Liver Flashcards

1
Q

acute hepatic failure, acute liver failure(ALF), or fulminant hepatic failure (FHF) are all the same things, t or f

A

true

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2
Q

**what does fulminant mean

A

a disease that has rapid and sudden onset

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3
Q

normal functioning of the liver

A

neutralizes toxins and waste and the cleaning of blood throughout the entire body

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4
Q

when we have pressure on the diaphragm due to inflammation of the liver, what is the pt predisposed to

A

respiratory problems

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5
Q

someone in acute liver failure has other dysfunctions what are they

A

hemodynamic instability - coagulopathies - high risk of bleeding making them predisposed to shock (hypo-volemic shock)
high risk for respiratory insufficiency/failure
risk for perfusion abnormalities
risk for renal failure
high risk for impaired immune responses and infection making them at high risk for infection then sepsis

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6
Q

why is the liver different r/t where it receives it blood supply

A

most vital organs get blood from arterial system

the liver gets it blood supply from arterial system (1/3) and venous system (2/3) making it a low pressure organ

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7
Q

what does we mean by a low pressure organ (liver)

A

inflammatory process causes decreased perfusion to the liver resulting in hypo-perfusion and high risk portal hypertension
+ ascites causes pressure on diaphragm causing resp problems - high risk for intravascular fluid depletion - decreased circulating blood volume due to low albumin causing fluid shift into abdomen - hypovolemia with ascites

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8
Q

if the liver fails acutely what are we going to have problems with

A

shock - sepsis - hypovolemia and bleeding

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9
Q

Acute hepatic failure defined as

A

Rapid deterioration of liver functioning (includes coagulopathies)
Coagulopathies result in bleeding and hemorrhage
Changes in mental status r/t decreased albumin and increased ammonia - increased ammonia levels cross the blood-brain barrier and causes severe confusion
Acute onset - no previous hx of chronic liver dysfunction

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10
Q

number 1 cause of acute hepatic failure

A

acetaminophen (Tylenol) overdose

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11
Q

additional cause of fulminant liver failure

A

Hep B or C exposure (second leading cause) or “Viral”
Tylenol overdose
ingestion of wild mushrooms thought to be edible

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12
Q

what is the antidote to Tylenol overdose

A

acetylcysteine N (Mucomyst)

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13
Q

Intervention for ALL HEPATIC FAILURE REGARDLESS OF CAUSE

A

acetylcysteine N (Mucomyst) - shown to improve outcomes

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14
Q

what should we ask a pt w/chg in LOC, bruising and bleeding with no previous hx of cirrhosis or liver dysfunction and the pt may be jaundice

A

assess exposure to all prescription and OTC meds (amoxicillin and ampicillin in children)
exposure to HEP B and C
what have they eaten - were they in Europe
assess alcohol consumption

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15
Q

definitive treatment for fulminant hepatic failure (FHF)

A

*liver transplant

mars is used as a bridge to transplantation

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16
Q

necrosis of cells results in

A

high risk for SIRS likely to result in MODS and ARDS - within 3-8 weeks - rapid process

17
Q

what do we base fluid resuscitation on

A

BP - MAP

18
Q

manifestations of acute hepatic failure

A

Destruction of liver cells - coagulopathies - PT60-100 - INR - 1.5 or > super high-risk of bleeding
Hyperbilirubinemia (definitive dx tool) - jaundiced - unconjugated because the liver conjugates bilirubin
Hypoglycemia - depression of glucose synthesis
Decreased lactate clearance - worsens metabolic acidosis - give NORMAL SALINE

19
Q

normal lab values r/t liver fxn tests (lab)

A

INR - 0.8 - 1.2
PT - 10-14 sec
clotting factors are not normal in FHF

20
Q

how do we assess coagulopathies in liver failure

A

PT and INR

21
Q

FHF fulminant hepatic failure occurs over this period of time

A

1-3 weeks - confusion, bruising

22
Q

hepatic encephalopathy (chg in mental status) can occur

A

as soon as 2 weeks after the onset of disease

23
Q

within 6-8 weeks of onset of FHF patients are

A

in a coma, dead or in need of a transplant

24
Q

in hepatic encephalopathy there are how many stages

A

4

25
Q

stage 1 coma grade s/s

A

mild confusion, slurred speech, normal EEG

26
Q

**stage 2 coma grade s/s

A

mild confusion, lethargy, marked asterixis

27
Q

stage 3 coma grade s/s

A

marked confusion, incomprehensible speech

28
Q

stage 4 coma grade s/s

A

responsive to deep stimuli to no response, coma

29
Q

how can we assess stage 4 coma

A

there is no gag reflex when suctioning patient when they are on the ventilator

30
Q

lab studies to know r/t FHF - fulminant hepatic failure

A

hyperbilirubinemia
liver enzymes (AST, ALT) are HIGH
serum ammonia levels are HIGH
**Albumin is LOW
PT, INR are HIGH
ABG - initially respiratory alkalosis progress to metabolic acidosis - initially hyperventilate, after increased WOB and hypoxemia dx as resp failure then increased PaCO2 - must be ventilated
Platelets are LOW - called thrombocytopenia - give vitamin K norm

31
Q

treatment for resp failure with high PaCo2

A

increase resp rate on ventilator to blow off excess CO2

32
Q

s/s with hepatic encephalopathy

A

confusion, headache, jaundice, personality chgs, palmar erythema, edema, spider nevi, liver flapping

33
Q

ammonia directly correlates to

A

worsening of encephalopathy - get levels down

34
Q

how do we decrease ammonia levels

A

lactulose - traps ammonia and propels it out

neomycin - decreases bacterial flora of the intestine thereby decreases ammonia formation

35
Q

complications r/t encephalopathy

A

high risk for GI bleed - give PPI prophylactic

36
Q

before the pt gets a central line what do we want to give

A

vitamin K - they have a big risk of bleeding

37
Q

how do you give vitamin K

A

sub q, IM, IV, PO

38
Q

mgmt for liver pt

A

protect pt from injury -bed low, seizure pads, 3 side-rails up, 1:1
neuro assessment q1hr
assess for resp failure
educate pt and family - scared