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Psychophysiology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

The two major aspects of drug influences

A

Drug effects (observable changes)

sites of action (binding sites)

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2
Q

Pharmacokinetics

A

What the body does to the drug

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3
Q

Endogenous vs exogenous

A

Endogenous: made in our body

Exogenous: produced outside our body

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4
Q

Pharmacokinetics vs pharmacodynamics

A

Pharmacokinetics: how drug moves through body

pharmacodynamics: biological response to drug

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5
Q

Four processes of pharmacokinetics

A

ADME

Absorption (how get in body)

Distribution (how moves trough body)

Metabolism (how is drug changed to an inactive form my enzymes)

Excretion (drug is excreted in urine by kidneys)

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6
Q
A

IV: fastest b/c it goes straight into your bloodstream

intraperitoneal: to your stomach (e.g., tubefeeding)

subcutaneous: into your fat

intracerebral: directly into your brain; bypass the blood-brain barrier; not really done in humans but on research animals

intracerebroventricular: straight into CSF
oral: one of the slowest ways; first pass metabolism (broken down in saliva, down to GI tract, etc); most common way for

psychotherapeutic drugs
sublingual: absorbing through capilaries below your tongue

intrarectal: bypassess “first pass” metabolism

inhalation: into your lungs

insufflation: absorbed by the mucous membrane in your nose (e.g.,
snorting cocaine)

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7
Q

Inhalation vs insufflation

A

inhalation: into your lungs - EX. weed

insufflation: absorbed by the mucous membrane in your nose (e.g.,
snorting cocaine)
- EX. cocaine

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8
Q

Blood flow

A

Entire volume of blood supply circulates every minute

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9
Q

Where do drugs exert their effects?

A

Sits of action

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10
Q

Most important factor in determining rate of absorbtion?

A

Lipid solubility – Lipid soluble materials pass through the most rapidly (pass through BBB)

heroin is more addictive b/c it has higher lipid solubility than morphine

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11
Q

Metabolism of drugs

A

most drugs are metabolized and deactivated by enzymes.

Enzymes sometimes transform molecules into more active versions
than the initial molecule. THIS INCREASES DURATION
- Ex. Prozac: body changes it to be more active, why takes two weeks to kick in (enzymatic activation)

LIVER: plays big role in enzymatic deactivation

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12
Q

Excretion of drugs

A

kidney is the primary organ of excretion

(GI, skin, lungs, and liver too)

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13
Q

Effictiveness of a drug is impacted by

A

sites of action

affinity at its site of action

Affinity: the capacity of a drug molecule to bind to a key site of action.

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14
Q

Affinity ratio for most desirable drug

A

Most desirable drug has high affinity for sites of action producing
therapeutic effects and low affinity for sites of action producing toxic side
effects

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15
Q

Dose Response Curve

A

Determines the point of maximum effect of a drug

After point of maximum effect of drug, increasing the dose does not produce a stronger effect

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16
Q

Margin of safety

A

The difference between therapeutic/desired effect of a drug and undesired effect

want the largest margin of safety

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17
Q

Therapeutic Index

A

A commonly used margin of safety

Two numbers obtained:
- Effective Dose 50 (ED50) = the dose that produces the desired effects in 50
percent of the individuals
- Toxic Dose 50 (TD50) = the dose that produces toxic effects in 50 percent of the individuals

Want ratio of TD/ED to be bigger than 10

Ex.

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18
Q

Low TI

A

ex. Lithium, Clozapine, Tricyclic antidepressants

have to get blood tested often

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19
Q

Neurotransmitter vs neuromodulator

A

Neurotransmitter: a chemical used for a neuron-to-neuron communication

Neuromodulator: a chemical that affects the neurotransmission of a whole group of neurons

GROUP VS INDIVIDUAL

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20
Q

Termination of a neurotransmitters

A

Through reuptake or enzymatic deactivation/degradation

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21
Q

Ligands

A

Neuromodulators that bind to a complementary receptor site

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22
Q

Agonists vs antagonists

A

Agonist a molecule that by binding to the receptor stimulates a
response = ↑ postsynaptic effects

Antagonists a molecule that by binding to a receptor blocks or
inhibits the response = ↓ postsynaptic effects

23
Q

Is a drug that blocks the re-uptake or enzymatic degradation of a
neurotransmitter an antagonist or agonist?

A

Agonist! because re-upatake is blocked, the neurotransmitters are jsut hanging in the cleft, still sending signals

24
Q

If the activation of a receptor causes vasoconstriction, what would happen if someone took an antagonist for that receptor?

A

Decreases vasoconstriction

25
Q

Direct vs indirect

A

Indirect: attatched to alternative binding site

Direct: attaches to direct binding site

26
Q

Neuromodulators are associated with… (direct or indirect)

A

Indirect

(b/c they bind to an alternative sites)

27
Q

Amino acid neurotransmitters in the brain

A

Glutamate - excitatory

GABA - inhibitory

28
Q

Amino acid neurotransmitters in the spinal chord and brain stem

A

Glutamate - excitatory

Glycine - inhibitory

29
Q

4 main glutamate receptors

A

NMDA, AMPA, Kainate, Metabotropic Glutamate

30
Q

NMDA Receptor

A

Receptor for glutamate!

Has 6 binding sites

Requirements for glutamate to bond:
- glycine must be attatched
- Mg must not be attatched (need it to be depolarized)

When channel opens, Na and Ca –> cell depolarizes

Ca is the secondary messenger

Alteration of the synapse (synaptic plasticity) =
building block of a newly formed memory

31
Q

Acetylcholine

A

PNS: central role in muscle contraction

CNS: Found in specific locations and pathways in CNS. Key role in REM sleep, perceptual learning, and memory.

32
Q

Facts about monoamines

A

Neuromodulators derived from a single amino acid.

Produced by several systems of neurons in the brain; mainly brainstem with widespread distribution around brain.

Mediate a variety of CNS fxns (e.g.,motor control, cognition, emotion, memory processing, and endocrine modulation)

33
Q

Three classes of monoamines and their chemicals (examples)

A

Catecholamines: dopamine, norepinephrine/noradrenalin, epinephrine/adrenalin

Indolamine: serotonin

Ethylamine: histamine

34
Q

Synthesis of catecholamines

A

Tyrosine -> L-dopa -> dopamine -> norepinephrine

35
Q

Precursors

A

Substances that can be chemically altered to become neurotransmitters

36
Q

What is the primary effect of dopamine?

A

movement, attention, learning, and reinforcing effects of substances

37
Q

What is the primary effect of norepinephrin?

A

Primary effect = vigilance/attentiveness

PNS: ANS regulation (heart rate, etc.)

(Dopamine in vesicles is converted to norepinephrine by a special enzyme)

38
Q

Locus Coeruleus (nucleus in the pons)

A

Where most noradrenergic systems begin

noradrenergic: involved in the body’s “fight or flight” response

39
Q

What are the primary effects of serotonin?

A

CNS: mood and pain regulation
control of eating, sleeping, arousal, and dreaming

PNS: involved in digestive tract

Precursor = Tryptophan

40
Q

What are the precursors of dopamine, norepinephrine, and serotonin?

A

Dopamine: tyrosine
Norepinephrine: dopamine
Serotonin: tryptophan

41
Q

Are dopamine, serotonin, and norepinephrine excitatory or inhibitory?

A

dopamine: excitatory and inhibitory

serotonine: inhibitory

norepinephrine: excitatory

42
Q

What are surplus and deficit effects of dopamine?

A

Surplus: Sz, substance addiction

Deficit: Parkinson’s, anxiety, memory, challenges, ADHD

43
Q

What are the surplus and deficit effects of serotonin?

A

Surplus: autism, mania

Deficit: depression and other mood d/os

44
Q

What are the surplus and deficit effects of Norepinephrine?

A

Surplus: anxiety

Deficit: several psychiatric conditions

45
Q

Primary effects of histamine

A

CNS: wakefulness

PNS: immunse response

46
Q

Primary effects of opiods

A

CNS: reinforcement, pain modulation

PNS: pain modulation

47
Q

Primary effects of Endocannabinoids

A

CNS: appetitie regulation

PNS: immune response

48
Q

Tolerance

A

A decrease in the effectiveness of a drug that is administered repeatedly. It is the body’s attempt to maintain homeostasis.

49
Q

Sensitization

A

An increase in the effectiveness of a drug as it is administered repeatedly.

(becasue your reward system gets so excited, the anticipation is so exicting and great)

50
Q

Pharmacokinetic tolerance

A

body breaks down drug preventing it from reaching
receptors.

51
Q

Pharmacodynamic tolerance

A

Decrease in receptor affinity for drug.

Damaged receptors

Receptor down-regulation (decrease in receptor)

52
Q

Dependence

A

The physical or psychological symptoms that occur that make someone feel like they must continue taking a substance; lack of substance results in withdrawal

53
Q

Placebo

A

an inactive/inert substance given as a control in substance
experiments.

Responses can be the result of motivation, expectation, classical conditioning

Viewing injection of placebo = ↓ post-operative pain

Informing participants, a placebo is a stimulant = ↑ HR and BP

Psychophysiology (13 decks)

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