Drugs Flashcards

Question

levertiracetam use, mOA, SE

Answer 1

USE: partial, toninc clonic MOA: unknown SE: fatigue, HA, psych issues

Answer 2

USE: all seizure types MOA: blocks Na, decreases glutamate SE: SJS

Answer 3

USE: partial,tonic clonic, migraine prophylaisis MOA: increases GABA SE: sedation, kidney stones

Answer 4

USE:partial, pheripheral neuropathy MOA: blocks Ca, GABA analog SE: sedation, ataxia

Answer 5

USE: tonic clonic MOA: blocks Na, increasea GABA SE: GI distress, hepatotoxicity, pancreatitis, trmor, weight gain tertogenissi: neural tube defects

Answer 6

USE: partial MOA: blocks Na, decreases glutamate SE: SJS, SIADH, diplopia, ataxia, agranucytosis tertogenissi: cleft palate

Answer 7

USE: gran-mal, status epilepticus MOA: blocks Na SE: SJS, SLE, diplopia, ataxia, mregloblastic anemia tertogenissi: fetal hydantoin syndrome

Answer 8

USE: partial, gran-mal MOA: increase GABA SE: sedation, tolerance/dependence, resp. depression

Answer 9

USE: status elipticas MOA: increase GABA SE: sedation, tolerance/dependence, resp. depression

Answer 10

USE: absences seizures MOA: blocks thalamic Ca channels SE: SJS, fatgiue, GI distress, HA, itiching

Answer 11

* Newborn: Ampicillin + gentamicin/cefotaxime * 2 – 50 y/o: Vancomycin + ceftriaxone/cefotaxime * \>50 y/o: Ampicillin + vancomycin + ceftriaxone/cefotaxime * Dexamethasone is indicated in bacterial meningitis

Answer 12

Abx (vancomycin/naficillin + ceftriaxone/cefotaxime + metronidazole) + drainage

Answer 13

antiretroviral therapy (ART)

Answer 14

penicillin

Answer 15

Amphotericin B + fluconazole

Answer 16

* Treatment: ganciclovir, valganciclovir, foscarnet

Answer 17

antiretroviral treatment for HIV

Answer 18

* Glatiramer acetate: decreases Th1 cells via Th reg cells * category B * IFN-beta: prevents T-cell migration * SE: flu * Fingolimod: prevents T-cell migration to CNS by holding lymphocytes in lymph nodes * Teriflunomide: decreased T-cell synthesis * Dimethyl fumarate: decreases inflammatory response via activation of Nrf2 pathway

Answer 19

* Natalizumab: binds integrin preventing T-cell migration * Risk of PML * Mitoxantrone: causes breakage in DNA à immunosuppression

Answer 20

botulin SE: dysphagia

Answer 21

* Treatment: pyridostigmine (AchE inhibitor), prednisone, IVIG, plasmapharesis

Answer 22

expondys 51

Answer 23

* Treatment: splints at nighttime (avoid flexion of wrist), steroid injection (outside of tunnel), surgery to open tunnel

Answer 24

* Treatment: supportive, mechanical ventilation if needed, plasmapheresis/IVIG (attacks ABs), NO steroids

Answer 25

* Treatment: Riluzone, Edavarone

Answer 26

* Dopamine precursor (Levodopa) * MOA: Dopamine precursor given orally à absorbed in duodenum * Bypasses rate-limiting step of dopamine synthesis * Side effects: dyskinesia (abnormal involuntary movements) after long-term use, nausea, GI upset, lowers BP * Carbidopa (prevents peripheral breakdown of Levodopa into dopamine) is now given in combination to minimize these side effects

Answer 27

* MOA: inhibits serotonin reuptake by serotonin transporters --\> increased serotonin in terminal * SE (fewer than TCAs): GI distress (most common 1st), SIADH, sexual dysfunction, suicidal thoughts (not contraindication)

Answer 28

* P450 reactions: fluoxetine, fluvoxamine paroxetine (less metabolism of drugs like Tamoxifen, TCAs, etc)

Answer 29

* Etiology: Due to excess serotonin secondary to SSRIs, stoppage of MAOI, combos of sertotnergic drugs (i.e. Tramadol, linezolid) * Signs/sx: AMS, GI sx, diaphoresis, myoclonus/hyperreflexia

Answer 30

* Suspect after: use of short-life drug (i.e. Paroxetine) * Sx: dizziness, HA, N/V, anxiety, paresthesias

Answer 31

* MOA: inhibits serotonin and norepinephrine reuptake by serotonin transporters à increased serotonin and norepinephrine in terminal * SE: HTN

Answer 32

* MOA: inhibits 5-HT and NE reuptake in CNS * SE: anticholinergic effects, antihistaminergic effects (sedation), alpha blockage (hypotension)

Answer 33

Nortriptyline, Desipramine, Maprotiline

Answer 34

Imipramine, Amitriptyline)

Answer 35

* Toxicity: cardiac arrhythmias/convulsions/coma (3 Cs) secondary to Na blockade, wide QRS (administer bicarb)

Answer 36

* MOA: Inhibits monoamine oxidase located on mitochondria --\> increases [NT] * SE: CNS stimulation, hypertensive crisis w/ ingestions of tyramine (a.a. in wine, cheese, and preserved meats)

Answer 37

* Indications * OCD: Fluvoxamine, Sertraline * Longest half-life: Fluoxetine (if non-compliant pt) * QTC prolongation: citalopram * Short half-life: Fluvoxamine, paroxetine * Less interactions: Citalopram

Answer 38

* Atypical antidepressants * Bupropion * MOA: inhibits reuptake of NE and dopamine * SE: seizures (people w/ eating disorders), tachycardia, insomnia * Uses: smoking cessation, sexual dysfunction * Mirtazapine * MOA: alpha-2 antagonist → increase release of NE and 5HT * Blocks 5HT2/3 and H1 receptors * SE: sedation, increased appetite/weight gain, dry mouth * Trazodone * MOA: blocks 5HT2, alpha1, and H1 receptors and inhibits 5HT reuptake * SE: sedation, priapism (traZZZobone) * Uses: insomnia * Nefazodone * MOA: blocks 5HT2, alpha1, and H1 receptors and inhibits 5HT reuptake * SE: hepatotoxicity

Answer 39

* Varenicline * MOA: nicotinic Ach agonist * SE: sleep disturbance, depress mood * Uses: smoking cessation * Vilazodone * MOA: inhibits 5HT reuptake + 5HT1A agonist * SE: HA, GI issues, weight gain, anticholinergic effects * Vortioxetine * MOA: inhibits 5HT reuptake + 5HT1A agonist * SE: nausea, sexual dysfunction, abnormal dreams, anticholinergic effects

Answer 40

**Typical Antipsychotics (-azine)** * MOA: block D2 receptor and secondary M1/H1/alpha-1 blockade * Storage: body fats (lipid soluble) – slowed to be removed

Answer 41

* Potency: * High (Effects: EPS): trifluoperazine, fluphenazine, haloperidol (Try 2 Fly High) * Low (Effect: anticholinergic/antihistamine/anti-alpha): chlorpromazine, thioridazine

Answer 42

* D2 blockade: EPS, endocrine changes, sexual dysfunction * EPS * **Hours to days: Dystonic reactions** * Description: uncoordinated spastic movements of muscle groups (i.e. trunk, tongue, face) * Tx: benztropine * **Days to months: Akathisia, Parkinsonism** * Akathisia: extreme restlessness and pacing; may lead to insomnia * Tx: beta blockers * Parkinsonism: tremors of extremities * Tx: Oral antiparkinsonian drugs * **Months to years: Tardive dyskinesia** * Description: involuntary and potentially irreversible movements around oral area * Dx: Abnormal Involuntary Movement Scale (AIMS) * Tx: benztropine; change dosage of meds

Answer 43

* Neuroleptic malignant syndrome (life-threatening) * Signs/sx (Malignant FEVER): Myoglobinuria (breakdown of muscles from movement), Fever, Encephalopathy, Vitals unstable, Enzymes increased, Rigidity of muscles * Tx: discontinuation of antipsychotic, Dopamine agonists (bromocriptine/dantrolene)

Answer 44

* H1 blockade: sedation, drowsiness, weight gain, hypotension * Alpha-1 blockade: postural hypotension, reflex tachycardia, dizziness * M1 blockade: blurred vision, dry mouth, sinus tachycardia, constipation, urinary retention, memory dysfunction * Other: corneal deposits (chlorpromazine), retinal deposits (thioridazine), QT prolongation

Answer 45

**Atypical Antipsychotics/Second-Generation (-apine, -peridone, -idone)** * MOA: post-synaptic blockade of D2 receptor and secondary 5HT-2A blockade * Equal efficacy as first-generation; less side effects

Answer 46

* \*\*Aripiprazole: partial D2 agonist * Hyperdopaminergic areas (mesolimbic area) → antagonist →+ sx * Hypodopaminergic areas (mesocortical area) → agonist → - sx

Answer 47

* Benefits: rare EPS, rare increase in prolactin, reduced negative sx * Side effects: prolonged QT

Answer 48

* -Apines: Metabolic syndrome * Clozapine: agranulocytosis, seizures, reduced risk of suicide, must monitor CBC * Risperidone: increased prolactin (only second gen), less weight gain * Olanzapine: weight gain * Ziprasidone: prolongs QT interval, dizziness, somnolence * Quetiapine: lenticular opacities, HA, increased AST

Answer 49

resistent pyshcosis.. when no other drug works

Answer 50

SSRi, clomipramine

Answer 51

SSRIs, and venlafaxine are first line. Prazosin can reduce nightmares.

Answer 52

lithium, valporate, carbamazepine, oxcarbazepine, lamotrigine

Answer 53

* Proposed MOAs: * Interactions with cation transport process by substituting for Na+ à direct effect on NTs (i.e. serotonin, dopamine, NE, Ach) OR inhibits PIP3 pathway * Side Effect * Teratogenicity (cardio malformations: Ebstein’s anomaly), goiter, hypotonia, CNS depression * SE: tremor, hypothyroidism (weight gain, GI distress, fatigue), nephrogenic diabetes insipidus (ADH inhibited à polyuria), metallic taste

Answer 54

Antidepressants, BZDz, Z drugs, beta agonists, buspirone

Answer 55

* MOA: enhance the effect of GABA by binding on GABA A receptor --\> increased rush of chlorine into post-synaptic * SE: tolerance (increased dose to produce effect), sedation, ataxia, anterograde amnesia, confusion, muscle weakness, withdrawal (anxiety, insomnia, muscle twitches/tremors, etc)

Answer 56

* Short half-life: alprazolam (Xanax), Triazolam, Lorazepam (Ativan) * Long half-life: diazepam (Valium), Chlordiazepoxide (Librium) orazepam has slowest absorption

Answer 57

* MOA: same as benzodiazepines * SE: less than benzos (no tolerance, no physical dependence, no sleep disturbance)

Answer 58

* MOA: partial agonist for 5-HT1A receptors in brain * Disadvantages: Slow onset of action; short half-life (needed 2-3x per day) * Advantages: no physical dependence, no abuse potential, less sedation, less interaction with alcohol

Answer 59

* First line: haloperidol (typical psychotic) * Benzos for withdrawal from alcohol/benzos/barbiturates or seizures * Cholinergic meds are only indicated in cases caused by anticholinergics or antihistamines (may have secondary anticholinergic effects) * Avoid anticholinergic drugs in treatment

Answer 60

* Cholinesterase inhibitors (Donepezil, Galantamine, Rivastigmine) * MOA: block cholinesterase à increased ACh * SE: GI sx (diarrhea), leg cramps, vivid dreams, bradycardia * Memantine * MOA: NMDA receptor antagonist * Anti-Amyloid-beta Antibody

Answer 61

* Examples: morphine/codeine, oxycodone (semi-synthetic opioids), fentanyl (synthetic opioid) * Demerol (Meperidine) dilates pupils (exception) * Tramadol: can cause serotonin syndrome (careful with SSRI); less addiction potential * MOA (euphoria): binds to Mu receptor → ↓ release of GABA → lack of GABA stimulation → dopamine release from neighboring neuron (Opioid = dope) * Acts at nucleus accumbens (reward) * MOA (analgesia): binds to Mu-GPCR→ hyperpolarization → ↓ NT → analgesia * Acts at anterior cingulate cortex, thalamus, periaqueductal gray (pain areas)

Answer 62

* Toxidrome (all decreases): ↓ HR/BP, ↓ RR (overdose risk), ↓ temp, ↓ pupil size (constriction), ↓ bowel sounds, ↓ sweating, euphoria * Tx: naloxone (opioid antagonist) * Withdrawal (opposite of toxidrome): dilated pupils, tachycardia/HTN, V/D, insomnia, sweating, craving for drug, dysphoria, piloerection (goosebumps), myalgia * Tx (not life-threatening) * Methadone (long-acting opioid full agonist) * Buprenorphine (partial opioid receptor agonist) * Naltrexone (competitive opioid antagonist)

Answer 63

* MOA: dopamine reuptake inhibitor * Toxidrome (all increases): ↑HR/BP, ↑RR, ↑Temp, ↑pupil size (dilation), ↑bowel sounds, ↑sweating * Complications: arrhythmias, MI, respiratory distress * Acute management for agitation: benzodiazepines or anti-psychotics (severe) * Withdrawal (opposite of toxidrome): constricted pupils, malaise, fatigue, hypersomnolence, depression, vivid dreams, psychomotor agitation * Tx: supportive (not life-threatening)

Answer 64

* Classic MOA: blocks reuptake → facilitates release of dopamine and NE from nerve endings → stimulant * Examples: methamphetamine (“speed”, “meth”), Ritalin, Dexedrin * Use: ADHD, narcolepsy, depression * Substituted (designer) MOA: release of dopamine, NE, and serotonin from nerve endings → stimulant, hallucinogen * Examples: MDMA (Ecstasy)

Answer 65

* Toxidrome (all increases): ↑HR/BP, ↑RR, ↑Temp, ↑pupil size (dilation), ↑bowel sounds, ↑sweating * Chronic use can lead to tooth decay (meth mouth)

Answer 66

* Benzodiazepine (BDZs) MOA – gamma unit: increases Cl- channel opening → more Cl- in post-synaptic cell → GABA potentiator * BZDs are not lethal alone * Examples: Diazepam (Valium), alprazolam (Xanax), Chlordiazepoxide (Librium), lorazepam (Ativan) * Barbiturate MOA - beta unit: increases Cl- channel opening → more Cl- in post-synaptic cell → GABA potentiator

Answer 67

* Toxidrome (all decreased – except eyes): ↓HR/BP, ↓RR, ↓Temp, ↓Bowel sounds, ↓Sweating, drowsiness, slurred speech, ataxia, * Tx: * BDZ: Flumazenil (short-acting BDZ antagonist) * Barbiturate: Na-HCO3 (promotes renal excretion) * Withdrawal (life threatening): HTN/tachycardia (medical emergency), hand tremor, psychomotor agitation, N/V, anxiety, irritability, sweating * Complications: tonic-clonic seizure * Tx: phenobarbital, clonazepam (anti-epileptics)

Answer 68

* MOA: activates GABA (alpha) and serotonin receptors in CNS → depressant * Metabolism: alcohol → acetaldehyde (via alcohol dehydrogenase) → acetic acid (via aldehyde dehydrogenase) * Asian glow: lack aldehyde dehydrogenase (less susceptible to dependence) * Toxidrome * \<50 mg/dL: impairment in skilled tasks, increased talkativeness, relaxation * \>100 mg/dL: ataxia, hyperreflexia, impaired judgement, lack of coordination, nystagmus, slurred speech * \>200 mg/dL: amnesia, diplopia, N/V, hypothermia, dysarthria * \>400 mg/dL: respiratory depression, coma, and death

Answer 69

* Delirium Tremens (DT): peaks 2-4 days after last drink; characterized autonomic hyperactivity (tachycardia/HTN, tremors, sweating, anxiety, etc) * Tx: BZDs (Chlordiazepoxide – Librium, Lorazepam, Diazepam) → taper * Wernicke’s encephalopathy: encephalopathy, oculomotor dysfunction, ataxia * Korsakoff’s syndrome (chronic dz from untreated Werkicke’s): * Pathophysiology: necrosis of mamillary bodies (often irreversible) Sx: Retrograde/anterograde amnesia, confabulation, unaware of illness

Answer 70

* Disulfiram * MOA: blocks aldehyde dehydrogenase (Asian glow – flushing, N/V) * Contraindicated in cardiac disease, pregnancy, LFTs must be monitored, adherence is low * Naltrexone * MOA: opioid receptor antagonist → decreases cravings and high associated with alcohol * Acamprosate * MOA: GABA-like agonist * Use: post-detox; indicated in patients with liver disease * Topiramate * MOA: GABA potentiator * Use: reduces cravings * Gabapentin (only if vital signs are stable)

Answer 71

* MOA: THC → binding to cannabinoid receptors on presynaptic neuron → inhibition of adenyl cyclase → release of inhibitory NT (GABA) * Toxidrome: impaired motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgement, conjunctival injection (red eyes), increased appetite, dry mouth, tachycardia * These symptoms cannot be explained by another substance or mental disorder * Complications: Cyclic vomiting syndrome (daily vomiting relieved by showering) * Dx: Stop marijuana use for two weeks to see if causal

Answer 72

* Examples: antihistamines (Benadryl). TCAs (Amitriptyline) * MOA: inhibition of Ach receptor * Toxidrome: ↑HR/BP, ↑Temp, ↑pupil dilated, ↓Bowel sounds, ↓Sweating, confusion, agitation * SE: Hot, dry, blind, red, mad

Answer 73

* LSD MOA: believed to act on serotoninergic receptors * Toxidrome: VS stable, perceptual distortion, depersonalization, anxiety, paranoia * PCP MOA: NMDA glutamate receptor antagonist → activates dopamine release * Toxidrome: anesthetic, dissociative, violence, impulsivity, tachycardia/HTN. Seizures * Tx: BZDs, rapid-acting anti-psyhotics * Other example: K2/synthetic marijuana, magic mushrooms, ketamine (anti-depressant effects), MDMA

Answer 74

* MOA: adenosine antagonist → increase in cAMP → stimulant effect via dopaminergic system * Toxidrome * 250 mg (2 cups): anxiety, insomnia, muscle twitching, GI problems, tachycardia * \> 1 g: tinnitus, agitation, cardiac arrhythmias * \>10 g: death secondary to seizures/respiratory failure * Withdrawal: headache, nausea, vomiting, depression, irritability

Answer 75

* Epidemiology: smoking common in patients with mental illness * Known to increase chronic pain * MOA: stimulates nicotinic receptors and autonomic ganglia of the SNS/PNS * Highly addictive via the dopaminergic system * Toxidrome: restlessness, insomnia, anxiety, increased GI motility * Withdrawal: cravings, dysphoria, anxiety, decreased HR, increased appetite, insomnia

Answer 76

* Nicotine replacement therapy (patches, gums, sprays) * Bupropion: antidepressant (partial agonist of nAChR & inhibits dopamine reuptake → reduces withdrawal sx) * Varenicline: antidepressant (partial agonist of nAChR → mimics nicotine → reduces withdrawal sx) * Nortriptyline: antidepressant

Answer 77

* MOA: modulates GABA à blocks neuroexcitation * Pharmacokinetics: rapid onset and metabolism * Organ system effects: respiratory depression, decreases cerebral flow à decreased ICP, _suppresses cortisol_ synthesis (adrenal insufficiency), increases _seizure risk_

Answer 78

* MOA: NMDA glutamate antagonist * Pharmacokinetics: rapid onset/short duration; lipid soluble (crosses BBB); liver excretion * Organ system effects: dissociation (disconnection from thoughts/memories); increased BP/HR; _increased ICP_ * SE: hallucinations/dreams, disorientation

Answer 79

* MOA: activates GABA-A receptors à Cl influx à hyperpolarization * Pharmacokinetics: rapid onset; eliminated through liver * Organ system effects: myocardial depression; hypotension; respiratory depression, _decreased ICP, decreases seizures_

Answer 80

depolarizing * MOA: Ach agonist --\> sustained depolarization --\> desensitization --\> prevents muscle contraction

Answer 81

* Examples (-cur-): Rocuronium, Atracurium, Pancuronium * MOA: competitive Ach antagonist

Answer 82

* Neostigmine given (cholinesterase inhibitor – causes bradycardia) * Atropine/glycoprolate (anti-muscarinics to counteract bradycardia)

Answer 83

* MOA: opioid agonist at mu-GPCR in CNS à increases K efflux à hyperpolarization à less pain transmission * SE: addiction, respiratory depression, hypotension, constipations, miosis

Drugs Flashcards

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