Liver Flashcards

1
Q

How many lobes does the liver have? How many Lobules?

A

2 lobes
thousands of lobules

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2
Q

What is the portal triad?

A

bile duct, portal vein and hepatic artery

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3
Q

What does the hepatic duct do?

A

move bile to gallbladder asnd duodenum

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4
Q

How much Cardiac output does the liver get?

A

25%

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5
Q

At what point can the liver no longer regenerate?

A

> 70% destruction

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6
Q

What does the liver mainly store?

A

B12, iron and others

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7
Q

What does the liver synthesize?

A

plasma proteins

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8
Q

What is bile needed for? How much is resorbed?

A

emulsify fat, cholesterol, elim wastes
95% resorbed

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9
Q

How is does bilirubin get produced?

A

RBC degradation

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10
Q

What is fulminant liver failure?

A

irreversible damage and insufficient hepatocytes to function

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11
Q

WHat is cholestasis?

A

failure of normal amount of bile
accumulation

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12
Q

What can cause cholestasis?

A

gall stones
tumor, alcohol, PBC,PSC

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13
Q

WHat is PBC?

A

slow autoimmune destruction of ducts

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14
Q

What is lead cause of liver trasnplant in women?

A

PBC

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15
Q

WHat is PSC?

A

genetic progressive inflammation and fibrosis of biliary tree

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16
Q

What condition is associated with PSC?

A

inflammatory bowel disease

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17
Q

Symptoms of Cholestasis?

A

pruritis, jaundice, dark urine, light stool, enlarged liver, growths under skin

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18
Q

What can we give for gall stone?

A

ursodiol- lowers cholesterol stauration

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19
Q

WHat can we give for pruritis?

A

cholestyramine, antihist (sedate) and Sertraline, Naltrexone and rifampin if refractory

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20
Q

What is hemochromatosis?

A

iron absorption is high, and can kill hepatocytes

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21
Q

What genetics will give you hemochromatosis?

A

homozygous for it

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22
Q

True or false: Liver enzyme measurments indicate level of function.

A

FALSE

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23
Q

If a patient gets lab work and ALP and GGT are elevated what condition do they have?

A

cholestasis

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24
Q

What conditions have high GGT?

A

LIVER PROBLEMS

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25
Q

If a patient had only ALP elevated what are we thinking?

A

could be due to bones

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26
Q

A patient has increased AST and ALT what condition is it?

A

Hepatocellular injury

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27
Q

Which enzyme ALT or AST is more specific?

A

ALT

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28
Q

Why might albumin level not change in acute liver problems?

A

takes 20 days to notice change

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29
Q

What is pre albumin?

A

transport protein and is more accurate and faster seen
NOT A PRECURSOR

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30
Q

What condition can cause an elevated bilirubin?

A

hemolytic anemia

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31
Q

What are the three LFTs?

A

albumin, bilirubin, PT

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32
Q

What is unconjugated bilirubin?

A

bound to albumin
not water sol
indirect

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33
Q

What is conjugated bilirubin?

A

free
sol in water
direct

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34
Q

Where does bilirubin become conjugated?

A

liver

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35
Q

What are the factors measure for PT?

A

1,2,5,7,9,10

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36
Q

When will you see a change in PT?

A

> 70% destruction

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37
Q

What enzymes show alcohol is the culprit?

A

<10x increase of enzymes
AST>ALT 2:1

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38
Q

What is the only cure for cirrhosis?

A

transplant

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39
Q

What is definition of cirrhosis?

A

chronic disease with fibrosis and nodular formation

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40
Q

What is NASH?

A

Non alcohol steatohepatitis

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41
Q

What is drink guidlines now?

A

Low risk= <2 drinks/week
Med risk= 3-6 drinks/week
high risk= >6 drinnks/week

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42
Q

Which gender gets more injuries when drunk?

A

male

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43
Q

Which gender is alcohol worse for? Why?

A

Women= absorb more alcohol

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44
Q

What is a drink equivalent?

A

341 ml of beer
43 ml of spirits
142 ml of wine

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45
Q

How can we diagnose cirrhosis?

A

Fib-4, APRI, uktrasound (first), elastography, biposy

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46
Q

What does compensated cirrhosis?

A

functions well despite scarring
may be asymptomatic
anorexia, loss of weight, weak, NDV

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47
Q

What is sx of decompensated cirrhosis?

A

confusion, edmea, fatigue, bleeding

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48
Q

What does the body to to decrease portal HTN?

A

RAAS and NO to dilate

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49
Q

What other organ becomes effected by portal HTN? What does it do?

A

spleen gets hiuge and destroys RBC

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50
Q

What are the consequences of portal shunting?

A

liver doesnt detoxify what we eat, malabsorb of fat,

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51
Q

What is ascites? What causes it?

A

collection of fluid in the peritoneal cavity
no albumin and retention of water

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52
Q

If the ascitic fluid has WBC what does that mean?

A

infection

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53
Q

What is SAAG? What level is liver related?

A

serum to ascitic albumin ratio
>11

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54
Q

What level of protein and SAAG indicates cardiac dysfunction?

A

> 25 and >11

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55
Q

What is inital therapy for ascites?

A

Na and watewr restrict
spirinolactone
furosemide

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56
Q

If initial therapy doesnt work for ascites what do we do?

A

paracentesis, TIPS, transplant

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57
Q

What is paracentesis? What else MUST be given?

A

remove fluid with needle
albumin must be given too

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58
Q

What is TIPS?

A

shunt in liver

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59
Q

At what level might we need fluid restriction?

A

Na <125

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60
Q

What dose is typical for ascites?

A

100 mg up to 400

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61
Q

S/e of spironolactone?

A

man boobs, lower libido, breast tender

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62
Q

What is dose of furosemide?

A

40 mg up to 160 mg

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63
Q

What diuretic do we give if cant tolerate spironolcaton?

A

amiloride

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64
Q

What can we add on if ascites is refractory?

A

metolazone

65
Q

What is refractory Ascites?

A

unresponsive to initial therpay and max dose of diuretics

66
Q

What drug can cause refracroy ascites?

A

NSAIDs

67
Q

What do we do if low urine sodium? what about high?

A

low= more diuresis
high= non adherence

68
Q

What is acceptable weight loss if edema and with?

A

none= 0.5 kg/day
more for with edmea

69
Q

What is spontaneous bacterial peritonitis?

A

infection with no cause, HIGH mortality

70
Q

What pathogens are common in bacterial peritonitis?

A

E coli, Klebsiella, strep pneumonia

71
Q

What is empiric therapy for community acquired and hospital acquired bacterial peritonitis?

A

Community- Cefotaxime or ceftriaxone for 5 days
Hospital- pip taz, meropenem +- vaancomycin

72
Q

Who should be on prophylactic treatment for bacterial peritonitis? What is the antibiotic?

A

if survived previous or high risk (low ascitic fluid protein or variceal hemorrhage)
Treat? norfloxacin, septra, ciprofloxacin

73
Q

What is hepatorenal syndrome?

A

renail failure due to liver dz, no pathological change to liver just vasoconstriction to kidney

74
Q

What are varices? At what mmHg can rupture occur?

A

high pressure in portal causes shunting and the small vessels become engorged especially in rectal, ab, esophagus
>12 mmHg

75
Q

How can we manage variceal bleeds?

A

give RBC, antibiotic for prophylaxis
octreotide/ somatostatin to vasoconstrict
band ligation
TIPS

76
Q

Are beta blockers useful in this condition?

A

YES non selective
Propanolol 20 mg BID
Nadolol 20 mg OD, Low CNS, renally unchanged
use until 55 bpm

77
Q

What is the most effective to stop bleeding in throat?

A

EVL

78
Q

How does encephalopathy occur in liver dz?

A

accumulate of ammonia and is neurotoxic

79
Q

How does encephalopathy present?

A

drowsy, mood change, confusion

80
Q

What are the grades of encephalopathy?

A

1= mild confusion and tremor, impaired motor
2= lethargy, mod confusion, ataxia
3= stupor, incoherent
4= coma, unresponsive

81
Q

What can make encephalopathy worse?

A

protein intake, gi bleed
diuretics
alcohol, infection, renal failure
metabolic acidosis

82
Q

How do we manage encephalopathy?

A

restrict protein intake
no depressants
LACTULOSE

83
Q

How does lactulose help encephalopathy?

A

reduce pH and reduces ammonia absorb
15-45 ml TID

84
Q

What is the goal with lactulose?

A

2-3 stools/day

85
Q

s/e of lactulose?

A

bloat, ND

86
Q

If lactulose doesnt work what can we do?

A

metronidazole- lowers production of ammonia
rifaximin- same MOA, costly

87
Q

What nutritional deficiencies occur in liver issues?

A

lower diet intake especially protein and fat soluble vitamins

88
Q

If heavy alcohol is involved what nutrients are deficient?

A

B1 (thiamine)-low absorption and intake give 200 mg/day
B6- 2 mg OD
folate- 400 ug OD

89
Q

Which hepatitis is a DNA virus?

A

Hep B

90
Q

How does Hep A spread?

A

fecal to oral

91
Q

WHat is the presentation of Hep A?

A

fever, jaundice

92
Q

Is there a vaccine for Hep A and how long does symptoms last for?

A

YES
3 months

93
Q

Post exposure of Hep A when is a vaccine good for? What can we give if no vaccine available?

A

good for 14 days after exposure
Ig

94
Q

Is Hep A something to be concerned about?

A

No. Feel ill just rest

95
Q

If a patient Has total anti-HAV what does this mean?

A

acute, resolved or immunity to hep A

96
Q

What is the marker for immunity for Hep A? what about for acute infection?

A

anti-HAV IgG
acute= anti_HAV IgM

97
Q

How does Hep B transmit?

A

fluids,

98
Q

True or false HIV is better transmissible through needles than Hep B?

A

FALSE

99
Q

IS there a vaccine for Hep B? Is it lifelong?

A

Yes
No may need booster

100
Q

Based on Age with Hep B what is the rates of chronic Hep b infection?

A

HIghest in kids

101
Q

What is symptoms of Hep B? What about for chronic?

A

usually sx
chronnic= cirrhosis, cancer in liver

102
Q

WHat is the first test we do for Hep B? what does it mean?

A

HBsAg= current infection

103
Q

What does anti HBs mean?

A

immunity

104
Q

What does HBV-DNA mean?

A

asses severity of infection
tells you if it is replicating

105
Q

How can we treat Hep B?

A

interferons
nucleoside analoguies= iamivudine, tenofovir, adefovir

106
Q

Pros and cons of interferons

A

pros= no resistance, better cure rate, short course
cons= , no in symptomatic cirrhosis, side effects bad

107
Q

Pros and cons of nucleoside analogues?

A

Pros= safer, oral
cons= less cure rates, longer therapy, resistance

108
Q

WHat is an issue with lamivudine?

A

resistance high

109
Q

What is issue with adefovir?

A

less potent

110
Q

When would we go for tenofovir therapy?

A

if resistance to lamivudine
very potent

111
Q

If there is resistance to lamivudine, can we add on entecavir?

A

NO- cross resistance

112
Q

How does Hep C transmit?

A

fluids

113
Q

Is there a vaccine for hep C?

A

NO

114
Q

WHat are the symptoms fo Hep C?

A

MOSTLY asymptomatic but if its the usual
chronic= cirrhosis and cancer

115
Q

What is Hep C usually co infected with?

A

HIV

116
Q

Which hepatitis has genotypes?

A

Hep C

117
Q

AFter exposure to Hep C when might you show symptoms?

A

30 yrs

118
Q

What marker shows infection of Hep C? What is 2 issues with it?

A

anti- HCV
takes 6 weeks to get the marker after exposure
stays for life despite removal of infection

119
Q

What is a more accurate test for acute infection of Hep C?

A

HCV PCR

120
Q

WHat is considered a cured Hep C?

A

NO HCV RNA

121
Q

How long is treatment for Hep C?

A

8 weeks generally

122
Q

WHat is Harvoni for? WHat are the drugs in it?

A

Hep C
ledipasvir, sofosbuvir

123
Q

What genotypes is harvoni for?

A

1,4,5,6

124
Q

What is an issue with Harvoni?

A

NO PPIs

125
Q

The drug zepatier is for…? What genotypes? What are the drugs?

A

Hep C geno 1,4
Grazo, ELbasavir

126
Q

WHat lab changes are seen with zepatier?

A

acute increase in ALT

127
Q

Epclusa is good for which genotypes? What drug interaction are we worried about? What are the drugs in it?

A

all except maybe 3
NO PPI
sofosbuvir and velpatasvir

128
Q

Which two treatments are the most common and act on all genotypes for Hep C?

A

Maviret and Epclusa
Vosevi also is all genomes

129
Q

What Hep C treatments need to be taken with food?

A

Maviret and Vosevi

130
Q

Common drug interactions with Hep C treatment?

A

PPI= epclusa
Phenytoin, CMZ
herbals!!!!!
contraceptives= for maviret

131
Q

Who should be screened for HepC?

A

People born in 1945-75, >18 once
PWID, jail,

132
Q

How does Hep D transmit? IS there a vaccine?

A

Fluids
Yes B vaccine works

133
Q

Treatment for Hep D?

A

interferon

134
Q

How does Hep E spread? Is there a vaccine?

A

fecal- oral
NO

135
Q

If Hepatitis infection what do you do for pain?

A

acet <2 gams a day

136
Q

What is the most common reason a drug is recalled? WHat gender is more affected?

A

hepatotoxicity
women

137
Q

What hepatoxicity agents are we generally say dont take?

A

herbals

138
Q

Why is it difficult to classify DILI?

A

usually caused by multiple pathways

139
Q

How quickly does hepatocellular DILI take? What drug is an example?

A

in one year
allopurinol

140
Q

What is steatonecrosis? What drug is an example that can cause this?

A

fatty liver- tetracyclines

141
Q

What drugs can cause cholestasis?

A

Erythromycin and CMZ

142
Q

What is clinically significant abnormalities of liver tests?

A

ALT> 3x
Bilirubin>2x

143
Q

What is the R value? How do we calculate it? What does the number mean?

A

R= (ALT/UL)/(ALP/UL)
>5= hepatocellular
<2= cholestasis

144
Q

What is an example of a intrinsic DILI?

A

Acetaminophen- well known`

145
Q

How is acetaminophen metabolized?

A

mostly glucuronidation or sulfation
if saturated then CYP= toxic metabolite that gets fixed by glutathione but that quickly gets depleted

146
Q

WHat is the toxic metabolite from acetaminophen?

A

NAPQ

147
Q

What are the 4 stages of acet toxicity?

A

1= 24 hours of GI
2= 1-3 days of ab pain, blood test abnormalities
3= asymptomatic or hepatic failure
4= recovery if survive

148
Q

True or fact overdosing on acetaminophen causes chronic hepatyic issues?

A

NO

149
Q

WHat levels of acet is toxic for adults and children?

A

> 7.5
150 mg/kg

150
Q

What are antidotes for Acetaminophen?

A

Syrup of ipecac
charcoal
acetylcystein

151
Q

WHat is an issue with syrup of ipecac and charcoal?

A

only help within first hour, charcoal is better than syrup tho

152
Q

How does acetylcysteine work?

A

enhances glutathione and promotes non toxic conjugation

153
Q

When do you administer Acetylcysteine?

A

when above treatment line of rumack-mathew nomogram

154
Q

What indicates allergic type DILI? WHat drugs?

A

sx of rash, fever, high eosinophils
anticonvulsants- phenytoin, Sulfa antibiotics, allopurinol

155
Q

When does non-allergic idiosyncratic DILI present? What are some drugs?

A

a week to a year
drugs= valproic acid, ketoconazole?

156
Q

What drug causes the most amount of DILI? WHy?

A

Amoxicillin because it is used SOOOOO much

157
Q

WHat child Pugh score is best survival and worst?

A

A=100%
C=45%

158
Q

TRue or false People with cirhhosis are more likely to be affected by DILI?

A

FALSE= just lower recovery

159
Q
A