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Multisystem Part 2 > drug classes in substance abuse > Flashcards

drug classes in substance abuse Flashcards

1
Q

classes that act through g protein coupled receptors?

A

opioids

cannabinoids

caffeine

LSD/mescaline

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2
Q

opiates act through…

A

the mu opioid receptor

GABA release inhibited and dopamine inreased

results in neuronal hyperpolarization –> disinhibition of dopamine release

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3
Q

cannabinoids act on…

A

cannabinoid receptors (CB1 and CB2)

similar to opioid receptors but located on different neurons

hyperpolarization –> disinhibition of dopamine release and inhibit Ca entry –> reduced transmitter release

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4
Q

LSD and mescaline act on…

A

partial agonist at serotonin 5HT2 receptor

acts through G protein (Gq) to increase IP3 –> causes depolarization and hallucinations

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5
Q

caffeine acts through…

A

antagonist at adenosine receptors (A1 and A2)

displaces adenosine at receptors so you dont get tired!

at A1 –> antagonism increases Gi/o activity

at A2 –> antagonism reduces Gs activity

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6
Q

classes that act through ion channel linked receptors?

A

nicotine

benzodiazepines

alcohol

ketamine/pcp

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7
Q

nicotine acts through

A

nicotinic acetylcholine receptor (nACH-R)

alpha4 beta2 subunit in brain is very sensitive to nicotine

increase in cation conductance –> depolarization allows dopamine release

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8
Q

benzodiazepines act through….

A

GABA-A-receptor at an allosteric site (not the same site as GABA)

potentiates the effect of GABA –> hyperpolarization of that ion channel

increased DA

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9
Q

alcohol acts through…

A

GABA-A receptor at allosteric site and potentiates GABA –> hyperpolarization (sedation)

and

blocks NMDA-receptor –> inhibits Glutamate effect –> euphoria and dopamine release

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10
Q

ketamine and PCP act through..

A

blocks NMDA receptors –> inhibits Glutamate effect –> disorientation, hallucinations, euphoria, dopamine release

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11
Q

drug classes that act through monoamine transporters?

A

cocaine

amphetamines

MDMA

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12
Q

cocaine acts through….

A

inhibits DAT, NET and SERT

increases extracellular DA, NE, and 5HT = high/euphoria

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13
Q

amphetamines act through…

A

blocks VMAT (displaces DA, NE and 5HT) –> increases extracellular DA, NE,, and 5HT

a high/euphoria and neurotoxicity

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14
Q

MDMA acts through… (ecstasy)

A

blocks SERT and displaces 5HT

increased extracellular 5HT and depletion = euphoria and neurotoxicity (serotonin)

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15
Q

chronic use of amphetamines/stimulants results in…

A

loss of stimulatory effects

depression/anxiety/hunger/weight gain

d/t down regulated monoamine receptors and depletion of monoamine vesicular stores (less transmitter and fewer receptors)

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16
Q

cocaine can produce what bad effect in overdose?

A

seizures, coma, intracranial hemorrhage

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17
Q

amphetamine overdose can cause?

A

psychotic episodes, paranoia, aggression, and skin/tooth/gum disease

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18
Q

cocaine and amphetamine withdrawal symptoms

A

relatively mild dysphoria, depression, hunger, and drug craving

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19
Q

MDMA

A

ecstasy/molly

lasts 3-6 hrs

sympathetic effects (tachycardia, NP, and alertness) dehydration and HTN

mildly hallucinogenic

OD –> hyperthermia/muscle breakdown, MI, stroke, neurotoxic

20
Q

nicotine

A

stimulant that acts on the nicotinic receptors (nACh) in brain at alpha4beta2 subunit

increases cation currents and increases extracellular DA levels

from smoke gets to brain very quickly

sympathetic effects on BP and HR

carcinogenic due to combustion products

21
Q

marijuana (THC)

A

peripheral effects: tachycardia, but little change in BP, dry mouth, hunger, flushing (vasodilation)

central effects: euphoria/high, distortion of visual/auditory stimuli, altered time perception, talk more, relaxing, sedation, psychomotor impairment

higher dose(edibles usually) = confusion, delusions, panic, paranoia

22
Q

what distinguishes THC from LSD?

A

THC induces a feeling of relaxation/sedation

23
Q

THC acts through

A

THC Receptors: CB1(in nervous system), CB2 (in immune cells)

G-protein coupled receptors, regulating Gi and Go - inhibit adenylyl cyclase - open K+ channels; reduce Ca2+ conductances

high concs CB1- receptors in brain

24
Q

therapeutic uses of THC (marijuana)

A
  • treatment of drug/radiation-induced nausea and vomiting in cancer chemotherapy
  • enhancement of appetite
  • reduction of intra-ocular pressure in glaucoma

use of CB1 antagonist, rimonabant, to control appetite

pain relief, either as analgesic, or as co-analgesic

25
Q

chronic mal-effects of smoking marijuana

A

respiratory problems

suppression of immune system

amotivational syndrome (memory loss and impaired mental performance)

26
Q

LSD

A

lysergic acid diethylamide synthetic

**partial agonist at 5HT2 receptors

somatic effects: dizzy, mydriasis, tremor

perceptual effects: blurred vision, altered colors and shapes, hallucinations mood swings, elation or dysphoria, panic, fear, detachment

**not addictive; dont ruin lifestyles/no compulsive use!!

27
Q

phencyclidine/PCP and ketamine

A

Glu NMDA receptor antagonists

channel blockers and reduce CA conductance

effects: intoxication, staggered gait, blank stare, muscle rigidity, analgesia (dont respond to pain), hypersalivation, sweating, bizarre/aggressive behavior, paranoia, convulsions

chronic effects: memory deficits, speech impairment

28
Q

ethanol metabolism (major pathway)

A

step 1 by alcohol dehydrogenase (ADH) and step 2 by aldehyde dehydrogenase

1) ethanol + NAD –> acetaldehyde + NADH + H
2) acetaldehyde + NAD –> acetic acid + NADH acetic acid –> calories

29
Q

ethanol metabolism (minor pathway)

A

by p450 enzyme (CYP2e

1) ethanol + NADPH –> acetaldehyde + NADP + H

then aldehyde dehydrogenase= acetaldehyde + NAD –> acetic acid + NADH

30
Q

fomepizole

A

inhibits ADH (alcohol dehydrogenase) by competing for NAD+

31
Q

more food in stomach DOES….what to alcohol absorption?

A

SLOWS it downs

32
Q

legal alcohol limit is

A

.8 mg/ml

33
Q

methanol metabolism

A

also metabolized by alcohol dehydrogenase and aldehyde dehydrogenase but it creates fairly toxic products–> formaledhyde and formic acid

34
Q

effects of ethanol on the liver -increases 3 things? -decreases 2 things?

A

increases NADH:NAD ratio (from heavy demand for NAD) increases rate of FA synthesis (since NADH is high)

increases plasma free FAs (d/t increases sympathetic activity)

decreases fatty acid oxidation (d/t lack of NAD) and decreases release of TGs from the liver results in accumulation of TGs

35
Q

ethanol: effect on gastric acid, sympathetic tone, and ADH

A

increases gastric acid secretion

increased sympathetic tone and vasodilation, increased heat loss

inhibits ADH secretiion –> diuresis!

36
Q

ethanol effects on CNS at .4-1 mg/ml 1-2 mg/ml 2-4 mg/ml 4-5 mg.ml

A

.4-1 mg/ml = mild euphoria, increased rxn time, impaired judgement, increased risk of accident

1-2 mg/ml = impaired gait, ataxia, loss of balance, slurred speech, analgesia, confusion, disinhibition, sedation

2-4 mg/ml = emesis, slow mental process, severe sedation, anesthesia, coma, respiratory depression

4-5 mg.ml = deep coma, death from respiratory depression at this range

37
Q

1 mg/ml ethanol =

A

0.1%

38
Q

what to give in order to retard methanol metabolism

A

ethanol or fomepizole (they compete for alcohol dehydrogenase and prevent bad methanol products from forming)

39
Q

benefits of alcohol?

A

elevates high density lipoproteins (HDL) which bind cholesterol reduction of plasma cholesterol

reduced risk of coronary heart disease, CV disease

improved cognition in elderly- Benefit seen with 1 - 15 g/day; 15 - 30 g/day did not increase effects ***antioxidants might play an important role

40
Q

resveratrol

A

from wine an antioxidant, anti-carcinogenic

decreases neuronal death following stroke; reduced platelet aggregation; decreased inflammatory responses • induction of apoptosis (protection against carcinoma) • CYP enzyme induction

Problems: Conc in wine is low - effective dose seems to be liters per day (not a good idea!) Bioavailability is low - poor absorption, very rapid metabolism in vivo

41
Q

SYNDROMES OF malnutrition due to chronic alcoholsim

A

peripheral neuropathy

pellagra (niacin deficiency) = GI disturbance, erythema, desquamation, CNS effects

amblyopia = partial loss of vision

Wernicke’s encephalopathy (thiamine deficiency) = disturbed eye movements, ataxia, tremor

Korsakoff’s psychosis (vitamin deficiency; other ?) severe memory loss, confusion

42
Q

fetal alcohol syndrome

A

low birth weight, poor growth, low IQ, impaired immune function, characteristic facial features

43
Q

alcoholic fatty liver

A

–fat accumulation (inhibition of tricarboxylic acid cycle; reduced oxidation of fat)

–accumulation of acetaldehyde (breakdown reduced because of reduced availability of NAD+)

  • increased lipid peroxidation
  • membrane damage
  • depletion of glutathione, vitamins, trace metals

–induction of CYP2E1

  • increased metabolism of many drugs; activation of carcinogens
  • result is necrosis and fibrosis: cirrhosis
44
Q

ethanol induces _____

A

CYP2E1

this activates procarcinogens

and

increases metabolism of drugs like acetaminophen

45
Q

alcohol withdrawal

day 1

day 2

day 3

A

1 - tremor and shakes; mild hallucinations (nondisorienting)

2 - tremors and hallucinations continue; tonic-clonic convulsions (potentially lethal)

3 - delirium tremens (DTs), autonomic symptoms (sweating, nausea, vomiting, disrrhea, fever)

**symptoms peak at 3-4 days then get better days 4-7

46
Q

synthetic canthinones

A

bath salts

release DA and 5HT

can cause severe rhabdomyolysis

Multisystem Part 2 (20 decks)

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