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Pharm- Nerv. System

Nervous System/Pharm/Affective Disorders I and II - OM-4

Some basic theories of Depression ? * Neurotrophic Hypothesis - loss of neurotrophic transport is cause from loss of BDNF -antidepressants increase BDNF * -
All available antidepressants effect ? *the monoamine system -enhance synaptic availability of serotonin, norepinephrine, or dopamine
Classes of Antidepressants ? *SSRIs * Serotonin-Norepinephrine Reuptake Inhibitors -SNRIs and Tricyclic Antidepressants * Serotonin Antagonists * Monoamine Oxidase Inhibitors * Tetracyclic and Unicyclic Antidepressants
Most common SSRIs ? * Fluoxetine * Sertraline * Paroxetine * Escitalopram
Most common SNRIs ? * Duloxetine * Milnacipran *Venlafaxine
Most common Tricyclic Antidepressants? * Amitriptyline
Most common Serotonin Antagonists? * Trazodone
Most common Monoamine Oxidase Inhibitors? * Phenelzine
Most common Tetracyclic/Unicyclic? * Buproprion
Most common Bipolar Drugs used ? * Lithium * Lamotrigine (others = Carbamazepine and Valproic Acid)
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
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
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
SSRI receptor/transporter effects ? * high affinity for SERT, so no real issue in effecting other transporters/receptors
Clinical Indications to use SSRIs ? *Major depression *Generalized anxiety disorder *PTSD *OCD *Panic disorder *PMDD (premenstrual dysphoric disorder) *Bulimia
SSRIs side effects ? *sexual dysfunction (low libido) *GI upset, N/D * weight gain (paroxetine)
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
SSRIs and enzyme inhibition ? *CYPD2D6 is inhibited by (paroxetine and fluoxetine) *CYP3A4 is inhibited by (fluvoxamine)
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
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)
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
SNRIs clinical indications to use? * Depression *Pain Disorders -Milnacipran – fibromyalgia -Duloxetine – diabetic neuropathic pain, and chronic musculoskeletal pain
SNRIs adverse side effects ? * SSRIs side effects * increased HR, BP, CNS (insomnia, anxious, agitation)
Toxicity that is higher in SNRIs over SSRIs ? * see higher cardiac toxicities with Venlafaxine)
If SNRIs are discontinued suddenly ? * see the similar Discontinuation Syndrome we see in SSRIs
SNRIs adverse drug interactions ? * fewer CYPP450 interactions than SSRIs *CYP2D6 is inhibited by Duloxetine
Contraindicated with SNRIs use ? * Contraindicated with monoamine oxidase inhibitors (MAOI), b/c it leads to serotonin syndrome
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
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
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
TCADs adverse side effects ? *Potent antimuscarinic effects--->dry mouth, constipation (anti-DUMBBELSS) *Potent antihistamine effects -weight gain and sedation *Sexual Dysfunction
TCAD that causes bed wetting in kids? *Imipramine
TCAD that can cause pain ? *Amitriptyline
TCAD prescribed often to relieve puritus (itching) ? *Doxepin
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
If TCADs are discontinued abruptly ? * Get Prominent discontinuation syndrome characterized by cholinergic rebound (dumbbelss) and flu-like symptoms
Anti-DUMBBELSS mnemonic for anti-muscarinic actions ? Constipation No Urination Mydriasis Bronchodilation Tachycardia No Emesis No Tearing Dry Mouth No Sweat
Muscarinic agonist DUMBBELSS mnemonic ? Diarrhea Urination Miosis Bronchoconstriction Bradycardia Emesis Lacrimation Salivation Sweating
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
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
Clinical indications when we would use TCADs? *Treatment of depression unresponsive to SSRIs and SNRIs
Serotonin Antagonist MoA ? *block 5-HT2A receptor (same target as LSD) -drug= Trazodone
5-HT2A Antagonist half life and drug adverse effects? *t 1/2 is short, need multiple doses *black box for SUICIDE
5-HT2A drug interactions ? *Trazadone is CYP3A4 substrate -Inhibitors can increase concentration of trazadone
5-HT2A clinical uses ? *Major depression (approved use; more historical) *Hypnotic (unlabeled but most common use)
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)
(review) MAO-A consists of ? *in dopamine and norepinephrine neurons -make Epi, NE, and Serotonin
(review) MAO-B consists of ? *in serotonin and histamine neurons -make tyramine, phenylethylamine, and benzylamine
Both MAO-A and B metabolize ? *tryptamine and dopamine
MAOI adverse drug side effects ? *orthostatic HTN and weight gain -top reasons drugs are stopped
MAOI sudden discontinuation causes? *a delirium like state (psychosis, excitement, confusion) -if given to the elderly, lower dose
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
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
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
MAOI clinical use ? *Treatment of depression unresponsive to other drugs
Unicyclic/Tetracyclic Drugs - Bupropion MoA ? * poorly understood - inhibits NE and Dopamine reuptake with no effect on Serotonin
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
Unique pharmakinetic action of Bupropion ? * biphasic elimination - 1st past lasts 1 hr and 2nd pass lasts 14 hours - so a good t 1/2
Buproion adverse side effects ? * agitation, insomnia, and anorexia
Buproion adverse drug interactions ? * its major metabolite, hydroxybupropion, is a moderate inhibitor of CYP2D6 *Avoid in ppl on MAOIs also
Clinical uses of Buproion ? * Depression not responsive to other agents and if sexual dysfunction is a side effect of another drug
Drug of Choice for Major Depressive Disorder ? * SSRIs or SNRIs
DOC for PTSD ? * SSRIs (according to USMLE First Aid)
DOC for Anxiety ? * SSRIs
Why TCADs and Buproion are 2nd line drugs ? * due to their adverse effectc
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
MoA of Lamotrigine in Bipolar Disorders? * Treats the DEPRESSIVE episode of Bipolar
Lithium absorption and metabolism ? * absorbed in 6-8 hrs * there is NO metabolism and it is excreted as Lithium
Lithium neurologic side effects ? *Tremor *Motor hyperactivity - uncontrolled mvts and ataxia *difficulty talking *Psychiatric - confusion
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
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
Lithium Adverse Drug Reactions ? * Thiazides and NSAIDS cause clearance to be slowed
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
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
Created by: thamrick800