UW revision acute liver failure , HE

Question 1

TRIAD acute liver failure?

Answer 1

Hepatic encephalopathy
Elevated transaminases
Impaired synthetic liver function (INR >= 1,5)

Question 2

Very important, that acute liver failure should occur in patients with normal liver - NO CIRRHOSIS OR UNDERLYING LIVER DISEASE

Answer 2

.

Question 3

What differentiates acute liver failure from acute hepatitis?

Answer 3

presence of hepatic encephalopathy

Question 4

ALF table. Etiology?

Answer 4

Viral hepatitis (HSV, CMV, HAV, B, C, D)
Drug toxicity (paracetamol, idiosyncratic)
Ischemia (shock liver, Budd-Chiari syndrome)
Autoimmune hepatitis
Wilson disease
Malignant infiltration

Question 5

ALF table. CP?

Answer 5

General symptoms - fatigue, lethargy, anorexia, nausea)
RUQ pain
Pruritus and jaundice due to hyperbilirubinemia
Renal insuff.
Thrombocytopenia
Hypoglycemia

Question 6

ALF table. Diagnostic requirements? 3

Answer 6

Severe acute liver injury (AST and ALT usually > 1000)
Signs of hepatic encephalopathy (confusion, asterixis)
Synthetic liver dysfunction

Question 7

Chronic HBV carriers, typically remain asymptomatic without evidence of underlying liver disease (eg fibrosis). In this case superinfection (HBV + HDV) –> carries high risk of ALF.

Answer 7

.

Question 8

Urine output in ALF?

Answer 8

decreased (due to intravascular volume depletion and decreased renal perfusion)

BUT NOT A PART OF ALF TRIAD DIAGNOSTICS

Question 9

Portal venous pressure in ALF?

Answer 9

Increased (due to incr. resistance to blood flow through the inflamed liver)

BUT NOT A PART OF ALF TRIAD DIAGNOSTICS

Question 10

Bilirubin in ALF?

Answer 10

Severe hyperbilirubinemia is common

BUT NOT A PART OF ALF TRIAD DIAGNOSTICS

Question 11

What virus cause cirrhosis?

Answer 11

HCV

Question 12

What viruses cause ALF?

Answer 12

HAV, HBV, HDV, HEV

Question 13

Renal failure common due to direct renal tubular toxicity (from acetaminophen)

Answer 13

.

Question 14

HE table. Precipitating factors?

Answer 14

Drugs (sedatives, narcotics)
Hypovolemia (eg diarrhea)
Electrolyte changes (eg hypokalemia)
Incr. nitrogen load (eg GI bleeding)
Infection (pneumonia, UTI, SBP)
Portosystemic shunting (eg TIPS)

Question 15

HE table. CP?

Answer 15

Asterixis, ataxia, altered mental status, sleep pattern changes

Question 16

HE table. Tx? 2

Answer 16

1. Correct precipitating factors (eg fluids, antibiotics)
2. Decr. blood ammonia concentration (lactulose, RIFAXIMIN)

Question 17

HE. ABs?

Answer 17

kinda Tx of underlying cause (eg pneumonia), bet turi but sisteminiai infekcijos pozymiai (temp, leu, tachy)

Question 18

wernicke vs HE?

Answer 18

In wernicke: Altered mental status, ataxia, NYSTAGMUS, NO ASTERIXIS.

in HE: altered mental status, sleep pattern changes, ataxia, ASTERIXIS

Question 19

Dont give high-proteins cirrhosis –> can precipitate HE by increasing ammonia levels.

Answer 19

.

Question 20

How hypokalemia can trigger HE?

Answer 20

Hypokalemia: exacerbate HE as resultant intracellular acidosis (K out, H in) causes increased NH3 production (glutamine conversion) in renal tubular cells.

Question 21

How metabolic alkalosis can trigger HE?

Answer 21

Metabolic alkalosis: exacerbate HE as it promotes conversion of ammonium (NH4+) [cannot enter CNS] to NH3 [can enter CNS].

Question 22

Proteins in cirrhosis?

Answer 22

Dont give high-protein diet - it cant precipitate HE

BUT also, these patients are malnourished, therefore do no give protein-free diet.

Protein restriction is generally for those with TIPS

Question 23

When give neomycin in HE?

Answer 23

Used to Tx HE in patients unresponsive to lactulose or cannot tolerate rifaximin.

Question 24

When is performed TIPS?

Answer 24

When ascites does not responds to medical Tx (eg diuretics) OR has ungoing active or recurrent variceal bleeding even after appropriate treatment with upper endoscopy. TIPS assoc. with HE in up to 35 proc. patients due to (NH3-rich) blood bypassing the liver.