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Pharm - Neuro/DA
Neuro/Drug Abuse Pharmacology from First Aid 2013
| Question | Answer |
|---|---|
| Name five classes of drugs used in the treatment of glaucoma. | Alpha-agonists - dec aqueous humor secretion Beta-blockers - dec aqueous humor secretion Acetazolamide - dec synthesis via CA enzyme Cholinomimetics - contract ciliary muscle to increase outflow Prostaglandin PGF2 - increase outflow |
| What are the side effects of epinephrine, brimonidine (a2) in glaucoma? | Mydriasis; do NOT use in closed-angle glaucoma. Blurry vision, ocular hyperemia, ocular pruritis. |
| What are some beta blockers used in glaucoma? What are their side effects? | Timolol, betaxolol, carteolol: no ocular SFX |
| What are the side effects of using acetazolamide to treat glaucoma? | Nothing. |
| What are some cholinergics used to treat glaucoma? What are their side effects? | Direct: Pilocarpine, carbachol Indirect: physostigmine, echothiophate Use pilocarpine in emergencies. All may cause miosis and ciliary muscle contraction, increasing outflow, but not halting secretion. |
| Which is the drug name of the prostaglandin PGF2 that is used in glaucoma to increase outflow? What is its side effect? | Latanoprost - darkening of the iris |
| What are the three opioid receptor classes? What is their cellular MOA? | Mu, kappa, and delta: they open K+ channels, close Ca2+ channels, and decrease synaptic transmission. They also inhibit the release of most NT's and substance P. |
| Name several full opioid agonists. | Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextramethorphan, diphenoxylate. |
| Which opiates are used for: 1. Diarrhea? 2. Cough suppression? 3. Addiction maintenance? 4. Acute pulmonary edema | 1. loperamide, diphenoxylate 2. dextramethorphan 3,4. methadone |
| What are the signs of opioid toxicity? What would you use to treat overdose? | respiratory depression, constipation, miosis ("pinpoint pupils"). Treat with: Naloxone, naltrexone |
| Butorphanol: MOA, Use, Tox | MOA: mu-opioid partial agonist, kappa agonist Use: severe pain (labor, migraine), less risk of respiratory depression Tox: Competes with full agonists and so can produce withdrawal symptoms if taken with other opiates. Not easily reversed. |
| Tramadol: MOA, Use, Tox | MOA: weak agonist, also an SNRI Use: chronic pain Tox: decreases seizure threshold |
| What are the symptoms of opioid withdrawal? | Sweating, dilated pupils, piloerection, vomiting, diarrhea, stomach cramps, rhinorrhea |
| What are the uses for Naloxone, Naltrexone? | Opioid toxicity. |
| What is the treatment for opioid withdrawal? | Nothing; treat symptoms. |
| What is the first-line treatment for simple, complex, and tonic-clonic seizures, and trigeminal neuralgia? | Carbamazepine |
| What is the first-line treatment for tonic-clonic seizures alone? | Valproate |
| What is the first-line treatment for absence seizures? | Ethosuximide |
| What is the treatment for status epilepticus? | Benzodiazepines (diazepam or lorazepam) |
| Seizures occurring as part of ecclampsia are classically treated with what? What epilepsy drugs may be added? | MgSO4, may add benzodizepines |
| Phenytoin: MOA, Use | MOA: blockade of Na channels and Glut release Use: Tonic-clonic szs, or as Class IB AA |
| What are some toxicities and side effects of phenytoin use? | Upreg CYP450, SLE-like syndrome, nystagmus, ataxia, diplopia, sedation, gingival hyperplasia, peripheral neuropathy, magaloblastic anemia, hirsutism, FHS |
| What is fetal hydantoin syndrome? | Maternal phenytoin use --> microcephaly, hypoplastic nails and phalanges, cardiac defects |
| Carbamazepine: MOA, Use, Tox | MOA: Na+ channel inactivation Use: 1st line for everything exc Absence sz Tox: diplopia, ataxia, blood dyscrasias, CYP450, SIADH, SJS |
| Ethosuximide: MOA, Use, Tox | MOA: blocks thalamic Ca2+ channels Use: absence seizures Tox: E-->FGH: Fatigue, GI, Headache |
| Valproate: MOA, Use, Tox | MOA: block Na, increase GABA Use: tonic-clonic or myoclonic seizures migraine prophylaxis Tox: GI, hepatotox, NT defects if pregnant weight gain |
| Topiramate: MOA, Use, Tox | MOA: block Na, increase GABA Use: 2nd line seizures, migraine prevention Tox: sedation, mental dulling, kidney stones, WEIGHT LOSS |
| Benzodiazepines: naming, MOA | Nom: -zepam, -zolam MOA: increase FREQUENCY of Cl- channel opening at GABA-A receptor |
| What are the clinical uses for benzodiazepines? | Anxiety, spasticity, status epilepticus, night terrors, sleep walking, hypnotic, alcohol withdrawal/detox |
| What are the toxicities of benzodiazepines? | Addiction, CNS depression with alcohol, less risk of respiratory depression than with barbiturates. |
| What is the treatment for benzodiazepine toxicity/overdose? | Flumazenil - competitive antagonist for GABA receptor |
| What is the treatment for alcohol withdrawal? | Benzodiazepines |
| What are the symptoms of benzodiazepine withdrawal? | Delirium, respiratory depression, seizure, anxiety, autonomic instability, cardiac arrest |
| Barbiturates: naming, MOA | Nom: -barbital, -pental MOA: increase DURATION of Cl- channel opening at GABA-A receptor |
| What are the clinical uses for barbiturates? | Anxiety, seizures, insomnia, induction of anesthesia (thiopental). |
| What are the toxicities of barbiturates? | Respiratory and CV depression, CNS depression with EtOH use, addiction, CYP450 interactions |
| What is the treatment for barbiturate toxicity/overdose? | Nothing; assist respiration and maintain BP |
| What are the symptoms for barbiturate withdrawal? | Same as for benzos: delirium, respiratory and cardiac depression, seizure, anxiety, autonomic dysregulation |
| What are some examples of non-benzo hypnotics? | Ambien (zolpidem), zaleplon, eszopliclone |
| How do non-Benzo hypnotics work? What are they used for? | They act via the BZI subtype of GABA receptors to treat insomnia. |
| What are the toxicities for non-benzo hypnotics, and how are they treated? | Ataxia, headaches, confusion. All of shorter duration and with less risk of dependence than other hypnotics. Immediately reversed with flumazenil. |
| General anesthetic induction, duration, and potency is governed by what variable? | Lipid-solubility: more hydrophobic = slower onset but high potency; less hydrophobic = faster onset and recovery time |
| In general anesthesia, what is MAC, and what is its relationship to potency? | Mean alveolar concentration = the concentration at which 50% are anesthetized. Potency = 1/[MAC] |
| Compare the potency and solubility of halothane vs. nitrous oxide. | Halothane (lipid solb) - slow induction, high potency N2O (less solb) - fast induction and recovery |
| Inhaled anesthetics: naming, MOA | Nom: halothane, N2O, "-flurane" MOA: unknown |
| Inhaled anesthetics: Effects, Tox | Eff: CV/Resp depression, N/V, increased cerebreal blood flow with decreased cerebral metabolic demand Tox: liver(halothane), kidney(methoxyflurane), convulsant(enflurane), malignant hyperthermia (all exc N2O) |
| How do you treat malignant hyperthermia, and what is its MOA? | Dantrolene: blocks the Ryr Ca2+ channel in the sarcoplasmic reticulum |
| What are the two classes of local anesthetics? | Esters: procaine, cocaine, teracaine Amides: lidocaine, et al (two I's in name) |
| What is the MOA and effect of local anesthetics? | MOA: block Na+ channels Block small nerve > larger nerve, myelinated > unmyelinated; lose pain, then temperature, then touch, then pressure. Need more with infected (acidic) tissue. Enhanced effect with vasoconstrictors. |
| Local anesthetics: Use, Tox | Use: minor surgeries, spinal anesthesia Tox: CNS excitation, HTN/hypoTN, cardiac toxicity, arrhythmias |
| What are the two classes of neuromuscular blocking agents? | Depolarizing (Succinylcholine) Non-depolarizing (-curium, -curonium) |
| Succinylcholine: MOA, Effect, Tox | MOA: Ach agonist, initial fasiculations, then blockade Phase 1: prolonged, depolarized Phase 2: repolarized but blocked Cholinesterase inhibitors will potentiate Phase 1, and reverse Phase 2. Tox: hyperCa, hyperK, malignant hyperthermia |
| Non-depolarizing NM blocking drugs: MOA, Tox | Competitive Ach antagonists, reversible with neostigmine or edrophonium |
| What are the symptoms of LSD intoxication? | CNS depression, anxiety, hallucination, delusion, flashbacks when sober, pupil dilation. |
| What are the symptoms of PCP/ketamine abuse? | Belligerence, fever, agitation, violent psychosis, vertical and horizontal nystagmus. |
| What are the symptoms of PCP/ketamine withdrawal? | Depression, anxiety, restlessness, disturbed sleep. |
| What is the treatment for PCP/ketamine withdrawal? | Benzodiazepines and haloperidol. |
| What are the symptoms for stimulant drug abuse? | increased mood, psychomotor agitation, insomnia, cardiac arrhythmia, tachycardia, anxiety, pupil dilations (cocaine and amphetamines) |
| What are the symptoms for stimulant withdrawal? | Depression, lethargy, somnolence, weight gain/hunger, headache, craving, suicidality (esp. cocaine) |
| What are the symptoms for depressant drug abuse? | Euphoria, decreased anxiety, sedation, behavioral disinhibition, respiratory depression. |
| What are the symptoms for depressant withdrawal? | Anxiety, tremor, seizures, insomnia |
| What is delirium tremens? What is its treatment? | Usually alcohol withdrawal with formication "crawlies," nightmares, hallucinations, diaphoresis, tremors, dysphoria. Treat with benzodiazepines. |
| What is the treatment strategy for Parkinson's Disease? | BALSA: B-Bromocriptine A-Amantadine L-L-Dopa (with Carbidopa) S-Selegiline A-Antimuscarinics |
| Bromocriptine: MOA, Use, Tox | Ergot-derived DA agonist. Used to increase DA in Parkinson's. Non-ergots (pramipexole, ropinirole) are preferred because ergots can cause vasoconstriction (CREST, Buergher's). |
| Amantidine: MOA, Use, Tox | MOA/Use: inc DA release in Parkinson's, also an antiviral for Influenza A and rubella Tox: ataxia |
| What is L-Dopa/Carbidopa used for? | L-DOPA: Converted to DA in Parkinson's. Carbidopa: peripheral decarboxylase inhibitor limits DA side effects peripherally |
| Selegiline: MOA, Use, Tox? | MOA: MAO-B inhibitor, prevent DA breakdown Also, COMT inhibitors Use: Parkinson's Tox: May enhance adverse effects of DA |
| What are side effects of long-term L-DOPA use? | Arrhythmia, dyskinesia, akinesia between doses |
| Which anti-muscarinic is used in Parkinson's? | Benzotropine: improves tremor and rigidity, no effect on bradykinesia |
| What two drug classes are given in Alzheimer's disease? | (1) NMDA antagonists: Memantine (2) Ach inhibitors |
| Memantine: MOA, Use, Tox | MOA: NMDA antagonist, prevents cytotoxicity Use: Alzheimers Tox: Dizziness, confusion, hallucination |
| Donezipil, galantamine, rivastigmine: Use, Tox | Use: Ach inhibitors for Alzheimer's Tox: Nausea, dizziness, insomnia |
| What drugs are used in the treatment of Huntington's? | In the dz: dec GABA, dec ACh, inc DA...so: Tetrabenazine and reserpine (inhibit VMAT to decrease DA packaging) Haloperidol (DA receptor antagonist) |
| Sumatripan: MOA, Use, Tox | MOA: 5HT agonist inhibits CN-V activation and induces vasoconstriction Use: acute migraines and cluster headaches Tox: Prinzmetal's vasospasm |
Created by:
wmwebb89
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