Therapeutics Exam 4 (Liver) Flashcards

1
Q

Blood enters the liver through via what?

A

hepatic artery AND portal vein

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2
Q

Blood leaves the liver through what

A

hepatic vein (central vein)

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3
Q

Drug metabolism usually happens in the liver:

Typically ______ medications but can sometimes _____ medications (______)

A
typically inactivates
CAN activate (prodrugs)
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4
Q

Liver Drug Metabolism:

What are phase 1 reactions

A

oxidation, reduction, or hydrolysis (activating or deactivating medications)

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5
Q

Liver Drug metabolism:

what are phase 2 reactions

A

conjugation (making a drug more water soluble— thus easier to excrete)

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6
Q

Liver Drug metabolism:

CYP enzymes seen in phase 1 or phase 2 reactions

A

phase 1

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7
Q

what is 1st pass metabolism

A

portion of medication that is metabolized BEFORE reaching systemic circulation….

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8
Q

what is extraction ratio

A

fraction of drug that is removed by the liver….

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9
Q

If a medication has a high ER it will have _____ bioavailbility

A

low

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10
Q

what are “pairs” of LFTs to look at for interpreting the liver

A

AST & ALT
Alk Phos & GGT
bilirubin (total, conjugated, unconjugated)
INR & Albumin

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11
Q

Normal Ranges:
AST
ALT

A

0 - 50 IU/L for both

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12
Q

Normal Ranges:
Alk Phos
GGT

A

Alk Phos: 30 - 120 IU/L

GGT: 0 - 50 IU/L

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13
Q

Normal Ranges:
Bilirubin Total:
Bilirubin (conjugated):
Bilirubin (unconjugated):

A

Total: 0 - 1.4 mg/dL
Conjugated: 0 - 0.3 mg/dL
Unconjugated: 0 - 1.1 mg/dL

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14
Q

Normal Ranges:
INR:
Albumin:

A

INR: 0.9 - 1.2
Albumin: 3.6 - 5 g/dL

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15
Q

AST or ALT

which one is more specific to the liver

A

ALT

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16
Q

AST and ALT can be elevated by what things?

A

viral infections
medications
ischemia

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17
Q

Ratio of ____ to ____ if > 2 = alcoholic liver disease

A

AST: ALT

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18
Q

if GGT and Alk Phos are elevated = what?

A

biliary tract injury

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19
Q

what things can elevate GGT and Alk Phos?

A

cholecystitis (inflammation of gall bladder)

obstruction (gallstone)

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20
Q

Bilirubin = the breakdown of _____

A

hemoglobin

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21
Q

Bilirubin is conjugated in the _____ to make it ______

A

in liver

to make it water soluble for excretion

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22
Q

_______ bilirubin is NOT assoc. with liver disease

A

unconjugated

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23
Q

elevated ______ bilirubin is associated with liver disease

A

conjugated

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24
Q

Unconjugated bilirubin is NOT assoc. with liver disease – it can be high when?

A

can be high when hemolysis is high (RBC/heme breakdown is high)

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25
Q

GGT or Alk Phos:

which one is more specific to the liver

A

GGT

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26
Q

INR will ______ in liver dysfunction - and why

A

increase because the liver is not making clotting factors = higher chance of bleeding

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27
Q

Albumin will ______ in liver dysfunction and why

A

decrease – because liver makes albumin…

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28
Q

______ and _____ are used as liver function indicators

A

INR and albumin

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29
Q

how to interpret LFTs?

A

look at how many times bigger the value is compared to the UPPER limit of normal

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30
Q

Cirrhosis:

reversible or irreversible

A

irreversible

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31
Q

Signs and Sxs of Cirrhosis

A
fatigue
wt loss
pruritis -- itching from built up bilirubin
jaundice
hepatomegaly/spleomegaly
encephalopathy
(pts can be asymptomatic)
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32
Q

what are some complications from cirrhosis/things that lead to increased morbidity and mortality

A
portal HTN
hepatic encephalopathy
ascites
Esophageal varices
spontaneous bacterial peritonitis
hepatorenal syndrome
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33
Q

5 things that could cause cirrhosis

A
Chronic alcohol consumption
Chronic viral hepatitis (Hep B and C)
Metabolic liver disease
Cholestatic liver disease
Drugs
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34
Q

what drugs can cause cirrhosis

A

amiodarone

methotrexate

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35
Q

what are some specific metabolic liver diseases that can lead to cirrhosis

A
hemochromatosis (high iron)
nonalcoholic steatohepatitis (fatty liver)
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36
Q

what is Child-Pugh Classification vs what is MELD Score

A

Child Pugh - classifies severity of cirrhosis

MELD: predicts mortality of pts with liver disease in next 3 months – helps rank pts on transplant list!!!

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37
Q

Child-Pugh Classification:

If mild disease: Class ___ and a score of ____

A

A

< 7

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38
Q

Child-Pugh Classification:

If moderate disease: Class ___ and a score of ____

A

B

7 - 9

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39
Q

Child-Pugh Classification:

If severe disease: Class ___ and a score of ____

A

C

10 - 15

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40
Q

what things are looked at/considered when finding the Child-Pugh Classification system

A
Bilirubin
Albumin
Ascites
encephalopathy
Prothrombin time
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41
Q

what does MELD score stand for

A

model for end stage liver disease score

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42
Q

what 3 things does MELD look at for predicting mortality

A

total bilirubin
SCr
INR

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43
Q

idea behind portal HTN

A

blood wont flow thru liver bc it is hard/fibrotic (thx cirrhosis) that the blood backs up and creates pressure

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44
Q

what is hepatic encephalopathy (HE)?

A

essentially confusion —

brain dysfunction due to liver insufficiency

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45
Q

why/how does hepatic encephalopathy occur?

A

Ammonia is produced by protein breakdown (normal thing to happen in body, dur)
liver NORMALLY makes ammonia –> urea but since liver sucks ammonia builds up
ammonia can cross BBB and cause neurotoxicity

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46
Q

Hepatic Encephalopathy:
FYI: Can be classified by type and severity, and its time course
(Type A,B,C and Grade I, II,III,IV, episodic, recurrent, persistent)

if ammonia level is _____ then it probably is NOT HE

A

ammonia level is normal - then probs not HE

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47
Q

what is asterixis

A

flapping tremor seen when the hands/arms are stuck out

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48
Q

Can be classified by what things?

A

by type and severity, and its time course, and if precipitated or not
(Type A,B,C and Grade I, II,III,IV, episodic, recurrent, persistent)

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49
Q

Treating Hepatic Encephalopathy:

when should you treat it?

A

always!! (doesn’t matter if spontaneous or precipitating)

50
Q

what things could precipitate hepatic encephalopathy

A
infections
electrolyte disorder
GI bleeding
diuretic overdose
constipation
51
Q

when do prophylaxis treatment for HE?

A

do secondary prophylaxis (aka if they ever get it - do prophylaxis…)

52
Q

Contaminant drugs to avoid when treating someones hepatic encephalopathy

A

benzos! (drugs that worsen confusion…)

53
Q

drugs used to treat hepatic encephalopathy (2 that are commonly used vs 2 that are not used as commonly)

A

commonly used: lactulose and rifaximin

not commonly used: neomycin and metronidazole

54
Q

MOA for lactulose to be used for hepatic encephalopathy

A

it increases ammonia elimination (via laxative effect)

makes environment more acidic = NH3 –> NH4- which means it cannot be absorbed

55
Q

Rifaximin MOA

A

eliminates ammonia producing bacteria

56
Q

Rifaximin or lactulose which one is more tolerated by patients

A

rifaximin

57
Q

Issues with lactulose?

A

they are pooping a lot
unpleasant taste
may cause dehydration, gas and bloating

58
Q

For acute or chronic treatment of hepatic encephalopathy:

titrate til you get to how many bowel movements a day?

A

2 - 4 / day

59
Q

Neomycin sucks for HE treatment why?

A

long term use = concern for ototoxicity or nephrotoxicity

60
Q

Metronidazole sucks for HE treatment why?

A

long term use = concern for neurotoxicity

61
Q

Ascites:

fluid (lymph) accumulation in the _______

A

peritoneal space

62
Q

what is SAAG stand for and why is it relevant to liver disease

A

SAAG = serum ascites albumin gradient

the SAAG score can help determine the cause of ascites

63
Q

how to find the SAAG value?

A

(albumin in serum) - (albumin in ascitic fluid)

64
Q

the SAAG value needs to be ____ to be cirrhosis

A

high or (> 1.1)

65
Q

how does a high SAAG value happen

A

portal HTN = more pressure = drive fluid into peritoneal space
since albumin is large it cannot pass the membrane

66
Q

1st line options for treating Ascites:

A
avoid alcohol
Na+ restriction 
avoid NSAIDs (leads to more Na+ and fluid retention)
diuretics
asses for liver transplant
67
Q

2nd line options for treating ascites

A

serial paracentesis

shunt

68
Q

what diuretics are used for ascites treatment

A

spironolactone

furosemide

69
Q

ratio of spironolactone and furosemide for treating ascites

A

100: 40

70
Q

spironolactone and furosemide:

which is superior by itself compared to the other

A

sprironolactone is superior alone

combo is superior is better overall

71
Q

Max doses of spironolactone and furosemide for ascites

A

spirono: 400 mg
furosemide: 160 mg

72
Q

if pt develops gynecomastia from spironolactone – what drugs can be used to replace it

A

eplerenone
amiloride
triamterene

73
Q

what is paracentesis

A

literally removing fluid straight from the ascites area

74
Q

Albumin and paracentesis:

give albumin when in relation to it?

A

AFTER

75
Q

Albumin and paracentesis:

use what ___ albumin

A

25% (more concentrated = less fluid you’re giving back)

76
Q

When is it indicated to give albumin to patients in relation to paracentesis

A

when over 5 L of fluid is removed!!

77
Q

how much albumin to give patients after paracentesis

A

6 - 8 g of albumin PER LITER of fluid removed

78
Q

what is SBP

A

spontaneous bacterial peritonitis

79
Q

Patients are at a higher risk of SBP if the have ______ in ascitic fluid

A

low protein

80
Q

Diagnosing SBP:
Done by taking a sample of ascitic fluid —
need to see an elevated _________ of (______ cells/mm3)

A

PMN count
(polymorphonuclear leukocyte)
> 250 cells/mm3

81
Q

Common abx for treating SBP

and treat for how long?

A

Cefotaxime and Olfloxacin

treat for 5 - 10 days

82
Q

For prevention of SBP:

do when recurrence rate is high —- what patients are high risk

A

if pts have low protein (<1.5 g/dL)
variceal hemorrhage
or
prior SBP

83
Q

For prevention of SBP:

Discontinue _________ because it is associated with increase rate of SBP

A

unnecessary PPIs

84
Q

what antibiotics can be used for SBP prevention and how often do you take them

A

Ciprofloxacin or SMT-TMP(bactrim)

take once daily

85
Q

In Cirrhosis — we will see (decreased or increased) INR - and what would make sense to give for this issue but we do not give it because it wasn’t actually effective…?

A

INCREASED INR – bc liver is not making clotting factors

do not give vitamin K

86
Q

Esophageal Varicies:

________ veins in the esophagus that leads to high risk of ______

A

enlarged

bleeding

87
Q

Esophageal Varicies: Treatment options?

A
blood transfusions (when Hgb hellla low)
Octreotide
EVL aka banding
Ceftriaxone 
(sorta PPIs)
88
Q

Esophageal Varicies Treatment:

Give Blood transfusions when?

A

to make sure Hgb stays above 7 g/dL

89
Q

Esophageal Varicies Treatment:
Octreotide is a ________ analogue

start when?

works by reduce _______ by causing ______

A

somatostatin analogue

start IMMEDIATELY if you suspect a variceal bleed

reduces portal pressure by causing vasoconstriction

90
Q

what is EVL? and another name for it?

and use it for what?

A

endoscopic variceal ligation aka BANDING

for treating esophageal varicies

91
Q

Esophageal Varicies Prohpylaxis options?

A

NSBB (non selective beta blockers)
EVL (the banding)
or TIPS – last line!

92
Q

Esophageal Varicies Prohpylaxis:

what to do for preprimary prophylaxis?

A

no treatment

93
Q

Esophageal Varicies Prohpylaxis

what to do for primary prophylaxis

A

NSBB OR EVL (not both!!)

definitely no TIPS

94
Q

Esophageal Varicies Prohpylaxis

what to do for secondary prophylaxis

A

NSSB + EVL = 1st line

TIPS = 2nd line

95
Q

T or F: for secondary prophylaxis of Esophageal Varicies Prohpylaxis once TIPS occurs you need to continue NSBB and EVL

A

false!! do not need them anymore

96
Q

what beta blockers are used for Esophageal Varicies Secondary Prohpylaxis

A

propranolol (BID
naldolol (QD)
carvedilol (QD to BID)

97
Q

For Esophageal Varicies Prophylaxis:

target a HR of ______ BPM

A

55 - 60

98
Q

For Esophageal Varicies Prophylaxis:

Hold or decrease dose when the SBP goes below _____

A

90 mmHg

99
Q

what is NASH stand for and what is it as a disease?

A

Non-alcoholic steatohepatitis

it is essentially “fatty liver”

100
Q

Risk factors for NASH?

A

metabolic diseases — obesity, T2DM, hyperlipidemia

101
Q

Treatment options for NASH?

A

lifestyle modification!! (wt loss and exercise)

possibly pioglitazone…?

102
Q

what does ALD stand for/what is

A

alcoholic liver disease — can be any injury ranging form steatosis to cirrhosis

103
Q

what are some additional risk factors that increase chance of ALD (other than large alcohol consumption)

A
type of alcohol (beer and liquor >wine)
timing (worse when not around mealtime)
binge drinking (4 -5 at a time)
obesity
genetics
104
Q

questionnaire for seeing if alcoholism

A

CAGE questionnaire (cut down, annoyed, guilty, eye opener)

105
Q

Prognostic score for ALD? it will give a sense of what?

A

MDF – maddrey discriminant function

predicts mortality

106
Q

ALD treatment?

A

abstain from alcohol - duh
supportive care
or prednisone or pentoxyfylline

107
Q

ALD Treatment:

if MDF Score < 32 give ________

A

supportive care only

108
Q

ALD Treatment:

if MDF Score > 32 give _____________

A

prednisone or pentoxifylne

109
Q

Signs and Symptoms of Alcohol Withdrawal

A
HA
tremors/SEIZURES (grand mal seizures)
elevated body temp
increased HR
N/V
irritability 
hallucinations
110
Q

T or F: delirium tremens is life threatening

A

true!!

111
Q

what is score is found in alcohol withdrawal based on symptoms

A

CIWA score (clinical institute withdrawal assessment)

112
Q

Drugs for treatment for alcohol withdrawal

A

Folic acid/Thiamine
Multivitamin
Benzo – PRN is best

113
Q
Definition of Acute Liver Disease:
Evidence of \_\_\_\_\_\_ abnormality
&amp;
any degree of \_\_\_\_\_\_in a pt without preesxisting cirrhosis
&amp;
illness is < \_\_\_\_\_ in duration
A

coagulation (INR of 1.5 or above)

degree of encephalopathy

< 26 weeks

114
Q

what drugs are direct toxins to the liver (she gave us a list of top 7)

A
APAP!
ASA
Niacin
Vit. A
Buprenorphine
Methylprednisolone
Tetracycline
115
Q

APAP posioning treatment:

3 things to possibly give?

A

activated charcoal
NAC (N-acetylcysteine)
Acetadote

116
Q

How does activated charcoal work for APAP toxicity

A

it binds to it in the STOMACH and prevents absorption

wont affect the APAP already absorbed tho :’(

117
Q

When to give NAC for APAP toxicity

A

all the time!!

even if you just suspect it, just give it!

118
Q

How does NAC work for APAP toxicity

A

NAC increases glutathione

*sometimes APAP –> NAPQI (which is toxic)

glutathione binds/detoxifies NAPQI

119
Q

T or F: NAC is not recommended if activated charcoal has already been given

A

false!!

give it still

120
Q

When adjusting a patients medications because of liver disease consider:
Extent of ________ of the med
Extent of liver disease (dose adjust recommended by _______ class)
Is the medication highly ______
avoid ______ meds

A

extent of hepatic extraction
child pugh class
highly protein?
avoid hepatotoxic

121
Q

Highly protein bound meds:
in liver disease —
____ protein/albumin = ____ unbound drug = ____ therapeutic effect

(each blank is high or low)

A

low albumin
high unbound drug
high effect