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Step 1 Drugs > Neurology > Flashcards

Neurology Flashcards

0
Q

Acetazolamide

A

Glaucoma also diuretic

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase

NO PUPILLARY OR VISION CHANGES

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1
Q

Methadone

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema, HEROIN ADDICTS

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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2
Q

Fentanyl

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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3
Q

Loperamide

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema, DIARRHEA

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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4
Q

Brimonidine

A

Glaucoma
Decrease aqueous humor synthesis

Side effects: Mydriasis; not used in closed angle glaucoma
ocular hyperemia, foreign body sensation, allergy reactions, ocular pruritus

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5
Q

Meperidine

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema

Toxicity: Respiratory depression, block urinary voiding reflexes. DILATES pupils in overdose.

DOESN’T CAUSE BILIARY COLIC

Constipation and miosis have no tolerance!

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6
Q

Timolol, betaxolol, carteolol

A

Glaucoma

Decrease aqueous humor synthesis

NO PUPILLARY OR VISION CHANGES

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6
Q

Latanoprost (PGFalpha)

A

Glaucoma: Prostaglandin

Increase outflow of aqueous humor

Darkens color of iris

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8
Q

Codeine

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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9
Q

Diphenoxylate

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema, DIARRHEA

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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10
Q

Physostigimine, echothiophate

A

Use in pilocarpine emergencies,

very effective at opening meshwork into canal of Schlemm

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11
Q

Glaucoma: Epinephrine

A

Alpha Agonist
Decrease aqueous humor synthesis via vasconstriction

Side effects: Mydriasis; not used in closed angle glaucoma
ocular hyperemia, foreign body sensation, allergy reactions, ocular pruritus

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13
Q

Morphine

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmission, inhibit adenylate Cyclase
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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14
Q

Naloxone

A

Opioid receptor antagonist
treats opioid toxicity
Displaces morphine from receptors (used acutely)

reverses analgesia, sedation, hypotension and respiratory depression

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15
Q

dextromethorphan

A

Opioid analgesic
Majority of OD related deaths

Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P

Clinical: pain, acute pulmonary edema, COUGH SUPPRESSION

Toxicity: Respiratory depression, block urinary voiding reflexes

Constipation and miosis no tolerance!

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16
Q

Tramadol

A

Weak opioid receptor agonist
Inhibits serotonin and NE reuptake

Clinical: chronic pain

Decreases seizure threshold, serotonin syndrome

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17
Q

Pentazocine

A

mu receptor agonist and weak antagonist
Competitively inhibits mu receptors and produces antagonistic effects leading to decreased opioid analgesic effects
Designed to produce analgesic effects with little abuse potential

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18
Q

Naltrexone

A

opioid receptor antagonist

Treats opioid toxicity

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19
Q

Ethosuximide

A

MOA: blocks thalamic T-type Ca2 channels

Clinical: absence seizures

Side effects: Fatigue, GI distress, Headache, Itching and Stevens-Johnson Syndrome
FGHIJ

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20
Q

Pilocarpine, carbachol

A

Glaucoma: cholnomimetic

increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

Side effects: miosis and cyclospasm

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21
Q

Benzodiazepines-seizure (diazepam, loazepam)

A

MOA: increase GABA action

Clinical: status epilepticus, eclampsia seizures, night terrors and sleepwalking, anxiolytic (Generalized anxiety disorder and panic attacks), short term for insomnia, seizures due to alcohol withdrawal, spasticity (muscle relaxant)

Side effects: sedation, tolerance, dependence, respiratory depression, impairs balance, decrease memory and concentration.

CI: alcohol, barbiturates, neuroleptics, and 1st gen antihistamines

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22
Q

Phenytoin

A

MOA: increased Na channel inactivation
Increase refractory period

Clinical: simple, complex, TONIC CLONIC (1st line), status epilepticus (1st line prophylaxis)

Side effects: ataxia, nystagmus, gingival hyperplasia (increased expression of PDGF), hirsutism, megaloblastic anemia (folate deficiency) fetal hydantoin syndrome, SLE-like syndrome, induction of cytocrhome P-450, lymphadenoapthy, SJ syndrome, osteopenia

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23
Q

Carbamazepine

A

MOA: increase Na channel inactivation

Clinical: first line for simple, complex and tonic clonic

Side effects: diplpia, agraunulocytosis, aplastic anemia, liver toxicity, teratogensis, induction of cytochrome P-450, SIADH, SJ syndrome

Monitor blood and LFTs

1st line for tirgeminal neuralgia

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24
Q

Valproic acid-seizures

A

MOA: increase Na channel inactiavtion
Increase GABA concentration by inhibiting GABA transminase

Clinical: Simple, complex, TONIC CLONIC (1st line), absence, juvenile myoclonic epilepsy

Side effects: GI distress, fatal hepatotoxicity, neural tube defects in fetus, weight gain, contraindicated in pregnancy

Also used for myoclonic seizures and bipolar disorder
Drug of choice for absence seizures associated with tonic clonic seizures

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25
Q

Gabapentin

A

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

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26
Q

Phenoarbital

A

MOA: increase GABA action

Clinical: simple, complex, tonic-clonic

Side effects: sedation, tolerance, induction of cytochrome P-450, cardiorespiratroy depression

1st line in neonates

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27
Q

Topiramate

A

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

28
Q

Tiagabine

A

MOA: Increase GABA by inhbiting re-uptake

Clinical: simple and complex

Also used for refractory partial seizures

29
Q

Vigabatrin

A

MOA: increase GABA by irreversibly inhibiting GABA transaminase

Clinical: simpe and complex

Also used for refratory partial seizures

30
Q

Barbituates

A

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)

31
Q

Halothane

A

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
32
Q

Levetiracetam

A

MOA: Unknown

Clinical: Simple, complex, tonic clonic

33
Q

Long acting Benzodiazepines

A

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)

34
Q

Medium acting Benzodiazepines

A

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)

35
Q

isoflurane

A

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

36
Q

Butorphanol

A

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

37
Q

Sevoflurane

A

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

38
Q

Short acting benzodiazepines

A

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)

41
Q

Midazolam

A

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

42
Q

Nonbenzodiazepine hypnotics

A

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

43
Q

Nitrous oxide

A

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

44
Q

Arylcyclohexylamines

A

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

45
Q

Thiopental

A

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

46
Q

Propofol

A

Used for sedation in ICU
Rapid anesthesia induction and short procedures

less postop nausea than thiopental

Potentiates GABA

47
Q

Local Anesthetics

A

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)

48
Q

l-dopa/carbidopa

A

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

49
Q

Fastest induction and recovery times for anesthetics

A

Low solubility in blood

49
Q

Greatest potency of anesthetics

A

Increased solubility in lipids (1/MAC)

50
Q

Succinylcholine

A

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

51
Q

Lamotrigine

A

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

51
Q

Enflurane

A

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

52
Q

Bromocriptine, pergolide, pramipexole, ropinirole

A

Bromocriptine, pergolide-ergot
pramipexole, ropinirole-non-ergot
Non ergots perferred due to longer half life

MOA: dopamine agonists

Treats parkinsons

53
Q

Methoxyflurane

A

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

53
Q

Dantrolene

A

MOA: prevent release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

Clinical: treat malignant hyperthermia and neuroleptic malignant syndrome-toxicity of antipsychotic drugs

55
Q

Selegiline

A

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

56
Q

Entacapone, tolcapone

A

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.

57
Q

Benzotropine and trihexyphenidyl

A

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

58
Q

Amantadine

A

treats Parkinsons
MOA: may increase dopamine release

AE: ankle edema and livedo reticularis

59
Q

Tubbucurarine, atracurium, mivacurium, pancuronium, vercuronium, recoroniuum

A

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

60
Q

Memantine

A

MOA: NMDA receptor antagonist, helps prevent excitotoxicity mediated by Ca2+

Clinical: Alzheimer

Toxicity: dizziness, confusion, hallucinations

61
Q

Donepezil, galantamine, rivastigmine

A

MOA: AChE inhibitors

Clinical: Alzheimers

Toxicity: nausea, dizziness, insomnia

Vitamin E-antoxidant helps slow functional loss of Alzheimers

62
Q

Tetrabenzine and reserpine

A

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

Clinical: Huntingtons

63
Q

Sumatriptan

A 
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,

64
Q

Ranibizumab

A

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

65
Q

Pryaptanib

A

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

66
Q

Riluzole

A

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

67
Q

Primidone

A

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)

Step 1 Drugs (15 decks)

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