McKeon article and Dipiro Flashcards
Identify changes in receptor density that are associated with complications of alcohol withdrawal syndrome (AWS)
Excessive exposure to EtOH upregulates NMDA receptors and downregulates GABAA which leads to tolerance. The exact opposite occurs during abstinence. (Enhanced NMDA receptor function and decreased GABAA receptor function)
Describe how complications of alcohol withdrawal are related to the pathophysiological effects of chronic alcoholism
Symptoms of withdrawal come from down regulation of GABAA receptors. GABA A and B are critical for the development of anxiety like behavior induces by repeated intoxications and withdrawal.
Dopaminergic transmission is enhanced during AWS and may play a role in hallucination
Identify clinical feature of alcohol withdrawal
Signs/symptoms occur within 1-2 days from their last drink. Abrupt cessation may lead to delirium tremens and withdrawal seizure.
Clinical findings: anxiety, tremor, HA, agitation, delirium, N/V, sweating, tachycardia, hyperventilation etc.
Identify clinical findings after examination of delirium tremens and Wernicke’s encephalopathy
Delirium tremens: Fast heart and breathing, hypertension, hyper-reflexia, sweating, agitation and delirium
Wernicke’s: Ataxia, amnesia and ophthalmoplegia
Explain the criterion of DSM-5 for alcohol withdrawal syndrome
Criterion A: Cessation of or reduction in alcohol intake, which has previously been prolonged/heavy
Criterion B: Must meet criteria above plus any of the 2 following symptoms (Autonomic hyperactivity, worsening tremor, insomnia, N/V, hallucinations, psychomotor agitation, anxiety, generalized tonic-clinic seizures)
Explain the rating scale used to assess the severity of alcohol withdrawal
Ten item scale that scores the severity of nausea, sweating, agitation, HA, tremor, anxiety, sensory disturbances, and orientation. > 9=BENZO. The score is repeated each hour until the score is < 10 and BENZO continues until they are < 9 (Then Q 8 hours until < 6)
Identify the complications of alcohol withdrawal
Alcohol withdrawal seizures, delirium tremens, electrolyte disturbance and dehydration, psychiatric problems (bipolar, schizo, panic, mania)
Identify biomarkers and lab values of heavy alcohol consumption
Gamma glutamyl transferase (GGT) and carbohydrate0deficient transferrin are both sensitive markers for EtOH use. Macrocytosis (increased MCV) Elevated ALT/AST Measurement of direct EtOH metabolites Elevated homocysteine levels
First line treatment for alcohol withdrawal syndrome, alcohol withdrawal seizures, delirium tremens and Wernicke’s encephalopathy
AWS: Benzos
Seizures: Benzos (lorazepam preferred over valium)
Delirium tremens: Lorazepam
Wernicke’s: IV high potency vitamin B-complex with thiamine
Compare and contrast the use of anti-epileptic drugs Vs benzos in a patient experiencing alcohol withdrawal
While benzos remain the first line therapy, they come with sedation and potential for addiction. Anti-epileptic drugs help with anxiety and depression
Identify the time course associated with a patient’s last drink as it relates to onset of alcohol withdrawal seizures
The seizure threshold declines on cessation of drinking and seizures may occur usually within 48 hours of abstinence.
Risk factors associated with alcohol withdrawal seizures
Elevated homocysteine levels, prior history of seizures, high total EtOH consumption and ,multiple previous detoxifications, electrolyte imbalances, hypoglycemia, CNS infection, illicit drug use.
Describe the relationship between thiamine, glucose, and Wernicke’s encephalopathy
Heavy alcohol consumption results in reduced thiamine absorption and increased thiamine excretion which may result in WE. Thiamine is a cofactor for enzymes required in glucose metabolism, and thus WE may be caused by administering glucose before thiamine.
