S&D
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
|---|---|---|---|---|---|
| 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
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
marshall19
Popular Pharmacology sets