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Summer FDTN Exam 5 > Liver > Flashcards

Liver Flashcards

1
Q

What is acute liver failure

A

Onset of liver injury, hepatic encephalopathy, and coagulopathy (INR >1.5) in patients w/ no prior h/o liver disease

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2
Q

Most acute liver cases arise from

A

massive hepatocyte necrosis; APAP overdose

-viral hepatitis, drugs, toxins, metabolic, vascular events, misc.

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3
Q

What are S/Sx of acute liver failure

A 
AMS (encephalopathy) 
cerebral edema 
coagulopathy 
multiple organ failure 
ascites, anasarca, shrinking liver on PE
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4
Q

What are the stages of encephalopathy (AMS)

A

Early: personality change, reverse sleep pattern
Progressing: lethargy
Late: coma

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5
Q

What is acute hepatic failure

A

acute onset liver failure with coagulopathy (INR >1.5) and jaundice
Encephalopathy w/in 1-4 weeks of liver injury!

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6
Q

What is subacute hepatic failure

A

Acute liver failure with encephalopathy developing 12-24 weeks after onset of liver injury

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7
Q

What are lab findings in acute liver failure

A

Severe coagulopathy (high PT/INR)- bleed easy
CBC: leukocytosis
BMP: hyponatremia, hypokalemia, hypoglycemia
LFT: marked elevation of bilirubin, ALT, AST

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8
Q

How do you treat acute liver failure

A

Hospitalization
Continuous monitoring
Supportive care
If recovery seems unlikely, prep for liver transplant

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9
Q

What is hepatitis

A

Acute or chronic hepatocellular damage

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10
Q

What causes acute vs chronic hepatitis

A

Acute: Viral!
Chronic: Viral!
so basically… VIRAL!!

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11
Q

How are different hepatitis forms contracted

A

A&E: fecal oral route (E from Mexico). But they are self limited!
B, C, D: parenterally, mucous membrane (IVDU, tattoos, infected mom, transfusion). these progress to chronic

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12
Q

What are categories of acute hepatitis

A

Self limited
Acute liver failure
Cholestatic hepatitis (HAV)
Relapsing hepatitis (HAV)

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13
Q

What is the pathophys of acute viral hepatitis

A

Cell mediated mechanisms cause hepatocyte injury by degeneration or apoptosis; CD8 and CD4 respond, and cytokines are produced

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14
Q

What are S/Sx of acute viral hepatitis (self limited)

A

Prodrome: malaise, anorexia, N/V, flu-like Sx. Abrupt onset in A&E, insidious in B-D
Wen prodromal Sx subside, jaundice sets in w/ dark urine and pruritis

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15
Q

What will self limited acute viral hepatitis show on PE

A

mild enlargement and ttp of liver

mild splenomegaly

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16
Q

What are S/Sx of cholestatic hepatitis (HAV acute)

A

severe jaundice
pruritis
anorexia and diarrhea
-BUT a good prognosis

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17
Q

What are S/Sx of relapsing hepatitis (HAV acute)

A 
Sx recur for wk-months 
arthritis 
vasculitis 
cryoglobulinemia 
-BUT, prognosis is excellent eventually
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18
Q

What are lab findings in acute viral hepatitis (self limited)

A 
ALT/AST >500 
Total bili: normal 
Alk Phos: normal 
Prolonged PT/INR: normal
Albumin: normal
WBC: normal 
\+/- lymphocytosis
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19
Q

What are cholestatic disease (acute viral) findings

A

Bilirubin 20+
Alk phos: high
ALT/AST: initially elevated, may decrease*

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20
Q

What are lab findings in relapsing acute viral hepatitis

A

ALT/AST: elevation after normalization
Bilirubin: elevation after normalization
-relapses usually don’t exceed previous levels

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21
Q

How do you treat acute viral hepatitis

A

Self limited and relapsing: outpt, unless severe dehydration. Plenty of fluids&kcal. No EtOH, rest, d/c non-essential drugs, if HCV doesn’t resolve in 3 months use antiviral, if HBV use tenofovir or entecavir if severe

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22
Q

How do you treat cholestatis acute viral hepatitis

A

Prednisone
Ursodeoxycholic acid
Cholestyramine for pruritis

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23
Q

Are HAV and HEV chronic

A

No, the virus can survive in bile and is shed in feces, but does NOT result in prolonged viremic or intestinal carrier states

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24
Q

What is the pathophys of hep A&E

A

Virus ingested, transported across intestinal epithelium, through mesenteric veins to liver
It enters hepatocytes, replicates, causes cell mediated injury, and is then shed into bile and travels to intestine

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25
Q

What are RF for Hep A

A

Live in Africa, Asia, or Latin America (poor sanitation, developing countries)
Close contact with infected person
MSM
Food outbreak (contaminated water, ice, shellfish)

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26
Q

What are S/Sx of HAV

A

28 day incubation: Fever, jaundice (2 weeks)
Cholestatic and relapsing hepatitis are common manifestations
Fulminant course NOT common

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27
Q

How can you diagnose Hepatitis A

A

IgM antibody to HAV (anti-HAV) 5-10 days before Sx. Stay high for 3-6 months
Lifelong IgG anti-HAV elevation means immunity**!

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28
Q

Positive anti-HAV IgG can indicate

A

Prior infection or recent disease

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29
Q

How do you treat Hep A

A

Supportive care

Nearly all will recover fully in 6 months

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30
Q

What info do you send the patient with Hep A home with

A

Wash hands after pooping and changing diapers
Dispose waste sanitarily
Safe food handling practices
Immunization if you are high risk
Avoid excess APAP and alcohol, eat a balanced diet
Kids: don’t go back to school until 1 week after illness onset

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31
Q

How can you prevent Hep A

A 
HAV vaccination (inactive) for: 
**All kids 1 y/o (CDC says healthy ppl 1-40) 
kids 2-18 in high risk areas 
Traveling to endemic area 
MSM
IVDU 
Occupational risk 
Hx of chronic liver dx 
Clotting factor disorder 
Household member has Hep A
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32
Q

What is Hep A prophylaxis

A

If you have been exposed to Hep A and are not vaccinated, Give prophylaxis w/in TWO WEEKS* of exposure
If <1 or >40, or immunocompromised, give immunoglobulin*

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33
Q

Key highlight on slide 42

A

Do it

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34
Q

What is the epidemiology of Hep E (where it’s found, how it’s spread, etc)

A

Endemic in: mexico, cuba, asia, africa, middle east
Spread by animals, MC swine and deer
Contaminated drinking water

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35
Q

What are Sx of Hep E

A

Abrupt onset prodromal Sx

Acute liver failure is common in pregnant ladies (esp in 3rd trimester)

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36
Q

How do you diagnose HEV

A

IgM anti-HEV detectable for 6 weeks
IgM replaced by IgG anti-HEV, detectable for 12-20 months (NOT immune longterm)
HEV RNA confirms presence of Hep E in serum or stool

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37
Q

How do you prevent Hep E

A

NO vaccine!! or immunoglobulin for prophylaxis! So:
Good sanitation
Avoid unpurified H2O
Avoid raw pork and venison (deer)

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38
Q

What is Hep B

A

a DNA virus that is transmitted by sex or mucosal route

Can develop limited (MC in adults) or chronically infected (MC in kids and perinatal) disease

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39
Q

Where is Hep B prevalent

A

West africa

South sudan

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40
Q

What are characteristics of Hep B

A

Outer envelope has: Hep B surface antigen (HBsAG)

In envelope: structural protein (HBcAg), non-structural (HBeAg), DNA polymerase (reverse transcriptase)

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41
Q

Hep B infection is influenced by

A 
age 
genetic factors 
presence of other viruses 
HBV mutation 
level of immunosuppression
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42
Q

How does Hep B manifest in different individuals

A

Neonates: 95% become chronic ASx carriers
Adult primary infection: 70% are ASx and self limited
Chronic HBV: risk of cirrhosis esp in older pts, or if co-infected with HCV, HDV, or HIV

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43
Q

What is the pathophys of Hep B

A

Liver injury occurs 2/2 host immune response to Hep B virus

Immune response is against Hep B structural protein (HBcAg)

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44
Q

Strong RF for Hep B are

A 
Perinatal exposure to Hep B mom 
Multiple sex partners 
MSM 
IVDU 
Asian, Eastern European, African 
FHx of HBV 
FHc of HCC 
Household contact with HBV
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45
Q

In order to diagnose Hep B you need

A

elevated clinical suspicion* in high risk individual

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46
Q

What are Sx of Hep B

A

Insidious onset

Serum sickness like syndrome: fever, chills, malaise, rash, n/v, arthralgias, arthritis

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47
Q

How does Chronic Hep B present

A

May be ASx OR signs of chronic dz:
Cirrhosis
HCC
liver failure

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48
Q

how do you diagnose acute Hep B

A

IgM antibody to Hep B core antigen (HBcAg) w/ Sx and elevated ALT
HBsAg and IgM anti-HBc 2wk-6mo after exposure

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49
Q

How do you know Hep B has resolved

A

ALT normalizes
No HBV DNA
Seroconversion to Anti-HBe and Anti-HBs, and IgG anti-HBc

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50
Q

How can you tell if someone has had a prior HBV infection

A

Will have both surface and core proteins!

anti-HBs, IgG anti-HBc, and anti-HBe

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51
Q

How do you diagnose chronic Hep B

A

HBsAg present for >6 months
HBeAg and HBV DNA persistence
Inactive carrier: ASx, normal ALT, low HBV DNA, anti-HBe

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52
Q

How do you treat chronic Hep B

A

Acute: self limiting
Fulminant: liver transplant
Chronic: anti-viral therapy

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53
Q

What are first line therapy options for chronic viral Hep B

A 
*Peginterferon alfa-2a: weekly subQ injection for 48 weeks  (best for young, non-cirrhotic, low HBV-DNA level) 
Nucleoside analogues (Entacavir, Tenofovir) to inhibit HBV replication: daily PO indefinitely
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54
Q

Goal of Hep B antiviral Tx is

A

Sustain low or undetectable HBV DNA

Seroconvert HBeAg and HBsAg and normalize ALT

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55
Q

How can you prevent Hep B

A

Hep B vaccine given once, then repeat 6 months later

Part of universal infant immunization, and for high risk individuals

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56
Q

What Hepatitis has vaccines

A

A and B!!!

NONE OTHERS

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57
Q

How can you prevent Hep B

A

Hep B immunoglobulin
Postexposure prophylaxis then HBV vaccine if sex w/ casual partner with HBV
Newborn w/ Hep B + mom: HBIG and HBV vaccine immediately after birth

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58
Q

What is secondary prevention of Hep B

A

Chronic HBV not immune to Hep A: Hep A vaccine
Chronic HBV: Avoid heavy alcohol
HBsAg positive: use barrier protection, don’t share toothbrush or razor, cover open cuts, clean blood with bleach, no blood, organ, or semen donation

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59
Q

What is the prognosis of Hep B

A

5 year risk for:
Cirrhosis= 10-20%
HCC= 5-10%
decompensated cirrhosis= 15%

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60
Q

Key highlights on slide 78

A

Go look

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61
Q

When should you suspect Hep D

A

Fulminant Hep B infection
Acute Hep B infection that improves then relapses
Progressive chronic HBV w/o active HBV replication

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62
Q

How do you get Hep D

A

You can only get it if you also have Hep B!

HDV is specific only in the presence of HBsAg

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63
Q

What do Hep D labs show

A

anti-HDV and HDV RNA
Co-infection: IgM anti-HBc
Superinfection: IgG anti-HBc

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64
Q

How do you treat Hep D

A

High dose interferon alpha and PEG IFN

therapy is not optimal 2/2 high risk of relapse

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65
Q

What is Hep C

A

a flavivirus

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66
Q

Per CDC, when should you screen for Hep C

A

If high risk for infection

If born between 1945-1065 regardless of risk

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67
Q

What is the pathophys of Hep C

A

Acute: self limited, most develop antibodies
Persistent viremia: hepatic inflammation and fibrosis. weak CD4 and CD8 cells can’t control viral replication
Chronic: liver damage 2/2 local immune response (inflammation) by hepatic stellate cells

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68
Q

In Hep C, cirrhosis is accelerate by

A

Chronic alcohol consumption

Coincidental viral infection

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69
Q

What are the types of Hep C

A

6 genotypes!
U.S.: Genotype 1
Middle east: genotype 4
South africa/asia: genotype 5&6

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70
Q

How is Hep C transmitted

A

Blood exposure, MV in IVDU

less common but still possible: sex, perinatal, accidental blood contact

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71
Q

Strong RF to Hep C are

A

IVDU
Blood transfusion before 1992
Clotting factor transfusion before 1987
HIV (more likely to progress to liver dz, esp w/ low CD4)

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72
Q

What is literally the worst news a hypochondriac could receive about Hep C

A

It can live outside the body for 3 weeks
YOU CAN GET HEP C FROM DRIED BLOOD!!!
So watch the damn tamp box in the bathroom, ya nasty

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73
Q

How does Hep C present

A

MC: ASx
Prodromal jaundice
Young women can spontaneously clear, but most develop chronic infection
Black are least likely to clear infection

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74
Q

What are acute function tests for Hep C

A

8 wks after exposure: HCV RNA (needed to Dx acute infection)
6-12 wks after: ALT and AST elevated
8 wks-months after: anti-HCV (hep C antibody) detectable

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75
Q

Who is more likely to spontaneously clear hep C (self limited dz)

A

IL28B genotype CC

IL28B CT&TT are LESS likely

76
Q

How can you diagnose chronic infection of HCV

A

HCV RNA in blood for min 6 months
Screening test by EIA detects Abs against virus. If +, it’s active
ASx
Likely have chronic liver disease, decompensated cirrhosis, and HCC

77
Q

What factors influence development of chronic progressive liver disease 2/2 HCV

A 
Older age 
Male 
Concurrent Hep B 
HIV 
high alcohol intake
78
Q

How do you use Hep C tests

A

Qualitative studies confirm viremia and have low limits of detection (RT-PCR detects 40-50 IU, TMA lower limit is 5IU)
Quantatitave tests give a wide dynamic range of viral loads

79
Q

What is a baseline HCV workup

A

Confirm HCV viremia (quantitative)
Eval for coexisting liver disease and HIV
Vaccinate for Hep A and B
Get viral genotype

80
Q

Goal in treating Hep C is

A

Clear virus from blood stream
Stabilize or improve liver histology
Sx control
Prevent complications (HCC, cirrhosis, decompensated dz)
If already cirrhotis: avoid passing to new liver, haver fewer complications, have less mortality

81
Q

What is NEW Hep C treatment

A

Telaprevir and Boceprevir: protease inhibitors that bind protease of HCV genotype 1 and inhibit replication
Sofosbuvir was more effective than any other medications
Direct acting antivirals: Simeprevir, Paritaprevir, Grazoprevir (second gen NS3-4 inhibitors)
-Can use ribavirin

82
Q

What determines Tx regimen for Hep C

A

HCV genotype
Has the patient been treated before
Do they have cirrhosis
(she said basically Sofosbuvir + another med)

83
Q

How can you tell Hep C is responding to Tx

A

RVR: HCV DNA undetectable by week 4 of Tx
EOT response: HCV DNA undetectable by end of Tx
SVR: sustained virologic response (best) means no HCV RNA 12 weeks after Tx is over
(Non-response means you have detectable RNA, Relapse means you were undetectable and now you are again)

84
Q

What reduces likelihood of achieving SVR

A

Cirrhosis
Previous nonresponse
HCV genotype 3
-In these, continue Tx by 24 weeks and add Ribavirin

85
Q

Hep C patient education is

A 
Dont share toothbrush or razors 
Cover bleeding wounds 
Don't donate organs or blood 
Use barrier protection 
Avoid IVDU
86
Q

Go over key highlights slide 128

A

do it

this was a shit show

87
Q

What drug classes are known to cause toxic hepatitis

A 
Antimicrobials* 
CNS agents 
Immunomodulators 
Analgesics 
Lipid lowering meds
88
Q

What specific drugs are known to cause toxic hepatitis

A 
APAP 
NSAIDs, ASA 
Augmentin, Sulfonamides 
Isoniazid, Rifampin 
Interferon, antiretrovirals for HIV 
OCP 
Carbamazepine, phenytoin, valproic acid 
Amiodarone 
TZD, Metformin 
Statins 
Methotrexate, Azathioprine 
Chemo 
Herbals 
Mushrooms 
Cocaine
89
Q

How does toxic hepatitis present

A

LFT elevation +/- acute liver failure
Liver injury w/in days-weeks of ingestion
Labs can look like hepatotoxic injury, cholestatic, or mixed

90
Q

How do you diagnose toxic hepatitis

A

H&P!

Exclude other causes

91
Q

How do you treat toxic hepatitis

A

Remove causative agent

+/- liver transplant for severe acute liver failure

92
Q

What is the MCC of acuute liver failure and drug induced liver injury

A

Tylenol!!!

Toxic dose is 10-20g (lower in alcoholics)

93
Q

How does APAP toxic hepatitis present

A

30 min-24 hours after ingestion: GI Sx
2 d after: R side abd pain and oliguria, elevated LFT, prolonged PT/INR
3-5 d after: hepatic necrosis w/ elevated aminotransferase, renal failure or acute liver failure
5-10 d after: recovery phase

94
Q

What increases the likelihood of death or need for liver transplant in an APAP OD

A

pH <7.3
Stage 3-4 encephalopathy w/ PT/INR >6.5 and Cr >3.4
Factor V level 10% or less

95
Q

How do you manage APAP OD

A

Get a serum APAP level
IV NAC
Charcoal w/in 1 hr of ingestion
Gastric lavage w/in 4 hours

96
Q

What are the types of alcoholic liver disease

A

Steatosis: fatty liver
Steatohepatitis: alcoholic hepatitis
Cirrhosis: fibrogenesis/scarring

97
Q

What are Sx of alcoholic liver disease

A

Portal HTN

Fever, anorexia, nausea, RUQ pain, tender hepatomegaly, jaundice

98
Q

What are lab findings in alcoholic liver disease

A 
AST high (AST>ALT) 
Alk phos: high 
Other LFT: normal 
Tg: high 
K, Phos, Mag: deficient 
Glucose: high
99
Q

How do you diagnose alcoholic liver disease

A

Hx of significant alcohol abuse
Exclude other forms
Liver biopsy

100
Q

How do you manage alcoholic liver disease

A

Abstinence can stop progression +/- reverse damage!

101
Q

What is Maddrey’s Discrimination function

A

A way to calc short-term prognosis in pts w/ worsening alcoholic hepatitis:
4.6 x (diff btwn pt’s PTT and control PTT) + SrBili
If DF >32, pt has 50% mortality during current hospitalization

102
Q

How do you manage acute worsening of alcoholic hepatitis

A

Stop drinking EtOH
Naltrexone, Acamprosate, or Baclofen lessen effects of withdrawal and decrease desire to drink
Counseling
Give carbs and calories (promote gluconeogenesis, prevent hypoglycemia)
Ntr support
Give folic acid, thiamine (prevent werneke’s), and zinc
Methylprednisolone PO x 1 month (reduce DF)
Pentoxifylline: PDE inhibitor to enhance circulation, reduce 4 week mortality

103
Q

What is NAFLD (hepatic steatosis)

A

Accumulation of Tg droplets in hepatocytes.

Can be benign if no significant inflammation or fibrosis on biopsy

104
Q

What is NASH

A

necroinflammatory change on liver biopsy, can progress to cirrhosis
Lipotoxic injury to hepatocytes

105
Q

RF for NAFLD are

A 
Insulin resistance 
Obesity 
DM2 
Lipid abnormalities 
Meds like Tamoxifen, and corticosteroids
106
Q

What increases the likelihood of death or need for liver transplant in an APAP OD

A

pH <7.3
Stage 3-4 encephalopathy w/ PT/INR >6.5 and Cr >3.4
Factor V level 10% or less

107
Q

How do you manage APAP OD

A

Get a serum APAP level
IV NAC
Charcoal w/in 1 hr of ingestion
Gastric lavage w/in 4 hours

108
Q

What are the types of alcoholic liver disease

A

Steatosis: fatty liver
Steatohepatitis: alcoholic hepatitis
Cirrhosis: fibrogenesis/scarring

109
Q

What are Sx of alcoholic liver disease

A

Portal HTN

Fever, anorexia, nausea, RUQ pain, tender hepatomegaly, jaundice

110
Q

What are lab findings in alcoholic liver disease

A 
AST high (AST>ALT) 
Alk phos: high 
Other LFT: normal 
Tg: high 
K, Phos, Mag: deficient 
Glucose: high
111
Q

How do you diagnose alcoholic liver disease

A

Hx of significant alcohol abuse
Exclude other forms
Liver biopsy

112
Q

How do you manage alcoholic liver disease

A

Abstinence can stop progression +/- reverse damage!

113
Q

What is Maddrey’s Discrimination function

A

A way to calc short-term prognosis in pts w/ worsening alcoholic hepatitis:
4.6 x (diff btwn pt’s PTT and control PTT) + SrBili
If DF >32, pt has 50% mortality during current hospitalization

114
Q

How do you manage acute worsening of alcoholic hepatitis

A

Stop drinking EtOH
Naltrexone, Acamprosate, or Baclofen lessen effects of withdrawal and decrease desire to drink
Counseling
Give carbs and calories (promote gluconeogenesis, prevent hypoglycemia)
Ntr support
Give folic acid, thiamine (prevent werneke’s), and zinc
Methylprednisolone PO x 1 month (reduce DF)
Pentoxifylline: PDE inhibitor to enhance circulation, reduce 4 week mortality

115
Q

What is NAFLD (hepatic steatosis)

A

Accumulation of Tg droplets in hepatocytes.

Can be benign if no significant inflammation or fibrosis on biopsy

116
Q

What is NASH

A

necroinflammatory change on liver biopsy, can progress to cirrhosis
Lipotoxic injury to hepatocytes

117
Q

What is Wilson’s disease

A

Auto recessive genetic abnormality leads to impaired copper transport
Results in hepatolenticular degeneration and cirrhosis, impaired biliary copper excretion, neuro complications

118
Q

How does NAFLD/NASH present

A

ASx!
+/- RUQ pain, hepatomegaly
Elevated eminotransferase levels

119
Q

How do you diagnose NASH/NAFLD

A

Macrovesicular steatosis w/ or w/o inflammation and fibrosis on liver bx
4 or less EtOH drinks x day

120
Q

How do you treat NASH/NAFLD

A

Weight loss
Dietary fat restriction
Exercise

121
Q

What is autoimmune hepatitis

A

Chronic hepatitis w/ high serum globulins

Presents w/ + ANA or amooth muscle antibosy

122
Q

What does autoimmune hepatitis respond to

A

Corticosteroids!
Prednisone and Azathioprine improve Sx and decrease:
Sr bili, Aminotransferases, gamma-globulin levels, reduce hepatic inflammation

123
Q

What are S/Sx of autoimmune hepatitis

A

Insidious onset
Fatigue, jaundice, hepatomegaly
+/- acutely severe or fulminant

124
Q

What lab findings indicate autoimmune hepatitis

A

Aminotransferase >1000
Total bili: increased
Alk Phos: increased
Sr gamma globulin: increased

125
Q

What do you need to diagnose autoimmune hepatitis

A

Autoantibodies: ANA or smooth muscle >1:40- anti-LKM1 if >1:40- anti-SLA +
High gamma globulin
No evidence of viral hepatitis
Liver bx

126
Q

Standard Tx for autoimmune hepatitis is

A

Prednisone taper from 30mg to 10mg in 1 month PLUS Azathioprine 50mg
or
Prednisone taper from 60mg to 20mg in 1 month, then 20mg maintenance

127
Q

When do you stop treating autoimmune hepatitis (end point for steroids)

A

Remission ideally: No Sx, nl AST/ALT, ULN), nl liver tissue (no hepatitis)
BUT- Tx can fail, you can have incomplete response, or drug toxicity

128
Q

When do you follow up on autoimmune hepatitis if remission is achieved

A

Hepatologist q3-6 months 2/2 high likelihood of recurrence

129
Q

Where does copper tend to accumulate in Wilson’s disease

A

Liver
Brain
Cornea (Kayser-Fleischer rings)

130
Q

Wilson’s disease has what specific lab findings

A

Decreased ceruloplasmin

131
Q

How do you treat Wilson’s disease

A

D-Penicillamine

Liver transplant if: fulminant hepatitis, hepatic insufficiency unresponsive to medical therapy, severe neuro Sx

132
Q

What is hereditary hemochromatosis

A

Inherited disorder w/ impaired intestinal iron absorption causing iron to deposit in multiple organs
GFE gene mutation
Suspected 2/2 FHx ot Hx of elevated iron saturation or Sr ferritin

133
Q

What is primary sclerosing cholangitis

A

Chronic thickening of bile duct walls leading to cholestatic liver disease
Inflammation, fibrosis, and stricturing of intra- and extra-hepatic bile ducts
Unknown pathogen, may be autoimmune
M>F, avg age 41

134
Q

How do you treat hemochromatosis

A

Serial phlebotomy to achieve iron depletion

If not Tx, can cause cirrhosis and HCC

135
Q

What is alpha-1 antotrypsin (AAT) deficiency

A

AAT is a protease inhibitor of proteolytic enzyme elastase

Deficiency manifests in lungs, liver, and rarely, skin

136
Q

How does AAT present in kids

A

Liver disease (elevated LFT, cholestasis)

137
Q

How do you diagnose AAT deficiency

A

Decreased AAT level

Genotypic Z protein (PiZZ is severe, PiMZ is intermediate)

138
Q

How do you treat AAT deficiency

A

No Tx!

139
Q

What is primary biliary cirrhosis

A

T cell attack on bile ducts causes gradual bile duct loss and portal scarring= cirrhosis
Commin in middle aged women

140
Q

How does primary biliary cirrhosis manifest

A

ASx
+/- fatigue and pruritis
Jaundice, cirrhosis, xanthelasma, xanthoma, steatorrhea

141
Q

What will primary biliary cirrhosis labs show

A

Alk phos: elevated
+ AMA
IgM: elevated
Cholesterol: elevated

142
Q

How do you diagnose primary biliary cirrhosis

A

Normal biliary imaging

Characteristic liver biopsy

143
Q

What are complications of ESLD

A 
Jaundice 
Fibrosis- then cirrhosis 
Palmar erythema 
Spider angioma 
Encephalopathy w/ asterixis (hands tremor when pointed up) 
Portal HTN 
Ascites, muscle wasting
144
Q

What is hepatic encephalopathy

A

Neuropsych abnormalities (I-short attention, II-personality change, III-confusion, IV-coma) 2/2 hepatocellular dysfxn causing increased ammonia levels (liver can’t convert ammonia to urea so ammonia crosses the BBB)

145
Q

How does PSC present

A

Pruritis, jaundice
Fatigue, weight loss, RUQ pain
Hepatomegaly, splenomegaly

146
Q

What do PSC labs look like

A

Cholestatic pattern: elevated alk phos and bilirubin, mild ALT/AST elevation (<300)
Atypical P-ANCA +

147
Q

How do you diagnose PSC

A

MRCP/ERCP: multifocal stricturing and dilation of intra/extrahepatic bile ducts (ERCP can also retrieve stones and place stents!)
Liver bx: support Dx and tells you level of cirrhosis

148
Q

How do you manage PSC

A

Stent for strictures (ERCP)

Ursodiol: reduce secretion of cholesterol from liver, may help Sx

149
Q

What is spontaneous bacterial peritonitis

A

Infection in abd ascites fluid or pleural fluid

Presents w/ fever, abdominal pain, AMS, or can be ASx

150
Q

What is the prognosis of PSC

A

Progress to cirrhosis, require liver transplant
10-12 year survival w/o transplant
Screen for cholangiocarcinoms q6-12 mo (CA 19-9, CT, or MRI)
If pt has UC: screen for colon cancer (CEA, colonoscopy)

151
Q

What diseases can lead to ESLD (cirrhosis) that have elevated ALT/AST

A 
HCV, HBV 
EtOH 
Steatohepatitis/NASH/NAFLD 
Autoimmune hepatitis 
Hemochromatosis 
Wilsin's disease 
AAT deficiency
152
Q

What diseases can lead to ESLD that have elevated Alk phos and Bili

A

PSC

primary biliary cirrhosis

153
Q

What are complications of ESLD

A 
Jaundice 
Fibrosis- then cirrhosis 
Palmar erythema 
Spider angioma 
Encephalopathy w/ asterixis (hands tremor when pointed up)
154
Q

What is hepatic encephalopathy

A

Neuropsych abnormalities (short attention, personality change, coma) 2/2 hepatocellular dysfxn leading to increased ammonia levels

155
Q

How do you treat hepatic encephalopathy

A

Grade I-II: Lactulose (want 2 BM/d) or Rifaximin

Grade III-IV: admit for Lactulose via NG tube until mental status improves

156
Q

What is portal vein thrombosis

A

Diminished blood flow in portal vein and changes in clotting factors that are normally cleared by liver causes thromboembolism

157
Q

How do you diagnose and treat portal vein thrombosis

A

Doppler US, CT, or MRI

Tx with anticoags (heparin or LMWH)

158
Q

How do you treat ESLD

A

1st line: Furosemide&Spironalactone (40mg:100mg)- compression stockings for LE edema

2: Paracentesis, thoracentesis
3: Transjugular intrahepatic Portosystemic Shunt (TIPS) creates channel between hepatic and portal vein to reduce portosystemic pressure to <12

159
Q

What is MELD (model of ESLD)

A

Determine transplant eligibility
3.8 (Srbili) + 11.2 (INR) + 9.6 (SrCr) + 6.4
MELD - Na - (0.025 x MELD x [140-Na]) +140
Total bili, INR, Cr, and Na are used bc they are strong predictors of 3 month mortality
Mortality decreases starting at MELD 15 (0 is least likely to die)

160
Q

What serology indicted ESLD

A 
Low Albumin and globulins (<6.3)
High PT/INR 
Low Sodium 
High Creatinine 
Thrombocytopenia
161
Q

What is albumin

A

60% of protein in serum! Should be 3.5-5
Carries small hydrophobic molecules (fatty acids, bili, drugs) and maintains osmotic pressure of blood
If low, think: nephrotic syndrome, malntr, chronic liver dz

162
Q

What is PTT

A

Thromboplastin +CaCl added to plasma to measure time to clot
Norm is 12-15 seconds
Need vitamin K for liver synthesis of thromboplastin!
If high think: chronic liver dz, acute liver failure, obstructive jaundice, vitamin K deficiency

163
Q

What is INR

A

Used to standardize PT

164
Q

Why is sodium low in ESLD

A

Indirect marker of portal HTN (chronically overloaded)! Marker of mortality
If w/ hyponatremia may lead to cerebral edema and neuro changes
Added to MELD score

165
Q

Why is Creatinine high in ESLD

A

Indicates worsening renal fxn

Vasodilation 2/2 portal HTN decreases blood flow to kidneys

166
Q

Why is thrombocytopenia present in ESLD

A

Coagulopathy of liver, TPO is dependent on liver function

Splenomegaly 2/2 portal HTN

167
Q

Score the progression of fibrosis

A

0: none
1: portal fibrous expansion
2: Thin fibrous septa
3: Septa bridge central veins
4: Cirrhosis

168
Q

What is MELD (model of ESLD)

A

Determine transplant eligibility

169
Q

How do you screen for cirrhosis complications

A

EGD to r/o varicies

Abdominal imaging to r/o HCC

170
Q

What is the serum marker for HCC

A

AFP!

Imaging you can do are CT/MR every 6 months

171
Q

MC RF for HCC is

A

Cirrhosis**

Other: chronic HBV, hereditary tyrosemia, Aflatoxin, Thorotrast

172
Q

How do you decide to transplant

A

MELD >15 is on the list
Ensure disease is not amenable to meds/surgery
Must have diminished QoL
Non-hepatic disease that would benefit from transplant (Amyloidosis)

173
Q

What is the epidemiology of HCC

A

one of MC malignancies worldwide
Highest in Asia an sub-saharan africa
Median age is 40
M>F

174
Q

How do you diagnose HCC

A

Screen: US or CT, AFP
confirm: Liver biopsy

175
Q

how do you manage HCC

A

No mets: liver transplant
Monitor growth w/ CT/MRI q6 months
Prevent growth w/ radiofrequency ablation and TACE

176
Q

What is cholangiocarcinoma

A

Cancer arising from bile duct epithelium
Intrahepatic (Klatskin tumors, perihilar) or Extrahepatic (distal)
Most are adenocarcinomas**

177
Q

What is the epidemiology of cholangiocarcinoma

A

MC in 50-70 y/o*

M>F

178
Q

What are some causes of cholangiocarcinoma

A 
chronic liver disease 
alcoholic liver dz 
Cirrhosis 
bile duct disease 
UC 
Choledocolithiasis 
HIV 
PSC 
chronic typhoid carrier 
heavy drinking 
exposure to: OCP, radionuclide, isoniazid
179
Q

How does cholangiocarcinoma present

A 
Painless jaundice 
weight loss 
abdominal pain 
pruritis 
palpable gallbladder 
hepatomegaly 
dark urine 
pale stools 
Triad*: fever, jaundice, RUQ pain
180
Q

How do you treat cholangiocarcinoma

A

Resect if candidate
If non-resectable: liver transplant w/ chemo +/- radiation
Chemotherapy +/- radiation, palliative care (if not transplant candidate)

181
Q

How do you decide to transplant

A

MELD >15 is on the list

182
Q

What are some post-transplant issues

A

Can pt survive post-op?
Can pt comply w/ complex med regimen s/p transplant?
Does pt have other comorbidities that will compromise the donor liver?

183
Q

Contraindications to liver transplant arw

A 
Active EtOH or drug abuse 
extrahepatic HCC 
Mets bile duct cancer 
non-hepatic malignancy 
Severe cardiopulmonary disease 
Co-morbidities reducing chance of survival (BMI >35) 
Unfavorable psych issues
184
Q

Who needs to eval patient for transplant

A 
Hepatology 
Social worker 
Psych 
ID, cardiology 
Transplant surgery 
Selection committee
185
Q

Who gets the liver first

A

Patient with most severe disease get it sooner than those w/ less severe disease!

Summer FDTN Exam 5 (12 decks)

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