Neuro: Test 1 : 28&29. Schriefer : Affective Disorders I & Ii

Front 1

what is the Monoamine hypothesis of depression?

Back 1

too little serotonin and epi lead to depression

Front 2

what is the Neurotrophic hypothesis of depression?

Back 2

BDNF regulate neural
plasticity,survival and and neurogenesis.

Depression decreases BDNF and antidepressants
increase BDNF.

Front 3

What type of depression is this:

Loss (Adverse life events). Physical illness (myocardial infarct, cancer). Drugs (antihypertensives, alcohol, hormones). Other psychiatric disorders (senility).

Back 3

Reactive

Front 4

What type of depression is this:

Precipitating life event not adequate for degree of depression. Autonomous (unresponsive to changes in life). May occur at any age (childhood to old age). Biologically determined (family history)

Back 4

Endogenous

this is where the neurotrophic hypothesis comes into play (that you have neuronal issue)

Will see more PHYSICAL symptoms

Front 5

What type of depression is this:

Characterized by episodes of mania. Cyclic: mania alone, rare; depression alone, occasional; mania-depression, usual

Back 5

Manic-depressive

Front 6

What kind of drug is Fluoxetine? used to treat?

Back 6

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 7

What kind of drug is Paroxetine? used to treat?

Back 7

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 8

What effects do SSRIs have on the ANS and CNS?

Back 8

Nothing significant!

This makes them safe, OD won't likely kill you

Front 9

what is the half life like for Paroxetine and Sertraline? What is important about this?

Back 9

Short as compareted to Fluoxetine (1 day vs 3 days)

so you have to make sure to wean them off it slowly or you can cause depression pretty quick

these are all SSRIs

Front 10

what do SSRIs do to the metabolism of other drugs?

Back 10

inhibit the metabolism of other drugs

Front 11

What is the major side effect of SSRIs? why

****TEST

Back 11

Nausea, headache, diarrhea are most common (stimulation of 5HT3 receptors)

note: another reason people may discontinue the drug is due to sexual dysfunction

Front 12

pt comes in on an SSRI with anxiety and motor restlessness, what drug(s) could have caused this?

Back 12

Fluoxetine, and to a lesser extent, sertraline

Front 13

Which SSRI ) may induce birth defects. Use during 3rd trimester may cause persistent pulmonary hypertension in newborns or withdrawal syndrome.

Back 13

paroxetine

Front 14

what do you have to worry about with kids taking SSRIs

Back 14

high risk of suicide

Front 15

What must you be careful of when you give an SSRI with SNRIs,TCA, MAOI, meperidine, or triptans?

****TEST

Back 15

SEROTONIN SYNDROME

mental status changes,(confusion to coma) disorders of motor activity (hyperreflexia, rigidity), and autonomic disturbances ( hyperthermia, hypertens.) All SSRIs)

more dangerous with fluvoxetine (long acting)

Front 16

PMDD, generalized anxiety disorder, panic, OCD, and bulimia can all be treated with what? (general)

Back 16

SSRIs

Front 17

Venlafaxine is what kind of drug?

Back 17

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 18

duloxetine is what kind of drug?

Back 18

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 19

which Serotonin and norephinephrine Reuptake Inhibitors (SNRI) should you avoid in pts with liver disease?

Back 19

Duloxetine – liver damage (rare) – avoid in pts with chronic liver disease or hepatic insufficiency

Front 20

Duloxetine does what to P450s?

Back 20

Duloxetine has greater potential than venlafaxine because it inhibits CYP2D6 and may increase drug levels of TCAs, Type 1C antiarrhythmics (e.g., flecainide) and phenothiazines.

INHIBITS METABOLISM

SNRI

Front 21

2 drug classes that can treat diabetic peripheral neuropathy?

Back 21

SNRIs and Tricyclics

Front 22

milnacipran is what kind of drug? Used to treat?

Back 22

SNRI

Fibromyalgia

note: all SNRIs can tx fibromyalgia, but milnacipran is used ONLY for fibromyalgia, not depression

Front 23

Trazodone MOA? Use?

Back 23

blocking 5HT2A receptors.

Most common use of trazodone is as hypnotic.
Side effects – arrhythmias and priapism

Front 24

Bupropion MOA? Use? Risk of causing?

Back 24

causes presynaptic release of DA and NE and blocks their reuptake.

Depression (used after SSRI)

Risk of seizures

note:Less sexual dysfunction, wt gain or sedation than other antidepressants.

Front 25

Mirtazapine MOA? Use? why it is liked?

Back 25

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

depression

liked: Less sexual dysfunction; more wt gain and sedation.

Front 26

Doxipen
Maprotiline
Amoxapine

are what kind of drugs

Back 26

second generation Tricyclic Antidepressants

Front 27

Imipramine
Desipramine
Amitriptyline

are what kind of drugs?

Back 27

first generation Tricyclic Antidepressants

Front 28

MOA of tricyclic antidepressant

Back 28

block the reuptake of NE and serotonin in the CNS, thereby potentiating transmitter action. This may be an early event in the mechanism of antidepressant action.

Front 29

which tricyclic has the strongest anticholinergic action?

Back 29

Amitriptyline

Front 30

What are the 3 ways you have adverse effects with Tricyclic antidepressants

Back 30

Antimuscarinic – e.g., dry mouth, constipation, blurred vision, Intensity varies with different drugs (amitriptyline strongest).

CNS – sedation, weakness, fatigue; may switch depressed patient to manic phase; tremor; seizures

Cardiovascular – orthostatic hypotension (a1 block), tachycardia, myocardial infarction, congestive heart failure, arrhythmias. May be less likely or less severe with 2nd generation drugs

Front 31

what can happen with acute poisoning of tricyclics? tx?

Back 31

Acute poisoning – life threatening; excitement and restlessness

Convulsions → coma → death. Must support vital functions. Physostigmine can reverse antimuscarinic, cardiotoxic, and neurotoxic effects.

Front 32

these drugs in addition to treating depression can be used to treat neuropathic pain, nocturnal enuresis, and fibromyalgia

Back 32

Tricyclics

nocturnal enuresis (imipramine), fibromyalgia (amitriptyline, doxipen).

Front 33

Tranylcypromine MOA? Use?

Back 33

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 34

Phenelzine MOA? Use?

Back 34

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 35

Isocarboxazid MOA? Use?

Back 35

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 36

2 main reasons we don't use MAOi?

***TEST

Back 36

Potentiate sympathomimetic amines

*****Dangerous interaction with tyramine (found in food)-->causes release of NE-->Hypertensive crisis

(MAO knocks out Tyramine, without it, it gets into the system and causes the release of NE, leads to hypertensive crisis)

Front 37

How does St. John's Wort help with depression? What are the problems associated with it?

Back 37

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 and suppress transplant rejection.

Front 38

MOA of Lithium Carbonate? Use?

Back 38

interferes with second messenger system, can't remake PIP2, SLOWS DOWN NEURONAL ACTIVITY

stabilize mood in bipolar pts

Front 39

A bipolar pt comes in complaining that they are constantly thirsty and peeing all the time...what drug is causing this? how?

***

Back 39

Lithium- Antagonizes ADH

leads to excessive thirst and urination

Front 40

Primary drug of choice for mood stabilization (bipolar)?

Back 40

VALPROATE (remember this is also an anti-epileptic!)

others that can be used: carbamazepine (na channel block), lamotrigine (na channel block)

Front 41

2 drugs that are first choice for depression?

Back 41

SSRIs or venlafaxine (SNRI)

Front 42

when is Electroconvulsive therapy (ECT) indicated

Back 42

when a person is a serious threat to kill themselves when depressed

Front 43

What are the first line choice drugs for bipolar

Back 43

Mood stabilizers are mainstays of treatment – Lithium, valproate or lamotrigine are first choice.

Carbamazepine also used.

Front 44

this is an antidepressant that can be added for severe depression, but don’t use alone. Can be used first line

Back 44

lamotrigine (another antiepileptic).

An antidepressant can be added for severe depression, but don’t use alone. Certain antidepressants may not be effective.

Front 45

for a manic episode, what drugs can be added to mood stabilizers?

Back 45

olanzapine or risperidone (atypical antipsychotics)

added to mood stabilizer (Lithium, valproate or lamotrigine).