Tx Of Affective Disorders Hupka Part 2

Front 1

THE ATYPICALS CAUSE LESS ___________

Back 1

SEXUAL DYSFUNCTION THAN OTHER ADs.

Front 2

blocks H1 receptors, presynaptic a2-adrenergic receptors
increases NE and 5HT release
blocks 5HT2 and 5HT3 receptors

WHAT DRUG ??

Back 2

MIRTAZAPINE (ATYPICAL)

Front 3

WHICH ATYPICAL AD CAN CAUSE SEIZURES?

Back 3

BUPROPION

Front 4

3 rings in chemical structure
Structurally and somewhat pharmacologically resemble phenothiazines (antipsychotics)

formerly the most commonly used antidepressants
Antidepressant efficacy = SSRIs but more AE
Less selectivity and more frequent AE limit usage

still widely used, but often for purposes other than depression.

WHAT DRUG?

Back 4

TCA (tricyclic antidepressant)

Front 5

examples of some commonly used TCAs?

Back 5

gen 1- impramine, amitryptaline

gen2 - amoxapine

Front 6

what is the early and late effect of TCAs?

Back 6

early - agents block the reuptake of NE and serotonin in the CNS, thereby enhancing transmitter action

late - Antidepressant effects develop after several weeks and may involve down regulation of receptors
Antidepressant effects develop after several weeks and may involve down regulation of receptors

considerable sedation.

Front 7

which class of ADs are known to have "prominent anticholinergic activity"?

Back 7

TCA of which amytryptiline has the strongest anticholinergic action.

Front 8

3 Cardiovascular effects of TCAs?

Back 8

hypotension - block a1

orthostatic hypotension - due to diminihsed cv reflexes, block a1

arrythmias - QRS widens, TCAs stabilize cardiac membranes similar to qundine tend to imapair cardiac conduction.

Front 9

how are TCAs absorbed, metabolized, and half life?

Back 9

oral absorption

high lipid solubility

metabolized in liver p450, followed by glucoronidation.

imipramine -> desimipramine (active metabolite)

amitryptaline -> nortryptiline.

LONG HALF LIFE (10-50 HR)

Front 10

WHY DO U WANT TO MONITOR BLOOD LEVELS OF TCAs?

Back 10

life threatening CV and CNS effects develop on a dose dependent basis and

Front 11

adverse effects of TCAs?

Back 11

dry mouth, constipation, blurred vision.

sedation, fatigue, can switch to manic, tremor, seizure, cv - hoTn, tachy, MI, CHF, arrtyhtmias.

less likely w/ gen2 drugs

most antimuscarnic seen w/ amytryptaline.

Front 12

acute OD on TCA. what can happen?

tx for those events?

Back 12

Seizures → coma → death
Potentially fatal arrhythmias


Physostigmine can reverse antimuscarinic, cardiotoxic, and neurotoxic effects

IV sodium bicarb can treat arrhythmia
Increases non-ionized form to decrease TCA binding to cardiac membrane sodium channels

.

Front 13

why can u not use hemodialysis to cure OD of TCAs?

Back 13

cannot use hemodialysis b/c of large VD and extensive binding to plasma protiens

Front 14

what happens if you use maoi + TCA?

Back 14

serotonin syndrome

Front 15

how do antipsychotics and SSRIs interfere w/ hepatic metabolism of TCAs?

Back 15

Antipsychotic drugs, SSRIs, interfere with hepatic metabolism of TCAs

Front 16

TCA for night time bed wetting?

Back 16

imipramine.

Front 17

TCA for fibromyalgia?

Back 17

amytryptaline (neuropathic pain)

Front 18

MAOIs are regarded as LAST CHOICE drugs, for the tx of depression, name some examples?

Back 18

tranylcypromine

phenelzine

Front 19

mechanism of MAOI?

Back 19

Block metabolism of naturally occurring monoamines (NE, 5HT) by binding" irreversibly" to MAO type A non selective inhibition.

Front 20

all body tissues contain some MAO, main one in brain is type
__ and in liver we see _____, what about plateletts?

Back 20

liver - both

brain - type a

plts - type a

Front 21

adv efx of maois?

Back 21

antimuscarinic, adrenergic blocking effects, other CNS effects
as well as interfering with conduction in heart

Irreversible inhibition of MAO produces long lasting effects

cns - direct stimulation simmilar to amphetamines.
Orthostatic hypotension (one of most common)
Weight gain
Central stimulation – tremors, insomnia
Overdose – agitation, hallucinations, convulsions, hypertensive crisis
Constipation, weakness, fatigue, skin rash, difficulty in urination, headache
High incidence of sexual dysfunction
hepatotoxicity

Front 22

majority of mao in body?

Back 22

type b

Front 23

transderm maoi used to tx depresison, selective maoB inhibitor.

Back 23

selegeline.

Front 24

name on drug interaction of MAOIs?

Back 24

Prolong the effects of tricyclics, central depressants, analgesics, anticholinergic agents

Front 25

hypertensive crisis can be brought on by interaction w/ a molecule found on food calld tyramine and . what other drug?

Back 25

maoi

tyramine- found in cheeses

Front 26

herbal remedy for mild to mod depression


Contains compounds that inhibit MAO and block 5HT reuptake
Drug interactions are a problem
Hyperforin, a P450 inducer found in St. J. W., increases metabolism of drugs used to treat AIDS (protease inhibitors) and suppress transplant rejection (cyclosporine)

Back 26

ST JOHNS WORT

Front 27

DIETARY SUPPLEMENT FOR WELL BEING?

Back 27

SAMe - s-adenosyl methionine

Front 28

most commonly use anti manic mood stabilizer?

Back 28

lithium carbonate


may produce anti-manic effects by action on inositol phosphates in nerve cell membranes
has no effects on normal person

elimnated in urine, absorbed GI (oral)

Front 29

therapeutic range for lithium use?

Back 29

0.6-1.25 Eq/L


1.6-2.0 mEq/L – fatigue, muscular weakness, slurred speech, ataxia, NVD, fine tremor, excessive thirst and urination (ADH antagonism – nephrogenic diabetes insipidus)


Above 2.0 mEq/L – CNS primarily affect → impaired consciousness and coma. Also muscular rigidity, marked tremor, and muscle fasiculations

Front 30

how do sodium levels effect lithitum levels?

Back 30

Sodium depletion can increase lithium levels and side effects

Front 31

name 4 other mood stabilizers besides lithium?

Back 31

valproate - Valproate is just as effective as lithium, is generally better tolerated, and is replacing lithium


lamotrigene (ANTIEPILECTIC)

carbamazepine

combo olanzapine (antipsych) + fluzoetine (ssri)

Front 32

when should pharmacological intervention be used for effective disorders?

Back 32

when the disorder is SEVERE


Affective disorders have high rate of spontaneous remission so drug treatment reserved for severe illnesses

Front 33

doc FOR DEPRESSION?

Back 33

SSRI - FLUXOETINE

SNRI - VENLAFAXINE

THEN ATPICAL THEN TCA THEN LAST MAOI


Recent studies suggest sertraline may serve as the initial drug choice for major depression
Choice of individual agent depends on patient and which side effects are to be used or avoided (use an SSRI in a patient with heart disease to avoid cardiac toxicity associated with tricyclics)

Front 34

CONCERN WITH SSRI AND AD IN GENERAL IN KIDS?

Back 34

SUICIDAL TENDENCIES.

Front 35

WHAT WOULD USE TO TX BIPLOAR DISORDER FIRST

WHAT IF YOU HAD A ACCOMPANYING DEPRESSIVE EPISODE?

WHAT ABOUT A MANIC EPISODE?

Back 35

Mood stabilizers are mainstays of treatment
lithium, valproate or lamotrigine are first choice
carbamazepine also used
Depressive episode – lamotrigine (another antiepileptic). An antidepressant can be added for severe depression, but don’t use alone
Manic episode – olanzapine or risperidone(ANTIEPILEPTIC) added to mood stabilizer