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75 Cards in this Set

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Mechanism behind tolerance to
1) Opiods
2)Barbituates
1) down regulation of postsynaptic receptor

2)enzyme induction
T/ F
CA STATE LAW MANDATES THAT ADEQUATE ANALGESIA MUST BE PROVIDED.
T
COCAINE:
LOCAL ANESTHETIC MECHANISM:
BLOCK NA+ CHANNELS – neuron doesn’t fire
COCAINE:
VASOCONSTRICTOR MECHANISM:
BLOCKS NE UPTAKE stimulates alpha 1 receptors to vasoconstrict
COCAINE:
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
(behavioral)

8) BACTERIAL or VIRAL ENDOCARDITIS, HEPATITIS & AIDS.
combination of ETOH & cocaine gives ______ which toxic effects can be greater
cocaethalene
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)

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.
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

c) Ataxia

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
Acamprosate
Disulfiram
Naltrexone (MOA)
opioid antagonist
Acamprosate (MOA)
restores balance between GABA & glutamate
Disulfiram
inhibits aldehyde dehydrogenase leading to an increase in acetaldehyde which results in nausea, vomiting, flushing, tachacardia upon ingestion of alcohol
Bhang
cheapest and least potent form of MJ. Low resin. From the tops of UNCULTIVATED plants. Most MJ grown in US is this type.
Ganja
Flowering tops & leaves of CULTIVATED plants. Higher quality and quantity of resin
Charas
Hashish. Highest grade. Made from RESIN ITSELF obtained from tops of mature plants.
Anandamide
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:
1) antiemetic
2) treat anorexia (CB1 agonist)
Rimonabant
CB1 antagonist in phase III clinical trials for weight loss
WHAT IS THE LAY TERM FOR AMPHETAMINES?
speed
MA-HUANG - ACTIVE INGREDIENT:
ephedrine
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)

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

CII- CONTROLLED SUBSTANCE
Methamphetamine (Desoxyn)
Street name:
Smokable form:
Ice
Crystal Meth
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?
euphoria?
alertness-NE
euphoria-dopamine
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
1)anorexiant
2) ADD/ADHD
3)Narcolepsy
Anorexiants
MOA & problems
MOA: increase DA/5HT release in lateral hypothalamus
Problem: not permamnent
Non Amphetamine anorexiants

any danger?
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
Orlistat (Xenical)

MOA
non-controlled substance alternative

MOA: inhibits lipases w/in GI tract therefor inhibiting conversion of dietary triglycerides into absorbable free fatty acids
ADD/ADHD
2-5% elementry school children

3-6X more commmon in boys

Characterized by:
-inappropriate attention
-impulsivity
-hyperactivity
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)
3)CV effects
4) Hyperpyrexia
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
Indolealkylamines
structurally similar to 5HT e.g. LSD
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
PHENYLETHYLAMINES
One of the two hallucinogen classes (the other is indolealkylamines)
1) Mescaline-peyote cactus
2) MDMA
DOM
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

street name
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:
leads to:
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
RHABDOMYOLYSIS
breakdown of mm fibers from inside out. PCP causes these direct effects on skeletal mm. violent behavor can cause severe mm damage.