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Unit 3: Pharm - Liza > Pharmacology of Substance Use > Flashcards

Pharmacology of Substance Use Flashcards

1
Q

How do CNS Depressants mostly act?

A

augment GABA-A receptor complex activity, to increase Cl- influx, hyperpolarizing the cell (inhibitory)

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2
Q

Alcohol is a tiny molecule! What does this mean for how it’s absorbed?

A

small so easy, rapid absorption by DIFFUSION through membranes; including mouth mucous membrane, stomach and MOST at small intestines

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3
Q

What does the rate of alcohol absorption depend on and what does this mean for BAC?

A

concentration of alcoholic beverage and whether the stomach is empty or full; empty stomach: peak BAC 3/4-1hr after last drink; full stomach: peak BAC 2-3 hrs after last drink

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4
Q

What exactly does food in the stomach do for alcohol?

A

it dilutes it, delays stomach emptying, increases effective rate of alcohol metabolism

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5
Q

Where is alcohol distributed? how is it eliminated? where is it metabolized?

A

1) distributed in total body water (it’s a tiny molecule)!
2) eliminated by METABOLISM
3) mostly in liver, some in stomach

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6
Q

Tell me about the hepatic pathway of ethanol oxidation

A

1) ethanol–>acetaldehyde (alcohol dehydrogenase mostly in liver cytoplasm)
2) acetaldehyde–>acetate (acetaldehyde dehydrogenase; ALDH1 in liver cytoplasm and ALDH2 in liver mitochondria)

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7
Q

What’s up with Asians and alcohol?

A

Asians possess atypical Beta2 allele w/enhanced rate of hepatic conversion of ethanol–>acetaldehyde; increased acetaldehyde causes facial flushing! Also, many Asians lack functional forms of ALDH2 so further elevating blood acetaldehyde levels (dizziness, nausea, etc)

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8
Q

Consumed alcohol is a tremendous load for the liver!! What are some metabolic effects?

A

all NAD dependent reactions are diverted, thus: impaired gluconeogenesis, increased lactic acid production, increased ketone body production, inhibited uric acid excretion, decreased fatty acid oxidation

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9
Q

What is the limiting factor determining the rate of alcohol oxidation (saturation/zero order kinetics)?

A

supply of NAD+

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10
Q

When do P450 enzymes (ie CYP2E1) come into play with alcohol oxidation?

A

more important factor at high levels of alcohol and with chronic alcohol consumption; this may enhance metabolism of some other drugs that are also metabolized by P450 (contributes to tolerance)

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11
Q

What three drugs have cross tolerance with their respect to actions on GABA?

A

alcohol, barbiturates and benzodiazepenes

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12
Q

What is considered the LD(50) for alcohol?

A

450-500 mg/dl (.45% BAC)

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13
Q

WHat is the progression of liver pathology regarding chronic heavy drinking?

A

inhibition of tricarboxcylic (TCA) cycle/oxidation of fat–>fatty liver–>hepatitis–>necrosis–>fibrosis –>cirrhosis–>hepatic failure–>death

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14
Q

What’s the word on cardiovascular effects of alcohol?

A

moderate consumption is protective (increases HDL, decreases coronary heart disease); i.e. 1 drink/day (more than that and no longer protective)

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15
Q

What’s the word on GI and Endocrine effects of alcohol?

A

chronic gastritis, decreased ADH secretion, hypogonadism/feminization/gynecomastia, suppreses uterine motility

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16
Q

How does disulfiram (antabuse) work?

A

Inhibits aldehyde dehydrogenase to cause acetaldehyde toxicity (nausea, vomit, headache etc)

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17
Q

What are some other alcohols that get abused?

A

methyl acohol (drygas)–>formaldehyde/formic acid–>severe acidosis/retinal toxicity

ethylene glycol (antifreeze)–>oxalic acid–>acidosis, nephrotoxicity

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18
Q

What are the main CNS stimulants and how do they generally act?

A

amphetamine, cocaine, caffeine, nicotine; most increase CNS catecholamine, especially dopamine activity

19
Q

What is the MOA of amphetamines and what are its current official therapeutic uses?

A

indirect sympathomimetic release of biogenic amines from nerve terminals in periphery and in CNS; dopamine potentiation most important

used to treat narcolepsy and ADHD

20
Q

What are the side effects to taking amphetamines?

A

Vasospasm leading to possible stroke or MI, arrhythmia, weight loss, tremor, anxiety, irritability, confusion, possible paranoid state

21
Q

What is the MOA of cocaine and what are its current official therapeutic uses?

A

blocks uptake transporters for dopamine (most important), norepi, and serotonin (thus increasing activity at those synapses)

used as topical anesthetic for URT (has combined vasoconstrictor/local anesthetic properties to shrink mucosa and provide anesthesia)

22
Q

How is cocaine broken down in the body?

A

It’s rapidly hydrolyzed by plasma cholinesterase

23
Q

What is the MOA of caffeine?

A

competitive antagonist at adenosine receptors (thus preventing adenosine’s sedative/anxiolytic etc effects); also inhibit phosphodiesterases (to increase cAMP)

24
Q

What can caffeine but used to treat?

A

vascular headaches (constricts blood vessels in the brain), asthma (relieves bronchoconstriction and reduces inflammation)

25
Q

What is the MOA of nicotine?

A

ganglionic stimulant and depolarizing ganglionic blocker

26
Q

What are considered to be the three Schedule I hallucinogens?

A

LSD, mescaline, psilocybin

27
Q

What is meant by Schedule I v Schedule II v Schedule III etc

A

Schedule I: drug has high potential for abuse and not accepted for medical use in US; Schedule II: may have high abuse potential but still accepted medical use (ex morphine); Schedule III “abuse less than Sched I or II)…etc

28
Q

What are the chemical categories of hallucinogens and what drugs fall under each category?

A

1) Indole alkyl amines: psilocybin and LSD

2) Phenylethylamines: Mescaline, MDMA

29
Q

What is the possible mechanism of action of all the hallucinogens?

A

agonist at 5HT2A receptors on Raphe cell body–> inhibition of Raphe Nuclei firing –> increased sensory input; also a partial dopamine agonist

30
Q

How is LSD oxidized? Is there cross tolerance between the hallucinogens?

A

LSD is oxidized int he liver; there is cross tolerance between LSD, mescaline and psilocybin (thus suggesting similar receptors)

31
Q

What are some of the side effects/toxicities of LSD?

A

bad trips (anxiety attack, panic attack), flashbacks, “street drug” lifestyle; note that no overdoses, birth defects of chronic psychoses ever linked to LSD

32
Q

What are some theoretical therapeutic effects of lSD?

A

helps w/pscyhoanalysis, alcoholism, autistic children, terminal cancer patients (may change attitude toward death)

33
Q

What is the name of the medication that blocks alcohol dehydrogenase in the treatment of methanol and ethylene glycol poisoning?

A

Fomepizole

34
Q

What is the mechanism of action for all the cannabinoids (marijuana, anandamide, dronabinol, nabilone)

A

all act on cannabinoid receptors CB1 and CB2 which are G protein coupled receptors

35
Q

Classify the cannabinoids and whether they are schedule I, II or III drugs

A

Marijuana - Cannabinoid - Schedule I

Anandamide - Endogenous Cannabinoid (thus no schedule)

Dronabinol - Synthetic THC - Schedule III

Nabilone - Synethetic THC - Schedule II

36
Q

What are the therapeutics of the cannabinoids?

A

anti-emetic, anti-nausea, appetite stimulating for cancer chemo and AIDS patients, analgesic for neuropathic pain;

possible: glaucoma, asthma, anxiolytic, migraine, MS treatment

37
Q

What are the side effects of cannabinoids?

A

vasodilation–>tachycardia, dilation of conjunctival vessels, bronchodilation, decreased intraocular pressure, hunger, impaired reproductive function, development, respiratory damage due to tar

38
Q

What is the active ingredient in marijuana and how is it metabolized?

A

active ingredient: delta-9-tetrahydrocannabinol

metabolized by P450 (can act as inducing enzyme with chronic use)

39
Q

What were the synthetic THC drugs (dronabinol and nabilone) created to treat?

A

anti-emetic, anti-nausea, appetite stimulate for cancer chemotherapy and AIDS patients

40
Q

Which of the synthetic THC analogs has the therapeutic effects of THC without the psychactive effects?

A

Nabilone

41
Q

What type of drug is Phencyclidine (PCP) and what is its MOA?

A

it’s a dissociative anesthetic that acts as an antagonist of ion channels associated w/NDMA receptors; it’s also an agonist at mu opioid receptors

42
Q

What are the effects of taking PCP?

A

violent behavior, coma, seizures, arrest, inexplicable psychoses, dissociation, confusion, ataxia, marked nystagmus; long half life due to its high lipid solubility and having active metabolites

43
Q

What type of drug is MDMA (Ecstasy)?

A

it’s a psychoactive substituted amphetamine with characteristics of: amphetamine + LSD + fluoxetine

44
Q

What type of drug is N-acetylcystine and what is it used for?

A

antioxidant; supplies sulfhydryl groups to glutathione; improves microcirculation, provides anti-inflammatory effect; used for acetaminophen overdoses

Unit 3: Pharm - Liza (14 decks)

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