Psycho Bio Exam 2 (Part2)

Front 1

Binding Affinity (or affinity)

Back 1

The degree of a chemical attraction between a ligand and a receptor
(can be high or low)

Front 2

Efficacy (or intrinsic activity)

Back 2

The ability of a bound ligand to ACTIVATE the receptor

(whether a drug is going to bind or not)

Front 3

Dose-response curve (DRC).

Wide vs Narrow therapeutic

ED & LD

Back 3

A graph of the relationship between drug doses and the effects.
-Wide therapeutic: More safe to take higher dose
-Narrow therapeutic: Small increase in dose can kill you
ED: EFFECTIVE DOSE
LD: LETHAL DOSE

Front 4

Metabolic Tolerance

Back 4

Organ systems become more effective at eliminating the drug

Front 5

Functional Tolerance

Back 5

Target tissue may show altered sensitivity to the drug by changing the number of receptors:
-Neurons DOWN REGULATE in response to agonist drug, making fewer recepetors available
-They UP-REGULATE in response to an antagonist

Front 6

Cross-tolerance

Back 6

tolerance to a drug becomes generalized to other drugs in its class

Front 7

How can a Drug alter the Presynaptic Neuron??

Back 7

Through:
-Transmitter Production
-Transmitter release (autoreceptors- more or less NT)
-Transmitter clearance (block re-uptake) & causes more NT out in synaptic gap

Front 8

How can a Drug alter the Postsynaptic Neuron??

Back 8

-Transmitter receptors (Block or Open)
-Effects on cellular processes (alters number of postmen. receptors & modulation of second messengers)

Front 9

Psychoactive Drugs: that can relieve symptoms of Antischzophrenics:

Back 9

(reduce synaptic activity by blocking receptors)

-Antipsychotic (neuroleptic) drugs: Selective antagonists of dopamine D2 receptors

-Atypical neuroleptics: Block serotonin receptors

Front 10

Psychoactive Drugs:
Antidepressant drugs: used to treat mood (affective) disorders

Back 10

(INCREASES synaptic transmission)
-MONOAMINE OXIDASE(MAO)-inhibitors prevents the breakdown of monoamines at the synapses -Accumulation of transmitters and prolonging their activity is a major feature of antidepressants.
-TRICYCLIC ANTIDEPRESSANTS: block reuptake of serotonin and norepinephrine (accumulates in synapse)(improves depression)
-SELECTIVE SEROTONIN REUPTAKE INHIBITORS(SSRIs): like Prozac or Celexa act specifically Blocks reuptake of transmitter at at serotonergic synapses.

Front 11

Psychoactive Drugs:
Anxiolytics

Back 11

-DEPRESSANTS: drugs that reduce nervous system activity (reduces excitability of neurons) (ex: alcohol & opium)
-BARBITURATES: early anxiolytic drug and sleep aid that acts as a depressant- Additive and easily overdosed
-BENZODIAZEPINE- acts as agonists on GABA(A) receptors and enhance inhibitory effects of GABA

Front 12

Psychoactive Drugs:
Opiates

Back 12

main ingredient: MORPHINE, an effective analegesic(or pain killer)
-Morphine and Heroin: both highly addictive

-Opiates(like morphine, heroin, & codeine) bind to OPIOD RECEPTORS in the brain, especially in the pariaqueductal gray.

-Endogenous Opioids-enkephalins, endorphins, & dynorphins: are peptides produced in brain, also additive

Front 13

Psychoactive Drugs: Alters consciousness
Nicotine

Back 13

from tobacco, acts as stimulant
-increases heart rate, blood pressure, digestive action, and alertness.
-Acts as an agonist on NICOTINIC ACh RECEPTORS on the ventral tegmental area(VTA)

Front 14

Psychoactive Drugs:
Alcohol

Back 14

-Effects are biphasic: Att first it acts as stimulant, but prolonged acts as depressant(inhibition of neural activity).
-Acts via agonist of GABA receptors
-Abuse damages nerve cells in many brain regions

FETAL ALCOHOL SYNDROME: Mother drinks while prego, causes damage to fetus; results in deformity, & stunted brain growth

Adults: Abuse affects frontal lobes, effects are reversible with abstinence

Bingeing may cause brain damage & reduce rate of neurogenesis

Front 15

Effects of chronic alcohol on brain:

Back 15

-Alcohol-related dementia
-Wernicke-Korsakoff syndrome (not direct effect)
confusion, disorientation, coordination, & movement problems. -Retrograde & anterograde amnesia. -confabulations
-Cardiovascular problems
-Liver damage: Fatty liver, alcoholic hepatitis, cirrhosis

Front 16

Psychoactive Drugs:
Marijuana

Back 16

main ingredient; delta-9-tetrahydrocannabinol (THC)
-Effects vary: include relaxation, mood alteration, stimulation, hallucination, & paranoia
-Brain contains specific cannabinoid receptors to mediate the effects of THC
-ENDOCANNABINOIDS-analogs of marijuana produced in the brain, such as ANANDAMIDE(which can produce hunger, poor memory, & reduced sensitivity to pain)

Beneficial? -Studies on effects: relieving pain & lowering blood pressure
CANNABINOID RECEPTORS:-presynaptic membranes. Found in Hippocampus, Basal ganglia, Cerebellum, Frontal Cortex

Front 17

Stimulants: What?
& Two examples

Back 17

-Increases nervous system activity, By increasing excitatory synaptic potentials (alert, activating affect) OR decreasing inhibitory activity.

1.CAFFEINE- blocks presynaptic adenosine receptors, resulting in increased transmitter release and then increases brain activity.
2.COCAINE- blocks monoamine transmitter reuptake (dopamine), which causes monoamines to accumulate in synapses

Front 18

Synthetic stimulants:

Back 18

Made in Lab. Amphetamine or methamphetamine:
Superficially resembles cocaine: accumulation of the synaptic monoamine transmitters norepinephrine & dopamine.
2STEP ACTION:
1st: Work in axon terminals, causing larger-than-normal release of transmitter
2nd: Amphetamine then interferes with breakdown of the transmitter and the synapses become potent in their effects on behavior
-Prolonged ude leads to symptoms that resemble those of schizophrenia or brain damage

Front 19

Psychoactive Drugs:
Hallucinogens

Back 19

Alters sensory perception and produces unusual experiences, (either in absence of stimulation or distorts existing perceptions).

LSD(acid)- strongly activates serotonin receptors in the visual cortex
-mescaline & psilocybin are similar and all produce strong visual effects
MDMA(Ecstasy)- hallucinogenic amphetamine derivative. -stimulates visual cortical serotonin receptors

Front 20

Psychoactive Drugs:
Dissociative Drugs

Back 20

Different from hallucinogens:
Produces feelings of depersonalization and detachment from reality.
-PCP and Ketamine: Both are antagonists at NMDA-type glutamate receptors

Front 21

Substance-related Disorders:
(2)

Back 21

DEPENDENCE: (addiction) the desire to self administer a drug of abuse (physical need)

SUBSTANCE ABUSE: a pattern of use that does not fully meet the criteria for dependence. (not dependent on the drug, but take it anyway)

Front 22

Models of Drug Abuse
(4)

Back 22

1. The MORAL MODEL- blames the abuser for lack of moral character of lack of self-control

2.DISEASE MODEL- says the abuser requires medical treatment; however, an abnormal condition in abusers has not been identified

3.PHYSICAL DEPENDENCE MODEL-says abusers use drugs to avoid withdrawal symptoms like dysphoria (strong negative feelings that can only be relieved by the drug

4.POSITIVE REWARD MODEL- says drug use is a behavior controlled by positive rewards, with no disease

Front 23

Medications to treat drug abuse

Back 23

Agonists: partially activate the same pathways

Antagonists: block effects of the abused drug that may produce withdrawal

Reward-blocking medications: block positive reward effects

Anti-craving medications: reduce appetite

Immunization: prompts immune system to remove targeted drugs from circulation before reaching brain