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Step1: Pharm from 1st AID > Neuro > Flashcards

Neuro Flashcards

1
Q

Zolpidem

A

MOA:

  • Bind to GABAa receptor and enhance inhibitory action of GABA on CNS
  • Same MOA as benzo’s

Use:

  • Short term Tx. of insomnia
  • Rapid onset of action (15 mins after admin)
  • Metabolized by P450 liver

Tox:
Less chance for tolerance and addiction

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2
Q

Chlorpheniramine
Diphenhydramine (Benadryl)
Promethazine
Hydroxyzine

A

MOA:
-1st gen H1-histamine receptor antagonist

Use:
-To tx. and prevent allergic rxns, motion sickness, anti emetics

Tox:
-Especially sedating when used with Benzo’s (Diazepam)

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3
Q

Diazepam

A

MOA:

  • Long acting benzo
  • Binds GABAa receptors

Use:
-Anxiolytic; Sedative hypnotic; Anticonvulsant; M. relaxant

Tox:

  • Sedation
  • Impaired coordination balance (avoid in elderly)
  • Decreased memory and [ ]
  • Confusion
  • Should not be used in combo with other CNS depressants*
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4
Q

Nimodipine

A

MOA:
-Ca2+ chan blocker

Use:
-Assist in prevention of cerebral vascular spasm following subarachnoid hemorrhage (SAH)… this is an alternative use to CCB’s

Tox:

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5
Q

Methyldopa

Clonidine

A

MOA:

  • Central sympatholytics
  • Stim. alpha-2A receptors centrally which causes a decreased in generalized sympathetic flow

Use:
-To decrease BP

Tox:
HypoTN

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6
Q

Valproic Acid

A

MOA:
-Suppresses abnormal electrical activity in the cortex by affecting GABA and NMDA receptors as well as Na+ and K+ channels

Use:
-Myoclonic seizures (a type of generalized seizure, except w/o loss of consciousness)

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7
Q

Antipsychotics & their associations

Thioridazine
Chlorpromazine
Haloperidol
Ziprazidone
Olanzapine
Clozapine
A
  • ->Retinal deposits that resemble retinitis pigments
  • ->Corneal deposits
  • ->Extrapyramidal symoptoms
  • ->Prolonged QT
  • ->Wt. gain
  • ->Agranulocytosis and seizures
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8
Q

Important antipsychotic SE’s

A

Extrapyramidal SE’s –> acute dystonic rxn; akathisia; drug induced parkinsonism

Tardive dyskinesia

Neuroleptic malignant syndrome

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9
Q

Modafinil

A

MOA:

  • Enhance dopaminergic signaling
  • Non-amphetamine stimulant

Use:
-Narcolepsy (low levels of stim NT, orexin (hypocretin), for maintaining wakefulness and suppressing REM sleep-related phenomena)

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10
Q

Cocaine

A

MOA:

  • Inhib’s presynaptic uptake of NE, DO, SE
  • Short acting sympathomimetic

Tox:

  • BP elevation
  • Chest pain 2ndry to coronary a. vasoconstriction
  • Agitation from CNS activation
  • Mydriasis
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11
Q

Buspirone

A

MOA:

  • anxiolytic agent
  • selective agonist of 5HT1a receptor

Use:

  • Generalized anxiety disorder
  • *clinical response is delayed up to 2wks of daily use**

Tox:

  • Dependence does not occur with chronic use
  • No m. relaxant or anticonvulsant properities
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12
Q

Phenelzine

Tranylcypromine

A

MOA:
-Monoamine oxidase inhibitors
-

Use:
-Atypical depression characterized by mood reactivity (improvement in mood in response to something positive), leaden fatigue, rejection sensitivity, increased sleep/appetite

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13
Q

What is the single most effective agent in treating TCA associated cardiac abnormalities?

A

Sodium bicarbonate

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14
Q

Carbamazepine

A

MOA:
-Blocks voltage gated Na+ chan’s in neuronal membranes

Use:

  • Simple partial, complex partial, and generalized tonic-clonic seizures
  • Mood stabilizer in bipolar disorder
  • Tx. trigeminal neuralgia
  • Diabetic neuropathy

Tox:

  • Bone marrow suppression
  • Hepatotoxic
  • Increase in ADH secretion may cause SIADH
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15
Q

Ethosuximibe

A

MOA:
-Blocks T-type Ca2+ chan’s and decreases Ca2+ current in thalamic neurons

Use:
-Absence seizures

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16
Q

Acetylecholinesterase inhib’s

A
  • Physostigmine (Tertiary amine–> works centrally & peripherally)
  • Neostigmine & Edrophonium (Quaternary ammonium structures that limits CNS penetration)
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17
Q

Phenytoin

A

MOA:
-Inhibits neuronal high-frequency firing of AP’s by blocking Na+ chain’s and prolonging their rate of recovery

Use:

  • Tonic clonic seizures (grand mal)
  • Status epilepticus

Tox:

  • Gingival hyperplasia
  • Hersuitism
  • Coarsening of facial features
  • Acneform skin rash
  • Generalized lymphadenopathy (pseudolymphoma)
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18
Q

Pentazocine

A

MOA:

  • Opioid narcotic
  • Partial agonist and weak antagonist activity at mu R’s

**b/c of its weak antagonistic affects, it can cause withdrawal symptoms in pt’s who are dependent or tolerant to morphine or other opioids

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19
Q

Cyproheptadine

A

MOA:
-Antihistamine with anti-serotonergic properties

Use:
-Serotonin syndrome

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20
Q

Lamotrigine

A

MOA:
-Anticonvulsant

Use:

  • Management of generalized tonic-clonic seizures
  • Bipolar disorder

Tox:
-Rash (discontinue drug immediately in children)

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21
Q

Drugs used for refractory partial seizures

A

Tiagabine–> inhib of GABA uptake

Topiramate–> blocks Na chan and enhances effect of GABA

Vigabatrin–> inhib GABA-transaminase and increase GABA [ ]

Gabapentin–> increase brain GABA [ ]

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22
Q

Methimazole

A

MOA:
-Inhib thyroid hormone synthesis by suppressing iodination and coupling of tyrosine

Use:
-Hyperthyroidsm

Tox:

  • Edema
  • Rash
  • Agranulocytosis
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23
Q

What is the main therapy for acute mania?

A

Mood stabilizers:

  • Lithium
  • Valoproic acid
  • Carbamazepine

Atypical antipsychotic:
-Olanzapine

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24
Q

Glaucoma drugs

A

↓ IOP via ↓ amt of aqueous humor (inhibit synthesis/ secretion or ↑ drainage)

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25
Q

Epinephrine

A

MOA:

  • α-agonist
  • ↓ aqeuous humor synthesis via vasoconstriction

Use:
-Glaucoma

Tox:
Mydriasis; do not use in closed-angle gluacoma

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26
Q

Brimonidine

A

MOA:

  • α2-agonist
  • ↓ aqeuous humor synthesis

Use:
-Glaucoma

Tox:
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

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27
Q

Timolol
Betaxolol
Carteolol

A

MOA:

  • β-blocker
  • ↓ aqeuous humor synthesis

Use:
-Glaucoma

Tox:
-No pupillary or vision changes

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28
Q

Acetazolamide

A

MOA:

  • Diuretic
  • ↓ aqeuous humor synthesis via inhibition of carbonic anhydrase

Use:
-Glaucoma

Tox:
-No pupillary or vision changes

29
Q

Glaucoma Cholinomimetics

Direct (pilocarpine, carbachol)

Indirect (physostigmine, echothiophate)

A

MOA:

  • ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
  • Use pilocarpine in emergencies—very effective at opening meshowrk into canal of Schlemm

Use:
-Glaucoma

Tox:
-Miosis and cyclospasm (contraction of ciliary muscle)

30
Q

Latanoprost (PGF2α )

A

MOA:
- ↑ outflow of aqueous humor

Use:
-Glaucoma

Tox:
-Darkens color of iris (browning)

31
Q

Opiod analgesics

Morphine
Fentanyl
Codeine
Loperamide
Methadone
Meeperidine
Dextromethorphan
Diphenoxylate
A

MOA:

  • Acts as agonists at opioid receptor (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission__ open K+ chan, close Ca2+ channel –> ↓ synaptic transmission
  • Inhib rlease of ACh, norepi, 5-HT, glutamate, substance P

Use:

  • Pain, cough suppression (dextromethorphan)
  • Diarrhea (loperamide and diphenoxylate)
  • Acute pulm edema, maintenance programs for heroin addicts (methodone)

Tox:

  • Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
  • Toxicity tx’ed w/ naloxone or naltrexone (opiod receptor antagonist)
32
Q

Butorphanol

A

MOA:
- Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia

Use:

  • Severe pain (migraine, labor, etc)
  • Causes less resp depression than full opioid agonists

Tox:

  • Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid)
  • Overdose not easily reversed with naloxone
33
Q

Tramadol

A

MOA:
-Very weak opioid; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters__ “tram it all” in with tramadol).

Use:
-Chronic pain

Tox:

  • Similar to opioids
  • Decreases seizure threshold
  • Serotonin syndrome
34
Q

Ethosuximide

A

MOA: Blocks thalamic T-type Ca2+ channels

Use: 1st line for Generalized (Absence) seizure.

Side effects: GI, fatigue, headache, urticaria, Steven-Johnson syndrome.

EFGHIJ= Ethosuximide, GI distress, headache, Itching, and steven-Johnson syndrom.

Notes: Sucks to have Silent (absence) Seizures

35
Q

Benzodiapzines (diazepam, lorazepam)

A

MOA: increase GABAa action

Use: 1st line prophylaxis for status epilepticus

Side Effects: sedation, tolerance dependence, respiratory depression

Notes: Also for eclampsi seizures (1st line if MgSO4)

36
Q

Valproic Acid

A

MOA: increase Na+ channel inactivation

Use: simple, complex (partial)seizures. 1st line for tonic clonic seizures, and absence

Side Effects: GI distress, rare but fatal hepatoxicity (measure LFTs), neural

Notes: Also used for myoclonic seizures, bipolar disorder

37
Q

Phenobarbital

A

MOA: incease GABAa action

Use: simple, complex, tonic-clonic seizures

Side Effects: sedation, tolerance, dependence, induction of cyt P-450, cardiorespiratory depression

Notes: 1st line in neonates

38
Q

Topiramate

A

MOA: Blocks Na+ channels, increases GABA action

Use: simple, complex, tonic-clonic seizures

Side Effects: sedation, mental dulling, kidney stones, weight loss.

Notes: Also used for migraine prevention

39
Q

Levetiracetam

A

MOA: Unknown; may modulate GABA and glutamate

Use: simple, complex, tonic-clonic seizures

40
Q

Tiagbine

A

MOA: Increase GABA by inhibiting re-uptake

Use: simple, complex seizures

41
Q

Vigabatrin

A

MOA: Increase GABA irreversibly inhibiting GABA transaminase

Use: simple, complex seizures

42
Q

Steven-Johnson syndrome

A
  • Prodrome of malaise and fever
  • Followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital).
  • Skin lesions progress to epidermal necrosis and sloughing
43
Q

Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital)

A

MOA: Facilitate GABAa action by increasing duratioin of Chloride channel opening, thus decreasing neuron firing. Contraindicated in porphyria.

Use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

Tox: Respiratory and cardiovascular depression (can be fatal); CNS depression ( can be exacerbated by alcohol use); dependence, drug interactions (induces cyt P-450).

Overdose tx is supportive (assist resp. and maintain BP).

44
Q

Benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxzepam, midazolam, chlordiazepoxide, alprazolam)

A

MOA: Facilitate GABAa action by increasing frequency of chloride channel opening. -decreases REM sleep.
-Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting –> higher addictive potential.

Use: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxifcation (esp. alcohol withdrawal – DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

Tox: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbituates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).

45
Q

Nonbenzodiazepine hypnotics (Zolpdem (ambien), Zaleplon, esZopiclone. “All ZZZz put you to sleep.”

A

MOA: Act via the BZI subtype of the GABA receptor. Effects reversed by flumazenil

Use: Insomnia

Tox: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzo.

46
Q

Anesthetics-general principles

A
  • CNS drugs must be lipis soluble (cross the blood-brain barrier) or to be actively transported.
  • Drugs with less solubility in blood = rapid induction and recovery times.
  • Drugs with more solubility in lipids = more potency =1/MAC

MAC = Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision).

47
Q

Inhaled anesthetics

A

MOA: Mechanism unknown

Use: Myocardial depression respiratory depression, N/V, increase cerebral blood flow (decreased cerebral metabolic demand).

Tox: Hepattoxicity (haothan(, nephrotoxicity (methoxyflurane), proconvulsant( enflurane), expansion of trapped gas in a body cavity (NO). Can cause malignanat hypernatremia -rare, life-threatening hereditary condition in which inhaled anesthetics (except NP0) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.

48
Q

Intravenous anesthetics, Barbituates

A

Theopental - high potency, high lipid solubility, rapid entry into brain.

Use: for induction of anesthesia and short surgical procedures.

Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat decreases cerebral blood flow

49
Q

Intravenous anesthetics, Benzodiazepines

A

Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics.

Tox: May cause severe postoperative respiratory depression, low BP (treat overdose with flumazenil), and anterograde amnesia.

50
Q

Intravenous anesthetics, Arylcylohexylamines (Ketamine)

A

PCP analogs that act as dissociative anesthetics.

MOA: Block NMDA receptors. Cardiovascular stimulants.

Side effects: Cause disorientation, hallucination, and bad dreams. Increases cerebral blood flow.

51
Q

Intravenous anesthetics, Opiods

A

Types: Morphine and Fentanyl

Use: Used with other CNS depressants during gen. anesthesia

52
Q

Intravenous anesthetics, Propofol:

A

MOA: Potentiates GABAa.

Use: Sedation in ICU, rapid anesthesia induction, and short procedures. less postoperative nausea than thiopental.

53
Q

Local Anesthetics
(Esters- procaine, cocaine, tetracaine).
(Amides- lIdocaiI, mepIvacaIne, bupIvacaIne ( amIdes have 2 I’s)

A

MOA: Block Na2+ channls by binding to specific receptors on inner portion of channel. Preferntially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3^o amine local aneshetics penetrate membrane in uncharged form, then bind to ion channels as charged form

Use: Can be given with vasoconstrictors (usually epinephrine) t enhance local action – decrease bleeding, increase ansesthesia by decreasing systemic concentration.

Used for minor surgerical procedures, spinal anesthesia. If allergic to esters, give amides.

Tox: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

54
Q

Neuromuscular blocking drugs(Depolarizing)

succinlyncholine

A

Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

MOA: Succinlycholine- strong ACh recepto agonist; produces sustained depolarization and prevents muscle contraction.

Reversal blockade:
-Phase I (prolonged depolarization) - no antidote!!. Block potentiated by cholinesterase inhibitors.

-Phase II (repolarized but blocked; ACh receptors are available, but desensitized) - antidote consists of cholinesterase

Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia

55
Q

Neuromuscular blocking drugs (Polarizing)

-Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

A

Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

MOA: competitive antagonsits - compete with ACh receptors.

Reversal of blockade - neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

56
Q

Dantrolene

A

MOA: Prevents the relase of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

Use: treat maligant hyperthermia and neuroleptic malignant syndrome( a toxicity of antipsychotic drugs).

57
Q

Parkinson disease drugs

A
  • Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity
BALSA:
Bromocriptine
Amantadine
Levopdopa (with carbidopa)
Selegiline (and COM inhibitors)
Antimuscarinics

for essential or familial tremors, use a β-blocker (e.g., propranolol).

58
Q

Bromocriptine (ergot), pramipexole, ropinirole (non-ergot)

A

MOA: dopamine agonists

non-ergots are preferred

59
Q

Amantadine

A

MOA: increase dopamine release

Use: antiviral against influenza A and rubella

Tox: ataxia

L-dopa/carbidopa is converted to dopamine in CNS

60
Q

Selegiline

A

MOA:
-Selegiline- selective MAO type B inhibitor, preferentially metabolizes dopamine over norpeinephrine and 5-HT, thereby increasing the availability of doapmine.

Use: adjunctive agent to L-dopa in treatment of Parkinson disease

Tox: May enhance effects of L-dopa

61
Q

Entacapone

A

MOA: COMT inhibitors, prevent L-dopa degradation –> increase dopamine availability.

Use: Parkinson Disease

62
Q

Tolcapone

A

MOA: COMT inhibitors, prevent L-dopa degradation –> increase dopamine availability.

Prevent dopamine breakdown

Use: Parkinson Disease

63
Q

L dopa (leveodopa)/ carbidopa

A

MOA: Increase dopamine in brain. Can cross blood-brain barrier, converted by dopa decarboxylase in CNS to dopamine.

-Carbidopa, a peripheral decarboxylase inhibitor, given with L-dopa to increase bioavailibility of L-dopa in brain and limit peripheral side effects.

Use: Parkinson Disease

Tox: Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia between doses.

64
Q

Benztropine

A

MOA: Antimuscarinic, curb excess cholinergic activity

Use: Parkinson disease, improves tremor and rigidity but has little effect on bradykinesia

**Park your mercedes- Benz.”

65
Q

Memantine

A

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).

Use: Alzheimer treatment

Tox: dizziness, confusion, hallucinations

66
Q

Donepezil, galantamine,rivastigmine

A

MOA: AChE inhibitors.

Use: Alzheimer treatment

Tox” Nausea, dizziness, insomnia

67
Q

Huntington drugs

A

Neurotransmitter changes in Huntington disease: low GABA, low ACh, high dopamine,

Treatments:
Tetrabenazine and reserpine -inhibit vesicular monoamine transport (VMAT); limit doapmine vesicle packaging release

Haloperidol- dopamine receptor antagonist

68
Q

Sumatriptan

A

MOA: 5-HT IB/ID agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half life <2 hours.

Use: Acute migraine, cluster headache attacks.

Tox: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.

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