Nervous System/Pharm/Affective Disorders I and II - OM-4
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| Some basic theories of Depression ? | * Neurotrophic Hypothesis
- loss of neurotrophic transport is cause from loss of BDNF
-antidepressants increase BDNF
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| All available antidepressants effect ? | *the monoamine system
-enhance synaptic availability of serotonin, norepinephrine, or dopamine
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| Classes of Antidepressants ? | *SSRIs
* Serotonin-Norepinephrine Reuptake Inhibitors
-SNRIs and Tricyclic Antidepressants
* Serotonin Antagonists
* Monoamine Oxidase Inhibitors
* Tetracyclic and Unicyclic Antidepressants
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| Most common SSRIs ? | * Fluoxetine
* Sertraline
* Paroxetine
* Escitalopram
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| Most common SNRIs ? | * Duloxetine
* Milnacipran
*Venlafaxine
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| Most common Tricyclic Antidepressants? | * Amitriptyline
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| Most common Serotonin Antagonists? | * Trazodone
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| Most common Monoamine Oxidase Inhibitors? | * Phenelzine
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| Most common Tetracyclic/Unicyclic? | * Buproprion
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| Most common Bipolar Drugs used ? | * Lithium
* Lamotrigine
(others = Carbamazepine and Valproic Acid)
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| SSRIs MoA ? | * allosterically binds to serotonin receptor, SERT, to produce a conformational change and blocks serotonin from being taken in to the cells to allow higher extracellular serotonin levels
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| SSRIs pharmakinetics ? | * rather long half lifes
* Fluoxetine has an active metabolite, Norfluoxetine, which has a 180 hour t1/2 !!!
* have interactions with CYP's, so if on other drugs metabolized by them, need to monitor dose, or get toxicities
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| With Fluoxetine, since its active metabolite lasts so long, what has to happen before given a treatment with a MAOI ? | * has to be discontinued for at least 4 weeks before MAOI tmt
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| SSRI receptor/transporter effects ? | * high affinity for SERT, so no real issue in effecting other transporters/receptors
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| Clinical Indications to use SSRIs ? | *Major depression
*Generalized anxiety disorder
*PTSD
*OCD
*Panic disorder
*PMDD (premenstrual dysphoric disorder)
*Bulimia
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| SSRIs side effects ? | *sexual dysfunction (low libido)
*GI upset, N/D
* weight gain (paroxetine)
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| What is Discontinuation Syndrome ? | * when a short half life SSRI (paroxetine, sertraline) is suddenly stopped
- get dizziness and paresthesias (tingling)
*so need to taper off of SSRIs
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| SSRIs and enzyme inhibition ? | *CYPD2D6 is inhibited by (paroxetine and fluoxetine)
*CYP3A4 is inhibited by (fluvoxamine)
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| SNRIs MoA ? | * Bind both SERT and norepinephrine transporter (NET) to do the same thing as SSRIs
* higher affinity to SERT
* little affinity for other receptors
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| Of the SNRIs, which is the only one that does not have balanced inhibition toward both receptors, but has low inhibition towards NET ? | * Venlafaxine
(others may be "balanced", but still have higher affinity to SERT)
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| SNRIs t1/2 and enzyme interactions? | * a little shorter t1/2 than SSRIs, so may have to give more often
*Duloxetine and Venlafaxine are metabolized by CYP2D6
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| SNRIs clinical indications to use? | * Depression
*Pain Disorders
-Milnacipran – fibromyalgia
-Duloxetine – diabetic neuropathic pain, and chronic musculoskeletal pain
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| SNRIs adverse side effects ? | * SSRIs side effects
* increased HR, BP, CNS (insomnia, anxious, agitation)
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| Toxicity that is higher in SNRIs over SSRIs ? | * see higher cardiac toxicities with Venlafaxine)
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| If SNRIs are discontinued suddenly ? | * see the similar Discontinuation Syndrome we see in SSRIs
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| SNRIs adverse drug interactions ? | * fewer CYPP450 interactions than SSRIs
*CYP2D6 is inhibited by Duloxetine
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| Contraindicated with SNRIs use ? | * Contraindicated with monoamine oxidase inhibitors (MAOI), b/c it leads to serotonin syndrome
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| Tricyclic Antidepressants(TCADs) MoA ? | * inhibits SERT and NET
*in antidepressant use, it inhibits 5-HT and NE reuptake
*within the TCADS, there is major variability in SERT and NET binding affinity
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| Main reason why TCADS are not popular to use ? | * b/c they interact with almost every type of receptor instead of specific ones
-get lots of side effects
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| TCADS t 1/2 and enzyme interactions ? | *dosed at night due to sedative effects
* shorter t 1/2
*all metabolized by CYP2D6, so can be an issue if other drugs also need CYP2D6 to be broken down
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| TCADs adverse side effects ? | *Potent antimuscarinic effects--->dry mouth, constipation (anti-DUMBBELSS)
*Potent antihistamine effects
-weight gain and sedation
*Sexual Dysfunction
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| TCAD that causes bed wetting in kids? | *Imipramine
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| TCAD that can cause pain ? | *Amitriptyline
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| TCAD prescribed often to relieve puritus (itching) ? | *Doxepin
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| A certain issue that TCADS can cause that is life threatening in people with cardiac issues ? | * TCADs cause an α-adrenergic blockade and can cause severe orthostatic hypotension
*avoid TCADs in ppl on antiHTN drugs
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| If TCADs are discontinued abruptly ? | * Get Prominent discontinuation syndrome characterized by cholinergic rebound (dumbbelss) and flu-like symptoms
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| Anti-DUMBBELSS mnemonic for anti-muscarinic actions ? | Constipation
No Urination
Mydriasis
Bronchodilation
Tachycardia
No Emesis
No Tearing
Dry Mouth
No Sweat
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| Muscarinic agonist DUMBBELSS mnemonic ? | Diarrhea
Urination
Miosis
Bronchoconstriction
Bradycardia
Emesis
Lacrimation
Salivation
Sweating
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| TCAD adverse drug reactions ? | *get high drug levels when other drugs are also using CYP2D6 or inhibiting it
*additive effects if also given anticholinergic or antihistamine
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| Since CYP2D6 can vary genetically, what can happen to TCADs? | *can cause rapid/slow metabolization of the drugs
-drug can have high effects in low doses or don't see any drug effects b/c being metab. too quickly
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| Clinical indications when we would use TCADs? | *Treatment of depression unresponsive to SSRIs and SNRIs
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| Serotonin Antagonist MoA ? | *block 5-HT2A receptor (same target as LSD)
-drug= Trazodone
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| 5-HT2A Antagonist half life and drug adverse effects? | *t 1/2 is short, need multiple doses
*black box for SUICIDE
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| 5-HT2A drug interactions ? | *Trazadone is CYP3A4 substrate
-Inhibitors can increase concentration of trazadone
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| 5-HT2A clinical uses ? | *Major depression (approved use; more historical)
*Hypnotic (unlabeled but most common use)
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| Monoamine Oxidase Inhibitors (MAOIs)MoA ? | * Drugs target MAO-A and MAO-B, non-selectively to increase monoamine content
(structurally resemble amphetamines and can cause CNS stimulation increase)
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| (review) MAO-A consists of ? | *in dopamine and norepinephrine neurons
-make Epi, NE, and Serotonin
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| (review) MAO-B consists of ? | *in serotonin and histamine neurons
-make tyramine, phenylethylamine, and benzylamine
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| Both MAO-A and B metabolize ? | *tryptamine and dopamine
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| MAOI adverse drug side effects ? | *orthostatic HTN and weight gain
-top reasons drugs are stopped
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| MAOI sudden discontinuation causes? | *a delirium like state (psychosis, excitement, confusion)
-if given to the elderly, lower dose
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| If MAOIS are given with SSRIs, SRNIs, or TCADS? | *get serotonin syndrome (cardiac, coma, clonus)
*Must have a 2 week drug free window before giving a MAOI and 2 week window after its use before giving a SSRIs, SRNIs, or TCAD.
-triad of the 3 C's
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| If MAOIs are given in the presence of tyramine ? | * tyramine is broken down by MAO, so we get high levels in blood
*causes HIGH BP (risk for MI, malignant HTN, or stroke)
*avoid aged cheeses and tap beer
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| If MAOIs are given in the presence of a Sympathomimetic (OTC cold meds) ? | * the containing pseudoephedrine and phenylpropanolamine in them cause a spike in HIGH BP
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| MAOI clinical use ? | *Treatment of depression unresponsive to other drugs
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| Unicyclic/Tetracyclic Drugs - Bupropion MoA ? | * poorly understood
- inhibits NE and Dopamine reuptake with no effect on Serotonin
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| Good reason why we might put someone on Bupropion ? | * does not cause Sexual Dysfunction
-so give it to someone have this side effect with the other drugs
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| Unique pharmakinetic action of Bupropion ? | * biphasic elimination
- 1st past lasts 1 hr and 2nd pass lasts 14 hours
- so a good t 1/2
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| Buproion adverse side effects ? | * agitation, insomnia, and anorexia
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| Buproion adverse drug interactions ? | * its major metabolite, hydroxybupropion, is a moderate inhibitor of CYP2D6
*Avoid in ppl on MAOIs also
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| Clinical uses of Buproion ? | * Depression not responsive to other agents and if sexual dysfunction is a side effect of another drug
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| Drug of Choice for Major Depressive Disorder ? | * SSRIs or SNRIs
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| DOC for PTSD ? | * SSRIs (according to USMLE First Aid)
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| DOC for Anxiety ? | * SSRIs
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| Why TCADs and Buproion are 2nd line drugs ? | * due to their adverse effectc
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| MoA of Lithium in Bipolar Disorders? | *Treats the MANIC phase of Bipolar
* not known
*Possibly Effect on electrolytes/ion transport, or Effects on inositol signaling, or effects on second messengers
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| MoA of Lamotrigine in Bipolar Disorders? | * Treats the DEPRESSIVE episode of Bipolar
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| Lithium absorption and metabolism ? | * absorbed in 6-8 hrs
* there is NO metabolism and it is excreted as Lithium
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| Lithium neurologic side effects ? | *Tremor
*Motor hyperactivity - uncontrolled mvts and ataxia
*difficulty talking
*Psychiatric - confusion
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| Other Lithium side effects ? | * low thyroid function - test TSH lvls
* Renal - Nephrogenic Diabetes Insipidus, Polydipsia and polyuria are common
* Cardiac - depresses sinus nodes (contraindicated in bradycardic pts.)
*Edema - most common
*Acne
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| Actions to take when treating someone with Lithium ? | * it has a slow onset, so give a benzo if in a severe manic episode til it kicks in
*Monitor serum levels since it has a narrow TI
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| Lithium Adverse Drug Reactions ? | * Thiazides and NSAIDS cause clearance to be slowed
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| Lithium in pregnant people ? | * It causes an increase in renal clearance, so after drug is given, it rapidly reverts back to low levels
* Can be transferred to newborns in breast milk - cause Lethargy, cyanosis, poor suck and Moro reflexes, hepatomegaly
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| Lithium Overdose level and how to fix ? | *usually get on a therapeutic dose due to low Na levels or start a thiazide/NSAID, etc.
* if serum Lithium exceeds > 2 mEq/L
* easily fixed on dialysis
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