Pharm-Drugs Of Abuse

Front 1

Mechanism behind tolerance to
1) Opiods
2)Barbituates

Back 1

1) down regulation of postsynaptic receptor

2)enzyme induction

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T/ F
CA STATE LAW MANDATES THAT ADEQUATE ANALGESIA MUST BE PROVIDED.

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T

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COCAINE:
LOCAL ANESTHETIC MECHANISM:

Back 3

BLOCK NA+ CHANNELS – neuron doesn’t fire

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COCAINE:
VASOCONSTRICTOR MECHANISM:

Back 4

BLOCKS NE UPTAKE stimulates alpha 1 receptors to vasoconstrict

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COCAINE:
EUPHORIA & ADDICITON MECHANISM:

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BLOCKS DOPAMINE UPTAKE IN MESOLIMBIC- MESOCORTICAL PATHWAYS (CELL BODIES IN NUCLEUS ACCUMBANS)

**seratonin also involved (will not get into)

Front 6

Chewing coca leaves leads to little abuse or dependence. WHY?

Back 6

Slow absorbance.
Distributed in blood stream and metabolised by plasma esterase.
Snorting or smoking has an fast, direct route to the brain.

Front 7

Crack cocaine (freebasing) -> rapid, intense high & ↑↑↑ risk addiction. WHY?

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Lungs have high surface area for absorption. Blood flow from lung goes to L ventrical to cerebral arteries and brain. Leading to rapid intense high.

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MEDICAL CONSEQUENCES OF COCAINE ABUSE:

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1. TREMORS, SEIZURES & CONVULSION (kindling)

RESPIRATORY DEPRESSION (blocks Na+ channels in resp. centers)

CRACK LUNG (signs & symptoms of pneumonia w/ no bacteria)

CARDIOVASCULAR – MI, arrhythmias, ↑ HR/BP, ischemic brain infarction, CVAs (blocks Na+, channel, & NE uptake and α receptors in heart also causes vasoconstriction (α Cx)

4. HYPERPYREXIA – (blocks NE uptake in thermoregulatory center of hypothalamus) can trigger seizure.

5) NECROSIS of NASAL SEPTUM & BOWEL ISCHEMIA & GANGRENE (vasocx from blocking NE uptake)

6) LOSS OF APPETITE -> effects on satiety center. – block NE re-uptake
7) HIV & AIDS
(behavioral)

8) BACTERIAL or VIRAL ENDOCARDITIS, HEPATITIS & AIDS.

Front 9

combination of ETOH & cocaine gives ______ which toxic effects can be greater

Back 9

cocaethalene

Front 10

EtOH can cause PARADOXICAL EXCITEMENT. WHAT IS THE PARADOX?

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Pharmacological effect is depressant. Inhibitory neurons are more sensitive. Inhibition of Inhibitory centers exite in small doses. High doses result in both inh & exit neuron inhibition.

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MECHANISMS OF ACTION of EtOh

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1) Increase binding of GABA to GABA A receptor – linked to Cl- conductace. INCREASED CLORIDE CONDUCTANCE hyperpolarizes neurons.

**GABA antagonists block the sedative ataxic effects of EtOH

2) Blocks Ca2+ influx -> decrease neurotransmitter release

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NALTREXONE (Trexan)

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Opioid antagonist that is approved for tx alcoholism. It ↓s the “high”, the craving, & the number of relapses.

Front 13

μ significance in alcoholism

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μ seems to be an important receptor in the addictive properties of EtOH. Mice that lack μ drink less EtOH. μ antagonists decrease reinforcing properties of EtOH & decrease dopamine release in nucleus acumbans

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Medical consequences of EtOH Abuse

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1. WARM, FLUSHING, SENSATION
(depresses vasomotor centers, ↑ cutaneous & gastric blood flow)

2. ENZYME INDUCTION -> ↑ in amt of enzyme ; ↑ in drug metabolism; ↑ drug interactions

3. DIURESIS MECHANISM: (↓ levels of ADH , decrease tubular absorption of H2O)

4. CARDIOVASCULAR EFFECTS:

GOOD NEWS: Chronic 1-2 drinks/day ↓ risk of cardiac death. ( small blood thinning effects)

BAD NEWS: (direct toxic effect on heart and vascular mm)

EtOH can constrict the coronary & cerebral vasculature.

5. RESPIRATORY DERESSION – (↑ GABA)

6. ESOPHAGITIS, GASTRITIS & DIARRHEA – (organic solvent-damage tissue- (Mallory-Weiss lesion)

7. CIRRHOSIS

8. FETAL ALCOHOL SYNDROME (FAS)

9. WERNICKE-KORSAKOFF SYNDROME

KORSAKOFF'S PSYCHOSIS:

10. NIACIN ENCEPHALOPATHY (PELLAGRA) – niacin deficiency. Chronic wasting (4Ds)-> Dementia (confusion, Disorientation, hallucinations, memory loss, psychoses), Dermatitis & Diarrhea.

Front 15

Mechanism of alcoholic cirrhosis

Back 15

15% of severe alcoholics

deceased protein intake results in mobilization of fat to liver. Liver needs NAD+ for fat metabolism but all NAD+ has been used in the metabolism of EtOH to acetaldehyde. Accumulation of reduced NADH, fat, and acetaldehyde results in liver damage.

Front 16

What is fetal alcohol syndrome. How does EtOH or its metabolite ACETALDEHYDE result in FAS(theories):

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FAS has been reported to result from as little as JUST ONE DRINK.

Child shows characteristic facial features, mental retardation, and problems with CV & GI systems.

Theories of damage:
a) inhibit embryonic cell proliferation.

b) damage placenta -> fetal malnutrition.

c) decrease fetal blood flow -> fetal hypoxia and growth retardation.

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WERNICKE'S ENCEPHALOPATHY is characterized by:

What is the treatment?

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a) Mental Sx: drowsy, inattentive, indifference, disoriented

b) Ocular Sx: abducens palsy, diplopia, strabismus, nystagmus

c) Ataxia

TX: Give Thiamine (B1)

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Korsakoff's psychosis

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Damage to mamillary bodies of posterior hypothalamus -> short-term memory loss.

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Niacin Encephalopathy (Pellagra)

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niacin deficiency--wasting -> dementia (confusion, disorientation, hallucinations, memory loss, psychoses), dermatitis & diarrhea.

Front 20

Rx treatment of alcoholism

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Naltrexone
Acamprosate
Disulfiram

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Naltrexone (MOA)

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opioid antagonist

Front 22

Acamprosate (MOA)

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restores balance between GABA & glutamate

Front 23

Disulfiram

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inhibits aldehyde dehydrogenase leading to an increase in acetaldehyde which results in nausea, vomiting, flushing, tachacardia upon ingestion of alcohol

Front 24

Bhang

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cheapest and least potent form of MJ. Low resin. From the tops of UNCULTIVATED plants. Most MJ grown in US is this type.

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Ganja

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Flowering tops & leaves of CULTIVATED plants. Higher quality and quantity of resin

Front 26

Charas

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Hashish. Highest grade. Made from RESIN ITSELF obtained from tops of mature plants.

Front 27

Anandamide

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endogenous cannabinoid. Binds CB1 & CB2 receptors. CB1 is responsible for analgesic effects of cannabinoids.

MOA: decreasess presynaptic Ca2+ influx and decreases NT release in dorsal horn.

Front 28

MARIJUANA IS NOT A HALLUCINOGEN b/c:

Back 28

1) rarely causes hallucinations
2)sedating not stimulating
3) doesn't dilate pupils, increase BP or temp like other hallucinagens
4) Need chronic/heavy use for tolerance/dependance and even after that w/drawl effects are mild
6)does not alter conciousness.

Front 29

How bad is MJ?

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Studies show no intellectual or neuro damage. no change in personality. no loss of will to work or participate in society. no effects of moderate-heavy use on learning perception, motivation after using for up to one year.
2003--Chronic use did not cause brain damage, learning, memory,attention, or language skills.

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Gateway hypothesis

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Use of MJ or EtoH early in life will use harder drugs later in life.

Front 31

Greatest risk of MJ

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LUNG DAMAGE--Inhale deeper & hold longer. Increase risk of bronchitis, emphysema, & lung cancer.

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Dronabinol (Marinol)

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FDA approved form of THC. Uses:
1) antiemetic
2) treat anorexia (CB1 agonist)

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Rimonabant

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CB1 antagonist in phase III clinical trials for weight loss

Front 34

WHAT IS THE LAY TERM FOR AMPHETAMINES?

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speed

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MA-HUANG - ACTIVE INGREDIENT:

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ephedrine

Front 36

KHAT (cathinone)

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-Amphetamine-like substance popular in the Middle East & Africa

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METHYLPHENIDATE (Ritalin)

Back 37

structurally similar to amphetamine with similar properties. Used for ADD/ADHD.

CII- CONTROLLED SUBSTANCE

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DEXMETHYLPHENIDATE (Focalin)

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d isomer of methylphenidate

CII- CONTROLLED SUBSTANCE

Front 39

DEXTROAMPHETAMINE (Dexedrine)

ADDERALL

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a mixture of amphetamine & dextroamphetamine salts. used for ADD/ADHD Longer acting than methylphenidate. Provides more steady control.

CII- CONTROLLED SUBSTANCE

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Methamphetamine (Desoxyn)
Street name:
Smokable form:

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Ice
Crystal Meth

Front 41

Mechanism of amphetamines & other stimulants (analeptics)

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1) increase NE & dopamine release
2) block NE/Dopamine uptake
3) stumulate NE/DA receptors
4) (amphetamines) Inhibit MAO A/B

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Feeling of Amphetamines & stimulants

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increase wakefulness & alertness, decrease sense of fatigue, increase intitiative,self-confidence & ability to concentrate. The elevate mood and cause elation & euphoria.

Front 43

What NTs are responsible for alertness?
euphoria?

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alertness-NE
euphoria-dopamine

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amphetamine psychosis

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results from high doses of amphetamines and increase DA/5HT release in mesolimbic pathway.

Front 45

Fatality of amphetemines.

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During same time period:
24 deaths w/Adderal
16 w/ Ritalin
10 w/ other amphetamines

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Legitimate medical uses of amphetamines

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1)anorexiant
2) ADD/ADHD
3)Narcolepsy

Front 47

Anorexiants
MOA & problems

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MOA: increase DA/5HT release in lateral hypothalamus
Problem: not permamnent

Front 48

Non Amphetamine anorexiants

any danger?

Back 48

1)diethylproprion(tenuate)CIV
2) benzphetamine (didrex)CIV
3 phendimetrazine(bondril PDM)CIII
4) Phentermine(adipex-P)CIV
5)Sibutramine (Meridia) CIV

CV complications & CNS stimulants subject to abuse

Front 49

Orlistat (Xenical)

MOA

Back 49

non-controlled substance alternative

MOA: inhibits lipases w/in GI tract therefor inhibiting conversion of dietary triglycerides into absorbable free fatty acids

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ADD/ADHD

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2-5% elementry school children

3-6X more commmon in boys

Characterized by:
-inappropriate attention
-impulsivity
-hyperactivity

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Atomoxetine (strattera)

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non stimulant treatment for ADHD
Not a controlled substance.
Mech: blocks NE uptake but does not effect dopamine (doesn't cause euphoria)

SE: increase risk of suicidal ideation & hepatotoxicity.

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Narcolepsy (hypersomnia)

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excessive daytime sleepiness & SLEEP ATTACKS brought on by strong emotional events

can be accompanied by cataplexy

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cataplexy -
what is it and what is tx

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-extreme muscle weakness or collapse while awake
-TX: Na+ oxybate (Xrem) --(GHP--CAUTION date rape drug)

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Modafinil (Provigil)

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Tx for narcolepsy

Actis by activating HYPOCRETIN/OREXIN PATHWAYS

A CIV controlled substance that can still have CV effects.

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Medical consequences of CNS stimulant abuse;

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1) Depletion of NE/DA (possibly 5HT)
2)CVA (secondary to increase BP)
3)CV effects
4) Hyperpyrexia
5) amphetamine psychosis

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Why is psychosis more prevalent with amphetamines than cocaine

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cocaine is short acting because of plasma esterases.

Front 57

common psychosis in amphetamine toxicity

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paranoias delusions

Front 58

Hallucinogenic properties are from stimulating _______ receptors in _______ brain areas.

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5-HT2A /cortical & limbic

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Indolealkylamines

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structurally similar to 5HT e.g. LSD

Front 60

LSD

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lysergic acid diethyl amide

an ergot fungus that grows on rye

generally causes ILLUSION (misinterpretation of actual stimuli) NOT HALLUCCINATIONS (interpreting something w/out an actual stimuli

LSD had a high therapeutic index. Deaths are usually accedental from perceptual distortions (thinking one can fly).

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Psilcybin & Psilocin

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naturally found indolealkyamines in MUSHROOMS

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PHENYLETHYLAMINES

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One of the two hallucinogen classes (the other is indolealkylamines)
1) Mescaline-peyote cactus
2) MDMA
DOM

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MDMA (methylenedioxymethamphetamine)
aka ECSTACY &
MDA (methylenedioxyamphetamine) aka EVE

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Designer amphetamines

synthetic compounds structurally similar to mescaline & amphetamine

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DOM (dimethoxymethylamphetamine)
aka STP (serenity, tranquility, peaca)

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Physiological effects:
mydriasis, hyperreflexia, increase BP & temp, tachycardia, & tremors, restlessness, anxiety, decreased appetite, dry mouth, insomnia

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Brain damage, chromosome abnormalities or teratogenic effects due to indole-like halucinogens or phenylethylamine mescalinr

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doesn't look like it

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MDMA danger

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degeneration of 5HT nerve terminals and long term depletion of 5HT

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PCP (phencyclidine) Phenyl-Cyclohexyl-Piperidine

street name

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angel dust

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PCP what is it?

Back 68

disociative anesthetic. pt is aware of but indifferent to surroundings, catatonic, flat face, open mouth, fixedd sightless stare, rigid but flexible posturing, no overt loss of consciousness.

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PCP mechanism

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stimulate PCP receptors which inhibits NMDA mediated glutamate releae. This enhances DA transmission in mesolimbic brain areas

high densities of NMDA glutamate receptors in hippocampus cause disturbances in attention, perception and association learning

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PCP effects

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can cause acute psychotic state (autistic, withdrawn, negativistic, bizarre, responses to behavioral tests) similar to schizophrenia. Causes NYSTAGMUS-- good DDX in PCP from organic psychosis

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PCP causes:
leads to:

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overwhelming sensory input leading to unpredictable , exaggerated, distorted & sometimes violent reaction to eviornmental stimuli.
Can lead to severe anxiety, panic, rage & aggression.

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Opisthotonos & siezures

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can result from PCP

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Tx for PCP

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put in a quiet envirnment
haloperidol (haldol) is often used

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ANTICHOLINERGIC ACTIVITY

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PCP has high anticholinergic activity so avoid neuroleptics w/ high anticholinergc activity

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RHABDOMYOLYSIS

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breakdown of mm fibers from inside out. PCP causes these direct effects on skeletal mm. violent behavor can cause severe mm damage.