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Antidepressants

S&D

QuestionAnswer
What decreases during pre-natal stress? Mineralocorticoid and Glucocorticoid receptors levels both decrease permanently in the hippocampus
What increases during pre-natal stress and maternal separation ? corticotropin-releasing hormone (CRH) mRNA in the Paraventricular nucleus (PVN) and CRH peptide in the amygdala and a stress response that does not turn off
Describe Glucocorticoid plasticity in the CNS Decreased GR in the hippocampus decreases the sensitivity of the negative feedback, increases the hypothalamic-pituitary-adrenal (HPA) activation for any given level of stress
What results can be seen in depressive behavioural consequences Excess CRH inhibits serotonergic release in the hippocampus
What is decreased in suicide victims Decreased 5HT1A levels in the hippocampus
Chronic glucocorticoid increase leads to ? Decreased post-synaptic 5HT1A in the hippocampus
Location of 5-HT1AR Hippocampus, Septum??, Entorhinal cortex
What receptors are hypothesised to be therapeutic target of antidepressant drugs Postsynaptic 5-HT1AR
What effects do TCA's have on post-synaptic 5HT1A receptors Sensitize them
5HT1A occupation allows for ? Dissociation aversive events (stress coping)
What is thought to be behind the loss of 5HT1A A tendency to dwell on negative outcomes, which might be an adaptive response to chronic stress
What decreases Neurogenesis? An overactive Hypothalamic-pituitary-adrenal axis
BDNR BRAIN DERIVED NEUROTROPIN FACTOR necessary for synapse formation in the hippocampus
Serotonoin acting on 5HT1A does what? In the hippocampus is beneficial in coping prob via upregulation of BDNF
What is increased in chronic stress? 5HT7
FLUOXETINE (PROZAC) SSRI treats depression in adults and children
IMIPRAMINE Tricyclic antidepressant
ESCITALOPRAM 5HT1A Agonist
SSRIs FLUOXETINE SERTRALINE CITALOPRAM VILAZODONE
TCAs IMIPRAMINE AMITRIPTYLINE* (OFTEN USED IN COMBO WITH NEUROLEPTICS OR BENZO) CLOMIPRAMINE (OCD) DESIPRAMINE NORTRIPTYLINE
Mixed 5HT, Norepinphrine reuptake inhibitors (SNRIs) VENLAFAXINE, DULOXETINE
NRIs & NDRIs BUPROPION (non-specific reuptake inhibition of Monoamines, glutamate and GABA)
What do TCAs and SNRIs block and SSRIs? TCA & SNRI block 5HT and NA transporters and SSRI are specific for serotonin
MONOAMINE RECEPTOR ANTAGONISTS (inhibit specific amine receptors including alpha2 and 5HT2A receptors) MIRTAZAPINE (Also 5HT1A agonist) TRAZODONE (5HT2A)
Monoamine oxidase inhibitors PHENELZINE SELEGILINE
SSRIs: MCA, Clinical use, Side effects MCA: Inhibit reuptake of 5HT at neuronal synapses, Clinical use: Major depression, OCD, anxiety disorders, bulimia nervosa Side effects: Inhibits liver enzymes, nausea, agitation, sexual dysfunction (anorgasmia), dystonic reactions
SNRIs: MOA, Clinical use, Side effects MOA: (-) reuptake of NE and 5HT @ neuronal synapses Clinical: Major depression, anxiety disorders, neuropathic pain (duloxetine), fibromyalgia (milnacipran), obesity (sibutramine) Side effects: Sedation, nausea, constipation, HT, mild sexual dysfunction
TCAs: MCA. Clinical use, Side effects MCA: Inhibit reuptake of NE and 5HT at neuronal synapses Clinical use: Major depression, OCD (Clomipramine), noctural enuresis (imipramine), panic disorder Side effects: Sedation, a-blocking effects (orthostatic hypotension), anticholinergic, coma
MAOis: MOA. Clinical use, Side effects MOA: Inhibit degradation of NE and 5HT at neuronal synapses Clinical use: atypical depression Side effects: Hypertension episodes with ingestion of tyramine-containing foods or beta agonist
NaSSA: MCA. Clinical use, Side effects MCA: A2-antagonist increases release of NE and 5HT Clinical use: Major depression (esp. with insomnia) Side effects: Weight gain, dry mouth, increased appetite, sedation Mirtazapine
SARI: MCA. Clinical use, Side effects MCA: Inhibits 5HT reuptake Clinical use: major depression (esp. with insomnia) Side effects: sedation, nausea, priapism, postural hypotension Trazodone (agonist to 5HT1A & antagonist 5HT2A)
MDD Drugs VORTIOXETINE (ATYPICAL SSRI, 5HT7 antag and 5HT1A agonist) VILAZODONE (SSRI, 5HT1A partial agonist) TRAZODONE SARI (5HT2A antag and 5HT1A agonist) BUPROPION NDRI DULOXETINE (neuropathic pain) SNRI*
Depression drugs CITALOPRAM (SSRI) CLOMIPRAMINE (TCA) VENLAFAXIN (SNRI) MIRTAZAPINE (NaSSA alpha2A antag and 5HT2a antag)
What do drugs that antagonize SERT or Alpha2 or inhibit MAO do to 5HT? They increase 5HT in various brain regions and increases side effects
What should be done in cases of SSRI non-responders? Treated with another class of antidepressant which utilize a different MAO
Most important serotonergic targets for antidepressant drugs? 5HT1A (decrease cAMP) 5HT2A, 5HT2C (icreases IP3) 5HT7 RECEPTOR (increases cAMP)
5HT1A Located in the raphe nucleus (presynaptic), hippocampus and periaqueductal grey.
SSRIs and MOA appear to do what? TCAs? Desensitize raphe 5HT1A autoreceptors without affecting post-synaptic 1A receptors TCAs facilitate or increase the sensitivity of post-synaptic 5HT1A receptors
5HT2A Located in the amygdala, nucleus accumbens (Nac), prefrontal cortex (PFC) Blocking 5HT2A is beneficial in depressed patients. Many serotonergic side effects are through 5HT2A including insomnia and sexual dysfunction
Blocking 5HT7 does what? Enable upregulation of BDNF which facilitates late LTP by interfering with NMDA mediated LTP in the hippocampus
BUPROPRION MOA blockade of Dopamine and NA uptake no sexual dysfunction, weight gain or sedation
SELEGILINE PATCH MOA blockage of DA breakdown, partially blocks NA and 5HT at high doses MOA appears to be blocked by D1 antagonists
5HT2A Antagonists Such as trazodone can enhance dopamine and noradrenaline release in the prefrontal cortex which decreasing dopamine release in the nucleus accumbens
_________ should not be used as monotherapy in bipolar depression or bipolar disorder (I or II) SSRIs
Side effects of SSRIs Nausea, diarrhea, agitation, insomia, headache, sexual dysfunction, axiety, inhibits metabolism of other drugs
What SSRI moderately inhibits CYP3A4? Fluoxetine
What SSRI is also a partial 5HT1A receptor agonist ? Vilazodone
Why are the effects of SSRIs delayed? Plastic change in following receptors take a few weeks: Desensitization of the 5HT1A in the Raphe Nuc, Down regulation of the 5HT2A receptors, Lowering of the 5HT7 receptor levels
What is the Black box warning from the FDA about SSRIs? warnings about increased risks of suicidal thinking and behavior (suicidality) in young adults ages 18 to 24 during initial treatment.
What are the 3 major antidepressant drugs for pediatric use? Fluoxetine, Escitalopram, Fluvoxamine
What antidepressant drugs treat GAD? Escitalopram,Duloxetin, Venlafaxine
What antidepressant drugs treat Panic? Fluoxetine (Prozac), Paroxetine, Sertraline (Zoloft), Venlafaxine
What antidepressant drugs treat OCD? Fluoxetine (Prozac), Paroxetine, Sertraline (Zoloft), Fluvoxamine, Clomipramine
What antidepressant drugs treat Social phobia/anxiety? Sertraline (Zoloft), Venlafaxine, Paroxetine
What antidepressant drugs treat PTSD? Paroxetine, Sertraline (Zoloft)
Serotonin release in the hippocampus is initially inhibited by 5HT1A autoreceptors in the ____. These autoreceptors are eventually down-regulated after a few weeks Raphe Nucleus
What is the initial consequence of the SSRIs on Raphe Nuc's effect on the Nuc. Accumbens, prefrontal cortex and amygdala that causing SUICIDES in 18-24 yrs? 5HT STIMULATES dopamine release in Nuc. Accumbens causing mania 5HT inhibits DA in the prefrontal cortex leading to apathy 5HT exacerbates anxiety in the amygdala
______ are contraindicated in bipolar disorder because they precipitate mania in susceptible individuals? SSRIs
What three receptors do TCAs have side effects on? Histamine, Adrenergic, Muscarinic
What are the 4 Cs in a TCA overdose? Circulatory failure, convulsions, coma, cardiac conduction defects
What is the cheese effect? MAOi leads to a build up of tyramine = NE release = hypertension crisis
What is serotonin syndrome ? The combination of 2 drugs (SSRIs, TCAs and MAOis) which increase serotonin levels leading to a potentially life threatening condition.
What are the symptoms of serotonin syndrome? Agitation, fever (hyperthermia), shivering, diarrhea, hyperreflexia, incoordination, muscle rigidity, monoclonus (twitching and jerking), tremor, seizures, and cardiovascular instability
How do you treat serotonin syndrome? First cease drug administration. Agitation, tremor and hypertonicity can be controlled with benzodiazepines. The serotonergic 2A blocker cyproheptadine is routinely used, although its usefulness is questioned
How does serotonin correlate with convulsion threshold? Low dose serotonin can raise the convulsion threshold.
Malignant hyperthermia clinical features and causal drug Diaphoresi, mottled skin, agitation, decreased bowel sounds, mascular rigidity, hyporeflexia. Halogenated inhalational anesthetics or depolarizing muscle relaxants
Neuroleptic malignant syndrome clinical features and causal drug Sialorrhea, diaphoresis, pallor, studor, mutism, coma, normal or decreased bowel sounds, lead-pipe rigidity,bradyreflexia. Trazadone, antipsychotic meds
Anticholinergic syndrome clinical features and causal drug Atropine type symptoms and decreased bowel sounds. TCAs, antidepressants and other anticholinergic drugs
What drugs carry a warning prolongation of the QT interval? TCAs: Amitriptyline, Desipramine, Imipramine. SSRIs: Citalopram, Fluoxetine, Paroxetine, Sertraline. SNRI: Venlafaxine. NaSSA: Mirtazepine. SARI: Trazodone
Describe anti-arrythmia medication effects They prolong the QT interval which creates a condition called Torsades de Pointe which may be congenital and can lead to ventricular fibrillation
Most frequent drugs to cause Antidepressant discontinuation syndrome (Withdrawal) Venlafaxine, Escilatopram (dizziness, muscle tension, chills, confusion or trouble concentrating, amnesia, crying) and Paroxetine
Drug that is contraindicated in anxiety, has sympathomimetic effects (sweating, dry mouth), dopaminergic (nausea and mania is a risk), hypertension and can increase seizure risk but does not cause sexual dysfunction or weight gain Bupropion
Drug that is primarily a 2A antagonist, blocks alpha1 and H1 at doses required for SERT antagonism, sedative effects via blockage of 5HT2A, enhances DA AND NE release in the PFC. ADR include orthostatic hypotension, hypnotic and sedation limits dosing Trazodone
Drug that antagonizes Alpha2, H1, AND 5HT2A. Increases serotonin, NE and DA. Side effects include severe sedation, constipation, dizziness, disturbed dreams, increased serum cholesterol, increased appetite, xerostomia Mirtazapine
Antidepressant interact most with what herbs? St John's Wort + SSRIs = delerium Ginseng (increases sex drive) + SSRIs = precipiate mania Ginkgo + SSRIs = serotonin syndrome and coma with trazadone
Drug that is an NMDA antagonist and addictive hallucinogen, dissociative anesthetic, and used for severe treatment-resistant depression and only used in patients who have exhausted all FDA-approved treatment with no history of substance abuse Ketamine
TCAs, trazadone and mirtazapine all cause what? Sedation via H1 blockage
TCAs, MAOis and trazadone all cause what? Orthostatic hypotension via Alpha1 block
TCAs, citalopram, venlafaxine, mirtazapine, trazodone all cause what? CVS Toxicity (TdP)
MOA OF 5HT AGONIST: triptans, the ergot alkaloids, & antidepressants may activate 5-HT1D/1B receptors on presynaptic trigeminal nerve endings to inhibit the release of vasodilating peptides
What do 5HT1D/1B agonist and 5HT1B receptors do? Inhibit the release of CGRP, Substantce P and neurokinin A; 5HT1B stimulates vasoconstriction
What is CGRP ? Calcitonin gene-related peptide causes vasodilation and inflammation of pial and dural vessels = activation of nociceptive trigeminal fiber
What constitute 85% of migraines in patients? Migraines without aura
what is the most efficacious drug used in migraine prophylaxis? Verapamil
What are the most widely used anticonvulsants drugs used for migraine prophylaxis? Topiramate and valproate
Name three andtidepressants used in migraine prophylaxis Fluoxetine (SSRI) Amitriptyline (TCA) Phenelzine (MAOi)
Name 4 NSAIDs used in migraine prophylaxis and their MOA Aspirin, Flurbiprofen, Naproxen, Meclofenamate VIA blocking thromboxane synthesis and platelet aggregation = reduce the release of serotonin
Name 5 B-blocker drugs used in migraine prophylaxis that lack intrinsic sympathomimetic activity atenolol, metoprolol, nadolol, propranolol, and timolol
What phase of a migraine do Verapamil, diltiazem, and nimodipine block? Vasoconstrictive phase of migraine headache
Name 2 drugs that have significant effects on cardiac as well as vascular Ca2+ channels Verapamil, Diltiazem
What Dihydropyridines have much greater affinity for vascular calcium channels than for Ca2+ channels in heart ALL OF THEM (Nifedipine, Amlodipine, Felodipine, Nicardipine, Nisoldipine, Nimodipine)
What migraine prophylaxis drug was approved by the FDA as pericranial injections in adult patients with chronic migraine? Onabotulinum Toxin A
MOA of Onabotulinum Toxin A Interrupts pain signals by decreasing levels of CGRP
Methylprednisolone usage ? cluster headaches but also migraine prophylaxis
Methylprednisolone MOA Blocks IL-1β-induced CGRP release. IL-1β induces PGE2 which stimulates CGRP, but glucocorticoids interfere with prostaglandin synthesis
How do abortive drugs treat acute migraine ? block the vasodilation and relieve pain and inflammation
What is the first line therapy for acute severe migraine attacks? Sumatriptan
What is the contraindication for Sumatriptan? Pts at risk for coronary artery disease
What drug may be helpful in pts with very severe nausea and vomiting ? Parenteral metoclopramide
5-HT1d/1b RECEPTORS AGONISTS in aborting migraine headache Dihydroergotamine, Ergotamine, Sumatriptan, Zolmitriptan
Ergotamine / Dihydroergotamine activation of presynaptic 5-HT1d/1b receptors in the trigeminal neurovascular system leads to ? Inhibition release of peptides that cause vasodilation - relieve migraine
Ergotamine / Dihydroergotamine activation of postsynaptic 5-HT1d/1b receptors in cerebral blood vessels leads to ? Vasoconstriction
Ergotamine / Dihydroergotamine stimulation of 5-HT1d/1b receptors in the brain stem leads to ? Prevents activation of trigeminal nerves involved in migraine headache (inhibitory receptor)
ADR of Ergotamine ? Ergot poisoning – bewitchment Nausea and vomiting Vasospasm via stimulating Alpha2 receptors - contraindicated in pts with IHD
When are TRIPTANS more commonly used in acute migraines? Early in an attack, when pain is still mild to moderate in intensity, compared to later use in 70-80%
TRIPTANS adverse effects: Coronary vasospasm, tingling or burning sensation in the skin covering various parts of the body, chest tightness, flushing, dizziness, drowsiness
Propranolol __________ concentration of Eletriptan, Rizatriptan and Zolmitriptan increases serum
A Triptan should not be used within ___________ after another triptan or an ergot alkaloid because vasoconstriction could be additive 24 hrs
TRIPTANS should not be used concurrently with _______ or _________ of stopping one MAO inhibitors, within 2 weeks
Rizatriptan and Eletriptan are modestly more effective than ________ whereas Naratriptan and almotriptan are better _______ Sumatriptan, tolerated
__________ is an opioid analgesic with serotonin re-uptake blocking properties (increases 5HT) used for aborting migraine headaches Tramadol
Created by: marshall19