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neuro 2 > final exam > Flashcards

final exam Flashcards

1
Q

what is the most commonly abused legal substance?

A

alcohol

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2
Q

what is the primary cause of the problem of alcohol?

A

CNS effect

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3
Q

alcohol causes an increase in —– fluidity

A

membrane

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4
Q

alcohol’s effect on GABA receptors

A

enhancement of inhibitory GABA at GABA a receptors (like benzodiazepines)

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5
Q

alcohol’s effect on glutamate

A

reduction of effect of excitatory glutamate on ion channels–inhibits NMDA receptors to glutamate

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6
Q

effect of alcohol on endogenous opiod peptides

A

causes release of endogenous opiod peptides and changes (increase) levels of dopamine and serotonin

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7
Q

what inhibits the desire for alcohol consumption?

A

opioid and dopamine receptor antagonists (naltrexone)

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8
Q

what does chronic use of alcohol do?

A

alters sensitivity/structure of NMDA receptor, leading to excitatory toxic effect upon acute withdrawal

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9
Q

NMDA receptor antagonists

A

reduce incidence of seizures occuring during ethanol withdrawal and ethanol consumption

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10
Q

major metabolite of alcohol

A

acetaldehyde

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11
Q

effect of alchol on CNS

A
  • early excitation due to disinhibition of inhibitory pathways (low dose)
  • high dose–> depressant–sedative/hypnotic effects
  • soporific effect (increases sleep time)
  • behavioral changes
  • disruption of motor activity
  • affects sexual function
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12
Q

effect of alcohol on cardiovascular system

A
  • increases catecholamines in blood
  • increased activity of vascular smooth muscle at low concentration but reduced activity at high concentration
  • increase in coronary blood flow
  • decrease in myocardial activity
  • heat loss
  • acetaldehyde formed –> increase in catecholamines, tachycardia, increase CO, increase BP
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13
Q

acute intoxication’s effect on liver

A

reversible decrease in microsomal metabolic enzyme activity

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14
Q

chronic intoxication

A

induction of liver enzyme activity (P450)

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15
Q

cirrhosis

A

overall decline in liver function

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16
Q

nutrition depletion bc of alc

A
  • inhibit vit A/D and decrease in pyridozine (b6)
  • depletion of Zn and selenium
  • marginal supply of calorie need without providing other nutritional rqments
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17
Q

alc’s effect on kidney

A

-inhibits ADH causing increased urine production and thirst

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18
Q

alc’s effect on sexual function

A

provokes desire but not performance

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19
Q

alc’s effect on HDL/LDL

A

increases it

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20
Q

alc’s effect on saliva and gastric

A

small doses increase salivation but higher reduce

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21
Q

alcohol retards absorption of ?

A

glucose, aa, thiamine, B12

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22
Q

alc causes – gland activation

A

adrenal gland

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23
Q

alcohol has rapid absorption where?

A

in stomach and intestine

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24
Q

> 20% alc ______ by inducing both gastric mucosal irritation and pylospasm

A

retards absorption

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25
Q

intoxication can also be achieved by?

A

inhalation (also exhaled)

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26
Q

metabolism of alc

A

> 95% of ingested alc is metabolized

  • by non-microsomal and microsomal pathways, latter applying to chronic
  • leads to production of actetaldehyde, which has multiple toxic symptoms
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27
Q

ethanol elimination follows —- order kinetics

A

zero

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28
Q

disulfiram

A

inhibits aldehyde dehydrogenase causing elevation in blood acetaldehyde levels–> hangover (flushing, headache, N/V, blurred vision, mental confusion)

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29
Q

how is alcohol related to heroin?

A

alc lowers the dose of heroin needed to overdose

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30
Q

short term ethanol use may cause exaggerated response to what?

A

oral anticoagulants and oral hypoglycemic agents

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31
Q

which drugs does ethanol influence absorption of?

A

benzo and diazepam

32
Q

aspirin + nsaids +alc

A

cause greater gastric irritation

33
Q

what can cause enhanced actaminophen toxicity?

A

in liver cirrhosis

reduction in drug met and depletion of glutathione

34
Q

high blood alc level inhibits metabolism of?

A

benzo

35
Q

other drugs like disulfiam

A

metrondazole, sulfonylurea

36
Q

abrupt withdrawal of alc

A

anorexia, nausea, GI upset, tremors, sweating

37
Q

neuromuscular hyperexcitability

A

gross tremors and grand mal convulsions

38
Q

autonomic hyperactivity

A

hyperthermia and circulatory collapse

39
Q

how is abstinence sydrome treated

A

long acting BDZ (diazepam)

-alternatives are clonidine and carbamazepine

40
Q

what is used in avoidance therapy?

A

disulfiram

41
Q

acetaldehyde

A

unconsciousness, hypotensive shock, sudden MI

42
Q

disulfram inhibits dopamine beta hydroxyase, preserving what?

A

dopamine (exaggerates schiz or depression)

43
Q

naltrexone

A

long acting
opiod antagonist
better tolerated than disulfiram

44
Q

acamprosate

A

alcohol dependence tment programs

-working a poorly understood mech

45
Q

methanol

A

used as industrial solvent and denaturing agent for ethanol

46
Q

metabolism of methanol

A

same enzymes as ethanol

zero order kinetic but products different

47
Q

toxicity of methanol

A

headache, nausea, visual disturbances, ab pain, resp disturbances –> coma/death

48
Q

poisoning of methanol

A

due to metabolites, formaldehyde and formic acid, which cause blindness

49
Q

cause of death of methanol

A

resp arrest

50
Q

treatment of methanol od

A

hemodialysis, peritoneal dialysis, bicarb infusion, ethanol admin/subst

51
Q

amphetamines are

A

cns stimulants

52
Q

what are indicated for ADHD

A

amphetamine, methylphenidate, methamphetamine, dextroamphetamine

53
Q

what are used for narcolepsy?

A

amphetamine, methylphenidate, dextroamphetamine

54
Q

appetite suppressants (anorectics)

A

methamphetamine

treat obesity by activating satiety center in hypothalamus

55
Q

major effect of amphetamines

A

CNS stimulation –> euphoria

-act at levels of cortex, subcortical areas, and spinal cord

56
Q

peripheral effects of amphetamines

A

increase sympathetic/adrenergic effects

57
Q

mech of action of amphetamines

A
  • highly lipophilic
  • rapid
  • release monoamine NT from presynaptic storage sutes (indirect-acting agents)
  • weak MAO inhibitors, uptake of NT’s and drugs
  • euphoria (increase in dopamine)
  • anxiety due to increase in NE
58
Q

methamphetamine

A
  • phenylalklyamine (parent compound)
  • in cold meds
  • “speed”
59
Q

why is methamphetamine preferred by abusers?

A
  • less adverse effects due to less NT

- free base –> easily smoked

60
Q

ecstacy

A
  • commonly abused (sched 1)
  • molly (designer drug)
  • serious effects –CV disorders and neurotoxicity
61
Q

how do abusers take amph?

A

iv or smoking

62
Q

chronic abuse of amph produces what?

A

tolerance

63
Q

acute overdose of amph

A

CV and CNS stim

increase symp stim

64
Q

chronic abuse of amph

A

anxiety, bad mood, fatigue

paranoid

65
Q

toxicity of amph tx

A

acidification of urine with NH4Cl which increases excretion of drugs

66
Q

dental issues of amph similar to?

A

cocaine

67
Q

high dose of amph

A

nervousness, can’t rest

convulsion with local anesthetics

68
Q

CV disorders

A

hypertension, vasoconstriction, hemorrhage

69
Q

meth mouth

A

caries and heavy plaque with xerostomia

70
Q

xanthine derivatives

A

caffeine, theophyline, theobromine

71
Q

—– is the only xanthine used primarily for its CNS effect

A

caffeine

72
Q

caffiene’s effect on CNS

A
  • greater stim of cortex, but least on spinal cord
  • clearer thougts
  • excessive–> spinal cord–> convulsions
73
Q

what stimulates the resp center in medulla?

A

caffiene

74
Q

net result of caffeine on CV system?

A

increase in BP

increase cardiac activity

75
Q

mech of action of caffiene

A
  • inhibition of phosphodiasterase–> increase camp–> cardiac stim and SM relax
  • adenosine antagonism–> bronchocnstriction, histamine release, CNS depression, methylxantines (caffiene) block effects of adenosine
  • stim of caetcholaime release
  • increase calcium mobilization
76
Q

doxapram

A

not xantine or amph

  • stim CNS –> greater efect on medullary resp centers (effect mediated via peripheral carotid chemorec)
  • tonic clonic convulsions in large doses
  • treats resp depression

neuro 2 (3 decks)

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