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PHM4482 > Hepatic encephalopathy > Flashcards

Hepatic encephalopathy Flashcards

1
Q

What is hepatic encephalopathy?

A

a syndrome in cirrhosis patients characterized by neuropsychiatric abnormalities (personality changes, intellectual impairment, depressed consciousness) after excluding brain disease.

Key prerequisite: portosystemic blood diversion.

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2
Q

What is the primary pathophysiological prerequisite for HE?

A

Diversion of portal blood into systemic circulation via portosystemic collaterals (spontaneous or surgical shunts).

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3
Q

What triad of symptoms characterizes hepatic encephalopathy?

A

Personality changes, intellectual impairment, and depressed level of consciousness.

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4
Q

What percentage of cirrhosis patients have subtle vs. overt HE?

A

Subtle signs in ~70%; overt HE in 30%-45%. Post-shunt surgery incidence: 24%-53%.

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5
Q

What is the survival rate for HE severe enough to require hospitalization?

A

42% at 1 year, 23% at 3 years.

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6
Q

What must be excluded to diagnose HE?

A

Primary brain disease (e.g., stroke, tumor, infection).

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7
Q

What percentage of end-stage liver disease patients experience severe encephalopathy nearing coma?

A

~30%.

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8
Q

What mechanisms contribute to brain edema in ALF-related HE?

A

Increased blood-brain barrier permeability, impaired cerebral osmoregulation, and elevated cerebral blood flow.

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9
Q

How does hepatic encephalopathy (HE) in acute liver failure (ALF) differ from HE in cirrhosis?

A

ALF-associated HE features prominent brain edema (due to blood-brain barrier dysfunction, impaired osmoregulation, increased cerebral blood flow), which is rare in cirrhosis. Brain edema in ALF is potentially fatal.

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10
Q

What life-threatening complication is unique to ALF-associated HE?

A

Severe brain edema causing cell swelling, leading to risk of herniation or death.

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11
Q

What defines Type A hepatic encephalopathy?

A

Encephalopathy associated with acute liver failure (ALF).

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12
Q

What characterizes Type B hepatic encephalopathy?

A

Encephalopathy due to portal-systemic bypass (e.g., surgical shunts) without intrinsic hepatocellular disease.

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13
Q

How is Type C hepatic encephalopathy defined?

A

Encephalopathy linked to cirrhosis with portal hypertension or portosystemic shunts. Subtypes: episodic, persistent, minimal.

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14
Q

What are the subcategories of Type C HE?

A

Episodic (acute flares), persistent (chronic symptoms), and minimal (subtle cognitive deficits).

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15
Q

What major pathophysiological difference separates ALF and cirrhosis-related HE?

A

Brain edema is central to ALF but absent/minimal in cirrhosis.

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16
Q

Why is distinguishing HE types (A, B, C) important?

A

Guides management (e.g., Type A requires urgent ALF treatment; Type B/C focus on reducing toxins/shunt closure).

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17
Q

What role do astrocytes play in hepatic encephalopathy (HE)?

A

Astrocytes regulate the blood-brain barrier, maintain electrolyte/nutrient homeostasis, and detoxify ammonia. Dysfunction (e.g., swelling, Alzheimer type II astrocytosis) contributes to HE.

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18
Q

How do astrocyte changes differ between cirrhosis and ALF in HE?

A

In cirrhosis: Alzheimer type II astrocytosis (swollen cells, pale nuclei, chromatin margination). In ALF: severe astrocyte swelling → brain edema (no Alzheimer type II features).

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19
Q

How is ammonia produced and detoxified in the body?

A

Produced in the gut via bacterial action/glutaminase. Detoxified in the liver (urea cycle) and muscle (glutamine synthetase). Brain astrocytes also metabolize ammonia but cannot upregulate detoxification.

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20
Q

How does skeletal muscle contribute to ammonia metabolism in cirrhosis?

A

Muscle expresses glutamine synthetase, converting glutamate → glutamine (trapping ammonia). Muscle wasting in cirrhosis reduces this detox pathway.

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21
Q

Why does hyperammonemia occur in cirrhosis?

A

Due to hepatocyte loss (reduced urea cycle) and portosystemic shunting, diverting ammonia to systemic circulation. Muscle wasting exacerbates it.

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22
Q

What supports and challenges the ammonia hypothesis in HE?

A

Supports: Treatments lowering ammonia improve HE. Challenges: 10% of HE patients have normal ammonia; elevated levels don’t always cause symptoms or EEG changes.

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23
Q

What is the revised role of GABA and neurosteroids in HE?

A

GABAergic tone was previously emphasized, but newer studies highlight neurosteroids (e.g., allopregnanolone) via peripheral-type benzodiazepine receptor (PTBR) activation, enhancing inhibitory neurotransmission.

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24
Q

Is HE fully reversible?

A

Traditionally yes, but studies show residual cognitive deficits post-recovery or transplant, especially with prior HE, diabetes, or alcohol-related cirrhosis.

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25
How do HE pathogenesis insights guide therapy?
Targeting ammonia (lactulose, rifaximin), neurosteroids (PTBR inhibitors), and managing cerebral edema in ALF (mannitol, ICP monitoring).
26
What did the University of Nebraska study find about ICP in cirrhosis?
Elevated ICP and cerebral edema (on CT) in 9/12 patients with grade 4 HE. Treatments like mannitol and hyperventilation provided transient improvement.
27
What are the two broad categories of HE, and how are they classified by grade?
Covert HE (CHE): Grades 0 (minimal) and 1. Overt HE (OHE): Grades 2–4. CHE is linked to poor outcomes.
28
What characterizes Grade 0 HE?
Subtle cognitive deficits (e.g., impaired attention, reaction time), normal mental status exams, abnormal psychometric tests (e.g., number connection, critical flicker test). No asterixis.
29
What physical finding is characteristic of Grade 2 HE?
Asterixis ("flapping tremor"). Also: lethargy, disorientation, slurred speech.
30
Describe Grade 1 HE symptoms.
Mild confusion, sleep disturbances, shortened attention span, euphoria/depression. Exam: Decreased short-term memory/concentration.
31
What causes fetor hepaticus?
Exhalation of mercaptans (sweet, musty breath odor).
32
What Parkinsonian symptoms may occur in HE?
Tremor, bradykinesia, cog-wheel rigidity, shuffling gait. Linked to manganese deposition in basal ganglia.
33
Describe hepatic myelopathy.
Rare complication of portosystemic shunting: spastic paraparesis, hyperreflexia, lower extremity weakness. Resistant to standard HE therapy; may improve with TIPS closure/transplant.
34
Name 4 tests used to diagnose minimal HE.
Number connection test, digit symbol test, block design test, critical flicker test.
35
Which HE-related symptom may respond to rifaximin?
Parkinsonian phenotype (e.g., tremor, rigidity).
36
How does hepatic myelopathy differ from typical HE?
Causes motor deficits (e.g., spastic paraparesis) rather than cognitive changes.
37
What is the classic laboratory finding in hepatic encephalopathy (HE)?
Elevated blood ammonia level (arterial or free venous sample). Tourniquet use can falsely elevate results.
38
When is ammonia testing useful vs. not useful in HE?
Useful: Supporting diagnosis in altered mental status. Not useful: Monitoring treatment response or checking in cirrhotic patients without HE.
39
What MRI finding is common in HE, and what causes it?
T1-weighted hyperintensity in the globus pallidus due to manganese deposition.
40
Why are CT/MRI performed in suspected HE?
To rule out intracranial lesions (e.g., hemorrhage, edema) rather than confirm HE.
41
How does renal failure worsen hepatic encephalopathy (HE)?
Reduces clearance of ammonia, urea, and nitrogenous compounds, exacerbating hyperammonemia.
42
Why does GI bleeding trigger HE?
Blood in the gut → increased ammonia absorption; transfusions may cause hemolysis → ↑ ammonia. Also, hypoperfusion → renal dysfunction.
43
Which drugs worsen HE? Name 4 classes.
Opiates, benzodiazepines, antidepressants, antipsychotics (CNS depressants that impair mental status).
44
How does protein intake affect HE?
Rare precipitant; excess protein → ↑ nitrogen load → gut bacteria produce more ammonia.
45
Why does alkalosis enhance ammonia toxicity?
Favors conversion of NH₄⁺ (less permeable) to NH₃ (lipid-soluble, crosses blood-brain barrier).
46
What clinical feature suggests hepatic encephalopathy (HE) over other causes of altered mental status in cirrhosis?
Improvement with lactulose and absence of focal neurologic signs.
47
How to distinguish intracranial lesions (e.g., stroke, hematoma) from HE?
Presence of focal neurologic deficits (e.g., hemiparesis, aphasia) and neuroimaging findings (CT/MRI).
48
Name 4 metabolic causes of encephalopathy to rule out in cirrhosis.
Hypoglycemia, electrolyte imbalance (e.g., hyponatremia), uremia, hypercarbia.
49
What defines organic brain syndrome vs. HE?
Chronic cognitive decline (e.g., dementia) without ammonia correlation or lactulose response.
50
What confirms HE diagnosis empirically?
Mental status improvement within 24–48 hours of lactulose administration.
51
What are the first-line therapies for managing HE?
Lactulose (to reduce ammonia via gut acidification/catharsis) and rifaximin (nonabsorbable antibiotic). Often used together for synergy.
52
How does lactulose reduce ammonia in HE?
Acidifies colonic lumen, converting NH₃ → NH₄⁺ (trapped in gut), and acts as a cathartic to reduce bacterial load.
53
When was rifaximin approved for HE, and what trial supports its use?
FDA-approved in 2010 (Bass et al. trial: 22% HE recurrence vs. 46% placebo when combined with lactulose).
54
Which antibiotics are used for HE, and what are their limitations?
Neomycin (2nd-line, risk of ototoxicity/nephrotoxicity) and rifaximin (safer, minimal absorption). Avoid long-term neomycin.
55
How do these agents reduce ammonia? Sodium Benzoate/Phenylbutyrate
Sodium benzoate binds glycine → hippurate (excreted). Phenylbutyrate converts to phenylacetylglutamine (excreted with ammonia)
56
What are risks of long-term neomycin vs. rifaximin?
Neomycin: ototoxicity/nephrotoxicity. Rifaximin: minimal side effects; rare C. difficile risk.
57
What agent improves sleep in HE patients, and what’s the caveat?
Hydroxyzine (25 mg) improves sleep efficiency but may worsen encephalopathy. Use cautiously.
58
How is grade 3/4 HE managed in the ICU?
Endotracheal intubation (aspiration risk), lactulose enemas (300 mL + 700 mL water), and correct precipitants (e.g., infection).
59
What is minimal hepatic encephalopathy (MHE), and what is its prevalence in cirrhosis?
MHE (covert HE) is low-level cognitive dysfunction in up to 70% of cirrhosis patients, marked by impaired attention, decision-making, psychomotor speed, and visuomotor skills. Often undetected without testing.
60
Why is MHE a concern for driving safety?
Patients show delayed reaction times and impaired executive function, increasing accident risk.
61
How does ammonia contribute to MHE?
Chronic hyperammonemia disrupts astrocyte/neuron function, causing subtle neuropsychiatric deficits.
62
What is a pragmatic approach to suspected MHE?
Consider empiric lactulose/rifaximin if psychometric testing is unavailable, especially in high-risk patients.
63
Why is MHE often missed clinically?
Symptoms are subjective/insidious; requires specialized psychometric testing not routinely performed.

PHM4482 (1 decks)

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