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final exam Flashcards

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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
intoxication can also be achieved by?
inhalation (also exhaled)
26
metabolism of alc
>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
27
ethanol elimination follows ---- order kinetics
zero
28
disulfiram
inhibits aldehyde dehydrogenase causing elevation in blood acetaldehyde levels--> hangover (flushing, headache, N/V, blurred vision, mental confusion)
29
how is alcohol related to heroin?
alc lowers the dose of heroin needed to overdose
30
short term ethanol use may cause exaggerated response to what?
oral anticoagulants and oral hypoglycemic agents
31
which drugs does ethanol influence absorption of?
benzo and diazepam
32
aspirin + nsaids +alc
cause greater gastric irritation
33
what can cause enhanced actaminophen toxicity?
in liver cirrhosis | reduction in drug met and depletion of glutathione
34
high blood alc level inhibits metabolism of?
benzo
35
other drugs like disulfiam
metrondazole, sulfonylurea
36
abrupt withdrawal of alc
anorexia, nausea, GI upset, tremors, sweating
37
neuromuscular hyperexcitability
gross tremors and grand mal convulsions
38
autonomic hyperactivity
hyperthermia and circulatory collapse
39
how is abstinence sydrome treated
long acting BDZ (diazepam) | -alternatives are clonidine and carbamazepine
40
what is used in avoidance therapy?
disulfiram
41
acetaldehyde
unconsciousness, hypotensive shock, sudden MI
42
disulfram inhibits dopamine beta hydroxyase, preserving what?
dopamine (exaggerates schiz or depression)
43
naltrexone
long acting opiod antagonist better tolerated than disulfiram
44
acamprosate
alcohol dependence tment programs | -working a poorly understood mech
45
methanol
used as industrial solvent and denaturing agent for ethanol
46
metabolism of methanol
same enzymes as ethanol | zero order kinetic but products different
47
toxicity of methanol
headache, nausea, visual disturbances, ab pain, resp disturbances --> coma/death
48
poisoning of methanol
due to metabolites, formaldehyde and formic acid, which cause blindness
49
cause of death of methanol
resp arrest
50
treatment of methanol od
hemodialysis, peritoneal dialysis, bicarb infusion, ethanol admin/subst
51
amphetamines are
cns stimulants
52
what are indicated for ADHD
amphetamine, methylphenidate, methamphetamine, dextroamphetamine
53
what are used for narcolepsy?
amphetamine, methylphenidate, dextroamphetamine
54
appetite suppressants (anorectics)
methamphetamine | treat obesity by activating satiety center in hypothalamus
55
major effect of amphetamines
CNS stimulation --> euphoria | -act at levels of cortex, subcortical areas, and spinal cord
56
peripheral effects of amphetamines
increase sympathetic/adrenergic effects
57
mech of action of amphetamines
- 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
methamphetamine
- phenylalklyamine (parent compound) - in cold meds - "speed"
59
why is methamphetamine preferred by abusers?
- less adverse effects due to less NT | - free base --> easily smoked
60
ecstacy
- commonly abused (sched 1) - molly (designer drug) - serious effects --CV disorders and neurotoxicity
61
how do abusers take amph?
iv or smoking
62
chronic abuse of amph produces what?
tolerance
63
acute overdose of amph
CV and CNS stim | increase symp stim
64
chronic abuse of amph
anxiety, bad mood, fatigue | paranoid
65
toxicity of amph tx
acidification of urine with NH4Cl which increases excretion of drugs
66
dental issues of amph similar to?
cocaine
67
high dose of amph
nervousness, can't rest | convulsion with local anesthetics
68
CV disorders
hypertension, vasoconstriction, hemorrhage
69
meth mouth
caries and heavy plaque with xerostomia
70
xanthine derivatives
caffeine, theophyline, theobromine
71
----- is the only xanthine used primarily for its CNS effect
caffeine
72
caffiene's effect on CNS
- greater stim of cortex, but least on spinal cord - clearer thougts - excessive--> spinal cord--> convulsions
73
what stimulates the resp center in medulla?
caffiene
74
net result of caffeine on CV system?
increase in BP | increase cardiac activity
75
mech of action of caffiene
- 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
doxapram
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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