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Psychopharmacology 552 > Exam 1 - Psychopharmacology > Flashcards

Exam 1 - Psychopharmacology Flashcards

1
Q

The use of psychotropic medications in the treatment of psychiatric disorders.

A

Psychopharmacology

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2
Q

Study of what the body does to drugs (i.e. absorption, distribution, metabolism and excretion)

A

Pharmacokinetics

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3
Q

Process by which the drug is metabolized by the cytochrome P450 enzymes (CYP 450) in the intestines and liver prior to going into the systemic circulation.

A

First pass metabolism:

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4
Q

Increase serum levels of other drugs that are substrates of that enzyme= cause toxic levels(SLOW METABOLISM)

e.g. Bupropion, Clomipramine, SSRIs, Ketoconazole, Grapefruit juice, Clarithromycin

A

Enzyme Inhibitors:

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5
Q

Decrease serum levels of other drugs that are substrates of that enzyme= can cause subtherapeutic drug levels (FAST METABOLISM).
e.g. Carbamazepine, St. John’s Wort, Tobacco, Phenobarbital, Phenytoin

A

Enzyme Inducers:

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6
Q

Study of what the drugs do to the body (i.e. target sites for drugs- receptors, ion channels, enzymes(MAOIs) and carrier proteins/reuptake pumps)

A

Pharmacodynamics:

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7
Q

Drug binds to receptors and activates a biological response

A

Agonist effect:

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8
Q

Drug causes the opposite effect of agonist

A

Inverse agonist effect:

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9
Q

Drug does not fully activate the receptors

A

Partial agonist effect:

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10
Q

Drug binds to the receptor but does not activate a biological response.

A

Antagonist effect:

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11
Q

Excitatory response:
Depolarization= The opening of Na+ and Ca+ channels so these ions go into the cell

A

-

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12
Q

Inhibitory response: Repolarization= The opening of Cl- channels so that Cl- goes into the cell, K+ leaves or both

A

-

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13
Q
A
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14
Q
A
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15
Q

-Nonmedicinal substances
-High abuse potential
-Not legally available by prescription

e.g. Heroin, Marijuana

A

Schedule 1

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16
Q

Medicinal drugs
High potential for abuse and dependency
Written prescription only
No telephone orders
No refills

e.g. Morphine sulfate, Methadone, Fentanyl, Oxycodone, Dilaudid

A

Schedule 2

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17
Q

-Medicinal drugs
Abuse potential
Refills limited to 5

e.g. testosterone, suboxone, appetite suppressants

A

Scheule 3

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18
Q

Medicinal drugs
Lesser abuse potential

e.g. Xanax, Librium, Klonopin, Ativan, Restoril,

A

Schedule 4

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19
Q

-Medicinal drugs
-Lowest abuse potential
-Handles like noncontrolled drugs

e.g. Lomotil

A

Schedule 5

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20
Q

___: Controlled studies show no risk
___: No evidence of risk in humans
___: Risk cannot be rule out
___: Positive evidence of risk
___: Absolutely contraindicated in pregnancy

A, B, C, D, X

A

A: Controlled studies show no risk

B: No evidence of risk in humans

C: Risk cannot be rule out

D: Positive evidence of risk

X: Absolutely contraindicated in pregnancy

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21
Q

Teratogenic risks common with psychiatric medications:

Benzodiazepines: Floppy baby syndrome, cleft palate

Carbamazepine (Tegretol): Neural tube defects

Lithium(Eskalith): Epstein anomaly

Divalproex sodium (Depakote): Neural tube deficits- specifically spina bifida, atrial septal defects, cleft palate and possible long-term developmental deficits

A
22
Q

Locus Cerelus: Key center of NE production

Ralphe Nuclei: Key center for 5HT production

A

-

23
Q

Key center of NE production

A

Locus Cerelus:

24
Q

Key center for 5HT production

A

Ralphe Nuclei:

25
Q

Essential for maintaining homeostasis; controls basic needs (eating, drinking, temperature regulation, sleep-wake cycles

Impairment:

Disturbed sleep, eating, changes in body temperature, emotional instability.

A

Hypothalamus

26
Q

Relay station for sensory information,

Impairment:

Sensory processing issues

A

Thalamus

27
Q

Memory, converting STM to LTM, learning

Impairment:

Impaired memory and attention

A

Hippocampus

28
Q

Regulates powerful emotions (fear, rage, sexual desires”

Impairment:

Irritability, anger, aggression

A

Amygdala

29
Q

Serotonin (5HT) “Calming NT)

Derived from Tryptophan

Made in the Ralphe Nuclei

Precursor of melatonin

Affects sleep, mood and behavior

7- 5HT receptor families w/ 15+ subfamilies

NOTE: 90% of serotonin in found in the GI tract

A

-

30
Q

Norepinephrine (NE)

Made in the Locus Cerulus

Key player in mediating the sympathetic nervous system (i.e. Fight or Flight)

Implicated in mood disorders, GAD, ADHD, PTSD etc.

Noradrenergic pathways

  • NE neurons innervates the amygdala and prefrontal cortex = areas important for anxiety and worry
A

-

31
Q

Dopamine (DA)

Produced in the Ventra Tegmental Area(Reward Pathway)

Associated with reward and pleasure

Involves 4 major pathways:

Mesolimbic Pathway

    • Associated with positive symptoms of schizophrenia (i.e. hallucinations, delusions etc)

Mesocortical Pathway

    • Associated with the negative symptoms of Schizophrenia (i.e. cognition, affect, apathy, behavior etc.)

Tuberoinfundibular Pathway

    • Note: Dopamine inhibits prolactin
      Therefore ↓DA= ↑ Prolactin

Nigrostriatal Pathway

    • Low levels of DA in this pathway produces increased motor movements
      e.g. EPS (Pseudo parkinsonism, Akathisia, dystonia & TD)
A

-

32
Q

Gamma-aminobutytric Acid (GABA) = “off”

Inhibitory at the postsynaptic neuron

Induces calmness and relaxation

Plays a role in anxiety disorders
e.g. Benzodiazepines & Barbiturates
GABA-a and GABA-b

A

-

33
Q

Glutamate = “on”

Excitatory at the
post-synaptic neuron

Pre-cursory of GABA

Involved in learning, memory, thought processing, sensory inputs.

A

-

34
Q

Acetylcholine (ACh)

Neurotransmitter of the parasympathetic autonomic nervous system and the sympathetic ganglia

Acts at the neuromuscular junctions

Involved in learning and memory (brain’s cholinergic neurons play a critical role in dementias)

A

-

35
Q

Antidepressants

Mood stabilizers

Antipsychotics

Anxiolytics

Psychostimulants

Benzodiazepines and Z-meds

Cognitive enhancers

Medications for
Substance-related and addictive disorders

A

Medication Classe

36
Q
  • Patient symptoms
  • Previous treatment responses by the patient or a family member to a particular med
  • Side effect profile
  • Comorbid(medical and psychiatric) conditions
  • Risk of suicide via overdose on the medication
  • Cost (newer meds may be prohibitively expensive)
A

Determinants of choice of medications

37
Q

Movement of drug from site of administration to the blood

A

Absorption

38
Q

Movement of drug from blood to rest of body

A

Distribution

39
Q

Breakdown of drug

A

Metabolism

40
Q

Removal of drug’s metabolic waste products from the body

A

Elimination

41
Q

Before the blood goes to the rest of the body from the GI tract, it passes through the liver

The liver is the major organ that breaks down drugs

Therefore, a certain amount of the drug will be inactivated or metabolized as it goes through the liver

Other routes may not be subject to this “first pass” effect (IV, IM, inhalation, subq)

A

First-Pass Metabolism

42
Q

CYP450

Inducer: leads to increased level of that enzyme

Inhibitor: leads to decreased level of that enzyme

Substrate: the enzyme works on the substrate to make the “product”

  • E.g. Venlafaxine is a substrate of CYP450 2D6 which converts it to desvenlafaxine
  • E.g. 1A2 can be induced by smoking: this means increased levels of 1A2, therefore any substrate of 1A2 will decrease in level
  • Major types affecting psych drugs: 1A2, 2D6, 3A4,
  • Many “newer” medications circumvent CYP450 issues
  • Genetic testing is often comprised largely of understanding the metabolism of this pathway for the individual
A

CYP450

43
Q

reduces the enzyme activity due to direct interaction with a drug=decreased metabolism of meds= increased Med levels

A

Inhibition

44
Q

increases the enzyme activity due to direct interaction with a drug =increased metabolism of meds= decreased Med level

A

Induction

45
Q

Major Inducers of CYP450

“COPS”

Carbamazepine (aut0inducer)
Oxcarbazepine
Phenytoin/phenobarbital
Smoking/St. John’s Wort

A

-

46
Q

Major Inhibitors of CYP450 Enzymes

“G-PACMAN”

Grapefruit
Protease Inhibitors
Antifungals
Cyclosporine/Cimetidine
Macrolides
Amiodarone (and dronederone)
Non-DHP CCBs (diltiazem & verapamil)

A

-

47
Q

What the drug does to the body

Drug-receptor interactions

Dose-response relationships

Potency and efficacy

Effects:

Side effects/Adverse effects

A

Pharmacodynamics

48
Q

Polypharmacy

  • Combining medications to improve therapeutic outcome
  • Also called “targeted drug combinations”
A

Drug Interactions

49
Q

Principles regarding drug interactions

Pharmacodynamic interactions: two drugs have the same or overlapping mechanism of action

Pharmacokinetic interactions: one drug affects the other’s absorption, distribution, metabolism, or excretion

Inadequate dosing: doses are too low because of side effects

Clinical evaluation and oversight: should be ongoing

A

-

50
Q

What is the Therapeutic Index?

A

Find and fill in data.

51
Q
A

Psychopharmacology 552 (7 decks)

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