Liver Failure Flashcards

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1
Q

What is Liver Failure?

A

liver shuts down d/t loss of more than 80% functional capacity

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2
Q

True or False: Liver Failure does not increase mortality rate of 50%

A

false

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3
Q

Is liver failure acute or chronic? (reversible or irreversible)

A

It can be acute (reversible) or chronic (irreversible)

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4
Q

Etiology of Liver Failure (3)

A
  • cirrhosis: decrease functional cells
  • severe hepatotoxicity eg alcohol
  • fulminant hepatitis eg Hepatitis C virus
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5
Q

What does Fulminant mean?

A

severe and acute

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6
Q

Patho: What is impacted/cause in LF? (4)

A
  1. Hematology
  2. Metabolism
  3. Hepatorenal Syndrome
  4. Hepatic Encephalopathy
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7
Q

Patho: Explain how LF affect hematology. Describe Manifestations (5)

A
  • hemostasis is impaired –> anemia: the ability to clot is lost
  • defective synthesis of clotting factors and fibrinogen: liver is unable to provide resources for clotting
  • depressed marrow function leading to thrombocytopenia and leukopenia: liver is unable to supply building blocks (clotting factors, proteins, and GFH) for blood cells in the marrow
  • inadequate clearance of activated clotting factors –> DIC = disseminated intravascular coagulation: widespread formation of blood clots in sm. vessels in body (thrombosis/embolus)
  • GI bleeds and hemolysis: caused by ruptured varices leading to hemorrhage
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8
Q

Inadequate liver fxn causes _______ failure.

A

multiorgan

Liver is a vital organ that help supplies resources for other organs

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9
Q

What is Hemolysis? Why does it occur in LF?

A

Hemolysis = lyses of blood cells predominantly RBC

b/c membrane of erythrocytes has defective properties d/t LF

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10
Q

Patho: Explain how LF affect Metabolism. Describe Manifestations (4)

A
  • inadeq. clearance of bilirubin: bilirubin cannot be broken down into excretable form in liver resulting in jaundice
  • defective urea cycle: liver is unable to process ammonia to be converted to urea resulting in hyperammonemia = acumm. of ammonia
  • hypoalbuminemia = deficiency of albumin: low albumin results in low osmotic pressure t/f fluid shift out of vessels resulting in edema and ascites
  • decrease estrogen catabolism: liver is unable to break down estrogen resulting in hyperestrogenism
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11
Q

What is bilirubin combined with to be converted to an excretable form? Where is it excreted?

A

Glucuronic acid

in kidneys

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12
Q

What is the consequence of hyperammonemia?

A

ammonia is toxic to body and gets into the circulation which eventually impact the brain

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13
Q

How does edema and ascites occur?

A

D/t deficiency of albumin, there is a decrease in OP which cause fluid to remain in tissues/interstitial space = edema

Increase fluid in interstitial space causes fluid to move into body cavity =ascites

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14
Q

What results in men and women in excessive levels of estrogen in circulation? Is it life-threatening?

A

Results are not life-threatening but produce significant problems.

Women and Men:

  • infertility
  • decrease libido
  • large breast
  • menstration issues
  • atrophy of testicles
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15
Q

Patho: Explain how LF cause hepatorenal syndrome. Describe Manifestations (3)

A
  • severe renal ischemia: vessels in hepatic portal system is dilated and systemic vessels are constricted –> acumm. of blood in splanchnic vessels –> less blood circulating to kidneys
  • renal failure: failure of liver is linked to kidney failure; reversed hepatic failure improves renal fxn (mechanism unknown)
  • oliguria, azotemia, and increase creatinine
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16
Q

What is oliguria?

A

inadeq. urine prod.

17
Q

What is azotemia?

A

build up of nitrogenous waste in circulation

affects heart and brain and cause toxicity

nitrogenous waste = nitrogen containing compound

18
Q

What is creatinine? What info does it give on kidneys?

A

creatinine = a waste product excreted in kidneys

measuring creatinine in blood gives info on kidney function

19
Q

Patho: Explain how LF cause hepatic encephalopathy. Describe Manifestations

A

toxic compounds are not detoxified b/c:

  • l/o fxn: liver is unable to detoxify waste in excretable form for the kidneys
  • portosystemic shunts: channels are established to divert blood away from portal HTN into the systemic veins AND toxic compounds bypass the liver and remain in circulation
  • early mnfst: asterixis and hyperreflexia
  • confusion, coma, and possibly death: toxic compounds travel to brain
20
Q

What is asterixis and hyperreflexia

A

Asterixis = flapping tremor of the hand when wrist is extended/bent back

Hyerreflexia = exaggerated reflexes found in px; hyperactive reflexes d/t toxic compound impacting the brain

21
Q

Treatment of LF (6)

A
  • treat underlying cause
  • symptomatic management
  • avoid complication
  • purgative
  • non-absorbent antibiotics
  • liver transplant
22
Q

What are purgatives?

A

potent laxatives - to evacuate proteins from bowel of large intestines which is a source of ammonia (nitrogen-containing compounds have proteins); to get rid of ammonia

23
Q

What are non-absorbable antibiotics?

A

Antibiotics are not absorbed and remain in dig tract to reach the large bowel (large intestine) to control the number of bacteria and minimize amount of ammonia

24
Q

What is required as a life-saving measure?

A

liver transplant