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Acute Liver Failure/Injury Flashcards

1
Q

Fulminant Hepatic Failure

A
  • clinical syndrome
  • massive necrosis of liver cells/dysfunction
  • preceding liver disease absent
  • duration <8 weeks
  • 66% mortality
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2
Q

Etiology of Fulminant Hepatic Failure

A
  • Viral (A,B,D,E, Herpes, CMV, EBV, Varicella, Adeno)
  • Drug & Toxin (acetaminophen, halothane, NSAIDS, herbals)
  • Ischemic (shock, Budd-Chiari)
  • Metabolic (Wilson, Fatty liver of pregnancy, Reye’s Syndrome)
  • Miscellaneous (Malignant Infiltration, Bacterial Infection)
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3
Q

Fulminant Hepatic Failure: Viral

A
  • most common cause
  • HAV rare usually > 40 years old
  • HBV: 50% coinfection w/delta, reactivation after immunosuppression
  • HEV: pregnant females
  • Immunocompromised: HSV, CMV, EBV, Varicella, Adenovirus
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4
Q

Fulminant Hepatic Failure: Vascular

A
  • Budd-Chiari: acute w/hepatic vein thrombosis
  • Hypotension: surgical shock, cardiac failure, septic shock
  • Hypoxia: hepatic artery occlusion, pulmonary failure
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5
Q

Fulminant Hepatic Failure: Metabolic

A
  • Wilson’s Disease: ceruloplasmin low, Cu high, hemolysis w/Hepatic Failure
  • Fatty Liver of Pregnancy: microvesicular fat with fatty acid metabolism abn.
  • Reye’s Syndrome: same above mitochondrial dysfunction
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6
Q

Fulminant Hepatic Failure: Infiltrative

A 
Malignant Infiltration
-Lymphoma (Burkitt's)
-Malignant histiocytosis
-CML, acute monoblastic leukemia
-massive infarction & necrosis
-Metastic cancer-small cell carcinoma of lung
Severe Bacterial Infection
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7
Q

FHF Investigations

A

Viral (HBsAg, HBcAb-IgM, HDV-Ab, HAV-IgM)
Metabolic-ceruloplasmin, anti-nuclear abs & smooth muscle abs
General-CMP, CBC, INR, AFP

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8
Q

Hepatotoxic Drugs

A

Mushroom poisoning

Herbal Remedies

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9
Q

Fulminant Hepatic Failure: Clinical

A
  • Jaundice not related to neuropsych abn.
  • Liver size large (small with collapse)
  • vomiting
  • inc. HR, BP, RR & fever are late signs
  • focal neurological signs, high fever may indicate alternative source of PSE
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10
Q

R/O Chronic Liver Disease

A
  • no liver history
  • small hard liver
  • splenomegally
  • vascular collaterals
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11
Q

Portosystemic Encephalopathy

A
  • Multifactoral: dec. glucose, perfusion, anoxia, change in electrolytes, edema
  • Neurotoxins: ammonia, GABA mercaptins, benzos
  • False Neurotransmitters: Aromatic Amino Acids (serotonin)
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12
Q

Encephalopathy & EEG

A

Stage 1: normal alert

2: inc. EEG amplitude with confusion
3: drowsy with dec. EEG wave frequency
4: coma w/triphasic EEG waves, diffuse slow waves

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13
Q

Neuropsychiatric: Fulminant Hepatic Failure

A
  • reticular stimulation (brain stem depression)
  • Early: personality change, anti-social, restless delerium (reticular stim)
  • Late: decerebrate rigidity (spasticity, extention of limbs), disconjugate gaze, Pupillary reflux loss, CVS collapse
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14
Q

Cerebral Edema

A

-common cause of death w/cerebellar & brain stem coning
-PaCO2 rises & blood flow inc
-Inc in ICP
-Death w/brain stem vascular interruption
-Decerebrate rigidity, extention posture
-Pupillary reflexes lost
(arching neck, erratic breathing, pronation of hands, seizure like activity, hyperextended extremities)

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15
Q

Fulminant Liver Failure: Hypoglycemia

A
  • seen in 40%
  • high plasma insulin levels
  • may lead to sudden death
  • lactic acidosis develops in 50%
  • due to inadequate tissue perfusion (+/- sepsis)
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16
Q

Fulminant Liver Failure: Good Indicator of Prognosis

A

INR

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17
Q

Fulminant Liver Failure: Other Effects

A

Acid-Base/Electrolytes
Renal Failure
Respiratory & CV failure
Infections

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18
Q

Fulminant Liver Failure: Prognostic Indicators

A 
age: 40 y/o
small liver
ascites
jaundice> 7 days before encephalopathy
hypoglycemia
hepatocyte necrosis >75% (biopsy) 
(Grade I or II encephalopathy 66%)
(Grade III or IV encephalopathy 20%)
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19
Q

Fulminant Hepatic Failure: Treatment

A
  • Vitals, Labs, LOC, I/O monitoring
  • Encephalopathy (Lactulose, mannitol, hyperventilation)
  • Coagulopathy
  • Nutrition (glucose, MVI, Elemental feeds)
  • Renal (ultrafiltration, dialysis)
  • Infections - treat as indicated
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20
Q

Artificial Hepatic Support

A
  • liver dialysis unit (don’t have)

- variations on charcoal hemoperfusion

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21
Q

Liver Transplantation

A
  • Neuroaxis intact
  • Survival 75%
  • No comorbid contraindications: cardiac, renal, respiratory, psychosocial
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22
Q

Common Causes of Hepatic Injury?

A 
alcohol
shock
tylenol
sepsis
antibiotics
pregnancy
viral hepatitis
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23
Q

What does portal vein do?

A

-brings blood from intestines and spleen to liver

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24
Q

Hepatic Blood Supply

A

Duel

  • Portal Vein (70%)
  • Hepatic Artery (30%)
  • less vulnerable to ischemia, but shock can cause ischemic hepatitis (especially from long term heart failure)
  • portal vein thrombosis can cause ischemia limited to liver
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25
Hepatic Vein Thrombosis
- Ischemic hepatitis (Budd-Chiari syndrome) - tender hepatomegaly - abdominal pain, ascites - hypercoagulable state (myeloproliferative disorder)
26
Shock Liver Causes?
- rapid rise in transaminases to a peak 25-250x normal - steady decline to normal in 7-10 days - Bilirubin rises only as transaminases are falling & rarely goes above 4x upper limit normal - Alkaline phosphatase rarely goes above 2xULN
27
Endothelium of Hepatic Sinusoids
-have fenestrations (windows) very in size, some let platelets pass
28
Hepatic Sinusoids: Open Circulation
- lined by fenestrated cells (no tight junctions or basement membranes) - no continuous diffusion barrier b/w plasma and hepatocytes' cell surface
29
Hepatic Sinusoids: Kupffer Cells
- intercalated b/w endothelial cells and forming part of sinusoidal lining - have phagocytic capacities & defend us by nabbing intestinal bacterial and products - stimulates them to release IL-1, TNF, IL-6, IL-8, IL-12, TGF-beta, interferon, PGD2, PGE2, thromboxane & complement (mediating sepsis)
30
Sepsis & Liver
- acute liver injury with inc. bilirubin & transaminases & alkaline phosphatase * **measures of liver injury***
31
Hepatic Sinusoids: Ito Cells
"perisinusoidal; fat storing or stellate cells" - underneath sinusoidal lining cells, with apparently random distribution - multipotential mesenchymal cells with the ability to differentiate into fibroblasts or myofibroblasts with chronic liver injury
32
Hepatic Sinusoids: Space of Disse
- b/w sinusoidal lining cells & hepatocyte cell membranes there is a tiny space ( - has some extracellular matrix glycoproteins & occasional collagen fibrils
33
Bile
- flows in reverse direction to afferent blood supply (central to portal) - hepatocytes secrete it into bile canaliculus, a structure formed by apposing lateral surfaces of 2 hepatocytes - canaluculi are sealed by tight junctions & actin filaments around the canaliculus provide some peristaltic action
34
Hepatocytes as Metabolic Detoxification sites
- vulnerable to injury - hepatocellular is most common form of drug-induced liver injury (inc. transaminases & moderately elevated alkaline phosphatase & bilirubin) - abx are most common type of drug for injury
35
Canaliculi drain into?
bile ducts - at interface b/w lobule and portal tirad, the ductules are lined by flattened epithelial cells; the oval cells that communicate with the bile ducts that eventually drain into the main bile duct - extracellular matrix in portal tirad stroma contains collagen (I, III, IV), glycoproteins, & proteoglycans
36
Oval Cell
-become ductal cell or hepatocyte
37
Canalicular Cholestasis
-preferentially affect bile canaluculi, interfering with their motility & resulting in canalucular bile "plugs"
38
hepatocellular Cholestasis
-impede secretion of bile into the canaliculi, resulting in the accumulation of bile in hepatocytes
39
Color of Bile
1. Green: most common, can be any shade 2. Yellow: common (gold/brown) 3. White Bile = mucus
40
Pregnancy induces Liver Disease
-1 in 1,000 pregnancies 3 forms 1) HEELP syndrome (hemolysis, elevated liver enzymes, low platelets) 2) Acute Fatty Liver in Pregnancy 3) Intrahepatic cholestasis of pregnancy (most common)
41
Intrahepatic Cholestasis of Pregnancy
- due to epiallopregnanolone sulfate inhibition of farnesoid X receptor mediated bile acid efflux - mild inc. bilirubin, inc. alk phos, maternal pruritis, modest fetal distress,premature birth & stillbirth, responds to ursodeoxycholic acid treatment
42
Cholestatic Liver Injury
- second most common drug-induced liver injury - inc. bilirubin & alkaline phosphatase, & moderately elevated transaminases - Psychoactive drugs (cause injury in hepatocellular or cholestatic pattern
43
3 Zones in Liver Lobule
- Periportal - Midzonal - Central
44
Centrolobular Hepatocytes
- "downstream" - receive blood with lower content of oxygen & metabolites than peri-portal hepatocytes - often first cells affected in many forms of hepatic injury
45
Midlobular Hepatocytes
-Intermediate with blood supply
46
Periprotal Hepatocytes
- best blood supply (rich in oxygen, nutrients) | - in severe injury they are only ones that survive
47
Tylenol Toxicity
- metabolized to toxic N-acetyl-p-benzoquinoneimine (NAPQI) - conjugated with glutathione to non-toxic compound (when run out it builds up) - centrolobular run out first - likely if >12g in day
48
Tylenol Toxicity Symptoms
- nausea, vomiting, sweating, pallor, lethargy, malaise - fine b/w 24-72 hrs then 72-96 re-appear with: - jaundice, confusion, bleeding
49
Location of necrosis: Acetaminophen
central
50
Location of necrosis: Yellow fever, mushrooms
midzone
51
Location of Necrosis: Phosphorus Compounds
periportal
52
Focal Necrosis
only few cells affected and with random distribution
53
Confluent Necrosis
affects large cell groups
54
Acute Viral Hepatitis also causes?
-swollen pale hepatocytes -portal & lobular infiltration by lymphocytes, macrophages (plasma cells) -Kupffer cell hypertrophy & hyperplasia +/- cholestasis
55
Symptoms of Viral hepatitis? (acute liver injury & necrosis)
- malaise, anorexia, nausea, fatigue - jaundice, transaminases are elevated - alkaline phosphatase usually do not rise as markedly
56
Autoimmune Hepatitis (liver injury)
not common - clinical similar to viral hepatitis but diagnostic abs - plasma cells more prominent
57
Microscopic: Alcohol cause of Acute Liver Injury
- ballooning degeneration - steatosis - Mallory bodies - feathery degeneration - apoptosis - acute inflammation
58
Chronic Liver Injury is Usually Associated with?
1. chronic inflammation & simultaneous ongoing 2. repair response 3. scarring (fibrosis)
59
Key players in Hepatic repair response?
- stellate cells (Ito) | - differentiate into myofirboblasts & secrete collagen and other extracellular matrix substances into the space of Disse
60
The end-stage of liver disease?
Cirrhosis
61
Spider Angiomas
- vascular lesions consisting of a central arteriole surrounded by many smaller vessels, most frequent on the trunk, face, arms - central arteriole can be seen pulsating when compressed with a glass slide
62
Most common causes of cirrhosis are?
1. alcohol 2. hepatitis C 3. non-alcoholic steatohepatitis 4. hemochromatosis

GI (19 decks)

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