ETOH withdrawal, AAT deficiency, Refeeding syndrome Flashcards

1
Q

ETOH withdrawal - pathophysiology

A

ETOH - increases GABA. Chronic ETOH –> enhances glutamate (excitatory)
Withdrawal = excess glutamate without GABA

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2
Q

ETOH withdrawal

Symptoms and timeline

A

Sx - insomnia, tremulousness, anxiety, GI upset, anorexia, headache, diaphoresis, palpitations, diaphoresis

seizures - 12-48 hours post
hallucinations - 12-24 hours post, resolved by 48 hours

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3
Q

Delirium tremens

A

Sx - Hallucinations, disorientation, tachycardia, hypertension, hyperthermia, agitation

Timeline - 24 to 96 hours post, lasts 1-5 days

Other have HypoK and HypoMa

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4
Q

Mx ETOH withdrawal

A

Benzo, long acting - Diazepam or Chlordiazepoxide

CLD - Lorazepam (available IV and PO) or Oxazepam (only PO)
If seizures - give IV

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5
Q

Refeeding syndrome - Pathophysiology, CF

A

Starvation = low insulin, high glucagon/cortisol - protein breakdown + gluconeogensis –>depletion of electrolytes

Sudden carb load = excessive insulin –> increase metabolism, takes everything into cell

CF - HypoPO4 (hallmark feature), hypoK, CCF, Rhabdo, seizures, CCF

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6
Q

AAT deficiency genetics

PiMM
PiMZ
PiZZ
Pi null null

A

• normal = PiMM
• homozygous PiMZ (50% normal A1AT levels)
• homozygous PiZZ (10% normal A1AT levels)
Homozygous Pi Null Null (NO production of AAT)

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7
Q

AAT function - Lung

Liver - effect

A
  • infection causes neutrophils to migrate to the lung and release “neutrophil elastase” which destroys elastin and kills bacteria
  • AAT stops elastase from going overboard and destroying lung elastin
  • AAT deficiency = uncontrolled destruction of lung tissue –> emphysema due to local inflammation and destruction of the lung

Malfunctioning AAT produced in liver –> gets stuck in sinusoids –> liver damage
*piZZ = no liver damage

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8
Q

Risk Factors AAT deficiency liver and lung issues

Treatment

A

Lung - smoking, asthma
Liver - ETOH, metabolic syndrome, male

Mx - Mx like COPD and CLD - supportive

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