Neuro 3 Flashcards
inability to control consumption of etoh, obtaining and consuming etoh is primary purpose, will have s/sx of withdrawal without it is defined as _______________
dependence
T/F: alcohol is a CYP450 inducer if consumed regularly
TRUE
______________ is a small water soluble molecule that is absorbed rapidly from the GI tract
ethanol
peak concentrations of ethanol are reached within _____________
30 min
why do women etoh concentrations peak before mens even with equal consumption
d/t lower total body water in females & differences in first pass metabolism
___________% of ethanol is oxidized in the liver
90
the remaining 10% of ethanol that is NOT oxidized in the liver is excreted through ________________ and ______________
lungs, urine
primary metabolism of etoh involves what enzyme?
alcohol dehydrognease
abuse of etoh typically leads to issues with what organs?
liver and pancreas (pancreatitis)
what is the primary pathway of ETOH metabolism?
Ethanol is converted to acetylaldehyde via oxidation reaction utilizing alcohol dehydrognease
what is the ethanol metabolism pathway chronic alcoholics
ethanol + NADPH + O2 –> microsomal ethanol oxidizing system (MEOS) –> acetaldehyde + NADP + H20
what is the second step in ethanol metabolism
Acetaldehyde dehydrogenase converts acetaldehyde to acetate.
if someone is allergic to alcohol they are lacking what enzyme
aldehyde dehydrogenase
what meds are used to tx alcoholism
- disulfuram 2. naltrexone
MOA of disulfram
inhibits aldehyde dehydrogenase (i.e. inhibits the conversion of acetaldehyde to acetate)
disulfram has been known to inhibit the metabolism of other drugs, such as:
- phenytoin 2. oral anti-coagulants 3. isoniazid
_______________ should not be given with other drugs medications that contain alcohol
disulfram
absorption of disulfram is _________________, and elimination is ________________
fast; slow (thus actions may persist for several days)
s/e of disulfram
- extreme discomfort in those who drink etoh 2. flushing 3. throbbing headache 4. N/V 5. sweating 6. hypotension 7. confusion
what is the MOA of naltrexone
- opioid receptor antagonist, blocks effects at mu opioid receptors 2. prevents the self administration of alcohol
how is naltrexone administered
PO or IM
what is the drug of choice in the tx of etoh-ism
naltrexone
DO NOT administer naltrexone in what situations?
- with disulfram 2. to pts with opioid dependance
in the treatment of etohism, __________________ will cause small increases in LFTs, and ______________________ will cause dose dependent hepatotoxicity
disulfram; naltrexone
meds that are not FDA approved that reduce cravings in chronic alcoholism
- ondansetron (zofran) 2. topiramate (topamax) 3. baclofen
which med has proven favorable for the relapse prevention and the tx of etoh dependence, esp when paired with psychological counseling
naltrexone
s/sx 6-8 hours into etoh withdrawal
- increased BP 2. tremor 3. anxiety 4. insomnia s/sx decrease after 1-2 days
etoh withdrawal has a large risk of seizures and hallucinations between days ______________
1-5
DT’s begin ______________ hours after last drink, and can last _________________ days
48-72; 5-10
s/sx of DT’s
- delirium 2. agitation 3. ANS instability 4. low grade fever 5. diaphoresis
goals of drug therapy with etoh withdrawal
- prevention of seizures 2. prevention of delirium 3. prevention of arrhythmias
drug therapy with alcohol withdrawal
- electrolyte imbalances need to be restored: K, Mg, phos (banana bag) 2. long acting sedative-hypnotic (Bz: librium, valium)
what is the sedative hypnotic of choice in tx of alcohol withdrawal
benzodiazepines: 1. chlordizepoxide (librium) 2. diazepam (valium)
if a pt comes in with liver dz, and etoh withdrawal, you should use ___________________ benzos, such as ______________ or _______________
shorter-acting; lorazepam (Ativan); Oxazepam (Serax)
what would molecularly explain why acute consumption of alcohol can cause “blackouts”
alcohol blocks glutamate action on the NMDA receptor
acute consumption of alcohol enhances the action of ______________ receptors
GABA-a
CNS effects of acute consumption of alcohol
- sedation 2. relief of anxiety 3. slurred speech 4. ataxia 5. impaired judgement 6. disinhibited behavior 7. intoxication
chronic effects of alcohol consumption on the CNS
- tolerance + physical/psychological dependence 2. dementia 3. wernicke-korsakoff syndrome 4. bilateral impaired visual acuity + blurred vision –> optic nerve degeneration
what is wernicke korsakoff syndrome caused by
thiamine deficiency secondary to chronic alcholism
what is wernicke korsakoff syndrome
rare degenerative brain d/o caused by chronic alcohol consumption
s/sx of wernicke korsakoff syndrome
- paralysis of external eye muscles 2. ataxia 3. confusion 4. coma 5. death
alcohol tolerance develops from ______________________ of neural pathway
up regulation
alcohol dependence results from over activity of the same neural pathway as _________________, after ethanol dissipates
tolerance
chronic consumption of etoh effects on PNS
- generalized symmetrical peripheral nerve injury 2. distal paresthesia of hands and feet 3. degenerative changes resulting in gait disturbances and ataxia
there is significant depression of myocardial contractility at BAC > _____________ mg/dl
100
CV effects of acute etoh consumption
- signifcant depression of myocardial contractility at BAC < 100 mg/dl 2. vasodilation secondary to CNS effects (even in cold environments)
CV effects of chronic etoh consumption
- dilated cardiomyopathy 2. ventricular hypertrophy 3. fibrosis 4. atrial and ventricular arrhythmias 5. HTN 6. raises HDL (thus prev CAD)
chronic etoh consumption interferes the therapeutic effects of what cardiac drug class?
beta blockers
T/F: ethanol previously was used IV to suppress premature labor
TRUE
acute consumption of etoh reproductive effects
releaxes the uterus
