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GI block > Pathophysiology- Acute Liver Failure > Flashcards

Pathophysiology- Acute Liver Failure Flashcards

1
Q

Fulminant hepatic failure general information

A
  • massive necrosis of liver cells/dysfunction
  • preceding liver disease absent
  • duration LESS than 8 weeks from onset of jaundice.
  • fulminant <2 weeks, sub fulminant is < 8 weeks.
  • 66% of mortality
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2
Q

What can cause acute liver failure?

A
  • viral, drug/toxin, ischemic, metabolic, misc like malignant infiltraiton and bacterial infection
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3
Q

most common cause of acute liver failure?

A

HEPATITIS B IS THE MOST COMMON CAUSE

  • viral
  • HAV rare and usually > 40
  • HBV usually have coinfection with HDV and reactivation after immunosuppresion
  • HEV–watch out for in pregnant females esp in 3rd trimester
  • immunocompromised ppl- HSV, CMV, EBV, Varicella, adenovirus
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4
Q

what other viral infections besides hep viruses can cause liver problems in immunocompromised patients?

A

HSV, CMV, EBV, Varicella, adenovirus

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5
Q

What is the 2nd most common cause of ALF? examples?

A

hepatotoxic drugs

anesthetics like halothane, non-steroidals, antituberculin like isoniazid, acetaminophen, mushroom poisoning, herbal remedies, alcohol

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6
Q

what kind of necrosis do you get with hepatotoxic drug induced ALF?

A

panlobular necrosis

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7
Q

what vascular problems can cause ALF? and what kind of necrosis does it cause?

A
  • centrilobular necrosis
  • budd chiari- acute w/ hepatic vein thrombosis
  • hypotension (shock, cards failure, septic shock)
  • hypoxia (hep artery occlusion, pulmonary failure.)
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8
Q

what are some metabolic causes of ALF?

A
  • wilson’s disease (ceruloplasmin low, high copper, hemolysis w/ hep failure)
  • fatty liver of pregnancy (microvesicular fat w/ FA metabolism)
  • Reye’s syndrome (mitochondrial dysfunction)
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9
Q

What infiltrative problems cause ALF?

A
  • lymphoma/burkitt’s
  • malignant histiopcytosis
  • CML, acute monoblastic leukemia
  • massive infarction and necrosis
  • mets ca- SCL
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10
Q

What tests do you do if you think you have pt w/ Fulminant Hepatic failure (FHF)??

A
  • general: CMP, CBC, INR, AFP
  • metabolic: ceruloplasmin, anti-nuclear antibodies, smooth muscle antibodies.
  • viral: HbsAG, HVcAB-IgM, HDV- Ab, HAV-IgM
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11
Q

What serological marker tests are you positive for w/ acute hepatitis b w/ recovery

A
  • postive HBsAg

&

  • positive anti-HBc
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12
Q

What does positive HBsAg tell you?

A
  • first serological marker post infection
  • it’s an ongoing infection
  • presence doesnt correlate with viral load or or severity
  • if persist >/= 6 mo then it indicates chronic infection
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13
Q

What does anti-HBc tell you?

A
  • indicates prior infection at some undefined time
  • IgM indicates recent infection
  • not associated with recovery or immunity
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14
Q

anti-HBs

A

marker of immunity and recovery

  • detectable after clearance of HBsAg
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15
Q

what serological test is most sensitive? which test always need to be exluded? (for hepatitis)

A

HBVsAg may be gone before antibody appear so core IgM is most sensitive

  • HDV- Ab (delta) always need to be exlcuded
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16
Q

clinical presentation of ALF

A
  • jaundice not related to neuropsych abnormality
  • liver size large –> small with collapse
  • vom common
  • increased HR, BP, RR, and fever are late signs
  • focal neuro signs, and high fever may indicate alternative source of PSE (portal system encephalopathy)
17
Q

what rules out chronic liver disease?

A
  • no liver hx
  • small hard liver
  • splenomegaly
  • vascular collaterals
18
Q

physical findings of ALF?

A
  • confusion, agitation or even hallucination –> deteriorate to coma soon after presentation
  • icteric/jaundice
  • no spidar angiomata (seen in cirrhosis)
  • tachy, tachypnea, hypotension
  • clear lungs, small shrunken liver
  • ascites in late stages
  • asterixis which is seen in chronic hepatic encephalopathy but rarely seen in this.
  • fetor hepaticus, sweet odor of breath, is observed here often
19
Q

portosytemic encephalopathy

A
  • multifactorial (decrease glucose and perfusion, anoxia, change in electrolytes, edema)
  • neurotoxins (ammonia, GABA mercaptins, benozs)*
  • false neurotransmitters (aromatic AA–> 5-ht)

*endogenous toxins are normally removed from portal and systemic circulation which may be directly toxic to neurons.

* lack of aromatic clearance —> production of increased inhibitory neurotransmitters

20
Q

encephalopathy and EEG - what are the different stages?

A
  • Stage 1: normal w/ alert pt
  • stage 2: increased EEG amplitude w/ confusion
  • stage 3: drowsy with decreased EEG
  • stage 4: coma with triphasic EEG waves, diffuse slow waves
21
Q

cerebral edema

A
  • common cause of death w/ cerebellar and brain stem coning
  • PaCO2 rises and blood flow increases
  • increase in ICP
  • death w/ brain stem vascular interruption
  • decerebrate rigidity, extention posture
  • pupillary reflex lost
22
Q

adverse effects of cerebral edema?

A
  • decreases cerebral blood flow –> brian anoxia

**cerebral perfusion pressure should be maintained above 40mmHG to presever brain oxygenation.

  • herniation of brain stem through falx cerebri is fatal

**erratic changes in bp, temp, or breathing pattern imply impending herniation

23
Q

hypoglycemia and lactic acidosis

A
  • lactic acidosis develop in 50% and hypoglyceia in 40%
  • high plasma insulin levels
  • may lead to sudden death
  • inadequate tissue perfusion –> +/- sepsis
24
Q

does cerebral edema lead to acidosis or alkalosis? hypoventilation or hyperventilation?

A

hypoventilation and aicidosis

25
Q

why is bleeding a frequent cause of death in ALF?

A
  • liver –> all factors except VIII and inhibitors.
  • with failure there is abnormal platelet production and function
  • PT/INR is indicator of prognosis
  • bleeding can happen in mucous membranes, gi tract, and brain
26
Q

why is infection common in advanced liver failure? where do you get infection? what kind of infection?

A
  • reduced immunity d/t impaired kupffer and PMN function. Reduced fironectin, compliment and opsonins.
27
Q

bad prognostic indicators of ALF?

A

both ends of age spectrum <10 or >40

small liver

ascites

jaundice > 7 days before encephalopathy

hypoglycemia

hepatocyte necrosis >75% on biopsy

28
Q

grading and prognosis?

A
  • grade 1 and 2 encephalopathy- 66%
  • grade 3 or 4 encephalopathy 2-%
29
Q

Fulminant hepatic failure treatment?

A
  • w/ encephalopathy- lactulose, mannitol, hyperventilation
  • nutrition- glucose, MVI, elemental feeds
  • renal: ultrafiltration, dialysis
  • infections- treat as indicated
30
Q

what are the 3 E’s for the triage, diagnosis, and treatment of acute liver failure?

A
  • establish the diagnosis, evaluate the etiology, estimate the severity of the illness
31
Q

survival rate in liver transplantation? criteria for liver transplantation?

A
  • 75% survival
  • neuroaxis intact
  • no comorbid contraindications

GI block (12 decks)

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