Glossary of pharm-drugs of abuse
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- Mechanism behind tolerance to
- 1) down regulation of postsynaptic receptor
- T/ F
CA STATE LAW MANDATES THAT ADEQUATE ANALGESIA MUST BE PROVIDED.
LOCAL ANESTHETIC MECHANISM:
- BLOCK NA+ CHANNELS – neuron doesn’t fire
- BLOCKS NE UPTAKE stimulates alpha 1 receptors to vasoconstrict
EUPHORIA & ADDICITON MECHANISM:
- BLOCKS DOPAMINE UPTAKE IN MESOLIMBIC- MESOCORTICAL PATHWAYS (CELL BODIES IN NUCLEUS ACCUMBANS)
**seratonin also involved (will not get into)
- Chewing coca leaves leads to little abuse or dependence. WHY?
- Slow absorbance.
Distributed in blood stream and metabolised by plasma esterase.
Snorting or smoking has an fast, direct route to the brain.
- Crack cocaine (freebasing) -> rapid, intense high & ↑↑↑ risk addiction. WHY?
- 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.
- MEDICAL CONSEQUENCES OF COCAINE ABUSE:
- 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
8) BACTERIAL or VIRAL ENDOCARDITIS, HEPATITIS & AIDS.
- combination of ETOH & cocaine gives ______ which toxic effects can be greater
- EtOH can cause PARADOXICAL EXCITEMENT. WHAT IS THE PARADOX?
- 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.
- MECHANISMS OF ACTION of EtOh
- 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
- NALTREXONE (Trexan)
- Opioid antagonist that is approved for tx alcoholism. It ↓s the “high”, the craving, & the number of relapses.
- μ significance in alcoholism
- 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
- Medical consequences of EtOH Abuse
- 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)
8. FETAL ALCOHOL SYNDROME (FAS)
9. WERNICKE-KORSAKOFF SYNDROME
10. NIACIN ENCEPHALOPATHY (PELLAGRA) – niacin deficiency. Chronic wasting (4Ds)-> Dementia (confusion, Disorientation, hallucinations, memory loss, psychoses), Dermatitis & Diarrhea.
- Mechanism of alcoholic cirrhosis
- 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.
- What is fetal alcohol syndrome. How does EtOH or its metabolite ACETALDEHYDE result in FAS(theories):
- 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.
- WERNICKE'S ENCEPHALOPATHY is characterized by:
What is the treatment?
- a) Mental Sx: drowsy, inattentive, indifference, disoriented
b) Ocular Sx: abducens palsy, diplopia, strabismus, nystagmus
TX: Give Thiamine (B1)
- Korsakoff's psychosis
- Damage to mamillary bodies of posterior hypothalamus -> short-term memory loss.
- Niacin Encephalopathy (Pellagra)
- niacin deficiency--wasting -> dementia (confusion, disorientation, hallucinations, memory loss, psychoses), dermatitis & diarrhea.
- Rx treatment of alcoholism
- Naltrexone (MOA)
- opioid antagonist
- Acamprosate (MOA)
- restores balance between GABA & glutamate
- inhibits aldehyde dehydrogenase leading to an increase in acetaldehyde which results in nausea, vomiting, flushing, tachacardia upon ingestion of alcohol
- cheapest and least potent form of MJ. Low resin. From the tops of UNCULTIVATED plants. Most MJ grown in US is this type.
- Flowering tops & leaves of CULTIVATED plants. Higher quality and quantity of resin
- Hashish. Highest grade. Made from RESIN ITSELF obtained from tops of mature plants.
- 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.
- MARIJUANA IS NOT A HALLUCINOGEN b/c:
- 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.
- How bad is MJ?
- 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.
- Gateway hypothesis
- Use of MJ or EtoH early in life will use harder drugs later in life.
- Greatest risk of MJ
- LUNG DAMAGE--Inhale deeper & hold longer. Increase risk of bronchitis, emphysema, & lung cancer.
- Dronabinol (Marinol)
- FDA approved form of THC. Uses:
2) treat anorexia (CB1 agonist)
- CB1 antagonist in phase III clinical trials for weight loss
- WHAT IS THE LAY TERM FOR AMPHETAMINES?
- MA-HUANG - ACTIVE INGREDIENT:
- KHAT (cathinone)
- -Amphetamine-like substance popular in the Middle East & Africa
- METHYLPHENIDATE (Ritalin)
- structurally similar to amphetamine with similar properties. Used for ADD/ADHD.
CII- CONTROLLED SUBSTANCE
- DEXMETHYLPHENIDATE (Focalin)
- d isomer of methylphenidate
CII- CONTROLLED SUBSTANCE
- DEXTROAMPHETAMINE (Dexedrine)
- a mixture of amphetamine & dextroamphetamine salts. used for ADD/ADHD Longer acting than methylphenidate. Provides more steady control.
CII- CONTROLLED SUBSTANCE
- Methamphetamine (Desoxyn)
- Mechanism of amphetamines & other stimulants (analeptics)
- 1) increase NE & dopamine release
2) block NE/Dopamine uptake
3) stumulate NE/DA receptors
4) (amphetamines) Inhibit MAO A/B
- Feeling of Amphetamines & stimulants
- increase wakefulness & alertness, decrease sense of fatigue, increase intitiative,self-confidence & ability to concentrate. The elevate mood and cause elation & euphoria.
- What NTs are responsible for alertness?
- amphetamine psychosis
- results from high doses of amphetamines and increase DA/5HT release in mesolimbic pathway.
- Fatality of amphetemines.
- During same time period:
24 deaths w/Adderal
16 w/ Ritalin
10 w/ other amphetamines
- Legitimate medical uses of amphetamines
MOA & problems
- MOA: increase DA/5HT release in lateral hypothalamus
Problem: not permamnent
- Non Amphetamine anorexiants
2) benzphetamine (didrex)CIV
3 phendimetrazine(bondril PDM)CIII
5)Sibutramine (Meridia) CIV
CV complications & CNS stimulants subject to abuse
- Orlistat (Xenical)
- non-controlled substance alternative
MOA: inhibits lipases w/in GI tract therefor inhibiting conversion of dietary triglycerides into absorbable free fatty acids
- 2-5% elementry school children
3-6X more commmon in boys
- Atomoxetine (strattera)
- 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.
- Narcolepsy (hypersomnia)
- excessive daytime sleepiness & SLEEP ATTACKS brought on by strong emotional events
can be accompanied by cataplexy
- cataplexy -
what is it and what is tx
- -extreme muscle weakness or collapse while awake
-TX: Na+ oxybate (Xrem) --(GHP--CAUTION date rape drug)
- Modafinil (Provigil)
- Tx for narcolepsy
Actis by activating HYPOCRETIN/OREXIN PATHWAYS
A CIV controlled substance that can still have CV effects.
- Medical consequences of CNS stimulant abuse;
- 1) Depletion of NE/DA (possibly 5HT)
2)CVA (secondary to increase BP)
5) amphetamine psychosis
- Why is psychosis more prevalent with amphetamines than cocaine
- cocaine is short acting because of plasma esterases.
- common psychosis in amphetamine toxicity
- paranoias delusions
- Hallucinogenic properties are from stimulating _______ receptors in _______ brain areas.
- 5-HT2A /cortical & limbic
- structurally similar to 5HT e.g. LSD
- 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).
- Psilcybin & Psilocin
- naturally found indolealkyamines in MUSHROOMS
- One of the two hallucinogen classes (the other is indolealkylamines)
1) Mescaline-peyote cactus
- MDMA (methylenedioxymethamphetamine)
aka ECSTACY &
MDA (methylenedioxyamphetamine) aka EVE
- Designer amphetamines
synthetic compounds structurally similar to mescaline & amphetamine
- DOM (dimethoxymethylamphetamine)
aka STP (serenity, tranquility, peaca)
- Physiological effects:
mydriasis, hyperreflexia, increase BP & temp, tachycardia, & tremors, restlessness, anxiety, decreased appetite, dry mouth, insomnia
- Brain damage, chromosome abnormalities or teratogenic effects due to indole-like halucinogens or phenylethylamine mescalinr
- doesn't look like it
- MDMA danger
- degeneration of 5HT nerve terminals and long term depletion of 5HT
- PCP (phencyclidine) Phenyl-Cyclohexyl-Piperidine
- angel dust
- PCP what is it?
- 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.
- PCP mechanism
- 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
- PCP effects
- 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
- PCP causes:
- overwhelming sensory input leading to unpredictable , exaggerated, distorted & sometimes violent reaction to eviornmental stimuli.
Can lead to severe anxiety, panic, rage & aggression.
- Opisthotonos & siezures
- can result from PCP
- Tx for PCP
- put in a quiet envirnment
haloperidol (haldol) is often used
- ANTICHOLINERGIC ACTIVITY
- PCP has high anticholinergic activity so avoid neuroleptics w/ high anticholinergc activity
- breakdown of mm fibers from inside out. PCP causes these direct effects on skeletal mm. violent behavor can cause severe mm damage.
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