Non viral hepatitis Flashcards

1
Q

MCC liver transplant

2nd MCC

A

Hep C

Etoh

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2
Q

first pass metabolism

A

Veinous drainage from stomach drains to portal vein before reaching systemic circulation
20% that goes from stomach goes directly to liver first from portal vein

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3
Q

this converts toxic alc to non toxic

A

ALDH2 is inhibited by Disulfiram (also Metronidazole, some Cephalosporins and Sulfonylureas)

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4
Q

Earliest response of the liver to chronic alcohol consumption

A

alcoholic fatty liver disease

Transaminases (LFT) often normal or transiently elevated

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5
Q

Generally the stage in-between fatty changes and cirrhosis

A

alcoholic hepatitis

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6
Q

lab values

A

AST:ALT usually >2.0
AST and ALT usually <300 iu/L (chronic so not that high)
increased Bilirubin in majority of pts with ETOH hepatitis
GGT very sensitive

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7
Q

chronic ETOH can lead to increased tylenol sensitivity

A

Suspect usage with transaminases >500 iu/L

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8
Q

with abstinence this can be reversed

A

non-fibrotic liver damage

alc hepatitis or steatosis

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9
Q

CIWA

A

etoh withdrawal assessment

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10
Q

classic triad of confusion/ataxia/ophthalmoplegia

wernicke’s encephalopathy

A

thiamine (b1) deficiency

75% develop Korsakoff’s encephalopathy anterograde/retrograde amnesia, confabulation

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11
Q

Fatty changes associated with obesity, hyperlipidemia, insulin resistance, malnutrition

A

Non alcoholic fatty liver disease

associated w/metabolic syndrome (insulin resistance, HTN, hyperlipidemia, low HDL)

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12
Q

NAFLD tx

A

Wt loss, correcting dyslipidemia (diet, statins), alcohol avoidance

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13
Q

Progression of fatty liver disease

Biopsy shows macrovesicular steatosis (fatty liver) and inflammation

A

non alcoholic steatohepatitis

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14
Q

Autosomal recessive genetic defect → Impaired copper transport → Copper deposition in
liver, brain and cornea

A

Wilson’d disease
Keyser-fleischer rings, neuro problems
DX: Ceruloplasmin level, 24-hour urine copper measurement
TX: chelation, oral zinc

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15
Q

Produced in the liver- protects the lungs from neutrophil elastase, an enzyme that can disrupt connective tissue
Liver, lung, dermatological and hematological manifestations

A

alpha 1 antitrypsin deficiency

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16
Q

AI hepatitis is commonly seen in this population

A

adolescent females

17
Q

viking disease

A

Hereditary Hemochromatosis, increased Fe absorption

therapeutic phlebotomy, chelation