Neuro 3 Flashcards

1
Q

inability to control consumption of etoh, obtaining and consuming etoh is primary purpose, will have s/sx of withdrawal without it is defined as _______________

A

dependence

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2
Q

T/F: alcohol is a CYP450 inducer if consumed regularly

A

TRUE

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3
Q

______________ is a small water soluble molecule that is absorbed rapidly from the GI tract

A

ethanol

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4
Q

peak concentrations of ethanol are reached within _____________

A

30 min

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5
Q

why do women etoh concentrations peak before mens even with equal consumption

A

d/t lower total body water in females & differences in first pass metabolism

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6
Q

___________% of ethanol is oxidized in the liver

A

90

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7
Q

the remaining 10% of ethanol that is NOT oxidized in the liver is excreted through ________________ and ______________

A

lungs, urine

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8
Q

primary metabolism of etoh involves what enzyme?

A

alcohol dehydrognease

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9
Q

abuse of etoh typically leads to issues with what organs?

A

liver and pancreas (pancreatitis)

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10
Q

what is the primary pathway of ETOH metabolism?

A

Ethanol is converted to acetylaldehyde via oxidation reaction utilizing alcohol dehydrognease

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11
Q

what is the ethanol metabolism pathway chronic alcoholics

A

ethanol + NADPH + O2 –> microsomal ethanol oxidizing system (MEOS) –> acetaldehyde + NADP + H20

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12
Q

what is the second step in ethanol metabolism

A

Acetaldehyde dehydrogenase converts acetaldehyde to acetate.

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13
Q

if someone is allergic to alcohol they are lacking what enzyme

A

aldehyde dehydrogenase

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14
Q

what meds are used to tx alcoholism

A
  1. disulfuram 2. naltrexone
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15
Q

MOA of disulfram

A

inhibits aldehyde dehydrogenase (i.e. inhibits the conversion of acetaldehyde to acetate)

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16
Q

disulfram has been known to inhibit the metabolism of other drugs, such as:

A
  1. phenytoin 2. oral anti-coagulants 3. isoniazid
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17
Q

_______________ should not be given with other drugs medications that contain alcohol

A

disulfram

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18
Q

absorption of disulfram is _________________, and elimination is ________________

A

fast; slow (thus actions may persist for several days)

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19
Q

s/e of disulfram

A
  1. extreme discomfort in those who drink etoh 2. flushing 3. throbbing headache 4. N/V 5. sweating 6. hypotension 7. confusion
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20
Q

what is the MOA of naltrexone

A
  1. opioid receptor antagonist, blocks effects at mu opioid receptors 2. prevents the self administration of alcohol
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21
Q

how is naltrexone administered

A

PO or IM

22
Q

what is the drug of choice in the tx of etoh-ism

A

naltrexone

23
Q

DO NOT administer naltrexone in what situations?

A
  1. with disulfram 2. to pts with opioid dependance
24
Q

in the treatment of etohism, __________________ will cause small increases in LFTs, and ______________________ will cause dose dependent hepatotoxicity

A

disulfram; naltrexone

25
Q

meds that are not FDA approved that reduce cravings in chronic alcoholism

A
  1. ondansetron (zofran) 2. topiramate (topamax) 3. baclofen
26
Q

which med has proven favorable for the relapse prevention and the tx of etoh dependence, esp when paired with psychological counseling

A

naltrexone

27
Q

s/sx 6-8 hours into etoh withdrawal

A
  1. increased BP 2. tremor 3. anxiety 4. insomnia s/sx decrease after 1-2 days
28
Q

etoh withdrawal has a large risk of seizures and hallucinations between days ______________

A

1-5

29
Q

DT’s begin ______________ hours after last drink, and can last _________________ days

A

48-72; 5-10

30
Q

s/sx of DT’s

A
  1. delirium 2. agitation 3. ANS instability 4. low grade fever 5. diaphoresis
31
Q

goals of drug therapy with etoh withdrawal

A
  1. prevention of seizures 2. prevention of delirium 3. prevention of arrhythmias
32
Q

drug therapy with alcohol withdrawal

A
  1. electrolyte imbalances need to be restored: K, Mg, phos (banana bag) 2. long acting sedative-hypnotic (Bz: librium, valium)
33
Q

what is the sedative hypnotic of choice in tx of alcohol withdrawal

A

benzodiazepines: 1. chlordizepoxide (librium) 2. diazepam (valium)

34
Q

if a pt comes in with liver dz, and etoh withdrawal, you should use ___________________ benzos, such as ______________ or _______________

A

shorter-acting; lorazepam (Ativan); Oxazepam (Serax)

35
Q

what would molecularly explain why acute consumption of alcohol can cause “blackouts”

A

alcohol blocks glutamate action on the NMDA receptor

36
Q

acute consumption of alcohol enhances the action of ______________ receptors

A

GABA-a

37
Q

CNS effects of acute consumption of alcohol

A
  1. sedation 2. relief of anxiety 3. slurred speech 4. ataxia 5. impaired judgement 6. disinhibited behavior 7. intoxication
38
Q

chronic effects of alcohol consumption on the CNS

A
  1. tolerance + physical/psychological dependence 2. dementia 3. wernicke-korsakoff syndrome 4. bilateral impaired visual acuity + blurred vision –> optic nerve degeneration
39
Q

what is wernicke korsakoff syndrome caused by

A

thiamine deficiency secondary to chronic alcholism

40
Q

what is wernicke korsakoff syndrome

A

rare degenerative brain d/o caused by chronic alcohol consumption

41
Q

s/sx of wernicke korsakoff syndrome

A
  1. paralysis of external eye muscles 2. ataxia 3. confusion 4. coma 5. death
42
Q

alcohol tolerance develops from ______________________ of neural pathway

A

up regulation

43
Q

alcohol dependence results from over activity of the same neural pathway as _________________, after ethanol dissipates

A

tolerance

44
Q

chronic consumption of etoh effects on PNS

A
  1. generalized symmetrical peripheral nerve injury 2. distal paresthesia of hands and feet 3. degenerative changes resulting in gait disturbances and ataxia
45
Q

there is significant depression of myocardial contractility at BAC > _____________ mg/dl

A

100

46
Q

CV effects of acute etoh consumption

A
  1. signifcant depression of myocardial contractility at BAC < 100 mg/dl 2. vasodilation secondary to CNS effects (even in cold environments)
47
Q

CV effects of chronic etoh consumption

A
  1. dilated cardiomyopathy 2. ventricular hypertrophy 3. fibrosis 4. atrial and ventricular arrhythmias 5. HTN 6. raises HDL (thus prev CAD)
48
Q

chronic etoh consumption interferes the therapeutic effects of what cardiac drug class?

A

beta blockers

49
Q

T/F: ethanol previously was used IV to suppress premature labor

A

TRUE

50
Q

acute consumption of etoh reproductive effects

A

releaxes the uterus