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Transplant Hep Boards > Alcohol Related Liver Disease > Flashcards

Alcohol Related Liver Disease Flashcards

1
Q

What is the definition of binge drinking`

A

Five drinks in men, four in women over two hours

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2
Q

What is the AUDIT?

A

10 questions on consumption, dependence, and any alcohol associated problems

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3
Q

What is AUDIT C

A
  1. How often did you have a drink containing alcohol in the past year
  2. How many drinks containing alcohol did you have on a typical day when you were drinking in the past year?
  3. How often did you have six or more drinks on one occasion in the past year?

Score >/= 4 –> intervention, referral should be offered

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4
Q

Which biomarkers can be prolonged in renal disease

A

ETG ethyl glucuronide
ETS ethyl sulfate
* so longer window of positive results after alcohol ingestion in patients with kidney disease

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5
Q

What is PETH?

A

phospholipid formed by the reaction of phosphatidylcholine with ethanol catalyzed by phospholipase D in the erythrocyte cell membrane

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6
Q

What is half life of PETH and what is detection time

A

10-14 days, but can be longer with more chronic, repeated heavy alcohol consumption.
Is not influenced by age, BMI, sex, kidney disease, or liver disease

Detection time is 2-3 weeks

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7
Q

What are the FDA approved medications for AUD?

A
  1. disulfiram- not recommended for patients with ALD
  2. Naltrexone 50 mg/d
  3. Acamprosate 660 mg TID
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8
Q

What are non FDA meds for AUD?

A
  1. Gabapentin
  2. Baclofen
  3. Topiramate
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9
Q

What are risk factors for ald

A
  1. alcohol dose above 1 drink/day (women) and 2 drinks/day (men)
  2. Pattern of consumption -daily drinking, binge drinking
  3. smoking cigarettes
  4. Women compared with men
  5. Genetics (PNPLA3,)
  6. Increased BMI
  7. Presence of comorbid conditions, chronic viral hepatitis, hemochromatosis, NAFLD, NASH
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10
Q

What are histologic features of AH?

A

Neutrophilic lobular inflammatio
Degenerative changes in hepatocytes (ballooning and Mallory Denk bodies)
Steatosis
Pericellular fibrosis

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11
Q

How to make a clinical diagnosis of AH?

A
  1. Onset of jaundice within prior 8 weeks
  2. Ongoing consumption of >40 (female) or >60 (male) g alcohol/day for more than six months with <60 days of abstinence before onset of jaundice
  3. AST>50, AST/ALT >1.5, both values <400
  4. Serum total bili >3.0

Definite AH: Clinically diagnosed and biopsy proven

Probable AH: Clinically diagnosed without potential confounding factors

Possible AH: Clinically diagnosed with potential confounding factors (ischemic hepatitis, drug induce, denies alcohol use, atypical lab findings)

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12
Q

What are components of Maddrey?

A

Bili
INR
Initiate steroids if >32

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13
Q

what are components of Lille?

A

Change in bili
INR
Cr
Age
Albumin
>/= 0.45 non response to steroids,

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14
Q

When should you start steroids in AH?

A

When MD > =32
MELD> 20
No contraindications:

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15
Q

What are genetic and environmental links to PBC?

A

Genetics: HLA associations + genes involved with innate immune system
Environmental: smoking, nail polish, infections

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16
Q

What does UDCA do in PBC?

A

Reduces disease progression and need for liver transplantation

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17
Q

What is the childhood equivalent to PBC?

A

There is none, it is an adult disease

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18
Q

Can AZA be used in AIH?

A

If no cirrhosis, then yes can be used. But can’t be used for induction therapy because it takes 6-8 weeks to take effect.
If compensated cirrhosis, need to check TPMT
Do not use in decompensated cirrhosis
Do not use in fulminant AIH

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19
Q

How do you use steroids in AIH?

A

Induction therapy:
-prednisolone or prednisone of 30 to 60mg/day, or up to 1 mg/kg/day as mono therapy
- combination therapy of 30 mg of red + 50 mg of AZA

Weaning:
- try to wean to Maintenace dose less than 20 mg/day

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20
Q

When to wean meds for AIH?

A

After two years of remission, can wean. Can do biopsy before withdrawing IS, because if inflammatory activity is present, relapse is almost universal, and therefore IS should be continued in the long term.

In adults, biopsy is not absolutely necessary before withdrawal. In children, it is strongly recommended

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21
Q

What if someone is treated for AIH, liver tests improve, but IgG remains elevated after two years of meds?

A

Can still try with withdrawal of meds, noting that IgG may be elevated in cases of cirrhosis

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22
Q

Can you use budesonide in AIH cirrhosis?

A

No- first pass metabolism is in the liver, and risk of PV thrombosis

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23
Q

What percentage of general population have a positive AMA?

A

0.5%

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24
Q

What lesion has a central scar

A

FNH

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25
Q

How to differentiate adenoma from FNH

A

eovist contrast
adenoma does not take up contrast, FNH does

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26
Q

When are adenoma at risk for rupture or transformation to HCC

A

when >5 cm

if <5 cm, imaging in six months. If stable, then annually. If growing >20 % increase in diameter or if >5cm –> surgical resection due to risk of hemorrhage

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27
Q

What is a cavernous hemangioma

A

benign tumor
female
multi centric
peripheral nodular arterial enhancement with fill in to center
no tx unless large/ Kasabach Merritt syndrome

if <5 cm –> no further imaging
if >5 cm, repeat imaging in 6-12 months and then if stable, no further imaging. If it grows, then repeat in 6-12 months. N oprereuiste for surgical interveion

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28
Q

What does FNH look like on imaging

A

central scar
rapid intest enhancement in arterial phase

no role in stopping OCP

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29
Q

What characteristic is associated with risk of malignant transformation to HCC in an adenoma

A

beta catenin mutation (can do stain, but clinically available too)

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30
Q

What happens to the biliary system in adenoma on biopsy or eovist imaging

A

absence of bile duct

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31
Q

What drug blocks signal 1

A

tacrolimus

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32
Q

What drugs inhibit purine synthesis

A

MMF
AZA

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33
Q

What drug deplete lymphocyte through complement mediated cell lysis

A

thymo

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34
Q

what is POA of pred

A

inhibits formation of arachidonic acid, a precursor of inflammatory cascade

NFAT

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35
Q

What drug blocks signal 2

A

anti ctla 4

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36
Q

What blocks signal 3

A

MTOR

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37
Q

How does HSV present post transplant

A

usually in first month
acute hepatitis

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38
Q

How does adenovirus present post transplant

A

respiratory symptoms, gastroenteritis, hepatitis UTI

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39
Q

how does Parvo B19 present post transplant

A

severe anemia

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40
Q

How can cryptococcal disease present and what must be done

What do you need to watch for

A

pneumonia
meningitis
disseminated

usually via lungs. but in Pulm disease, have to rule out CNS disease

rapid decreasing IS and treating with anti fungal can lead to reconstitution inflammatory syndrome

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41
Q

What are risk factors for PNF

A

female donor
advanced age donor
pre-perfusion allograft steatosis
cold ischemia time

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42
Q

What cytokine aids with tolerance

A

Il 10

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43
Q

Does Hep E cause ALF

A

not typically, but in pregnancy associated with high mortality. can cause chronic hepatitis and cirrhosis

44
Q

What is treatment of Hep E

A
  1. lower IS
  2. ribavirin
45
Q

What type of renal disease is HRS

A

pre-renal
due to splanchnic vasodilation

46
Q

What are pressure in SOS/post sinusoidal

how is this different than sinusoidal or pre-sinusoidal

A

wedged- increased
free- normal
HVPG- increased

in sinusoidal, it is same pattern

in pre-sinusoidal, everything is normal

47
Q

What are risk factors associated with post transplant renal dysfunction

A

Strongest: older age and post transplant creatinine levels

maybe female
sex

other include: pretransplant cr, hep c

48
Q

How does GVHD present

A

rash
cytopenia
GI compliaints

49
Q

What are risk factors for GVHD

A

0- 1- class 1 HLA

HLA DQR or more than 2 HLA class 1 was not associated with GVHD

50
Q

What does baby need in a mother with high viral load of Hep B

A

HBIG and vaccination at birth

51
Q

What is the most common pathologic finding in cystic fibrosis

A

hepatic steatosis

52
Q

What are risks of HAT

A

duration of hepatectomy
aortic conduit
multiple transfusions

53
Q

What are down staging rules for HCC

A
  1. residual disease has to fall into Milan
    2, one lesion 5-8 cm
  2. 2-3 lesions:
    - at least one greater than 3 cm
    -each lesion less than or equal to 5 cm
    - total diameter of all lesions less than or equal to 8 cm
  3. four or five lesions
    - each less than 3
    total diameter less than or equal to 8 cm
  4. AFP<1000
54
Q

What graft has best outcome in LDLT

A

no survival difference in left lobe or right lobe

55
Q

What does tamoxifen do to liver

A

fatty liver, typically after 1-2 years

56
Q

Which hep c drug cannot be given in renal dysfunction or dialysis patients

A

anything with soft

57
Q

What can be used for treatment in someone treated with interferon and cirrhosis

A

soft/vela, epclusa, in cirrhosis need duration of 12weeks

58
Q

What should you give household contacts of someone with Hep A

A

post exposure prophylaxis
for hepatitis A infection vary by age and
health status. For healthy people over 12 months
to 40 years old, hepatitis A vaccine is preferred
over IG due to likelihood of response, long-term
protection, and equivalent efficacy to IG. IG is
recommended within TWO WEEKS of exposure for
persons over 40 years old due to lack of knowledge
on vaccine performance and possibility of more
severe presentation in patients with older age.WHAT HEP

59
Q

What can happen to Hep B when getting treated with DAA

A

can cause flare

60
Q

Which hep c drugs interact with ppi

A

epclusa
harvoni

61
Q

How do you manage someone with HbcAb+ getting four weeks of prednisone 20 mg

A

treat for ppl hep b during treatment and at least six month post treatment

62
Q

What do you do in someone with cirrhosis who goes from Hep B eAg+ to Hep B eAb+

A

continue tif indefinifintiely because there is cirrhosis

if no cirrhosis, could do therapy for 12 months and then stop (consolidation)

63
Q

AST ALT in the 1000’s but bili disprportionatey low

A

herpes,

fevers

64
Q

What can you get from boar

A

Hep E

tx in immunocompetent patients is supportive care

immunocompromised –> ribavirin

65
Q

what do you do for immunesuppresed patients who are exposed to hep a

A

Immunoglobulin
is particularly important to give to immunosuppressed
patients exposed to hepatitis A given the
risk of fatal hepatitis A infection and reduced
response to vaccination in this population.

66
Q

WHAT DRUG INTERFERES WITH mavyret

sofo

A

statin

amiodarone, BB(just need to watch HR)

67
Q

What does Vit E help with

A

steatosis and inflammation. does not improve fibrosis

68
Q

what conditions are associated with microvesicular steatosis (7)

A
  1. tetracycline
  2. cholesterol ester storage disease
  3. fatty liver of pregnancy
  4. aspirin
  5. valproate / mitochondrial
  6. HIV meds
  7. cocaine
69
Q

What is dubin johnson

A

cannot export conjugated bilirubin so marked conjugated hyperbilli at birth

black liver

normal LFTs, no liver failure

ABCC2 gene

70
Q

Criger Nagar

A

increase in unconjugated bili

UGT1A1

type 1 is absent enzyme so more severe than type 2

71
Q

Which PFIC has elevated GGT

A

type3

(three three more beer)

72
Q

which PFIC is associated with HCC

A

type 2

73
Q

What does urso do in PBC

A

reduces LDL (Not HDL)

reduces risk of variceal bleeding

reduces risk of progression

reduces risk of needing transplant

does not help with osteoporosis or fatigue (note phlebotomy does help with fatigue in HH)

74
Q

What grade of HE is asterixes seen?

A

Mininal and Grade 1 is covert HE

Grade 2 is asterixsis and overt

Grade 4 is coma

75
Q

How is overt HE defined? How is covert defined?

A

Grade 2
Asterixsis
Disorientation

Covert: diagnosed with psychomotor or neuropsychological testing

76
Q

How do you use ammonia in HE?

A

Increased blood ammonia alone does not add any diagnostic, staging, or prognostic value for HE in patients with CLD. A normal value calls for diagnostic reevaluation however

77
Q

What type of hemorrhage is seen in HE

A

Intracerebral hemorrhage is five times more likely in patients with HE. So a CT isn’t needed to diagnose HE, but should be used to rule out other diseases like a bleed

78
Q

When should rifaximin be used in HE?

A

Not enough data for rifaximin alone, should be used in conjunction with lactulose for prevention of recurrence of HE

Rifaximin added to lactulose is the best-documented agent to maintain remission in patients who have already experienced one or more bouts of OHE while on lactulose treatment after their initial episode of OHE

79
Q

What are alternative regimens for HE?

A

IV LOLA Oral (not IV) BCAA for additional or alternative treatment
ORAL BCAA may have more of an effect on promotion of lean body mass rather than treatment of HE
Metronidazole or neomycin for alternative treatment

80
Q

What type of HE do you treat?

A

Overt only

81
Q

How do you prevent post TIPS HE

A

Routine prophylaxis is NOT recommended

82
Q

When can prophylactic therapy for HE be discontinued?

A

Under circumstances where the precipitating factors have been well controlled (i.e., infections and VB) or liver function or nutritional status improved, prophylactic therapy may be discontinued

83
Q

What influences the risk of repeated episodes of HE?

A
  1. overall liver function
  2. body habitus/ muscle mass
  3. controlling precipitins factors

If these are all controlled, prophylactic therapy may be able to be stopped

84
Q

What are the daily energy intakes for HE?

A

35-40 kcal/kg ideal body weight

85
Q

What are the daily protein intake for HE?

A

1.2-1.5 g/kg/day

86
Q

What is the most common pediatric liver tumor

A

hepatoblastoma

Can be asymptomatic or painful from a larger tumor

87
Q

What is the best thing for survival in kids with hepatoblastoma

A

resection (but this has to be possible anatomically)

AFP is a great biomarker for tumor

88
Q

Who does Biliary atresia affect

A

-neonate
- female predominance
- higher rate in non-white

89
Q

What other abnormalities are seen in biliary atresia

A

situs inversus, splenic malformation
intestinal malrotation
cardiac anomalies
pancreatic anomalies

90
Q

What is seen at birth in those with BA

A

elevated bilirubin on Day of life 1

91
Q

What is the triangular cord sign

A

seen in biliary atresia
increased echogenicity along anterior wall of portal vein

92
Q

What is the gold standard dx for BA? What are other helpful tests

A

Intraoperative cholangiogram or PTC- want to see dye go into the liver and out of intestine

U/S - triangular cord sign
HIDA - want to see good excretion into intestine

Liver biopsy- not diagnostic, will see bie duct proliferation that detects extra hepatic biliary obstruction

93
Q

What is kasai

A

all extra hepatic biliary tissue excised

creation of roux en y

roux jejunum anatomiste to portal plate

restores bile flow

94
Q

What determines need for transplant in BA after kasai

A

time to kasai
those who got kasai within 30 days DOL were more likely to survive with native liver than those who got kasai >90 day of life

Total bili <2 at 3 months post kasai associated with higher survival with native liver

95
Q

What is the definition of ALF in peds

A
  1. absence of pre-existing liver disease
  2. biochemical evidence of acute liver disease

–coagulopathy not corrected by vit k
—-INR >1.5 + HE
or
INR>2 –> status 1A

96
Q

Vit A deficiency

A

ocular changes: dry eyes and night blindness

Skin changer: poor wound healing, hyperkeratosis

growth retardation

*if not responding well to supplementation, can give zinc as well

97
Q

what is therapeutic target of vit D

A

> 30ng/mL

98
Q

How is it best to supplement vit D in children?

A

D3, because it has better water solubility and therefore better absorption

99
Q

Vit E defiiciency

A

Hemolytic anemia
Nuerologic deficits (ataxia, peripheral neuropathy)
muscle pain

High doses antagonize Vit A and adversely affect wound healing and platelet function

100
Q

Thiamine or B1 deficiency

A

dry beriberi (loss of feeling, difficulty walking, loss of muscle function)

wet beriberi (high output cardiac failure)

Wernicke/Korsakoff (confusion, ataxia, ocular abnormalities)

101
Q

Niacin or B3 deficiency

A

pellagra: dry skin and bright red tongue

Neuro: memory loss, abnormal behavior

102
Q

Pyridoxine or B6 deficiency

A

paresthesia, seizure
oral changes (glossitis, ulcerations)

103
Q

zinc deficiency

A

rash
alopecia
poor wound healing
myopathy
altered sense and test
?HE

104
Q

selenium deficiency

A

cardiomyopathy
myositis and cramps

105
Q

What happens if <18 and listed, but then turn 18 while waiting for a liver

what if <18, listed, then delisted, then turn 18

A

-classified as 12-17

-must be registered as an adult

106
Q

What can be added to steroids in severe AH

A

NAC
- may improve 30 day mortality

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