Pathophysiology- Acute Liver Failure Flashcards
(31 cards)
Fulminant hepatic failure general information
- 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
What can cause acute liver failure?
- viral, drug/toxin, ischemic, metabolic, misc like malignant infiltraiton and bacterial infection
most common cause of acute liver failure?
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
what other viral infections besides hep viruses can cause liver problems in immunocompromised patients?
HSV, CMV, EBV, Varicella, adenovirus
What is the 2nd most common cause of ALF? examples?
hepatotoxic drugs
anesthetics like halothane, non-steroidals, antituberculin like isoniazid, acetaminophen, mushroom poisoning, herbal remedies, alcohol
what kind of necrosis do you get with hepatotoxic drug induced ALF?
panlobular necrosis
what vascular problems can cause ALF? and what kind of necrosis does it cause?
- centrilobular necrosis
- budd chiari- acute w/ hepatic vein thrombosis
- hypotension (shock, cards failure, septic shock)
- hypoxia (hep artery occlusion, pulmonary failure.)
what are some metabolic causes of ALF?
- 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)
What infiltrative problems cause ALF?
- lymphoma/burkitt’s
- malignant histiopcytosis
- CML, acute monoblastic leukemia
- massive infarction and necrosis
- mets ca- SCL
What tests do you do if you think you have pt w/ Fulminant Hepatic failure (FHF)??
- general: CMP, CBC, INR, AFP
- metabolic: ceruloplasmin, anti-nuclear antibodies, smooth muscle antibodies.
- viral: HbsAG, HVcAB-IgM, HDV- Ab, HAV-IgM
What serological marker tests are you positive for w/ acute hepatitis b w/ recovery
- postive HBsAg
&
- positive anti-HBc
What does positive HBsAg tell you?
- 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
What does anti-HBc tell you?
- indicates prior infection at some undefined time
- IgM indicates recent infection
- not associated with recovery or immunity
anti-HBs
marker of immunity and recovery
- detectable after clearance of HBsAg
what serological test is most sensitive? which test always need to be exluded? (for hepatitis)
HBVsAg may be gone before antibody appear so core IgM is most sensitive
- HDV- Ab (delta) always need to be exlcuded
clinical presentation of ALF
- 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)
what rules out chronic liver disease?
- no liver hx
- small hard liver
- splenomegaly
- vascular collaterals
physical findings of ALF?
- 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
portosytemic encephalopathy
- 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
encephalopathy and EEG - what are the different stages?
- 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
cerebral edema
- 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
adverse effects of cerebral edema?
- 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
hypoglycemia and lactic acidosis
- lactic acidosis develop in 50% and hypoglyceia in 40%
- high plasma insulin levels
- may lead to sudden death
- inadequate tissue perfusion –> +/- sepsis
does cerebral edema lead to acidosis or alkalosis? hypoventilation or hyperventilation?
hypoventilation and aicidosis
