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Pharm > Liver > Flashcards

Liver Flashcards

1
Q

cirrhosis is caused by what two things?

A

chronic hepatic inflammation or cholestasis

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2
Q

5 most common causes of chronic liver disease?

A

chronic viral hep C, alcoholic liver disease, non alcoholic fatty liver disease, chronic hep B, autoimmune induced hep

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3
Q

what are six complications of liver disease?

A

1) . portal HTN
2) . Ascites
3) . hepatic encephalopathy
4) . esophageal varices
5) . spontaneous bacterial peritonitis
6) . hepatorenal syndrome

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4
Q

portal HTN causes what two things?

A

inc pressure within the portal venous system and complications of cirrhosis

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5
Q

what is ascites?

A

accumulation of fluid within peritoneal cavity

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6
Q

what happens in hepatorenal syndrome?

A

arterial vasodilation in splanchnic circulation, from portal hypertension, decreases GFR and subsequent failure

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7
Q

what two things can cause ascites?

A

inc resistance within the liver pushes lymphatic drainage into abdominal cavity OR reduced osmotic pressure (hypoalbuminemia)

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8
Q

what are the four tx options for ascites?

A

sodium restriction, diuretics, paracentesis, albumin

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9
Q

sodium restriction guidelines for ascites

A

<2000 mg/day; some may need <500 mg/day

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10
Q

what happens when sodium is restricted too much? what does this put muscle at risk for?

A

protein and caloric consumption decreases as well; puts muscle at risk for wasting

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11
Q

what are the two preferred agents for ascites diuretics? what is the dosing of each

A

furosemide (Na/K+ excretion) and spironolactone (K+ sparing)

**40 mg/100 mg

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12
Q

what three things do you need to monitor when giving diuretics for ascites?

A

electrolyte imbalances, renal impairment, and gynecomastia (spironolactone)

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13
Q

hepatic encephalopathy: impaired hepatic clearance or portal-systemic shunting leads to (5)

A

accumulation of ammonia or glutamine (leads to swelling), benzodiazepine-like substances activating GABA receptors, zinc deficiency, altered cerebral metabolism

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14
Q

if removing >5 L at one time for ascites, what should you administer?

A

albumin (try to correct plasma balance)

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15
Q

if a pt still has refractory ascites, what do you add to diuretic combination

A

midodrine (vasopressor-constricting)

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16
Q

what group of meds contribute to sodium and water retention (and therefore will stop when having ascites)

A

NSAIDS

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17
Q

what two drugs should you avoid to prevent renal failure when a pt has ascites

A

ACEs and ARBs

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18
Q

what is important to look for before administering drugs for hepatic encephalopathy?

A

other causes of altered mental states

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19
Q

on the child-Turcotte-pugh classification for cirrhosis severity, what is indicated by a pt who scores more points?

A

more cirrhosis, more severe liver disease, more complications

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20
Q

covert hepatic encephalopathy is stages ____ through ____ (better); overt is stages ___ and ____

A

covert- 0-2

overt 3&4

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21
Q

1st choice agent for hepatic encephalopathy

A

lactulose

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22
Q

MOA lactulose

A

colon bacteria convert lactulose to acetic & lactic acid, creating an acidic pH; acidic pH causes GI tract ammonia to be reduced to ammonium ion (inhibits diffusion of ammonia into blood)

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23
Q

dosing of lactulose

A

45 mL q 1-2 hr until loose stool AND titrate further until pt has 2-3 BMs per day

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24
Q

lactulose can be continued ___ _____ for prevention

A

long term

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25
Q

10 gm of Kristalose is ___ mL of lactulose

A

15 mL

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26
Q

what is goal of ABX therapy for hepatic encephalopathy

A

reduce urease producing bacteria that lead to excess NH3

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27
Q

three ABX used for hep encephalopathy

A

rifaximin, neomycin, metronidazole

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28
Q

dose, absorption, tolerance of rifaximin

A

550 mg BID; minimal, good toleration

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29
Q

dose, absorption, and monitoring for neomycin

A

3-6g/day for 1-2 weeks then 2 g/day maintenance; very little absorption, monitor in renal patients

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30
Q

dose for metronidazole; what can it cause

A

250 mg BID, peripheral neuropathy

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31
Q

4 other tx for hepatic encephalopathy besides lactulose and ABX

A

Miralax, zinc supplementation, nutritional interventions, dietary changes

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32
Q

miralax dosing for hepatic enceph and when to use

A

4L over 4 hrs; use in acute situation to get symptoms under control (faster improvement than lactulose)

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33
Q

what are the two specific dietary supplementations given for hepatic enceph?

A

BCCA or LOLA

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34
Q

esophageal varices are often a consequence of ________ _________, commonly due to ________

A

portal HTN; cirrhosis

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35
Q

pts with esophageal varices have a tendency to develop _______ and are associated with ______ mortality rates

A

develop bleeding and high rates

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36
Q

tx options for esophageal varices depend on what three things?

A

acute bleed vs primary prophylaxis vs secondary prophylaxis after a bleed

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37
Q

acute management for esophageal varices: surgical and medication

A

endoscopy with band ligation or sclerotherapy; octreotide (somatostatin analog) and ceftriaxone

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38
Q

primary prevention of bleed (esophageal varices) medication

A

non selective BB

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39
Q

secondary prevention of bleed (esophageal varices): surgical and medication

A

band ligation; non selective BB +/- nitrates

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40
Q

BB MOA (B1 and B2)

A

Decrease cardiac output (β1)

Decreasing vasodilation of splanchnic arteries (β2)

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41
Q

how do BB help esophageal varices?

A

slow down their growth and lowers incidence of first bleed or repeat bleed

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42
Q

how to use BB for esophageal varices

A

continue indefinitely; titrate HR to 55 bpm or 25% below baseline (OR until side effects)

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43
Q

why do nitrates help with esophageal varices?

A

used in combo with BBs to potentially decrease bleeding rate

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44
Q

what resistance does nitrate use help decrease?

A

intrahepatic

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45
Q

MOA of octreotide

A

mimics somatostatin by inhibiting release of serotonin, gastrin, VIP, insulin, glucagon, secretin, pancreatic polypeptide, motilin, and growth hormone; inhibition leads to vasoconstriction and dec splanchnic blood flow

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46
Q

ADRs of octreotide

A

bradycardia, hyperglycemia, pruritus, hypersensitivity rxn, fatigue, HA, diarrhea

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47
Q

what should you use octreotide in combo with?

A

ABX- ceftriazone (1 gr qd for a week, crosses the blood brain barrier)

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48
Q

what is SBP? what organisms can cause it?

A

infection of ascetic fluid; organisms are usually GRAM NEG (E coli and Klebsiella), but can be gram pos (strep pneumo, S aureus)

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49
Q

dx of SBP depends on…

A

> 250 polymorphonuclear cells/mm3

50
Q

what are the two options for acute tx of SBP?

A

ABX (cefotaxime or ceftriaxone) or albumin

51
Q

how long do you administer ABX for acute SBP? dosing of each is?

A

5-10 days
Cefotaxime (2 g q 8-12 hours)
Ceftriaxone (2 g qd)

52
Q

dosing for albumin for SBP

A

1.5 g/kg day 1 and then 1 g/kg on day 3

53
Q

when do you consider using albumin for acute SBP tx? (3 things)

A

1) . SCr >1 mg/dL
2) . BUN >30 mg/dL
3) . total bili >4 mg/dL

54
Q

what are ABX used for SBP prevention?

A

fluoroquniolones- cipro or norfloxacin

OR bactrim

55
Q

when does a pt get prophylactic ABX for SBP?

A

if pt survives the first episode of SBP then get ABX to prevent another episode

56
Q

what do we use to tx patients with alcoholic liver disease? what is specific drug and dosing?

A

corticosteroids- only thing we can give them; 4 week course of prednisone 40 mg, followed by 2 week taper

57
Q

Hep A virus is what type of virus? this does not result in _________ infection

A

RNA virus; chronic

58
Q

how is Hep A transmitted? (2 ways)

A

person to person through fecal-oral or consumption of contaminated food/water

59
Q

Hep A resolves within ___ months of infection because…

A

2; death of hepatocytes results in elimination of the virus

60
Q

what are the preexposure prophylaxis measures for Hep A?

A

vaccination- Havrix/Vaqta

Twinrix (Hep A and B combo)

61
Q

what is postexposure prophylaxis for Hep A? (2)

A

Hep A immune globulin or HAV vaccine

62
Q

what type of virus is Hep B? what two types of disease can it be?

A

DNA; acute and chronic

63
Q

chronic infection of Hep B increases risk of what?

A

hepatocellular carcinoma

64
Q

prevention strategies for Hep B

A

vaccination:
3 dose schedule (0, 1 & 6 months) of recombivax and Engerix-B
OR HEPLISAV-B for adults only (2 dose series, 2nd dose 1 month later)

65
Q

are alfa interferons good for tx of chronic Hep B virus?

A

nope, tx lasts for 48 weeks and lots of ADRs so not preferred

66
Q

when are alfa-interferons considered the preferred option for Hep B?

A

for initial tx of chronic HBV infection in tx naïve adults (never been tx for hep B before)

67
Q

what are the five NRTI drugs for chronic Hep B tx?

A 
lamivudine (epivir)
entecavir (baraclude)
telbivudine (tyzeka)
adefovir (hepsera)
tenofovir alafenamide (vemlidy)
68
Q

are ABX for hepatic encephalopathy always added to lactulose?

A

not always, in later stages of disease you might add ABX BUT these ABX are very expensive and isn’t the current guidelines

69
Q

what are the two 1st choice options for chronic Hep B tx in tx-naïve adults?

A

entecavir (baraclude) and tenofovir alafenamide (vemlidy)

70
Q

how long should tx for chronic Hep B be for?

A

12 months after pts have seroconversion to HBV- negative (some people might need to take indefinitely)

71
Q

which chronic Hep B drug is used less often due to increased resistance within 1st year of use?

A

lamivudine (epivir-HBV)

72
Q

which chronic Hep B drug should only be initiated if other antivirals are contraindicated or not available?

A

telbivudine (tyzeka)

73
Q

which chronic Hep B drug should not be used in combination with interferon alpha because of neurologic side effects?

A

telbivudine (tyzeka)

74
Q

which chronic Hep B drug inhibits DNA polymerase/reverse transcriptase and is effective against lamivudine resistant HBV?

A

adefovir (hepsera)

75
Q

what is goal of therapy for chronic Hep C?

A

eradicate virus plus prevent progression of fibrosis and development of cirrhosis

76
Q

what is considered a cure for chronic Hep C?

A

undetectable HCV RNA for 12 weeks after completing therapy

77
Q

what is the most prevalent HCV genotype?

A

Type 1- 75% (type 2&3: 20-25%, Type 4,5,6 <2%)

78
Q

what are the three direct acting antivirals used for Hep C tx?

A

NS3/4A (protease) inhibitors, NS5A inhibitors, and NS5B inhibitors

79
Q

what are the protease inhibitor drugs?

A 
"pr" in middle of names*
simeprevir
paritaprevir
grazeoprevir
glecaprevir
voxilaprevir
80
Q

what are the NS5A inhibitor drugs?

A

have “asvir” ending

ledipasvir, daclatasvir, obitasvir, elbasvir, velpatasvir, pibrentasvir

81
Q

what are the NS5B inhibitor drugs?

A

have “buvir” ending

sofosbuvir, dasabuvir

82
Q

how do protease inhibitors and NS5A inhibitors target Hep C virus?

A

prevent viral replication

83
Q

how do NS5B inhibitors target Hep C virus?

A

act as a chain terminator so virus cant finish replication cycle

84
Q

when is peginterferon alfa-2b used for chronic Hep C tx?

A

used in combo with ribavirin with compensated liver disease and/or HIV infection (not used much anymore though)

85
Q

when is ribavirin used for chronic Hep C tx?

A

combo therapy in interferon alfa with compensated liver disease and /or HIV infection (not used much anymore)

86
Q

what is the boxed warning for ribavirin?

A

hemolytic anemia

87
Q

can ribavirin be used in pregnancy?

A

no, its a teratogen; there are two forms of barrier tx during pregnancy and 6 months after (used for men and women)

88
Q

what are the four preferred drugs for tx of HCV?

A

Epclusa, Harvoni, Zepatier, Mavyret

89
Q

what are the two indications for use of Epclusa?

A

tx of chronic HCV genotypes 1-6 in adults:

1) . without cirrhosis or with compensated cirrhosis (stage A of cirrhosis)
2) . decompensated cirrhosis (stage B and C) combined with ribavirin

90
Q

how long do you use epclusa for tx? what is dose?

A

12 weeks; one tab per day (with or without food)

91
Q

main ADR of epclusa

A

can reactivate HBV

92
Q

what are drug-drug interactions for epclusa?

A

agents that induce P-gp and CYP3A4 (dec concentration of epclusa)

93
Q

what are two indications of use for Harvoni?

A

tx of chronic HCV genotypes 1,4,5,6 (tx naive/experience with or without cirrhosis OR tx w cirrhosis) OR tx of chronic HCV in pts coinfected with HIV

94
Q

what is the main drug drug interaction with Harvoni?

A

amiodarone (levels are increased by Harvoni)

95
Q

what are the two indications of use for zepatier?

A

tx of chronic HCV genotypes 1 or 4 in adults or tx of patients with HIV coinfection

96
Q

severe potential ADR of zepatier

A

increase in ALT >5x normal in 1% of subjects

97
Q

2 indications of use for Mavyret

A

tx-naïve pts with HCV genotypes 1-6 without cirrhosis and compensated cirrhosis OR HCV genotype 1 previously treated

98
Q

can you get an acute or chronic liver injury from drugs?

A

both

99
Q

what is the most common cause of acute liver failure in the US?

A

drug induced liver injury

100
Q

what is intrinsic hepatotoxicity associated with?

A

ingestion of toxic dose (acetaminophen, tetracycline, anabolic steroids)

101
Q

intrinsic hepatotoxicity is _________ and dose ___________

A

predictable and dose dependent

102
Q

what is the most common type of drug induced liver injury?

A

idiosyncratic hepatotoxicity

103
Q

idiosyncratic hepatotoxicity is ___________ and has a ________ ________ before sensitivity reaction

A

unpredictable; latent period (1-3 months usually, can be up to a year)

104
Q

what are the two types of idiosyncratic hepatotoxicity?

A

non immune mediated and immune mediated

105
Q

how does non immune mediated IH cause injury?

A

drug metabolites interfere with protein/enzyme activity, which disrupts cell function & leads to cell death

106
Q

how long does it take for toxicity to develop in non immune mediated IH?

A

weeks or months OR develop several weeks after discontinuing

107
Q

ex of drugs that cause non immune mediated IH

A

amiodarone, diclofenac, isoniazid, ketoconazole, valproate

108
Q

how does immune mediated IH cause injury?

A

involves drug, its metabolite and immune system leading to hepatocyte necrosis or apoptosis (cytokines are also released)

109
Q

how long for onset of symptoms for immune mediated IH?

A

delayed: 1-8 weeks

110
Q

what is the severe condition that can be caused by immune mediated IH?

A

Stevens-Johnson’s syndrome

111
Q

what is symptom recurrence for immune mediated and non immune mediated IH rechallenge

A

immune mediated- recurrence is quick

non immune mediated- injury may or may not occur again

112
Q

what are 5 common causative agents of acute hepatocellular injury?

A

acetaminophen, valproic acid, nefazodone, venlafazine, lovastatin

113
Q

how do drugs cause acute hepatocellular injury?

A

liver cells are injured by the drug releasing enzymes found primarily in the liver cells in the blood (elevation of enzymes in serum indicates injury)

114
Q

how do drugs cause acute cholestasis injury?

A

drug interferes with bile metabolism inside the cell, increased bile levels in the cells leads to cell injury

115
Q

how soon after discontinuing the offending agent does acute cholestasis resolve symptoms?

A

within a few weeks have full resolution

116
Q

what are five common causative agents of acute cholestasis injury?

A

amoxicillin/clavulanic acid, erythromycin, carbamazepine, chlorpromazine, anabolic steroids

117
Q

what is mixed pattern acute hepatic injury? what are AST/ALT and alkaline phosphatase labs?

A

combo of hepatocellular and cholestasis; ast/alt >8x and alka phos >3x

118
Q

what are some common causative agents of mixed pattern acute hepatic injury?

A 
NSAIDs
Macrolides (azithromycin) 
Nitrofurantoin
Sulfonamides (Bactrim)
Amoxacillin/clavulanic acid
Cyclosporine
Carbamazepine
119
Q

what are the two steps of dechallenge to determine DILI?

A

1) . remove current drug from regimen

2) . if 50% decrease in AST/ALT in 8 days, you found the offending agent

120
Q

what do you do for acetaminophen toxicity?

A

administer n-acetylcysteine (which increase glutathione and clears Tylenol from system)

Pharm (10 decks)

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