Exam I: Psychopharm & Research Methods Flashcards

1
Q

Methods of Agonistic and Antagonistic Drug Effects

A

(1) Effects on Production of Neurotransmitter-lrvel of nucleus
Agonistic (Step 1): Drug serves as Precursor–more ingredients, more opportunity
Antagonistic (Step 2): Drug inactivates Synthetic Enzyme

(2) Effects on Storage and Release of Neurotransmitter-
Antagonistic (Step 3): Drug prevents Vesicle Storage-problem getting cake in box
Agonistic (Step 4): Drug stimulates NT release on Proteins
Antagonistic (Step 5): Drug prevents NT release on Proteins

(3) Effects on Receptors
Agonistic (Step 6): Drug mimics effect of NT (Direct Agonist)
Antagonistic (Step 7): Drug blocks receptor (Direct Antagonist)
• Competitive binding. Direct agonist and direct antagonist act directly on post-synaptic binding site (steps 6, 7)
• Noncompetitive binding. Indirect agonist and indirect antagonist act indirectly on post-synaptic binding site.
Antagonistic (Step 8): Drug stimulates autoreceptors: inhibits synthesis/release
Normal situations, autoreceptors
Agonistic (Step 9): Drug blocks autoreceptors: increase synthesis/release

(4) Effects on Reuptake or Destruction of Neurotransmitter-after axion
Agonistic (Step 10): Drug blocks reuptake
Agonistic (Step 11): Drug inactivates acetylcholinesterase

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2
Q

(1) Effects on Production of Neurotransmitter-lrvel of nucleus

A

Agonistic (Step 1): Drug serves as Precursor–more ingredients, more opportunity
Antagonistic (Step 2): Drug inactivates Synthetic Enzyme

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3
Q

(2) Effects on Storage and Release of Neurotransmitter-

A

Antagonistic (Step 3): Drug prevents Vesicle Storage-problem getting cake in box
Agonistic (Step 4): Drug stimulates NT release on Proteins
Antagonistic (Step 5): Drug prevents NT release on Proteins

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4
Q

(3) Effects on Receptors

A

Agonistic (Step 6): Drug mimics effect of NT (Direct Agonist)
Antagonistic (Step 7): Drug blocks receptor (Direct Antagonist)
• Competitive binding. Direct agonist and direct antagonist act directly on post-synaptic binding site (steps 6, 7)
• Noncompetitive binding. Indirect agonist and indirect antagonist act indirectly on post-synaptic binding site.
Antagonistic (Step 8): Drug stimulates autoreceptors: inhibits synthesis/release
Normal situations, autoreceptors
Agonistic (Step 9): Drug blocks autoreceptors: increase synthesis/release

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5
Q

(4) Effects on Reuptake or Destruction of Neurotransmitter-after axion

A

Agonistic (Step 10): Drug blocks reuptake

Agonistic (Step 11): Drug inactivates acetylcholinesterase

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6
Q

Factors that impact rate at which drug reaches sites of action within the brain:

A

(1) Lipid (Fat) solubiliity: Blood-brain barrier in effect for water-soluble molecules only; Fat-soluble molecules may pass through capillaries into CNS
> For instance: heroin > fat-soluble than morphine; IV injection produces greater effect as function of rate of action
> Opiods, narcotics
> Therapeutic effects in small doses, assist in pain releif

(2) Extent of depot binding
> More drug on albumin, more powerful the effect

(3) Inactivation and Excretion
> Keep your eye on metabolism and excretion
– Especially in aging population who have been on same prescription for a long time because ineffective excretion

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7
Q

Psychopharmacology

A

The study of the effects of drugs on the nervous system and on behavior.

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8
Q

Drug effect

A

The changes a drug produces in an animal’s physiological processes and behavior.

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9
Q

Sites of action

A

The locations at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells.

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10
Q

Pharmacokinetics

A

The process by which drugs are absorbed, distributed within the body, metabolized, and excreted.

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11
Q

intravenous (IV) injection

A

Injection of a substance directly into a vein.

Different trajectory,

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12
Q

intraperitoneal (IP) injection, into gut

A

Injection of a substance into the peritoneal cavity – the space that surrounds the stomach, intestines, liver, and other abdominal organs.

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13
Q

intramuscular (IM) injection

A

Injection of a substance into a muscle.

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14
Q

subcutaneous (SC) injection

A

Injection of a substance into the space beneath the skin.

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15
Q

oral administration

A

requires more the drug
– Administration of a substance into the mouth, so that is swallowed. A drug is most effective for oral administration when drug molecules are:
• Small in size, Weakly acidic, Water & fat soluble, Potent in small amounts, and not easily degraded

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16
Q

sublingual administration

A

Administration of a substance by placing it beneath the tongue.

17
Q

intrarectal administration

A

– Administration of a substance into the rectum.

18
Q

inhalation

A

Administration of a vaporous substance into the lungs.

19
Q

topical administration

A

– Administration of a substance directly onto the skin or mucous membrane.

20
Q

intracerebral administration

A

—requires very little amount of the drug

–Administration of a substance directly into the brain.

21
Q

intracerebroventricular (ICV) administration

A

– Administration of a substance into one of the cerebral ventricles.

22
Q

depot binding

A

– Binding of a drug with various tissues of the body or with proteins in the blood (e.g., albumin).
– Free ride into brain, importance of being fat soluble

23
Q

albumin

A

A protein found in the blood; serves to transport free fatty acids and can bind with some lipid-soluble drugs.

24
Q

dose-response curve

A

A graph of the magnitude of an effect of a drug as a function of the amount of drug administration.

25
Q

therapeutic index

A

The ratio between the dose that produces the desired effect in 50 % of the animals and the dose that produces toxic effects in 50 % of the animals. *alcohol changes the safety v danger rates

26
Q

affinity

A

The readiness with which two molecules join together.

27
Q

tolerance

A

A decrease in the effectiveness of a drug that is administered repeatedly.

28
Q

withdrawal symptom

A

The appearance of symptoms opposite to those produced by a drug when the drug is administered repeatedly and then suddenly no longer taken. Delirium tremens, seizures, etc.

29
Q

sensitization

A

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

30
Q

Placebo

A

(p for positive)
(double-blind random control trial placebo
– An inert—technically inactive—substance that is given to an organism in lieu of a physiologically active drug; used experimentally to control for the effects of mere administration of a drug.
– Expectancy effects

31
Q

nocebo

A

When the “placebo effect” has a negative effect

n for negative

32
Q

Drug

A

“An exogenous (born from without) chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body (neurons) when taken in relatively low doses” (Carlson, 2007, p. 103).

33
Q

MRI v CT:

MRI Advantages

A
Greater Imaging Ability
Greater resolution
Detect smaller objects
Distinguish white/gray matter
3 Planes: Coronal, Axial, Sagittal
No Distortion from Bone
Display posterior fossa, pituitary, optic nerves, spinal cord
Does not utilize Ionizing Radiation
Applied to Intra- and Extra-cranial arteries
Identify White Matter Plaques
MS
PML
AVM
Mesial-temporal sclerosis
MRA-surrounding arteries, find aneurysms
34
Q

MRI v CT:

MRI Disadvantages

A

Expense: MRI Costs 2-3 times more than CT
Duration: 40 minutes instead of Pacemaker
> Aneurysm clips
> Cochlear implant

35
Q

Parkinson’s & TRAP

A

Parkinson’s disease is a movement disorder that results from degradation of cell bodies and dopaminergic neurons within the substantia nigra (component of basal ganglia)

Symptoms/Signs:
Tremor (characteristically resting)
o different than action, essential, born out of degradation
o Upper extremity, starts and moves down same side

•Rigidity (diminished fluid motion of limbs, ‘cog-wheel’)

•Akinesia/Bradykinesia (psychomotor slowing)
o Absence of movement or slow movement
o Slow thinking also

•Postural Instability
o Fall risk
o Natural reflex might break down