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Pharm of Abused Drugs > Abused Drugs > Flashcards

Abused Drugs Flashcards

1
Q

Depressants

A

Ethanol, Benzos, Barbs, Solvents, GHB

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2
Q

Stimulants

A

Cocaine, Amphetamines, Me-phenidate

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3
Q

Opioids

A

Heroin, hydromorphone, oxycodone, fentanyl, methadone, W-18

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4
Q

Psychadelics

A

LSD, Mescaline, Psilocybin, Synthetics

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5
Q

Others

A

Cannabis and synthetic CBs, Bath Salts, PCP/Ketamine, Steroids, Nicotine, Caffeine

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6
Q

SUD Spectrum

A

Mild 2-3/11, Moderate 4-5/11, Severe 6+/11

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7
Q

Trend of Alcohol Use

A

Current drinking increases and binge drinking decreases with age

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8
Q

What is the neurobiological system of reward?

A

Mesotelencephalic DA system

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9
Q

What is the path of the Mesolimbic DA system?

A

VTA to NAcc

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10
Q

Changes in the craving state

A

Cues from hippocampus, amygdala, and stress from insula drive; PFC is compromised and normal executive fxn impaired –> enhances drug use behavior

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11
Q

Which drugs of abuse act on the VTA?

A

Opioids, ethanol, barbiturates, benzos

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12
Q

Which drugs of abuse act on the NAcc?

A

Amphetamines, cocaine, opioids, cannabinoids, phencyclidine

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13
Q

Which drugs act on GPCRs? Where?

A

Opioids, THC, GHB; VTA

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14
Q

Which drugs act on channels? Where?

A

Benzos, nicotine, ethanol; VTA

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15
Q

Which drugs act on transporters?

A

Cocaine, amphetamine, ecstasy

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16
Q

Ethanol distribution attributes

A

Rapid/wide in aqueous compartments, freely permeable across BBB and placenta, no protein binding/sequestration, no uptake into fat depots

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17
Q

Primary pathway of alcohol metabolism

A

Hepatic ADH (cytosolic) – NAD+ dependent (rate limiting), non inducible, some in stomach

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18
Q

What can block ADH?

A

Fomepizole

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19
Q

Secondary pathway of alcohol metabolism

A

CYP450 2E1>1A2>3A4 (MEOS – uses NADPH cofactor), high threshold, low capacity, but inducible

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20
Q

Acetealdehyde metabolism

A

ALDH – mitochondrial, NAD+ dep;

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21
Q

What blocks ALDH?

A

Disulfram

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22
Q

Acute actions of hydrocarbon inhalants

A

Rapid onset euphoria and short duration (similar to EtOH – early excitation and loss of inhibition followed by risky behavior, then dazed/drunk; later headache. bloodshot eyes(

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23
Q

Acute effects of nitrite inhalants

A

Vascular/smooth muscle dilation, hypotension, increased CBF

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24
Q

Adverse effects of inhaled hydrocarbons

A

Anxiety, decreased appetite, tinnitus, marrow & CNS pathology, tolerance, withdrawal symptoms (similar to EtOH)

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25
Q

Adverse effects of inhaled nitrites

A

Methemoglobinemia, decreased BP, HA

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26
Q

Effects of EtOH

A

Biphasic on NE/DA turnover, actions at GABA-A and NMDA-Glu receptors, action at cation channels, AC, and PI PLC

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27
Q

Acute psychological effects of EtOH

A

Dose-related excitation –>depression; alters cognitive, emotional, and behavioral functions, state dependent learning, labile affect, attention decreased and actions disorganized

28
Q

Acute neurological effects of EtOH

A

Anterograde amnesia, positional nystagmus, EEG changes

29
Q

Acute CV effects of EtOH

A

Myocardial depression, labile BP, arrhythmias, CVA potential, vasodilation, elevation of HDL3

30
Q

Acute renal effect of EtOH

A

Diuresis (decreased ADH release)

31
Q

Acute endocrine effects of EtOH

A

Increased release of CRF, ACTH, Cortisol, Oxytocin, PRL; Decreased release of GNH and GH

32
Q

Attributes of pharmacodynamic tolerance

A

Membrane changes, GABA-R and GLU(NMDA)-R and Ca2+ channels

33
Q

Attributes of metabolic tolerance

A

Induction of CYP450s (2E1, 3A4, 1A2)

34
Q

Symptoms of EtOH abstinence syndrome

A

Craving, hyperirritability, anxiety, tremor, insomnia, nausea, sweating, hallucination, seizure

35
Q

Delirium Tremons

A

Confusion, disorientation, agitation, hyperpyresis (fever, dehydration)

36
Q

Tx of Alcohol OD

A

Supportive therapy, flumazenil if w/ benzos

37
Q

Tx of methanol tox

A

Antagonize ADH w/ fomepizole or EtOH

38
Q

Tx of withdrawal/abstinence syndrome

A

Sub therapy: BDZ, phenobarb
Symptomatic therapy: phenytoin, gapapentin
Supportive therapy: thiamine, NSAIDS

39
Q

EtOH Recovery management

A

Discontinue sed/hyps, disulfram (aversive), naltrexone (anti-craving), acamprosate (anti-craving – is NMDA antagonist and GABA-A agonist)

40
Q

PK of Cocaine

A

Liphophilic but charged; widely H2O distributed but redistributes to fat depots as well (Metabolism limited)

41
Q

Metabolism of cocaine

A

Ester hydrolysis to polar products (cholinesterases); N-demethylation to active norocaine metabolite

42
Q

Adverse effects of cocaethylene

A

seizures, immune system depression, hepatic damage

43
Q

Cocaine excretion

A

Renal

44
Q

Cocaine MOA

A

Blocks GNA (no change in RP); sypathomimetic effects indriectly by blocking presynaptic NE uptake; blocks DAT, NET, and 5HT transporters

45
Q

Actions of cocaine

A

LA, vasoconstriction, psychomotor stimulant

46
Q

Difference between amphetamine MOA and cocaine MOA

A

Amphetamines also block VMAT and reverse DAT so they secrete cytoplasmic rather than vesicular DA

47
Q

Effects of cocaine

A 
CV: Increased BP, HR, CO
Respiration: hyperpnea
Smooth M: Increased GI/UG tone
Eye: mydriasis and cycloplegia
Themoreg: hyperthermia
Appetite: Suppression
CNS: general arrousal> desynchronization> seizure
48
Q

Cocaine order of events with behaviors

A

Euphoria –> dysphoria –> hallucinosis –> psychosis

49
Q

Cocaine OD

A

Profound CNS excitation (hypervigilence –>extreme agitation –> seizure), cardiac arrhytmia, hypertensive crisis, respiratory paralysis

50
Q

Stages of triphasic withdrawal syndrome in cocaine dependence

A

Crash (hours) –> subacute (days-weeks) –> extinction (months-years)

51
Q

Opiate effects

A

CNS: euphoria (rush) –> sedation (nod), analgesia
Respiration: depression of CO2 drive/responsiveness
GI Smooth m: increased resting tone w/ decreased peristalsis/secretion
Eye: Miosis
Nausea/Emesis: stimulation of CTZ
CV: reduced TPR, orthostatic hypotension, cerebral vasodilation (increased CO2)

52
Q

Opiate tox triad

A

Coma, respiratory depression, miosis

53
Q

Acute abstinence syndrome for opioids

A

Mydriasis, sweating, piloerection, tachycardia, diarrhea, yawning, HTN, fever, craving, irritability, nausea, cramps, muscle/bone aches, dysphoria, insomnia –> protracted: periodic anxiety, insomnia, craving

54
Q

Opiate OD Tx

A

Support vital fxns (esp respiration), naloxone

55
Q

Opiate withdrawal tx

A

Methadone detox (cross dependence), clonidine detox + acetaminophen, decrease dose by 20-25%/d

56
Q

Long term management of opiate abuse

A

Agonist maintenance: methadone (dosage issues)
Buprenorphine (+naloxone)
Antagonist tx: naltrexone
OIC Rx: MeNTX and naloxegol

57
Q

MJ Absorption

A

Inhalation – 10-50% in circ, peak in 10-20 min

Oral – slow uptake, peak 1-3 hrs

58
Q

MJ Distribution

A

95-99% plamsa protein bount – high distribution in lipid tissues; rapidly distributed into lipid environments (terminal t1/2 is almost a full day) – extended w chronic admin because extends half life

59
Q

MJ Metabolism

A

Lungs and liver – lots of 1st pass; alkyl hydroxylation – active 11-OH THC (25% more potent); oxidative rxn –> inactive OH/COOH metabolisms

60
Q

MJ Excretion

A

1/3 urine –> glucuronide and metabolites

2/3 fecal –> enterohepatic recirc

61
Q

MJ Intox Syndrome

A

Euphoria, altered perception, intensified sensorium
—>
impaired goal-direction, lapse of attention, sedation
—>
Anterograde amnesia, narrowed visual field, poor coordination/rxn time
—>
anxiety, dysphoria, panic etc.

62
Q

Acute MJ Effects on CNS

A

State-dependent learning, analgesia, thermoreg –> hypothermia, stimulates appetite, suppresses NV, suppresses REM sleep, decreases intraocular pressure

63
Q

Acute MJ effects on CV

A

Tachycardia (20-100% increase in HR for 1-3hrs, dose-related), CO increase in supine position, postural hypotension

64
Q

Acute MJ Effects on resipiratory, endocrine, and immune systems

A

Respiratory: bronchodilation, irritation of mucosa
Endocrine: less T and spermatogenesis in males, less PRL, LH, FSH, GH in females
Immune: impares cell and humoral responses (increases susceptibility)

65
Q

NT and Molecular MOA for MJ

A

NT: catecholamines, GABA, opioids, serotonin, glutamate, ach

Molecular: AC inhibition (Gi), calcium channel inhib, K channel activation

66
Q

Signs/Symptoms of MJ Dependence (Withdrawal syndrome)

A

Irritability, restlessness, insomnia anorexia nausea, diarrhea, sweating, increased Tb, weight loss, hand tremor, salivation, tearing, REM rebound, sleep disturbances (usually gone w/in 48 hrs)

Pharm of Abused Drugs (1 decks)

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