Neurology Flashcards

Question

Gabapentin

Answer 1

MOA: Inihibits voltage activated Ca channels GABA analog Clinical: Simple, complex, tonic clonic Side effects: sedation, ataxia also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

Answer 2

MOA: increase GABA action Clinical: simple, complex, tonic-clonic Side effects: sedation, tolerance, induction of cytochrome P-450, cardiorespiratroy depression 1st line in neonates

Answer 3

MOA: blocks Na channels Increase GABA action Clinical: simple, complex, tonic clonic Side effects: mental dulling, kidney stones, weight loss Used for refractory partial seizures, and migraine prevention

Answer 4

MOA: Increase GABA by inhbiting re-uptake Clinical: simple and complex Also used for refractory partial seizures

Answer 5

MOA: increase GABA by irreversibly inhibiting GABA transaminase Clinical: simpe and complex Also used for refratory partial seizures

Answer 6

Phenoarbital, pentoarbital, thiopental, secobarbital MOA: facilitate GABA by increasing DURATION of Cl- channel opening decreasing neuron firing Contraindicated in porphyria Clinical: sedative for anxiety, seizures, insomnia, induction of anesthesia (theopental) Toxicity: respiratory and cardiovascular depression (can be fatal), CNS depression (exacerbated by alcohol use), dependence Induce cytochrome P-450 Overdose treatment is supportive (assist respiration and maintain BP)

Answer 7

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Bronchodilation properties used in patients with asthma ``` Toxicity: Hepatotoxicity-extensive hepatic necrosis (autoAb damage), Increased AST, ALT and bilirubin Malignant hyperthermia (+succinylcholine) induce fever and severe muscle contractions-Treat with dantrolene ```

Answer 8

MOA: Unknown Clinical: Simple, complex, tonic clonic

Answer 9

Diazepam, temazepam, Chlorodiazepoxide, clorazepate, flurazepam MOA: Facilitate GABA by increasing frequency of Cl- channel opening Decreases REM sleep Clinical: anxiety, spasticity, status epilepticus (diazepam), detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia) Diazepam and chlrodizepoxide are first line treatment for seizures assoicated with alcohol withdrawal Toxicity: Less dependence (due to slower clearance), Higher daytime drowsiness (increased chance of falls), additive CNS ddepression effects with alcohol, less risk of respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly) decreased memory and concentration Avoid with alcohol, barbituates, neuroleptics and 1st gen antihistamines Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

Answer 10

Estazolam, lorazepam, temazepam 10-20 hour duration MOA: facilitate GABA action by increasing frequency of CL- channel opening Decrease REM sleep Clinical: anxiety, spasticity, status epilepticus (lorazepam), detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia) Toxicity: dependence, additive CNS depression with alcohol, less respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly), decreased memory and concentration Treat overdose with flumazenil (competitive antagonist at GABA benzodizepine receptor)

Answer 11

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Toxicity: malignant hyperthermia AD (+succinylcholine) induces fever and severe muscle contractions-treat with dantrolene

Answer 12

Mu-opioid receptor partial agonist and kappa-opioid receptor agonist, produces analgesia Clinical: severe pain (migraine, labor) Toxicity: less respiratory depression can cause opioid withdrawal symptoms

Answer 13

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Bronchodilation properties used in patients with asthma Toxicity: Malignant hyperthermia-AD (+succinylcholine) induces fever and severe muscle contractions-treat with dantrolene

Answer 14

Triazolam, Oxazepam, midazolam and alprazolam (TOM and Al are short) MOA: facilitate GABA action by increasing frequency of Cl- channel opening Decrease REM sleep Clinical: anxiety, spasticity, detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia) Toxicity: dependence, additive CNS depression with alcohol, less respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly), decreased memory and concentration LESS DROWSINESS SEVERE WITHDRAWAL SYMPTOMS AND HIGHER ADDICTIVE POTENTIAL Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

Answer 15

Benzodiazepine used for IV anesthetics Used for endoscopy Used with gaseous anesthetics and narcotics may cause severe postop respiratory depression Decrease BP (treat overdose with flumazenil) anterograde amnesia

Answer 16

Zolpidem (Ambien), Zaleplon, eszopiclone MOA: act via the BZ1 subtype of the GABA receptor. Effect reversed by flumazenil Rapid onset of action Clinical: insomnia Toxicity: ataxia, headaches confusion less risk of dependence than benzodiazepines No antconvulsant or muscle relaxing acitivity Rapid metabolism by liver enzymes

Answer 17

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Toxicity: expansion of trapped gas in a body cavity

Answer 18

Ketamine PCP analogs that act as dissociateive aneshtetics MOA: block NMDA recpetors Cardiovascular stimulants Cause disorientation, hallucination and bad dreams Increase cerebral blood flow Also used in treating morphine tolerance

Answer 19

Barbiturate IV anesthetic High potency and high lipid solubility-rapidly enters brain Great for recovery used of induction of anesthesia and short surgical procedures effect terminated by rapid redistribution into tissue (skeletal muscle and fat) Decreased cerebral blood flow

Answer 20

Used for sedation in ICU Rapid anesthesia induction and short procedures less postop nausea than thiopental Potentiates GABA

Answer 21

Esters: procaine, cocaine, tetracaine Amides: lidocaine, mepivacaine, bupivacaine (amides have 2 i's) MOA: block Na channels by binding to receptors on inner portion of channel Preferentially bind to activated Na channels so most effective in rapidly firing neurons Clinical: with epinephrine to enhance local action leading to decrease bleeding, increase anesthesia by decreasing systemic concentration Cannot penetrate membrane effectively in infected tissue due to acidic environment Affect small diameter fibers and myelinated fibers (size matters more) more than large and unmyelinated Order of loss: pain-temp-touch-pressure Use: minor surgical procedures, spinal anesthesia Toxicity: CNA excitation, severe cardiovacular toxicity (bupivacaine), hypertesnion, hypotension and arrhytmmias (cocaine)

Answer 22

MOA: increase dopamine in brain l-dopa can cross BBB and converted by dopa decarbocylase in the CNS to dopamine Carbidopa: peripheral decarboxylase inhibitor-increases L-dopa bioavalability in the brain limits peripheral side effects not anxiety, agitation, insomnia, confusion, delusions and hallucinations Clinical: parkinsons-will experience on/off phenomenon (unpredictable) Toxicity: arrhytmias from increase peripheral formation of catecholamines can lead to dyskinesia following administartion and akinesia bewtee doses also dystonia (all occur after 5-10 years of use) Somnolence, confusion, hallucinations (first in older people) Do not take with vitamin B6 due to increase peripheral metabolism of levodopa decreasing its effectiveness

Answer 23

Low solubility in blood

Answer 24

Increased solubility in lipids (1/MAC)

Answer 25

Depolarizing neuromuscular blocking drug MOA: strong ACh receptor agonist: produces sustained depolarization and prevents muscle contraction -Not degraded by AChE Reversal of blockade Phase I: (prolonged depolarization)-no antidote potentiated by cholinesterase inhibitors Phase II: (repolarized but blocked-Ach receptors are available but desensitized)-antidote cholinesterase inhibitors Clinical: muscle paralysis in surgery or mechanical ventilation-selective for motor nicotinic receptor Complications: hypercalcemia, hyperkalemia (can lead to rhabdomyolysis especially with halothane) and malignant hyperthermia arrhythmias

Answer 26

MOA: blocks voltage gated Na channels Clinical: simple, complex, tonic clonic, absence Side effects: SJ syndrome Also used for refractory partial seizures, and Bi-polar disorder

Answer 27

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Toxicity: proconvulsant Malignant hyperthermia: AD (+succinylcholine) induces fever and severe muscle contractions-treatment dantrolene

Answer 28

Bromocriptine, pergolide-ergot pramipexole, ropinirole-non-ergot Non ergots perferred due to longer half life MOA: dopamine agonists Treats parkinsons

Answer 29

Inhaled anesthetic MOA: unknown Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow Toxicity: nephrotoxicity Malignant hyperthermia-AD (+succinylcoline) induce fever and severe muscle contractions-treat with dantrolene

Answer 30

MOA: prevent release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle Clinical: treat malignant hyperthermia and neuroleptic malignant syndrome-toxicity of antipsychotic drugs

Answer 31

MOA: selectively inhibits MAO-B which metabolizes dopamine over NE and 5HT increasing the availability of dopamine Clinical: adjunctive agent to L-dopa in treatment of Parkinson toxicity: may enhance adverse effects of L-dopa MPTP produces Parkionsonism (MPP+ created by MAO-B causes damage) can be prevented by pretreatment with selegiline

Answer 32

MOA: COMT inhibitors prevent L-dopa degradation via methylation leading to dopamine availability Clinical: parkinsons Tolcapone can lead to hepatoxicity Dyskinesia, hallucinations, confusion, nausea and ORTHOSTATIC hypotension.

Answer 33

MOA: antimucarinic Clinical: improves tremor and rigidity but has little effect on bradykinesia in Parkinson's Drug induced Parkinson's AE: dry mouth, blurred vision, constipation, nausea and urinary retention

Answer 34

treats Parkinsons MOA: may increase dopamine release AE: ankle edema and livedo reticularis

Answer 35

Nondepolarizing neuromuscular blocking drugs MOA: competitive antagonists of ACh receptors Reversal of blockade: neostigmine (given with atropine to prevent muscarinic effects), edrophonium and other cholinesterase inhibitors Clinical: muscle paralysis in surgery or mechanical ventilation-selective for motor nicotinic receptor Use vecuronum or recuroniium in burns, myopathies, crush injuries and denervation to avoid hyperkalemia

Answer 36

MOA: NMDA receptor antagonist, helps prevent excitotoxicity mediated by Ca2+ Clinical: Alzheimer Toxicity: dizziness, confusion, hallucinations

Answer 37

MOA: AChE inhibitors Clinical: Alzheimers Toxicity: nausea, dizziness, insomnia Vitamin E-antoxidant helps slow functional loss of Alzheimers

Answer 38

MOA: inhibit vesicular monoamine transporter (VMAT Limit dopamine vesicle packaging and release Clinical: Huntingtons

Answer 39

``` MOA: 5Ht agonist Inhibits trigeminal nerve activation prevents vasoactive peptide release Induces vasoconstriction half-life < 2 hours ``` Clinical: acute migraine and cluster headache attacks Toxicity: coronary vasospasm (contraindicated in patients with coronary artery disease or Prinzmetal angina), mild tingling Increases BP Avoided in cardiac or cerebrovascular disease,

Answer 40

Anti VEGF Used for age related wet macular degeneration slows choroidal neovascularization

Answer 41

Anti VEGF Used for age related wet macular degeneration slows choroidal neovascularization

Answer 42

Modestly increases survival of Lou Gehrig disease by decreasing presynaptic glutamate release

Answer 43

Metabolized to phenobarbital and phenylethylmalonamide (PEMA) both of which are anticonvulsants Used for epilepsy, 2nd line essential tremor Causes lethargy, acute intermittent porphyria (abdom pain, neuro, psych)