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GI > Acute Liver Failure/Injury > Flashcards

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
Q

Hepatic Vein Thrombosis

A
  • Ischemic hepatitis (Budd-Chiari syndrome)
  • tender hepatomegaly
  • abdominal pain, ascites
  • hypercoagulable state (myeloproliferative disorder)
26
Q

Shock Liver Causes?

A
  • 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
Q

Endothelium of Hepatic Sinusoids

A

-have fenestrations (windows) very in size, some let platelets pass

28
Q

Hepatic Sinusoids: Open Circulation

A
  • lined by fenestrated cells (no tight junctions or basement membranes)
  • no continuous diffusion barrier b/w plasma and hepatocytes’ cell surface
29
Q

Hepatic Sinusoids: Kupffer Cells

A
  • 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
Q

Sepsis & Liver

A
  • acute liver injury with inc. bilirubin & transaminases & alkaline phosphatase
  • measures of liver injury*
31
Q

Hepatic Sinusoids: Ito Cells

A

“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
Q

Hepatic Sinusoids: Space of Disse

A
  • b/w sinusoidal lining cells & hepatocyte cell membranes there is a tiny space (
  • has some extracellular matrix glycoproteins & occasional collagen fibrils
33
Q

Bile

A
  • 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
Q

Hepatocytes as Metabolic Detoxification sites

A
  • 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
Q

Canaliculi drain into?

A

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
Q

Oval Cell

A

-become ductal cell or hepatocyte

37
Q

Canalicular Cholestasis

A

-preferentially affect bile canaluculi, interfering with their motility & resulting in canalucular bile “plugs”

38
Q

hepatocellular Cholestasis

A

-impede secretion of bile into the canaliculi, resulting in the accumulation of bile in hepatocytes

39
Q

Color of Bile

A
  1. Green: most common, can be any shade
  2. Yellow: common (gold/brown)
  3. White Bile = mucus
40
Q

Pregnancy induces Liver Disease

A

-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
Q

Intrahepatic Cholestasis of Pregnancy

A
  • 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
Q

Cholestatic Liver Injury

A
  • second most common drug-induced liver injury
  • inc. bilirubin & alkaline phosphatase, & moderately elevated transaminases
  • Psychoactive drugs (cause injury in hepatocellular or cholestatic pattern
43
Q

3 Zones in Liver Lobule

A
  • Periportal
  • Midzonal
  • Central
44
Q

Centrolobular Hepatocytes

A
  • “downstream”
  • receive blood with lower content of oxygen & metabolites than peri-portal hepatocytes
  • often first cells affected in many forms of hepatic injury
45
Q

Midlobular Hepatocytes

A

-Intermediate with blood supply

46
Q

Periprotal Hepatocytes

A
  • best blood supply (rich in oxygen, nutrients)

- in severe injury they are only ones that survive

47
Q

Tylenol Toxicity

A
  • 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
Q

Tylenol Toxicity Symptoms

A
  • nausea, vomiting, sweating, pallor, lethargy, malaise
  • fine b/w 24-72 hrs then 72-96 re-appear with:
  • jaundice, confusion, bleeding
49
Q

Location of necrosis: Acetaminophen

A

central

50
Q

Location of necrosis: Yellow fever, mushrooms

A

midzone

51
Q

Location of Necrosis: Phosphorus Compounds

A

periportal

52
Q

Focal Necrosis

A

only few cells affected and with random distribution

53
Q

Confluent Necrosis

A

affects large cell groups

54
Q

Acute Viral Hepatitis also causes?

A

-swollen pale hepatocytes
-portal & lobular infiltration by lymphocytes, macrophages (plasma cells)
-Kupffer cell hypertrophy & hyperplasia
+/- cholestasis

55
Q

Symptoms of Viral hepatitis? (acute liver injury & necrosis)

A
  • malaise, anorexia, nausea, fatigue
  • jaundice, transaminases are elevated
  • alkaline phosphatase usually do not rise as markedly
56
Q

Autoimmune Hepatitis (liver injury)

A

not common

  • clinical similar to viral hepatitis but diagnostic abs
  • plasma cells more prominent
57
Q

Microscopic: Alcohol cause of Acute Liver Injury

A
  • ballooning degeneration
  • steatosis
  • Mallory bodies
  • feathery degeneration
  • apoptosis
  • acute inflammation
58
Q

Chronic Liver Injury is Usually Associated with?

A
  1. chronic inflammation & simultaneous ongoing
  2. repair response
  3. scarring (fibrosis)
59
Q

Key players in Hepatic repair response?

A
  • stellate cells (Ito)

- differentiate into myofirboblasts & secrete collagen and other extracellular matrix substances into the space of Disse

60
Q

The end-stage of liver disease?

A

Cirrhosis

61
Q

Spider Angiomas

A
  • 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
Q

Most common causes of cirrhosis are?

A
  1. alcohol
  2. hepatitis C
  3. non-alcoholic steatohepatitis
  4. hemochromatosis

GI (19 decks)

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