd-Chiari Syndrome caused by (X) and is example of (pre-hepatic/hepatic/post-hepatic) cirrhosis.

A

X = Hepatic v thrombosis

Post-hepatic

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12
Q

Of all the clinical signs in decompensated cirrhosis, (X) is the most dramatic and cause of death in up to (Y) of all patients with cirrhosis.

A 
X = esophageal varices bleeding
Y = 1/3
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13
Q

List the 5 main parameters used in “Child” criteria to assess severity/mortality with bleeding varices in cirrhosis.

A

Acronym: ABCPE

Albumin, BR, asCites, PT, Encephelopathy

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14
Q

Patient actively bleeding from esophageal varices requires emergent:

A
  1. Endoscopy (variceal ligation)

2. Resuscitation (IV fluids, blood)

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15
Q

Which drugs used for Rx in acute esophageal variceal bleeding?

A

Octreotide (long-acting somatostatin analog)

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16
Q

Cirrhosis: (X) cells are responsible for the ECM deposition and fibrosis.

A

X = hepatic stellate cells (which act as myofibroblasts)

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17
Q

Cirrhotic liver pathophysiology: sinusoidal fenestrations are (normal/wider/narrower).

A

Narrower (lost!) - hence increased resistance to blood flow within sinusoid lumen

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18
Q

(High/low) platelets may be marker of portal HTN. Why?

A

Low;

Blood backs up to spleen (splenomegaly) and platelets sequestered there

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19
Q

Increased intrahepatic resistance in cirrhosis is caused by both architectural and functional alterations. What are examples of functional alterations?

A

Active contraction of stellate/myofibroblast and vascular smooth muscle cells (modifiable by drugs)

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20
Q

Octreotide used in cirrhosis patients for treatment of (X) complication. What are the mechanisms by which it does this?

A

X = esophageal varices bleeding (somatostatin analog)

  1. Decrease post-prandial hyperemia (by inhibiting glucagon release)
  2. Direct vasoconstriction of splanchnic arteriolar muscle (decrease collateral flow)
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21
Q

Screening followed by primary prophylaxis for variceal bleeding includes (X) drugs/procedure.

A

X = non-selective beta-blockers OR endoscopic band ligation (EBL)

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22
Q

Esophageal variceal bleeding prophylaxis: (selective/non-selective) beta blockers used only for which effects?

A

Non-selective;

B1: decreases CO and splanchnic blood flow
B2: Allows unopposed alpha1 splanchnic vasoconstriction

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23
Q

T/F: Part of treating active variceal bleed is to give antibiotic prophylaxis.

A

True

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24
Q

All patients with ascites should undergo (X) diagnostic procedure.

A

X = paracentesis (of 50cc fluid)

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25
Q

T/F: Chronic liver disease accounts for 40-50% of ascites cases.

A

False - almost 80%!

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26
Q

Ascites: albumin in ascites fluid is (lower/equal/higher) compared to that in plasma.

A

Lower

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27
Q

Which three measurements are taken from paracentesis of ascites fluid?

A
  1. Albumin
  2. Total protein
  3. Cell count
28
Q

(X) gradient is calculated following paracentesis of ascites fluid. If it’s greater than 1.1, what are the main potential causes of the ascites?

A

X = SAAG (serum-ascites albumin gradient/gap)

  1. Cirrhosis
  2. Cardiac
29
Q

List the four main etiologies that are responsible for 99% of ascites cases.

A
  1. Cirrhosis
  2. Cardiac
  3. Malignancy
  4. Infection
30
Q

(X) gradient is calculated following paracentesis of ascites fluid. If it’s less than 1.1, what are the main potential causes of the ascites?

A

X = SAAG (serum-ascites albumin gradient/gap)

  1. Malignancy
  2. Infection
31
Q

Since both cirrhoses and (X) ascites have SAAG (greater/less) than 1.1, (Y) is used to differentiate between them.

A

X = cardiac
Greater;
Y = total protein

(Cirrhosis will have TP under 2.5 and cardiac greater than 2.5)

32
Q

Treatment of ascites: (star the most important factor)

A
  1. Na restriction
  2. Diuretics*
  3. (Maybe) large V paracentesis
33
Q

T/F: Fluid restriction doesn’t help treat ascites.

A

True - just Na restrict; fluid restrict only if hyponatremic

34
Q

What’s spontaneous bacterial peritonitis?

A

Spontaneous infection of ascitic fluid without any apparent intraabdominal source of infection

35
Q

(X) is used to diagnose spontaneous bacterial peritonitis.

A

X = paracentesis (WBC over 500 with PMNs over 50% in ascetic fluid)

36
Q

Rx for spontaneous bacterial peritonitis.

A
  1. Antibiotics (ceftriaxone)
  2. IV albumin (circulatory support)
  3. Secondary prophylaxis (antibiotics)
37
Q

T/F: ICP is elevated in hepatic encephalopathy and anatomic lesions can be found in MRI.

A

Partly false - ICP elevated, no lesions

38
Q

T/F: Most severe form of hepatic encephalopathy (coma) is irreversible in 80% of patients.

A

False - reversible in up to 50%

39
Q

Main toxin responsible for hepatic encephalopathy is (X), which is produced by (Y) and normally metabolized to (Z) in a functional liver.

A 
X = ammonia
Y = colonic bacterial ureases
Z = urea
40
Q

Mortality of untreated SBP can be greater than (X)%.

41
Q

T/F: Elevated ammonia levels are used to make diagnosis of hepatic encephalopathy.

A

False - level does not correlate to severity

42
Q

Hepatic encephalopathy treatement:

A
  1. Lactulose

2. Rifaximin (antibiotic)

43
Q

How does lactulose treat hepatic encephalopathy?

A

Metabolized by gut flora to FAs that lower colonic pH (ammonium formed and excreted)

44
Q

Liver Disease classification: list the acute etiologies causing lobular disease.

A

Viral, drug, toxin

45
Q

Liver Disease classification: list the chronic etiologies causing lobular disease.

A
  1. Steatohepatitis
  2. Viral
  3. Autoimmune
  4. Metabolic
46
Q

Liver Disease classification: list the acute etiologies causing duct disease.

A
  1. Obstruction

2. Cholangitis

47
Q

Liver Disease classification: list the chronic etiologies causing duct disease.

A
  1. Primary biliary cholangitis
  2. Biliary stricture
  3. Sclerosing cholangitis
48
Q

Viral and drug etiologies of liver disease cause (X) type of cell degeneration. Alcohol and metabolic etiologies cause (Y) type.

A 
X = hydropic (ballooning/swelling) degeneration
Y = steatosis (fatty accumulation)
49
Q

Viral and drug etiologies of liver disease cause (X) type of cell death. Alcohol and metabolic etiologies cause (Y) type.

A 
X = apoptosis and necrosis
Y = necrosis and necroptosis
50
Q

Liver pathology: Inflammatory response with high PMNs should make you think of (X) etiology.

A

X = alcohol

51
Q

Liver pathology: (Purple/pink), acidophilic bodies indicative of (X) cell (degeneration/death).

A

Pink;

X = apoptosis (death)

52
Q

Liver pathology: Mallory’s hyaline indicative of (X) cell (degeneration/death).

A

X = necroptosis (death)

53
Q

List the four necrosis patterns seen in liver disease (pathologically).

A
  1. Spotty
  2. Zonal
  3. Piecemeal
  4. Massive
54
Q

Liver pathology: List the four “zones” that can be necrotic in zonal necrosis pattern.

A
  1. Centrilobular
  2. Mid-zonal
  3. Peri-portal
  4. Bridging necrosis
55
Q

List the three etiologies that come to mind when centrilobular necrosis seen in liver disease.

A
  1. Viral hepatitis (acute)
  2. Drug/toxin-mediated (acetaminophen)
  3. Ischemia
56
Q

List the three most important causes of massive/fulminant hepatic necrosis.

A
  1. Viral hepatitis
  2. Toxicity (acetaminophen esp)
  3. Idiosyncratic drug reaction
57
Q

Liver pathology: (X) drugs can cause cholestasis without inflammation, resulting in (normal/elevated) (BR/ALT/AST/ALP).

A

X = anabolic steroids (androgens, estrogen)

Normal ALT/AST, elevated BR, ALP

58
Q

T/F: Fibrosis is part of the histological pattern in steatosis.

A

True - pericellular and septal fibrosis

59
Q

Ito cells in liver play a role in which pathological process?

60
Q

Non-alcoholic fatty liver disease related to (X) syndrome.

A

X = metabolic (insulin resistance)

Triad: DM (II), obesity, dyslipidemia

61
Q

List the 3 main inherited metabolic diseases causing deposits and liver pathology. What accumulates in each? Star the most common.

A
  1. Hemochromatosis (Fe)*
  2. Wilson’s (Cu)
  3. Alpha-1 antitrypsin def (a-1 antitrypsin)
62
Q

Liver biopsy: (X) stain for iron shows its abundant presence in (hepatocytes/ducts/scar tissue). What color would this patient’s liver be?

A

X = Prussian blue
All;
Rust-colored

63
Q

Wilson’s disease associated with mutation in (X). What are some prominent histological features you would expect to see?

A

X = ATP7B (metal ion transporter)

Mallory’s hyaline, steatosis, vacuolated nuclei

64
Q

PAS-diastase positive inclusions in liver suggests which disease?

A

Alpha-1 antitrypsin def (abnormal protein can’t leave hepatocyte ER)

65
Q

The hallmark histological lesion for (X) disease is a portal duct-centered inflammatory process that is typically granulomatous.

A

X = primary biliary cholangitis/cirrhosis

GI DRx (11 decks)

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