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GI- Week 3 > Pathophysiology Acute Liver Failure > Flashcards

Pathophysiology Acute Liver Failure Flashcards

1
Q

What is the tx for all cases of acute liver failure?

A

transplant

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2
Q

What is fulminant hepatic failure?

A

aka acute liver failure, a syndrome of massive necrosis of liver cells without preceding liver disease (i.e. complete failure occuring within 8 weeks of onset of disease)

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3
Q

How deadly is ALF?

A

•66% mortality!!! Get to transplant

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4
Q

What are the causes of ALF?

A
  • viral
  • drug and toxin (Viral and toxic account for 75% of cases)
  • ischemic
  • metabolic
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5
Q

What are the possible viral causes of ALF?

A

•A(rare), B, D (gotta have B), E(pregnant), Herpes (immuncompromised), CMV, EBV (uncommon), Varicella, Adeno

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6
Q

What are the main drug causes of ALF?

A

Acetaminophen, Halothane, NSAIDS, Herbals

Isoniazid

Mushroom poisoning

Alcohol

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7
Q

What are some ischemic precipitators of ALF?

A

•Shock (prolonged hypotension/heat-stroke), Budd-Chiari (OCs= clots in hepatic veins)

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8
Q

What are some metabolic causes of ALF?

A

•Wilson (chronic but present acutely),

Fatty Liver of Pregnancy (abortion needed),

Reye’s Syndrome

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9
Q

What is the most common viral cause of ALF?

A

Hep B

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10
Q

Most examples of hepatotoxicity caused by drugs occur when?

A

within the first 4 to 8 weeks of beginning use.

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11
Q

Describe the metabolism of acetaminophen?

A

Acetaminophen in therapeutic doses undergoes sulfation and glucuronidation (phase II reactions) but is metabolized by cytochrome P450 2E1 (phase I reaction) to N-acetyl-p-benzoquinoeimine (NAPQI) if the capacity of the phase II reactions is exceeded or if the cytochrome is induced.

Glutathione-S-transferase (GSH) is capable of detoxifying NAPQI to mercapturic acid if glutathione is available.

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12
Q

Hypotension can cause ALF. What are some common sources?

A
  • Surgical shock
  • Cardiac Failure
  • Septic Shock
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13
Q

Hemolysis with Hepatic Failure is highly suggestive of what?

A

Wilson Disease. Wilson’s is genetically determined and usually presents before age 35.

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14
Q

T or F. Malignant infiltration of the kidneys can also cause ALF

A

T. In cases of lymphoma, CML, small cell carcinoma of the lung, etc.

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15
Q

Acute hepatitis B is characterized by what serology wise?

A

a positive surface antigen test (HBsAg) and a positive core antibody test (anti-HBc)

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16
Q

What is the first serologic marker to appear in Hep B infection?

A

HBsAg. ·Indicator of ongoing infection

·Presence does not correlate with viral load or severity of infection

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17
Q

·Persistence of HBsAG for 6+ months indicates what?

A

chronic infection

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18
Q

Anti-HBc (Antibody to hepatitis B core antigen) indicates what?

A

prior infection at some undefined time

· IgM indicates recent infection

· Not associated with recover or immunity

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19
Q

What is anti-HBs (Antibody to HBsAg)?

A

·Marker of recovery and immunity detectable AFTER clearance of HBsAg

20
Q

HBsAg seroconversion follows HBeAg seroconversion and maybe delayed by months, sometimes taking years for HBsAg seroconversion in chronic infection

A
21
Q

HBV surface antigen may be gone before anti-HbSAg antibody appears thus core IGM most sensitive

A
22
Q

What are the symptoms of ALF?

A

Typical features observed in the patient with acute liver failure include confusion, agitation, or even hallucination. Mental status often deteriorates to coma soon after presentation, making history-taking impossible.

Most patients will be icteric, although some barely so, and spider angiomata as seen in cirrhotic patients should be absent.

Tachycardia, tachypnea, and relative hypotension are common. Asterixis, so commonly observed in chronic hepatic encephalopathy, is rarely seen.

23
Q

What other things may be seen in ALF?

A

Fetor hepaticus, a sweet odor caused by mercaptans excreted in the breath, is often observed.

Percussion over the rib cage to detect hepatic dullness reveals that the liver span is considerably decreased, and there may be no dullness appreciated, as evidence of the loss of hepatic mass. At autopsy, the normal liver mass of approximately 1600 g may be reduced to as little as 600 g.

Edema (ascites) is not observed initially but may develop in the hospital. Although the extremities are often cold, after resuscitation warm shock is the rule.

24
Q
A
25
Q

What are the neuropsychiatric symptoms of PSE?

A

•Reticular stimulation ®brain-stem depression

•Early

  • Personality change, anti-social
  • Restless delerium ( reticular stim.)

•Late

  • Decerebrate rigidity leading to spasticity, extention of limbs
  • Disconjugate gaze, Pupillary reflex loss, CVS collapse.
26
Q

What is a very common cause of death in ALF?

A

cerebral edema and herniation causing brain stem vascular interruption

27
Q

What things suggest impending herniation in ALF pts with cerebral edema?

A

Erratic changes in blood pressure, temperature, or breathing

28
Q

What are some physical findings Physical findings in patients with advanced hepatic encephalopathy and cerebral edema?

A

Typically, patients will experience a brief period of agitation before the development of coma. Hepatic coma is usually graded as I through IV-grade I is signified by altered personality and subtle changes in cognition; grade II typically demonstrates confusion, slurred speech and possibly asterixis, but the patient remains able to follow commands; grade III is characterized by deepening coma responsive to strong stimuli with some purposeful movements; grade IV patients are totally unresponsive.

Hyperventilation is universal in all stages of hepatic coma. In grade IV coma, decerebrate posturing, changes in breathing patterns, seizures, and pupillary abnormalities all occur in the presence of cerebral edema.

29
Q

In grade IV coma, decerebrate posturing, changes in breathing patterns, seizures, and pupillary abnormalities all occur in the presence of cerebral edema. These signs, alone or in association with systemic hypertension, warrant immediate intervention with what?

A

mannitol and pursuit of transplantation, if available. Corticosteroids, hyperventilation, and use of phenobarbital, although recommended for head trauma patients to decrease cerebral edema, are of little benefit in acute liver failure. Diuretics have been used in addition to mannitol but are of uncertain value.

30
Q

How is glucose affected by ALF?

A

hypoglycemia is common, with high insulin levels due to inadequate tissue perfusion

Lactic acidosis may occur

31
Q

What acid-base abnormalities are seen in ALF?

A
  • hyponatremia
  • hypokalemia due to urinary loss and poor intake
  • respiratory alkalosis due to hyperventilation

•Cerebral edema leads to hypoventilation and acidosis

32
Q

Why do Hypotension and tachycardia occur in ALF?

A

Decreased systemic resistance following by cardiac compensation

33
Q

Why is bleeding a common cause of ALF?

A

Liver synthesizes clotting factors

34
Q

Why is infection common in late ALF?

A

there is reduced immunity due to Kupffer and OMN dropout and reduced compliment production

35
Q

Where is infection common in late ALF?

A

blood, lungs, and urine

36
Q

What types of bugs are commonly responsible for infection in ALF?

A

66% gram positive

Fungal common

37
Q

What are some poort prognostic indicators in ALF?

A
  • Age: <10 or >40y.o.
  • Small liver
  • Ascites
  • Jaundice > 7 days before encephalopathy
  • Hypoglycemia
  • Hepatocyte necrosis > 75% (biopsy)
38
Q

What cause of ALF historically has the best survival rate?

A

Acetaminophen and other drugs

39
Q

T or F. Wilson Disease is likely to spontaneously resolve

A

T. Transplant is needed or death occurs

40
Q

What are the standard txs for FHF encephalopathy?

A

•Lactulose, mannitol, hyperventilation

41
Q

For most people, its Medical suppport until transplant

A
42
Q

How should a person with confirmed ALF via icnreased INR, altered mental status, etc. be handled initially?

A

Admit to ICU where they are evaluated for both etiology AND severity

43
Q

What is the tx for acetaminophen OD?

A

N-acetylcysteine

44
Q

What is the tx for mushroom OD?

A

Pencillin, silibinin antidote

45
Q

What is the tx for Wilson disease?

A

Transplant

46
Q

What pts are eligible for transplant in ALF?

A

Those with deteriorating liver function, okay brain function, and hx of alcohol/drugs, no co-morbidities that are likely to kill the pt

GI- Week 3 (15 decks)

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