ETOH withdrawal, AAT deficiency, Refeeding syndrome Flashcards
ETOH withdrawal - pathophysiology
ETOH - increases GABA. Chronic ETOH –> enhances glutamate (excitatory)
Withdrawal = excess glutamate without GABA
ETOH withdrawal
Symptoms and timeline
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
Delirium tremens
Sx - Hallucinations, disorientation, tachycardia, hypertension, hyperthermia, agitation
Timeline - 24 to 96 hours post, lasts 1-5 days
Other have HypoK and HypoMa
Mx ETOH withdrawal
Benzo, long acting - Diazepam or Chlordiazepoxide
CLD - Lorazepam (available IV and PO) or Oxazepam (only PO)
If seizures - give IV
Refeeding syndrome - Pathophysiology, CF
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
AAT deficiency genetics
PiMM
PiMZ
PiZZ
Pi null null
• normal = PiMM
• homozygous PiMZ (50% normal A1AT levels)
• homozygous PiZZ (10% normal A1AT levels)
Homozygous Pi Null Null (NO production of AAT)
AAT function - Lung
Liver - effect
- 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
Risk Factors AAT deficiency liver and lung issues
Treatment
Lung - smoking, asthma
Liver - ETOH, metabolic syndrome, male
Mx - Mx like COPD and CLD - supportive