drug classes in substance abuse

Question 1

classes that act through g protein coupled receptors?

Answer 1

opioids

cannabinoids

caffeine

LSD/mescaline

Question 2

opiates act through…

Answer 2

the mu opioid receptor

GABA release inhibited and dopamine inreased

results in neuronal hyperpolarization –> disinhibition of dopamine release

Question 3

cannabinoids act on…

Answer 3

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

Question 4

LSD and mescaline act on…

Answer 4

partial agonist at serotonin 5HT2 receptor

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

Question 5

caffeine acts through…

Answer 5

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

Question 6

classes that act through ion channel linked receptors?

Answer 6

nicotine

benzodiazepines

alcohol

ketamine/pcp

Question 7

nicotine acts through

Answer 7

nicotinic acetylcholine receptor (nACH-R)

alpha4 beta2 subunit in brain is very sensitive to nicotine

increase in cation conductance –> depolarization allows dopamine release

Question 8

benzodiazepines act through….

Answer 8

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

Question 9

alcohol acts through…

Answer 9

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

and

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

Question 10

ketamine and PCP act through..

Answer 10

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

Question 11

drug classes that act through monoamine transporters?

Answer 11

cocaine

amphetamines

MDMA

Question 12

cocaine acts through….

Answer 12

inhibits DAT, NET and SERT

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

Question 13

amphetamines act through…

Answer 13

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

a high/euphoria and neurotoxicity

Question 14

MDMA acts through… (ecstasy)

Answer 14

blocks SERT and displaces 5HT

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

Question 15

chronic use of amphetamines/stimulants results in…

Answer 15

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)

Question 16

cocaine can produce what bad effect in overdose?

Answer 16

seizures, coma, intracranial hemorrhage

Question 17

amphetamine overdose can cause?

Answer 17

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

Question 18

cocaine and amphetamine withdrawal symptoms

Answer 18

relatively mild dysphoria, depression, hunger, and drug craving

Question 19

MDMA

Answer 19

ecstasy/molly

lasts 3-6 hrs

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

mildly hallucinogenic

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

Question 20

nicotine

Answer 20

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

Question 21

marijuana (THC)

Answer 21

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

Question 22

what distinguishes THC from LSD?

Answer 22

THC induces a feeling of relaxation/sedation

Question 23

THC acts through

Answer 23

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

Question 24

therapeutic uses of THC (marijuana)

Answer 24

• 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

Question 25

chronic mal-effects of smoking marijuana

Answer 25

respiratory problems suppression of immune system amotivational syndrome (memory loss and impaired mental performance)

Question 26

LSD

Answer 26

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!!

Question 27

phencyclidine/PCP and ketamine

Answer 27

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

Question 28

ethanol metabolism (major pathway)

Answer 28

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

Question 29

ethanol metabolism (minor pathway)

Answer 29

by p450 enzyme (CYP2e 1) ethanol + NADPH --\> acetaldehyde + NADP + H then aldehyde dehydrogenase= acetaldehyde + NAD --\> acetic acid + NADH

Question 30

fomepizole

Answer 30

inhibits ADH (alcohol dehydrogenase) by competing for NAD+

Question 31

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

Answer 31

SLOWS it downs

Question 32

legal alcohol limit is

Answer 32

.8 mg/ml

Question 33

methanol metabolism

Answer 33

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

Question 34

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

Answer 34

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

Question 35

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

Answer 35

increases gastric acid secretion increased sympathetic tone and vasodilation, increased heat loss inhibits ADH secretiion --\> diuresis!

Question 36

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

Answer 36

.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

Question 37

1 mg/ml ethanol =

Answer 37

0.1%

Question 38

what to give in order to retard methanol metabolism

Answer 38

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

Question 39

benefits of alcohol?

Answer 39

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

Question 40

resveratrol

Answer 40

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

Question 41

SYNDROMES OF malnutrition due to chronic alcoholsim

Answer 41

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

Question 42

fetal alcohol syndrome

Answer 42

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

Question 43

alcoholic fatty liver

Answer 43

–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

Question 44

ethanol induces \_\_\_\_\_

Answer 44

CYP2E1 this activates procarcinogens and increases metabolism of drugs like acetaminophen

Question 45

alcohol withdrawal day 1 day 2 day 3

Answer 45

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

Question 46

synthetic canthinones

Answer 46

bath salts release DA and 5HT can cause severe rhabdomyolysis