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CNS II > Pharm Stimulants > Flashcards

Pharm Stimulants Flashcards

1. List the prototype methylxanthines, describe their mechanism of action and pharmacological effects, and list their major side effects. 2. List the prototype psychomotor stimulants, cocaine, and nicotine, describe their mechanism of action and pharmacological effects, and list their major side effects. 3. Describe the pattern and nature of abuse observed with psychomotor stimulants, cocaine and nicotine, the degree of tolerance and dependence, and the treatment of the abuse. 4. Describe the

1
Q

strychnine class

A

convulsant

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2
Q

picrotoxin class

A

convulsant

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3
Q

pentylenetetrazol class

A

convulsant

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4
Q

MOA of strycninie

A

blocks gly receptos in spinal cord resulting in disinhibition

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5
Q

MOA of picrotoxin and pentylenetetrazol

A

non-competitively blocks Cl-channels of GABA, resulting in disinhibition

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6
Q

sx of strychnine poisoning

A

( opisthotintus (tenatny) and risus sardonicus

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7
Q

treatment for strychninie poisoning

A

IV diazepam, reduced envoronmental stress and activated charchol

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8
Q

caffeiene class

A

methylxanthine

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9
Q

theophylline class

A

methylxanthine

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10
Q

theobromine class

A

methylxanthine

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11
Q

cognitive effetcs of methylxanthines

A

increases capacity for intellectual effort and decreases reaction time, decreases fine motor coordination, timing skills ans possibly math

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12
Q

CNS actions of methylxanthine

A

increase sensitivity of medullary respiratory centers to CO2 - increases ventilation

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13
Q

CV actions of methylxanthine

A

increase HR (slight), dialates peripherial vasculatire, constricts cerebral vasculature

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14
Q

muscle effects of methylxanthine

A

smooth - dilates brochioles

skeletal - increased capacity for work, some performance enhancing effects

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15
Q

GI effects of methylxanthine

A

stimulates peristalsis

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16
Q

MOA of methylxanthine at high levels

A

mobilization of intracellular Ca++/inhibits phostphodiasterase

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17
Q

clinical MOA of methylxanthine

A

antagonism of Adenosine receptors

18
Q

presence of food in GI will do what with methylxanthine

A

reduce rate of absorption but decrease gut irritation

19
Q

increases t 1/2 of methylxanthine

A

hepatic disease, pregnancy and OCPs

20
Q

decreases t 1/2

A

smoking , phenytoin, barbos

21
Q

methylxanthine t 1/2 is longest in

A

pre-term infants

22
Q

sx of methylxanthine toxicity

A

nervousness, insomnia, delirium, convulsions, olfactory.gustatory hallucinations

23
Q

caffiene can cause headaches in people who

A

are non-tolerent

24
Q

varenicline MOA

A

partial agonistat nicotinic receptor

25
Q

use of varenicline

A

smoking cessation

26
Q

effect of varenicline

A

blunting of rewarding effects of nicotine

27
Q

rimobabant MOA

A

atagonist/inverse agonistat CB1 cabbabinoid receptors

28
Q

SE of rimonabant

A

depression and suicidal idealation

29
Q

methylphenidate class

A

psychomotor stimulant

30
Q

stereochemical form of psychomotor stiumulants most active

A

L version

31
Q

most potent psychomotor stiumulants

A

meth

32
Q

least potent psychomotor stiumulants

A

cocaine/methylphenate

33
Q

CNS effects of psychomotor stiumulants

A

stimulate medullary respiratory centers, increase motor activity, elevate mood, reduce fatigue, insomnia

34
Q

MOA of anphetamines

A

release catecholamines and 5-HT, inhibit reuptake of same

35
Q

MOA of methylphidate and cocaine

A

inhibit reuptake of MOA via blockade of transporters

36
Q

psychomotor stiumulant that the “high” tracks alongside plasma levels

A

cocaine

37
Q

perception of “high” dependant upon

A

uptake into brain

38
Q

thereputic uses of amphetamines

A

weight loss (not legit)
ADHD
narcoplepsy

39
Q

non-stimulant treatment of narcolepsy

A

modafinil

40
Q

toxicity of ampetamines sx

A

psycotic reacton (visual hallucinations, paranoia, change in affect) sympathomimetic increase

41
Q

primary NT receptor MDMA effects

A

5-HT

42
Q

active ingrediant in “bath salts”

A

cathinone

CNS II (25 decks)

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