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Pharm II Exam 4 > Liver Disease Agents > Flashcards

Liver Disease Agents Flashcards

1
Q

What is liver cirrhosis?

A

Chronic degenerative disease characterized by replacement of normal liver tissue w/ diffuse fibrosis that disrupts structure & function of liver

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2
Q

Types of Cirrhosis?

A

Alcoholic (MC): from chronic alcoholism
Post-necrotic: from previous infection (acute viral hepatitis)
Biliary: from chronic biliary obstruction/infection (LC)

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3
Q

Precipitating factors/predisposition of cirrhosis?

A

Malnutrition, Excess alcohol, bile excretion impairment (obstructed liver/bile duct, gallstones), necrosis (toxins, hepatitis), CHF

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4
Q

Pathophysiology of cirrhosis?

A

Liver cell damage –> inflammation & hepatomegaly –> slow hepatic impairment –> obstructed venous b/f –> portal HTN –> regeneration attempts –> fibrosis/small nodular liver

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5
Q

Complications of cirrhosis?

A

Spider angioma, Hepatomegaly, Splenomegaly, Fingernail changes, Bruising/bleeding, Asterixis, Hepatic enceph, Portal HTN, Esophageal varices, ascites, Bacterial peritonitis, Hepato-renal synd.

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6
Q

What is Asterixis?

A

Flapping tremor

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7
Q

How does Child-Turcotte-Pugh (CTP) Classify liver disease?

A

Grades degree of disease based on labs & clinical manifestations
(encephalopathy, ascites, bilirubin, albumin, PTT)

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8
Q

Encephalopathy CTP points?

A

(+1) none, (+2) mild-mod grade 1/2, (+3) severe grade 3/4

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9
Q

Ascites CTP points?

A

(+1) none
(+2) mild-mod diuretic response
(+3) severe diuretic refractory

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10
Q

Bilirubin CTP points?

A

(+1) <2
(+2) 2-3
(+3) >3

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11
Q

Albumin CTP points?

A

(+1) >3.5
(+2) 2.8-3.5
(+3) <2.8

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12
Q

PTT (seconds prolonged) CTP points?

A

(+1) <4
(+2) 4-6
(+3) >6

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13
Q

PTT (normalized ratio) CTP points?

A

(+1) <1.7
(+2) 1.7-2.3
(+3) >2.3

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14
Q

Class A CTP?

A

5-6 points (least severe)

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15
Q

Class B CTP?

A

7-9 points (mod-severe)

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16
Q

Class C CTP?

A

10-15 points (most severe)

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17
Q

1 and 2 year survival of Class A CTP?

A

1 yr: 100%
2 yr: 85%

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18
Q

1 and 2 year survival of Class B CTP?

A

1 yr: 80%
2 yr: 60%

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19
Q

1 and 2 year survival of Class C CTP?

A

1 yr: 45%
2 yr: 35%

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20
Q

What is hepatic encephalopathy?

A

Protein rich foods (meat) absorbed involving normal flora, unable to metabolize urea in liver –> ammonia (NH3) build-up in blood & crosses BBB causing s/sx of encephalopathy

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21
Q

S/sx of encephalopathy?

A

Confusion, Inverted sleep cycle, Jerking limbs, Personality changes

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22
Q

What is a common admission to acute care?

A

Episodic overt encephalopathy

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23
Q

Tx for 1st acute encephalopathy episode & outpatient prevention of 2nd event?

A

Lactulose

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24
Q

Combo Tx for 2nd encephalopathy event in hospital & outpatient prevention for future events?

A

Lactulose & Rifaximin

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25
Q

Primary prevention pharm agents for encephalopathy?

A

None (no data)

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26
Q

What is portal HTN?

A

Diseased liver doesn’t allow venous flow –> backup flow increases BP in portal vein –> esophageal area creates collateral veins (varices) that enlarge as dz progresses/cause frank bleeding in stomach

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27
Q

What can portal HTN cause?

A

Esophageal varices & ascites (can lead to bacterial peritonitis

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28
Q

Importance of maintaining hepatic portal HTN?

A

Development/progression of varices, minimizes risk of varices rupture & risk of ascites

29
Q

Goal of treatment w/ portal HTN?

A

Slow progression of cirrhosis (cure/reversal not possible)

30
Q

Cornerstone of tx for portal HTN?

A

BB (propanolol, nadolol)

31
Q

Primary goal of BB tx for portal HTN?

A

Prevent varices

32
Q

Use of BB with portal HTN is dependent on what?

A

Varices status

33
Q

Window hypothesis for early cirrhosis BB use?

A

Use not indicated
Cardiac reserve, SNS/RAAS @ baseline
Low risk for bacterial translocation/death

34
Q

Window hypothesis for decomp cirrhosis BB use?

A

Use indicated for prophylaxis (primary & secondary for variceal bleeds)
SNS/RAAS inc. to compensate for low arterial BP
Inc. risk for bacterial translocation/death

35
Q

Window hypothesis for end-stage cirrhosis BB use?

A

Stop BB if: ascites, SBP >400, MAP </= 82, serum Na+ <120, acute kidney injury hepatorenal synd., spontaneous bacterial peritonitis, sepsis, severe alc. hepatitis, poor follow ups/adherence
-Cardiac reserve impaired
-SNS/RAAS max stimulation
-Gut bacterial translocation/death

36
Q

What is ascites?

A

Dec. intravascular volume stimulates RAAS to increase intravascular volume –> don’t stay in vessels d/t albumin shortage (from diseased liver) & high aldosterone (inc. SNS/RAAS holds onto Na+/H2O)

37
Q

1 yr mortality w/ ascites?

A

15%

38
Q

5 yr mortality w/ ascites?

A

45%

39
Q

Non-pharmaceutical tx of ascites?

A

Sodium/H2O restriction (no added table salt, <1L of free water/day)

40
Q

Med tx for ascites?

A

Diuretics (Spironolactone, Furosemide)

41
Q

What is bacterial peritonitis?

A

Infection of ascitic fluid w/o definitive intra-abdominal source

42
Q

What is the most common life-threatening infection with cirrhosis?

A

Bacterial peritonitis

43
Q

Most common bacteria that cause bacterial peritonitis?

A

E. coli (*MC), Klebsiella pneumo, Pneumococci, Strep. viridans, S. aureus, misc gram (-) and (+)

44
Q

3 implicated factors of bacterial peritonitis?

A

-Altered gut microbiota
-Inc. gut permeability
-Impaired immunity

45
Q

How is gut microbiota altered in bacterial peritonitis?

A

Increased enterobacteria & SI bacterial overgrowth

46
Q

Increased gut permeability with bacterial peritonitis?

A

Impaired GI motility w/ flora disturbance –> dec. immunity –> flow of pathogens/endotoxins to mesenteric nodes

47
Q

Impaired immunity with bacterial peritonitis?

A

Inadequate bacterial activity in ascitic fluid, compromised defense mechanisms

48
Q

Active bacterial peritonitis tx?

A

3rd gen cephalosporin: Cefotaxime & Albumin (to dec. risk of renal failure/hepato-renal synd.)

49
Q

Alternate med for bacterial peritonitis if Cefotaxime allergy?

A

Oxofloxacin

50
Q

Consider discontinuing what med w/ bacterial peritonitis?

A

BB (may improve life expectancy)

51
Q

Med for prevention of bacterial peritonitis w/ severe liver disease (2+ events of ascites, bili >3mg/dL, several encephalopathy events)?

A

Ceftriaxone daily

52
Q

Med for prevention of bacterial peritonitis for less severe liver disease?

A

Norfloxacin

53
Q

Prescriber trends for cirrhosis?

A

-Pain management
-PPI’s
-Sedatives
-Statins (pravachol)

54
Q

Avoid which meds w/ cirrhosis?

A

NSAIDs (high risk of GI bleed, renal failure, worsened ascites)

55
Q

MOA of Lactulose w/ hepatic encephalopathy?

A

Antidiarrheal:
-increases peristalsis to dec. ability to absorb ammonia/proteins from foods
-May absorb some existing ammonia/protein from the blood

56
Q

ADRs of Lactulose?

A

Diarrhea (given 3-4x/day and monitored for loose stools daily), Non-compliance

57
Q

Rifaximin MOA?

A

ABx w/ little systemic absorption, decreases flora in intestines/prevents conversion of food to ammonia type chemicals

58
Q

ADRs of Rifaximin?

A

Chronic use: abx resistance

59
Q

Protein restriction in tx for hepatic encephalopathy?

A

1g/kg/day

60
Q

How do propanolol and nadolol lower portal vein HTN?

A

Have vasoconstricting action limiting blood to the liver (decreases portal vein pressure)

61
Q

Why are propanolol and nadolol used specifically for portal HTN?

A

Non-specific BB: lower HR (B1 action)
Goal HR: 55-65bpm

62
Q

ADRs of propanolol and nadolol?

A

Dec. HR –> indirectly dec. BP
Also have B2 activity: asthma/COPD exacerbations

63
Q

Ratio of Spironolactone:Furosemide for ascites?

A

2.5:1

64
Q

How do diuretics counteract pathology of ascites?

A

Counteract high levels of aldosterone

65
Q

ADRs of diuretics for ascites?

A

BP changes
Furosemide: dec. in Na+, K+, Ca
Spironolactone: inc. in K+

66
Q

Method for pain management in cirrhosis?

A

Start low, go slow

67
Q

Risk w/ PPIs?

A

Increased SBP

68
Q

Risk w/ sedatives?

A

Fall risk

Pharm II Exam 4 (3 decks)

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