Hepatitis/Liver Disease Flashcards

1
Q

Workup for liver disease

A

US!
CBC w/ diff & PT/INR (anemia, platelets, albumin, bilirubi, AST, ALT, ALP)
Acute Hep panel
TSH
Iron/TIBC and Ferritin (hereditary hemochromatosis)
AMA + IgM (PBC) - autoimmune destruction of bile ducts
anti-trypic & phenotype (alpha-1-antitrypsin deficiency)
TTG, IgA (celiac)
Ceruloplasmin (wilson’s) +/- 24 hr copper
ANA, ASMA, LKMA, Anti-LC1, Anti SLA/LPA, IgG (autoimmune hepatitis)
HIV, CMV, mono – in those hospitalized where everything else is normal

consider sepsis, rhabdo

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2
Q

Ceruloplasmin

A

Wilson’s disease

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3
Q

TTG, IgA

A

celiac

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4
Q

Iron, TIBC, ferritin

A

hereditary hemochromatosis

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5
Q

AMA, IgM

A

PBC

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6
Q

AST/ALT levels:

A
Normal: <30-40
Cirrhosis: 30-100
Chronic Hep B/C: 40-150
EtOH: 100- 800
Hep A/B/C acute: 300-3,000
Shock liver or acetaminophen toxicity: >1000 - 10,000
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7
Q

Most common liver disease in US

A

NAFLD (nonalcoholic steatohepatitis 2nd)

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8
Q

Abnormal LFTs for liver disease

A

Hepatocellular pattern (<10x ULN)
Increased ALT & AST (liver transaminases)
+/- elevated ALP (NASH)

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9
Q

General guidelines for interpreting aminotransferases

A

AST: ALT > 2 = Alcoholic Liver Disease (ALD)

ALT > AST = NASH (rario usu. <1), acute or chronic viral hepatitis

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10
Q

Cholestatic pattern of LFT

A

increase in ALP/GGT

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11
Q

NAFLD aka

A

fatty liver
hepatic steatosis
Non-alcholic steatohepatitis (NASH) - fatty liver WITH inflammation of liver w/ hepatocyte injury

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12
Q

NASH

A

fatty liver w/ inflammation of liver w/ hepatocyte injury
Worse prognosis as higher risk of developing fibrosis & cirrhosis

Bx GOLD STANDARD but not often used

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13
Q

what is considered non-alcoholic

A

<20 g ETOH/day (less than 2-3 drinks/day)

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14
Q

Subtypes of NAFLD

A

Isolated Steatosis (NAFL) - w/o injury of fibrosis of hepatocytes on bx; risk of progression to cirrhosis is MINIMAL

NASH - fatty liver + inflammation = hepatocyte injury; bx +/- fibrosis; risk of PROGRESSION of fibrosis, cirrhosis is SIGNIFICANT

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15
Q

More likely to progress to cirrhosis

A

NASH

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16
Q

NAFLD/NASH are associated w/ increased death concurrent w/

A

CVD

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17
Q

Risk factors for NAFLD

A
• Abdominal Obesity
• DM2 (insulin resistance)
• Hyperlipidemia (high TG and Low HDL) 
• Metabolic Syndrome* 
others (not important)
• Genetic Factors (PNPLA3, TM6SF2)
• Age
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18
Q

Strongest predictor of NAFLD

A

metabolic syndrome

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19
Q

Symptoms of NAFLD/NASH

A

asymptomatic
fatty infiltration of imaging
no significant ETOH hx

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20
Q

Liver bx for NAFLD/NASH

A

combo of steatosis and inflammation +/- fibrosis (rarely get– get fibroscan or MRE instead)

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21
Q

Labs for NASH

A
hepatocellular pattern
mild ALT/AST (rarely >300)
Normal albumin, bilirubin, INR
Ferritin elevated (marker of inflammation)
HLD (lipid panel)
Glucose (elevated of dx of DM2)
ALP elevated in 1/3 (GGT elevated)
\+/- weakly positive autoimmune factor (bx to confirm)
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22
Q

Marker of inflammation

A

ferritin

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23
Q

Management for NASH

A

exclude other causes of elevated LFT

order Fibroscan/calculate FIB-4

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24
Q

Tx for NASH

A
exercise &amp; weight loss (main tx!!!!)
Minimize ETOH and CVD risk factors
Control DM and HLD (statins ok)
Monitor LFT/Liver tests after implementation of management
Vaccinate Hep A and Hep B if not immune
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25
Liver bx use for NASH
confirm dx (before tx w/ meds) exclude concomitant liver disease assess degree
26
What is hereditary hemochromatosis?
Genetic mutation results in increased GI absorption of iron → leads to accumulation of iron in the liver, pancreas, heart, adrenals, testes, pituitary, skin & kidney
27
Clinical findings for hereditary hemochromatosis
family hx or incidentally note increased AST/ALT No specific sx (fatigue, malaise, RUQ discomfort) Late sx (4th-5th decade): hepatomegaly, hepatic insufficeincy, cirrhosis, DM, impotence, arthralgia (2nd/3rd MCP), bronze pigment of skin, cardiomegaly w/wo CHF Bronze DM: Triad of DM, bronze pigment of skin, cirrhosis
28
Bronze DM
Dm Bronze pigment of skin Cirrhosis Associated w/ hereditary hemochromatosis
29
Hereditary hemochromatosis most common in
caucasians of Northern european origin
30
Labs for hereditary hemochromatosis
``` elevated LFT (AST, ALT, ALP); modest Serum Fe & TIBC & ferritin (Fe/TIBC = Transferrin saturation) - TS 45+ and/or Ferritin >200 (men), >150 (women) --> proceed to GI (HFE mutation analysis) ```
31
Tx for hereditary hemochromatosis
Therapeutic phlebotomy
32
Dx of hereditary hemochromatosis
genetic testing +/- liver bx | after finding TS >45, or Ferrin >200 (men), >150 (female
33
Tx for hereditary hemochromatosis
* Avoid Vit C and iron supplements * Avoid uncooked shellfish especially oysters ( w/ iron testing elevated) * Avoid ETOH * Regular phlebotomy*** (usu. managed by hematologist ) * Risk of cirrhosis (increased with ETOH or other liver disease) * w/ cirrhosis screen q 6 months (US +/- AFP)
34
When to screen for hereditary hemochromatosis
HFE genotype & iron testing in 1st degree relatives
35
Who to screen for HH
Elevated Liver tests (AST/ALT) Abnormal iron studies First degree relative dx with HH Evidence of liver disease* Suggestive symptoms of HH
36
Wilson's disease: what is it?
auto recessive mutation Genetic defect results decreased excretion of copper into bile and accumulation of copper in liver Once the liver’s capacity for copper is exceeded, copper is released into the bloodstream → accumulates in brain, cornea, joints, kidney, heart, and pancreas
37
Clinical findings of wilson's disease
age 3-55 hepatic, neuro and psych manifestations (tremor, dysarthria, incoordination/ataxia, parkinsonism, personality/behavior changes) KAYSER-FLEISCHER RING + neuro manifestations = PATHOGNOMONIC
38
Pathognomonic for wilson's
kayser-fleischer ring + neuro sx
39
Kayser-Fleisher ring
Fine pigmented granular deposits in the cornea (brownish/gray-green) Get optho exam if WD is suspected
40
Dx of WD
``` Mild elevation of AS/ALT ALP normal or LOW SERUM CERULOPLASMIN (reduced in WD - copper carrying protein) <5 ug/dl Opto eval (K-F) 24-hour urine copper (increased) ``` Dx confirmed w/ liver bx +/- molecular testing
41
Tx for WD
chelating agents | D-penicillamine and trientine
42
Severe alpha-1-antitrypsin iis considered
<11 micromole/L
43
Risk w/ alpha-1-antitrypsin deficiency
severe lung disease chronic liver disease * increase w/ cigarette smoking and onset is accelerated
44
infant/children presentation w/ alpha-1-antitrypcin deficiency
severe liver disease
45
When to suspect Alpha-1-antitrypsin deficiency
non-smoker w/ emphysema <45 YO neonatal cholestasis childhood cirrhosis
46
Who to screen for alpha-antitrypsin
Emphysema - less than 45 YO - non smoker/minimal smoker - predominant basilar changes on CXR Adult onset asthma Clinical findings or hx of unexplained chronic liver disease (elevated LFTS, cirrhosis) Family hx of emphysema/liver disease Hx of panniculitis (skin manifestation)
47
Panniculitis associated w/
a1 anit-tryspin deficiency
48
Dx for a1 anti-trypsin
mildly elevated AST/ALT Serum a1-antitrypsin (decreased) a1 antitrypsin phenotype/genotype (MM is "wildtype"= normal)
49
Tx for a1 antitrypsin deficiency
liver transplant
50
presentation of acute severe liver disease
hepatomegaly + tenderness jaundice splenomegaly fever (Rare)
51
Dx for autoimmune hepatitis
ANA, ASMA, LKMA (liver-kidney microsomal antibody), LKC-1 (Liver cytosol), IgG SLA (anti-soluble liver antigen) & anti-liver pancreas antigen (LPA) -- IN CHILDREN AST, ALT 7-10x nml elevated bili, ALP, PT/INR albumin decreased
52
Management of autoimmune hepatitis
Prednisone + Azathioprine (Imuran) - continue until remission (normal LFT) - maintain on lowest does of Imuran for continued remission (take off steroid) - monitor DEXA (steroid use) Liver transplant in fulminant liver failure
53
Acute viral hepatitis types
A and E
54
causes HCC
B
55
Fecal-oral route
E and A
56
Vaccines available
A | B
57
always chronic
C
58
Seen concurrently
B and D (dependent on B)
59
Fatal in pregnancy
E
60
HAV transmission
areas w/ inadequate sanitation Asia & African homeless Fecal-oral route
61
Presentation of Hep A
children <6 YO: asymptomatic Adults: symptomatic - flu like prodrome - icteric phase (jaundice, dark urine, pruritus, light colored stool) - hepatomegaly & jaundice most common
62
When does jaundice occur
1 week after sx onset
63
Incubation for hep A
28 days
64
Labs for hep A
``` elevated AST/ALT (>1000 or 15x ULN) inc. bilirubin inc. ALP + IgM anti-HAV @ onset of sx (acute infection) IgG anti-HAV = immunity ```
65
Tx for hep A
supportive - fluid + rest; full recovery by 6 months infection precautions notify local health dept (post exposure prophylaxis) Vaccination
66
Who should be hospitalized w/ hep A
elderly multiple comorbidities underlying liver disease fulminant liver failure
67
Transmission of hep B
blood/blood derived body fluids Sexual contact parenteral contact peri-natal
68
Leads cauing of cirrhosis and hepatocellular carcinoma
Hep B
69
S/Sx of acute hep B
N/V, RUQ pain, jaundice, malaise, arthralgias, fever INCREAED BILI, ALP significantly increased transaminases (ALT >15x)
70
Chronicity of hep B
rare in adults | if infected as an infant - most will become chronic
71
Tx for acute hep B
supportive- most recover w/ immunity | +/- antiviral (acute liver failure or protracted course)
72
When to hospitilize those w/ acute hep B
underlying liver disease multiple comorbidities sigsn of liver failure & need to be transferred to transplant center Older/elderly (more severe >60 YO)
73
Chronic hep B sx
usually asymptomatic
74
Labs for chronic hep B
``` hep B surface Ag positive >6 months Transaminases eleved (mild or normal) ```
75
Complications of hep B
cirrhosis | HCC
76
When does acute hep B usually become chronic
immunocompromised | exposed to infant or child <5 y
77
Labs for hep B
``` HBsAg: (+) active disease (acute or chronic) anti-HBs (+) immunity (vaccine or resolved infection) Anti-HBc: - IgM anti-HBc = acute exposure - IgG anti-HBc = previous exposure - Total anti- HBc (previous exposure) HBeAg anti-HBe ```
78
HBsAg
(+) before onset of sx detectable in the blood after exposure (1-9 weeks) Hallmark of active infection (acute or chronic) HBsAG > 6 mo = chronic
79
How long do you have IgM anti-HBc
4 months
80
IgG anti-HBc
persists indefinitely
81
Immunity from hep B infection lab results
Anti-HBs (+) | Anti-Hbc IgG (+)
82
Immunity from Hep B vaccine labs
Anti-HBs (+) | Anti-Hbc (IgG) (-)
83
Use of HBeAg
index od disease infectivity - marker of replication associated w/ higher levels of HBV DNA anti-HBe w/ HB e Ag negative = lower levels of virus
84
How to monitor for cirrhosis and imaging
Fibroscan | MRE
85
Most common cause of liver transplant
Hep C
86
Risk factors for hep C
``` IV Drug use, tattoos, piercing*** recipient of clotting factors (prior to 1987) Blood transfusion (prior to 1992) HIV infection Hemodialysis Known exposure (needle stick) children born to HCV mother Sexual contact (rare, greater in MSM) ```
87
Usually becomes chronic
Hep C
88
Sx of Hep C
``` usually asymptomatic (jaundice, fever, fatigue, n/v, RUQ discomfort) AST/ALT in 100's (< 300) Bilirubin elevated (-) Hep C Ab w/ (+) RNA viral load OR (+) Hep C Ab prio had (-) Hep C Ab ```
89
Dx of chronic Hep C
elevated LFR/liver tests (mild)
90
Most common cause of hep C in your 20's
IVDU
91
Who to screen for Hep C
persons born 1945-1965 w/o prior assesment of risk **** Blood transfusion/transplant before 1992 or clotting factor before 1987 Person who injected/intra-nasal drugs long term dialysis born to HCV mother Healthcare workers/public safety after exposure Evidence of chronic liver disease Annually in those that inject pregos (unregulated) tattoo/piercing incarcerated HIV infection Sexually active people about to start PEP
92
Dx of Hep C
elevated transaminases cirrhosis: AST > ALT acute: in 100's
93
Tx for Hep C
``` avoid ETOH screen for hep A and B -- vaccinate Screen for HIV Regular imaging for cirrhosis Refer to GI ```
94
Med tx for Hep C
oral meds (8-12 weeks in duration) Direct-acting anit-virals (DAA) treatable/curable in most pts
95
DNA virus
Hep B
96
RNA virus
Hep C
97
Seen only in conjunction w/ Hep B
Hep D
98
Dx of Hep D
delta virus RNA w/ +HBsAg
99
Tx for hep B
eradicate Hep B (refer to GI/hepatology)
100
Hep E transmission
fecal-oral
101
Presentation of Hep E
acute hepatitis sx- similar to hep A | travel to developing countries in last 1-2 months
102
Dx of Hep E
Hep E RNA
103
Hep E fatality
20% of PREGNANT! | otherwise not severe
104
Tx for Hep E
supportive
105
Acute
A & E | B,C,D can present acutely
106
Fecal-oral
A and E
107
Vaccine
(ABle to get vaccine) | A and B
108
Chronic
hep C
109
dependent on Hep B
D
110
Fatal in pregnancy
E