First Aid Pharm - Neuro
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74 terms
Terms | Definitions |
|---|---|
 Opiod receptors are this type of receptor, and have these classes: | G-protein coupled receptors (mu, delta, kappa) (μ, δ, κ) |
| Receptor that binds morphine and endorphins? | Mu (μ) opiod receptor |
| Receptor that binds enkephalins? | Delta (δ) opiod receptor |
| Receptor that binds dynorphins? | Kappa (κ) opiod receptor |
| This drug category/class is used for cough suppression, diarrhea; SE: respiratory depression, miosis, CNS depression (coma), constipation | Opiod analgesics |
| Opiod drug; MOA: full mu (μ) agonist; SE: histamine release | Morphine |
| Opiod drug; MOA: full mu (μ) agonist; other: useful for maintenance, long duration, orally active | Methadone |
| Opiod drug; MOA: full mu (μ) agonist; SE: muscarinic antagonist (doesn't cause miosis), don't combine with SSRIs or MAOIs | Meperidine |
| Opiod drug; MOA: full mu agonist (the other commonly used opiod drug besides morphine) | Fentanyl |
| Opiod drug; MOA: partial mu agonist; given in combination with NSAIDS; antitussive | Codeine |
| What are the OTC opiod analgesics? | Dextramethorphan (antitussive), diphenoxylate (antidiarrheal), loperamide (antidiarrheal) |
| This opiod antagonist has a short half-life; IV; used for acute (emergency) opiod overdose (heroin) | Naloxone |
| Opiod antagonist; PO; used to reduce ethanol craving (given to alcoholics); also used for long-term opiod addiction | Naltrexone |
| What symptoms does abstinence syndrome (withdrawal from opiods) feature? | Anxiety, GI distress, gooseflesh, muscle spasms, rhinorrhea, sweating |
| Epilepsy drugs that block Na channels | Phenytoin, carbamazepine, topiramate, lamotrigine, valproic acid |
| This epilepsy drug blocks Na channels; SE: gingival hyperplasia, hirsutism, hydantoin fetus, megaloblastic anemia (↓ folate absorption) | Phenytoin |
| This epilepsy drug blocks Na channels; SE: Steven-Johnson syndrome | Lamotrigine |
| What is a partial seizure? | Simple partial: sensory disturbances; Complex partial: incontinence, post-ictal confusion, déjà vu, lip smacking |
| What is the DOC for treatment of partial seizures, its MOA and SE? | Carbamazepine (stabilizes the inactivated state of sodium channels and ↑ GABA); SE = blood dyscrasias, teratogenic |
| What is a tonic-clonic seizure and its DOC? | "Grand-mal" (freeze/jerk); DOC = Valproate (Valproic acid) |
| What is the MOA and SE of Valproate (Valproic acid)? | ↑ GABA; blocks Na channels and T-type Ca++ channels; SE = rare fatal hepatotoxicity, causes fetal NTDs |
| What is an absense seizure and its DOC? | Blank stare, EEG = 3-Hz spike and wave; DOC = Ethosuximide |
| What is the MOA and SE of Ethosuximide? | Blocks T-type Ca++ channels; SE: fatigue, GI, headache, Steven-Johnson Syndrome |
| What is status epilepticus and its treatment? | Continuous seizures >20min. Treatment: Lorazepam → Phenytoin → Phenobarbital → Midazolam/Intubation |
| What is a febrile seizure and its DOC? | Kids, occurs during rise in temp, not peak temp; DOC = Acetaminophen |
| What is a temporal seizure and its DOC? | Have hallucinations before seizure; DOC = Carbamazapine |
| What is a myotonic seizure? | Increased muscle tone, arms fling forward; DOC = Valproic acid (Valproate) |
| What is a Lennox-Gasteau seizure and its treatment? | Hundreds of seizures every day; DOC = EEG, then lobectomy |
| This epilepsy drug blocks Na channels and ↑ GABA; SE: kidney stones | Topiramate |
| These epilepsy drugs block thalamic T-type Ca++ channels | Ethosuximide, Valproic acid |
| These epilepsy drugs increase GABA | Topiramate, Valproic acid, Benzodiazepines, phenobarbitol, gabapentin |
| This epilepsy drug ↑ GABA; SE: dependence (first line for acute seizures) | Benzodiazepines (diazepam, lorazepam) |
| This epilepsy drug ↑ GABA; SE: dependence (first line for pregnant women, children) | Phenobarbitol (barbiturate) |
| This epilepsy drug ↑ GABA; SE: sedation, ataxia | Gabapentin |
| Which acts faster, highly blood soluble anesthetics or low blood soluble anesthetics? | Low solubility in blood = Rapid induction and recovery. |
| What effect does lipid solubility have on anesthetics? | High lipid solubility = high potency |
| What effect does minimal alveolar concentration of anesthetics have on their potency? | As MAC increases, potency decreases. |
| List the inhaled anesthetics and their MOA. | Halothane (→ hepatitis), isoflurane (used in heart sx), NO2 (→ diffusion hypoxia); these block Na channels from inside! |
| What inhaled anesthetic has hepatotoxicity? | Halothane |
| What inhaled anesthetic has nephrotoxicity? | Methoxyflurane |
| What inhaled anesthetic is a proconvulsant? | Enflurane |
| This class of drugs increases the duration of Cl- channel opening, thereby facilitating GABA-A action (↓ neuron firing) | Barbiturates |
| This class of drugs increase the frequency of Cl- channel opening, thereby facilitating GABA-A action (↓ neuron firing) | Benzodiazepines |
| List the benzodiazepines (3ish) | -zepams, zolams, and chlordiazepoxide |
| This drug is used to treat benzodiazepine overdose and acts as a competitive antagonist at GABA receptor | Flumazenil |
| List the short-acting benzodiazepines (3) | triazolam, oxazepam, midazolam ("TOM thumb") |
| List the intravenous anesthetics (5ish) | B.B. King on OPIATES PROPOses FOOLishly (Barbiturates, benzodiazepines, Ketamine, opiates, propofol) |
| This high potency barbiturate is used for induction of anesthesia in short procedures, decreases cerebral blood flow (IV anesthetic) | Thiopental |
| This benzodiazepine is the most common drug used for endoscopy; may cause severe postoperative respiratory depression (IV anesthetic) | Midazolam |
| A PCP analog used as a dissociative anasthetic; decreases cerebral blood flow (IV anesthetic) | Ketamine (arylcyclohexamines) |
| 2 opiates used with other CNS depressants during general anesthesia (IV anesthetics) | Morphine, fentanyl |
| Used for rapid induction of anesthesia and short procedures, less postoperative nausea than other drugs (IV anesthetic) | Propofol |
| What fibers are affected first by local anesthetics? | Small, myelinated fibers. Pain first, Pressure is last. |
| What do you co-administer with local anesthetics and why? | Vasoconstrictors [Epi] to enhance local action (except cocaine!) |
| What are the local anesthetics (5) with a short half-life? | Esters (cocaine, benzocaine, procaine, tetracaine, novacaine) |
| What are the local anesthetics (5) with a long half-life? | Amides ("two i's" - Lidocaine, Prilocaine, Mepivacaine, Bupivacaine) |
| Local anesthetics MOA | Block Na channels (preferentially bind activated Na channels) |
| What local anesthetics causes CNS excitation and severe cardiovascular toxicity? | Bupivicaine |
| What are neuromuscular blocking drugs used for? | Muscle paralysis in surgery or mechanical ventilation. |
| What receptor do NMJ-blocking drugs target? | NMJ-blocking drugs block transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles, either by acting presynaptically via the inhibition of ACh synthesis/release or by acting postsynaptically at the ACh receptors. |
| What is the only depolarizing NMJ-blocking drug and what are its two phases? | Succinylcholine. Phase 1 = prolonged depolarization. Phase 2 = Repolarized but bloacked. |
| Effect of giving cholinesterase inhibitors in each phase of succinylcholine action. | Phase 1: Cholinesterase inhiitors makes it worse. Phase 2: Reversed by cholinesterase inhibitors |
| What are the nondepolarizing NMJ blockers? | Have cur in the name (end in cararine, curium or curonium) |
| How do you reverse a nondepolarizing NMJ block? | ACh-E inhibitors (neostigmine, edrophonium) |
| How do you treat malignant hyperthermia or neuroleptic malignant syndrome? (same drug) | Dantrolene (prevents release of Ca2+ from SR) |
| What causes malignant hyperthermia? | Using inhaled anesthetics (except NO2) + succinylcholine) |
| What are the drugs used for Parkinson's treatments? | BALSA (Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics) |
| What are the 4 treatment classes for Parkinson's? | Agonize dopamine receptors (bromocriptine), ↑ Dopamine (Amantadine, L-dopa/carbidopa), Prevent dopamine breakdown (MAO-B inh, selegiline), Curb excess cholinergics (benztropine, no effect on bradykinesia) |
| What is the treatment for essential or familial tremors? | β-blockers |
| How does the L-dopa/carbidopa treatment work? | L-dopa crosses the blood brain barrier and is converted in CNS to dopamine. Carbidopa inhibits peripheral decarboxylase. |
| What Parkinson drug causes arrhythmias? | L-dopa (when it's converted to dopamine in periphery) |
| What drug is co-administered with L-dopa in Parkinson's but may enhance its side effects? | Selegiline (MAO-B inhibitor) |
| DOC for treatment of migraines, its MOA and SE? | Sumatripan. 5-HT 1D agonist. Causes vasoconstriction. Short half-life. SE: coronary vasospasm |
| Contraindications for sumatripan? | CAD or prinzmetals (causes coronary vasospasm) |
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