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Psychopharmacology Test 3 > Psychopharm Test 1 - Intro/Mood/MDD/Bipolar > Flashcards

Psychopharm Test 1 - Intro/Mood/MDD/Bipolar Flashcards

1
Q

Classic Neurotransmission aka Anterograde

A

The stimulation of presynaptic neuron causes electrical impulses to be sent to the axon terminal. The electrical impulses are converted to chemical messengers & then stimulate the post synaptic neuron

** Communication between neurons is chemical (L to R; presynpatic to postsynaptic)

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2
Q

Retrograde Transmission

A

post synaptic neuron communicates with the presynaptic neuron. From R to Left.

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3
Q

Volume Transmission

A

occurs without a synpase at all - diffusion transmission
Ex. In prefrontal cortex - not a lot of dopamine reuptake pumps so dopamine will diffuse away to other dopamine receptors throughout the brain and stimulate them.

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4
Q

What are the 6 key neurotransmitters targeted by psychotropic drugs?

A

Serotonin
Norepinephrine
GABA
Dopamine
Glutamate
Acetylcholine

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5
Q

How are neurotransmitters recycled?

A

Via Transporters
Ex. SERT - reuptake of serotonin
DAT - reuptake of dopamine
NET - reuptake of NE

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6
Q

What are the 5 transduction cascades?

A
  1. Transmembrane
  2. G Protein Linked
  3. Enzymes
  4. Voltage Gated Ion Channels
  5. Ligand Gated
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7
Q

What psychotropic durgs use 12 transmembrane transporters?

A

SSRI/SNRI/DNRI

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8
Q

What psychotropic drugs use G protein linked transduction?

A

D2, 5HT2A, 5HT2C, 5HT1A, 5HT7
** 30% of meds we use like the D2 receptors

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9
Q

What psychotropic drugs target enzymes?

A

MAOI’s (mostly used in major depressive disorder)

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10
Q

What psychotropic drugs target Ligand Gated Channels?

A

5HT3 (benzos), NMDA, GABA-A neurosteroid sites

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11
Q

What psychotropic drugs target Voltage Gated ion channels

A

Anticonvulsants and Mood Stabilizers

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12
Q

Which two conduction cascades use the Agonist spectrum?

A

G protein linked and Ligand Gated (** all the receptor sites ones)

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13
Q

How do neurons adapt to medications?

A

Via upregulation/downregulaton & sensitizaton/desensitization

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14
Q

Upregulation

A

A mechanism for the increased or decreased sensitivity to agonists and antagonist drugs suggests that decreased exposure to an agonist results in an increase in the number of receptors (upregulation).
Ex. if you give somone a antagonist (receptor blocker) the receptors sense there is a decrease in the # of receptors and upregulated/make more receptors available. At the same time the receptors now become more sensitive, so there is sensization

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15
Q

Downregulation

A

Increased exposure to an agonist can result in a decrease in the number of receptors (downregulation). Body senses the receptors are stimulated too much decreases the number of receptors available. The overstimulation results in desensitization is as why you may need to increase a dose of medication

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16
Q

Epigenetic’s and gene expression

A

neurotransmission, drugs, and the ENVIRONMENT we are exposed to determined if certain genes in our body are expressed or silenced.
*Depending on what happens in a persons life (i.e sex abuse, trauma, dietary deficiencies, drugs etc) genes can change and be silenced or activated (in good an bad ways - like substance abuse, or coping mechanisms).

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17
Q

Full Agonist

A

Bind to receptor site and act just like the endogenous agonist made in the body that would normally bind to it. It produces the full response at the receptor site

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18
Q

Partial Agonist

A

binds to the receptor site that the endogenous agonist would normally bind to, but only generates a fraction of the response that the actual endogenous agonist would generate

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19
Q

Inverse agonist

A

binds to the same site as the endogenous agonist, but instead of agonizing it produces the opposite effect & causes a decrease in signaling at the receptor site

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20
Q

Antagonist

A

will bind to the receptor site, but not activate the receptor; instead it prevents/competes for the site and limits the amount of agonists that can bind to the site

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21
Q

Allosteric Modulators

A

bind to a different site than the endogenous agonist, but by binding to a different receptor site they alter the ability of the receptor to bind with it’s agonist. This can cause an increase or decrease in the ability of an agonist to bind to the receptor, or reduce the affects an agonist has when it does bind. Sometimes when allosteric modulators bind to a different site they can also activate the receptor on its own.

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22
Q

Pharmacokinetics

A

science of how drugs are absorbed distributed to tissues in the body and eliminated.
**Metabolism of CYP450 enzymes

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23
Q

Pharmacodynamics

A

How the drug that is metabolized/absorbed works in the body. (Mechanism of action of drug)
Ex. Agonists, Antagonists etc.

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24
Q

Therapeutic Index

A

area between a drugs lethal dose and effective dose. The wider the distance is the safer the drug tends to be.

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25
Q

Direct Agonists

A

directly bind to and activate receptor sites

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26
Q

Indirect Agonists

A

work to increase the # of neurotransmitters synthesized/released
OR
inhibit reuptake

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27
Q

What do MAOInhibitors do?

A

prevent the breakdown of neurotransmitters (dopamine, serotonin, NE)

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28
Q

What are the two types of allosteric modulators

A

postive allosteric modulators - boost what the neurotransmitter does
negative allosteric modulators - blocks what the neurotransmitter does

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29
Q

Monoamine Hypothesis of Depression

A

depression is due to a deficiency in the neurotransmitters: dopamine, norepinephrine, serotonin
1. s/t monoamine neural degeneration in hippocampus/frontral cortex does not allow for appropriate production of neurotransmitters
2.s/t inhibition of the auto receptors bec pts with major depression may have an increased # of autoreceptors

30
Q

How do antidepressants work for MDD

A

Downregulates autoreceptors, but it takes time for this to occur bc you are going to increase the amount of neurotransmitter (serotonin, NE, DA etc) which in turn will increase the autoreceptors, but as you keep giving the medication and stimulating the sites, autoreceptors become tired and downregulate and desensitize, thus allowing more serotonin, NE, DA, to stay in the cleft.

31
Q

What brain circuits are malfunctioning in MDD?

A

Prefrontal Cortex -
Nucleus Accumbens - decreased interest; low motivation
Striatum - psychmotor fatigue
Hypothalamus - sleep/appetite changes
Cerebellum - psychomotor effects (slow thinking/slow body mvmts)

32
Q

What medications are used to treat MDD?

A

Tricyclic Antidepressants
MAOIs
SSRI/SNRIs
NDRI/SARI

33
Q

How do Tricyclic Antidepressants work?

A

Binds to NET and SERT (the NE and serotonin reuptake transporters), thus blocking normal reuptake and increasing the length that NE and serotonin are in the synaptic cleft.

**DOWNREGULATION of presynaptic autoreceptors = upregulation in BNDF synthesis

34
Q

Examples of Tricyclic Antidepressants

A

Amiltriptyline
Clopipramine
Despiramine
Doxepin
Imipramine
Nortriptyline
Protriptyline
Trimipramine

35
Q

Mechanism of Action of Tricyclic antidepressants

A

Blocks NET & SERT
antagonist 5HT2A, 5HT2C
antagonists: H1 receptors, alpha-1 adrenergic receptors, and muscarinic cholinergic receptors
Block voltage-sensitive Na+ channels

36
Q

Side effects of Tricyclic Antidepressants:

A

Blockade—H-1 receptor— sedation, weight gain,
Blockade— Muscarinic cholinergic receptor—anticholinergic actions (dry mouth, blurred vision, urinary retention, constipation)
Blockade— Alpha-1 receptor— orthostatic hypotension, dizziness

weakly block voltage-sensitive sodium channels in heart and brain at therapeutic doses; in over-dose, cause of coma/SZ d/t CNS actions, cardiac arrhythmias, cardiac arrest, death d/t peripheral cardiac actions

37
Q

What substrate does Amiltryptiline block

A

2C9 (breaks down warfarin)

38
Q

What substrate does Clopipramine, Desipramine, Nortriptyline, & Protriptyline block

A

2D6

39
Q

What substrate does Imipramine effect?

A

1A2 & 2C19

40
Q

What substrate does Doxepine work on

A

2C9 & 2C19
Inhibitor of 2D6

41
Q

What does Monamine Oxidase do and why are inhibitors important for the tx of depression

A

Monoamine oxidase removes neurotransmitters NE, DA & serotonin in the brain, so when you give an MAOI inhibitor it allows NE, DA, and serotonin to stay in the cleft longer and combats depression

MAOa removes amine group from NE, dopamine and serotonin

MAOb removes amine group from dopamine and phenethylamine; less specificity for NE, 5TH (only at high concentrations)

42
Q

Besides Depression what else can MAOI’s treat?

A

Panic disorder
Anxiety disorder
Social anxiety

43
Q

What is the lag time from initiation of an MAOI to therapeutic effects?

A

2 weeks.
Pts should take the medication for at least 6 months for maximal therapeutic benefits

44
Q

Examples of MAOIs

A

Isocarbazid
Phenelzine
Selegiline
Tranycypromine

45
Q

What do SSRIs do?

A

blocks the reuptake of serotonin thus leaving more serotonin available to engage with pre and post synaptic receptor sites for a longer duration of time

**5HT1A autoreceptor is believed to be overexpressed in MDD, resulting in excessive inhibition of serotonergic neurons in the rakhi nucleus, amygdala, hippocampus

46
Q

Besides MDD what else do SSRIs treat?

A

anxiety disorders, PTSD, PCD, PDD, ED

47
Q

Citalopram (Celexa)
(SSRI)
Inhibitor: 1A2 & 2C19
Substrate: 2C19 3A4/5

A

No specific serotonin subtype, 5HT1, 5HT2, 5HT3.

dose increases is limited s/t prolonging QTC = cardiotoxic

48
Q

Sertraline (zoloft)
(SSRI)
Substrate: 2B6, 2C9, 2C19, 3A4
Inhibitor: 2D6

A

weak DAT inhibition
DAT inhibition = may improve energy, motivation, concentration
favorite to add wellbutrin too, adding together the weak DAT inhibition
approved for anxiety, OCD

49
Q

Escitalopram (Lexapro)
(SSRI)

A
50
Q

Fluoxetine (PROZAC)
(SSRI)
Substrate: 2C9, 2D6 3A4/5
Inhibitor:2C19

A

LONGEST 1/2 life of SSRIs (about 1 week) Do not need to taper

antidepressive, ED (Anti-bulima)
generally activating, detect energizing/fatigue reducing effects, improves concentration and attention

Best matched for pt with reduced positive affect, hypersomnia, psychomotor retardation, apathy, fatigue
Less matched for pt with agitation, insomnia, anxiety

Adding olanzapine, 5HT2C antagonist actions, leads to further enhanced DA/NE release in cortex to mediate antidepressant actions.

51
Q

What areas of the brain are effected in bipolar disorder?

A

prefrontal cortex, amygdala & striatum

52
Q

Criteria for Dx of Bipolar

A

DIGFAST = manic/hypomanic episodes
Distractibility
Irritable
Grandoise
Flight of ideas
Activity Increase
Sleep deprived
Talkative

** Abnormal elevated mood should last >1 week & need at least 3 of DIGFAST

53
Q

Pathology of Bipolar

A

Decreased expression of serotonin transporter gene

54
Q

Pts with bipolar have ______ lateral ventricles which indicates loss of ______ ______.

A

Enlarged

Neural tissue

55
Q

FDA Meds approved for Bipolar

A

Lithium (Mood Stabilizer)
Valproic Acid (Anticonvulsant)
Lamotrigine
Carmazapine
Aripiprazole
Olanzipine
Olanzipine-fluoxetine
Risperidone
Quetiapine
Asenapine

56
Q

Lithium

A

“gold standard” in tx in bipolar MANIA, but NOT bipolar depression
> age 7
Takes 1-3 weeks to start working
Check kidney function (repeat kidney function q 1-2 years)
Monitor q 6-12 months
EKG for pts >50 before starting

57
Q

Valproic Acid/Valproate

(Anticonvulsant/Mood Stabalizer/Migraine Prophylaxis/Voltage Sensitive Na Modulator)

A

Inhibts the reuptake of GABA which increases the release of dopamine in prefrontal cortex (but not in nucleus accumbens)

Inhibits glutamate NMDA (in mania and sezures NMDA is thought to be excessive)

58
Q

What is Valproic Acid used for

A

Acute Mania
Bipolar depression & bipolar disorder maintenence
Migraine prophylaxis
Adjunctive therapy in schizo and psychosis

59
Q

What channels does Carbamazepine block?

A

Na and Ca at alpha subunit
Inhibits the release of glutamate

60
Q

What is Carbamazepine used for?

A

Acute/mixed mania
Bipolar maintenance
Seizures

(will need to check Na levels) watch for hypoNa

61
Q

What is important about the bipolar medication valproic acid in women of child bearing age?

A

Neurotoxic - do not use in women of childbearing age
** counsel women on taking birth control
High risk of causing spina bifida, disability, autism etc.

62
Q

What is important to remember about Valproic Acid (bipolar med)liquid form?

A

absorbed in stomach so causes more GI symptoms
Using a delayed release (DR) can help combat this.

63
Q

Valproic Acid is _______ bound.
Why is this important?

A

Protein
be careful with pts who have low protein bc then it would leave too much valproic acid in body = toxicity
(hypoalbumin)
*also eating disorders

64
Q

What are the two FDA drugs approved for Bipolar DEPRESSION

A

Quetiapine
Olanzipine-Fluoxetine

65
Q

Which 2 biplar medications are NOT approved for bipolar mania

A

Lamotrigine
Olanzinpine-Fluoxetine

66
Q

Which bipolar medication can be given as a long acting injection?

A

Risperidone

67
Q

When you give lithium for bipolar what labs must be checked?

A

thyroid (TSH)
kidney
calcium level

** do not want pts to end up with hypercalcemic

68
Q

Does Lithium upregulate or down regulate 5HT2a

A

DOWNREGULATES in raphi nucleus

69
Q

Carbamazapine is an ________ of all CYP enzymes

A

pan INDUCER = NEED TO CHECK BLOOD LEVELS 7-10 DAYS AFTER STARTING and may need to adjust blood levels;

Can also cause hypoNA - confusion/ataxia/seizures etc.

70
Q

Olanzipine (Bipolar medication) puts patient’s at risk for _______ _______ & _______ _______.

A

metabolically toxic - risk for DM and weight gain; check a lipid panel and TG level;
** need to start metformin

71
Q

What is the only bipolar/antipsychotic medication that comes in a patch form?

A

Asenapine

72
Q

What is a major risk when taking lamotrigine for bipolar?

A

Steven’s Johnson syndrome
Also 1/10 patients develop a papular rash.
approved for bipolar maintenence

Psychopharmacology Test 3 (4 decks)

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