Neurology Flashcards

Question

Hypnotics | Zolpidem, Zaleplon, Eszopiclone

Answer 1

MOA: act via BZ1 subtype of GABA receptor Use: Insomnia Avd. effects: ataxia, headaches, confusion modest day-after psychomotor depression and few amnestic effects less dependence risk than benzodiazepines sleep cycle less affected than with benzo Effects reversed by flumazenil

Answer 2

inhaled anesthetic low blood and lipid solubility -----> fast induction and low potency

Answer 3

inhaled anesthetic high lipid and blood solubility ------> high potency and slow induction

Answer 4

MOA: unknown ``` Effects: Myocardial depression Respiratory depression Nausea / Emesis Increase cerebral blood flow (decrease cerebral metabolic demand) ``` ``` Adv. effects: Hepatotoxicity (Halothane) Nephrotoxicity (Methoxyflurane) Proconvulsant (Enflurane) Expansion of trapped gas in a body cavity (N2O) Malignant hyperthermia ```

Answer 5

life threatening Inhaled anesthetics or succinylcholine induce fever and severe muscle contractions Susceptibility can be inherited as AD w/ variable penetrance. Mutations in voltage-sensitive ryanodine receptor cause increase Ca2+ release from sarcoplasmic reticulum. Treatment: Dantrolene (ryanodine receptor antagonist)

Answer 6

Intravenous anesthetic High potency, high lipid solubility, rapid entry into brain Used for induction of anesthesia and short surgical procedures Effect terminated by rapid distribution into tissue and fat Decrease cerebral blood flow

Answer 7

Intravenous anesthetic Used for endoscopy Used adjunctively w/ gaseous anesthetics and narcotics May cause severe postoperative respiratory depression, decrease BP (treat overdose w/ flumazenil), anterograde amnesia

Answer 8

Intravenous anesthetic PCP analogs that act as dissociative anesthetics Block NMDA receptors Cardiovascular stimulants Cause disorientation, hallucination, bad dreams Increase cerebral blood flow

Answer 9

Intravenous anesthetic Used for sedation in ICU, rapid anesthesia induction, short procedures Less postoperative nausea than thiopental Potentiates GABAa

Answer 10

Intravenous anesthetic | Morphine, fentanyl used with other CNS depressants during general anesthesia

Answer 11

MOA: Block Na+ channels (bind inner portion of channel) Most effective in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form. Can be given with vasoconstrictors (like epinephrine) to enhance local action - decrease bleeding, increase anesthesia by decreasing systemic concentration. In infected tissue - alkaline anesthetics are charged and cannot penetrate membrane effectively --> need more anesthetic Order of nerve blockade: small-diameter fibers > large diameter fibers Myelinated fibers > unmyelinated fibers small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers Order of loss: pain, temperature, touch, pressure Use: Minor surgical procedures, spinal anesthesia If allergic to esters, give amides ``` Adv. effects: CNS excitation Severe cardiovascular toxicity (bupivacaine) Hypertension Hypotension Arrythmias (cocaine) Methemoglobinemia (benzocaine) ```

Answer 12

Strong ACh receptor agonist Produces sustained depolarization and prevents muscle contraction ``` Reversal of blockade: Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors Phase II (repolarized but blocked; ACh receptors are available, but desensitized) - may be reversed with cholinesterase inhibitors ``` Use: Muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor. Complications include hypercalcemia, hyperkalemia, malignant hyperthermia

Answer 13

Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium - Competitive antagonists - compete with ACh for receptors Reversal of blockade - neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

Answer 14

MOA: prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor Use: Malignant hyperthermia Neuroleptic malignant syndrome (toxicity of antipsychotic drugs)

Answer 15

MOA: Activates GABAb receptors at spinal cord level, including skeletal muscle relaxation ``` Use: Muscle spasms (ex. acute low back pain) ```

Answer 16

MOA: Centrally acting skeletal muscle relaxant Structurally related to TCA, similar anticholinergic side effects Use: Muscle spasms

Answer 17

Ergot Dopamine agonist Parkinson drug

Answer 18

Non ergot Dopamine agonist Parkinson drug

Answer 19

Increase dopamine release Decrease dopamine reuptake Toxicity = ataxia, livedo reticularis Use: Parkinson

Answer 20

``` MOA: Increase level of dopamine in brain Prevent peripheral (pre-BBB) L-dopa degradation --> Increased L-DOPA entering CNS --> Increased L-DOPA available for conversion to dopamine Carbidopa blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase; also reduces side effects of peripheral L-dopa conversion into dopamine (nausea, vomiting) ``` Use: Parkinson

Answer 21

Act centrally (post-BBB) to inhibit breakdown of dopamine MOA: Prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT Tolcapone works centrally to block conversion of dopamine to 3-OMD by inhibiting central COMT Use: Parkinson

Answer 22

Act centrally (post-BBB) to inhibit breakdown of dopamine MOA: Blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B. Use: Parkinson

Answer 23

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+) Adv. effects: Dizziness, Confusion, Hallucinations Use: Alzheimer's

Answer 24

MOA: AChE inhibitors Adv. effects: Nausea, dizziness, insomnia Use: Alzheimer's

Answer 25

MOA: Inhibit vesicular monoamine transport (VMAT) --> decrease dopamine vesicle packaging and release Use: Huntington's

Answer 26

D2 receptor agonist Use: Huntington's

Answer 27

Treatment for ALS that modestly increase survival by decreasing glutamate excitotoxicity via an unclear mech. "For Lou Gehrig disease, give riLOUzole"

Answer 28

``` MOA: 5HT 1B/1D agonists Inhibit trigeminal nerve activation Prevent vasoactive peptide release Induce vasoconstriction ``` Use: Acute migraine Cluster headache attacks Adv. effects: Coronary vasospasm Mild paresthesia Contraindicated in patients with CAD or Prinzmetal angina