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Neuro FirstAid > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Glaucoma drugs

A

Decr IOP via decr amount of aqueous humor (inhibit synthesis/secretion or incr drainage).

alpha-agonists: epinephrine, brimonidine (alpha 2)
beta-blockers: timolol, betaxolol, carteolol
diuretics: acetazolamide
cholinomimetics:
-direct: pilocarpine, carbachol
-indirect: physostigmine, echothiophate
prostaglandin: lantaprost (PGF2a)

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2
Q

Epinephrine (glaucoma)

A

alpha agonist
MOA: decr aqueous humor synthesis via vasoconstriction
SE: dydriasis: do not use in closed-angle glaucoma

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3
Q

Brominidine (glaucoma)

A

alpha 2 agonist
MOA: decrease aqueous humor synthesis
SE: blurry vision, ocular hyperemia, foreign body sensation, ocular allergic run, ocular pruritis

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4
Q

Timolol, betaxolol, carteolol (glaucoma)

A

beta blocker
MOA: decrease aqueous humor synthesis
SE: no pupillary or vision changes

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5
Q

Acetazolamide (MOA, SE)

A

diuretic
MOA: inhibit carbonic anhydrase–> decr aqueous humor synthesis
SE: no pupillary or vision changes

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6
Q

Pilocarpine, carbachol (direct)
Physostigmine, echothiophate (indirect)
(MOA, SE)

A

cholinomimetic
MOA: increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
SE: miosis and cyclospasm (contraction of ciliary muscle)

Use pilocarpine in emergencies - very effective at opening meshwork into canal of Schlemm

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7
Q

Lantanoprost (PGF2a) (MOA, SE)

A

Prostaglandin
MOA: Increase outflow of aqueous humor
SE: darkens color of iris (browning)

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8
Q

Opioid analgesics (MOA, clinical use, toxicity)

A

Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate.

MOA: Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission—open K+ channels, close Ca2+ channels–> decr synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

Clinical use: Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone).

Toxicity: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to mitosis and constipation.

Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)

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9
Q

Butorphanol (MOA, clinical use, toxicity)

A

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

Clinical use: Severe pain (migraine, labor, etc.). Causes less respiratory depression than full opioid agonists.

Toxicity: Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.

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10
Q

Tramadol

A

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

Clinical use: chronic pain

Toxicity: Similar to opioids. Decreases seizure threshold. Serotonin syndrome

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11
Q

Ethosuximide

A

1st line for absence seizures (generalized)
MOA: Blocks thalamic T-type Ca2+ channels
SE: GI, fatigue, headache, urticaria, Steven-Johnson syndrome. EFGHIJ—Ethosuximide causes Fatigue, GI distress, Headache, Itching, and Stevens-Johnson syndrome

Sucks to have Silent (absence) Seizures

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12
Q

Benzodiazepines (diazepam, lorazepam)

A

1st line for acute status epilepticus seizure
MOA: increase GABA(A) action
SE: Sedation, tolerance, dependence, respiratory depression
Also for eclampsia seizures (1st line is MgSO4)

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13
Q

Phenytoin

A

Seizure tx for:
simple, complex (partial focal)
1st line for tonic-clonic (generalized)
1st line prophylactic for status epilepticus
MOA: incr Na+ channel inactivation; zero-order kinetics
SE: Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, Stevens- Johnson syndrome, osteopenia
Notes: Fosphenytoin for parenteral use

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14
Q

Carbamazepine

A

Seizure tx:
1st line for simple, complex (partial focal)
tonic-clonic (generalized)
MOA: incr Na+ channel inactivation
SE: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome
Notes: 1st line for trigeminal neuralgia

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15
Q

Valproic acid

A

Seizure tx:
Simple, complex (partial focal)
1st line Tonic-clonic, absence (generalized)

MOA: incr Na+ channel inactivation, incr GABA concentration by inhibiting GABA transaminase
SE: GI, distress, rare but fatal hepatotoxicity (measure LFTs),
neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy
Notes: Also used for myoclonic seizures, bipolar disorder

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16
Q

Gabapentin

A

Simple, complex, tonic-clonic seizure tx
MOA: Primarily inhibits highvoltage- activated Ca2+ channels; designed as GABA analog
SE: Sedation, ataxia
Notes: Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

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17
Q

Phenobarbital

A

Simple, complex, tonic-clonic seizure tx
MOA: incr GABA(A) action
SE: Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression
Notes: 1st line in neonates

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18
Q

Topiramate

A

Simple, complex, tonic-clonic seizure tx
MOA:Blocks Na+ channels, incr GABA action
SE: Sedation, mental dulling, kidney stones, weight loss
Notes: also used for migraine prevention

19
Q

Lamotrigine

A

Simple, complex, tonic-clonic, absence seizure tx
MOA: Blocks VG Na+ channels
SE: Stevens-johnson syndrome (must be titrated slowly)

20
Q

Levetiracetam

A

Simple, complex, tonic-clonic seizure tx

MOA: unknown, may modulate GABA and glutamate release

21
Q

Tiagabine

A

Simple, complex seizure tx

MOA: incr GABA by inhibiting reuptake

22
Q

Vigabatrin

A

Simple, complex seizure tx

MOA: incr GABA by irreversibly inhibiting GABA transaminase

23
Q

Barbiturates (names, MOA, clinical use, toxicity)

A

Phenobarbital, pentobarbital, thiopental, secobarbital

MOA: Facilitate GABAA action by incr duration of Cl− channel opening, thus incr neuron firing (barbiturates incr duration).
Contraindicated in porphyria.

Clinical use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).

Toxicity: Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450). Overdose treatment is supportive (assist respiration and maintain BP).

24
Q

Benzodiazepines (names, MOA, clinical use, toxicity)

A

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.

MOA: Facilitate GABAA action by incr frequency of Cl− channel opening. Decr REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting–> higher addictive potential).

“Frenzodiazepines” incr frequency. Benzos, barbs, and EtOH all bind the GABA(A) receptor, which is a ligand-gated Cl− channel.

Clinical use: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

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

25
Q

Nonbenzodiazepine hypnotics (names, MOA, clinical use, toxicity)

A

Zolpidem (Ambien), Zaleplon, esZopiclone.
“All ZZZs put you to sleep.”

MOA: Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil

Clinical use: Insomnia

Toxicity: 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. Decr dependence risk than benzodiazepines.

26
Q

Anesthetics- general principles

A

CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
Drugs with low solubility in blood = rapid induction and recovery times.
Drugs with high solubility in lipids = high 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). Examples: N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has high lipid and blood solubility, and thus high potency and slow induction

27
Q

Inhaled anesthetics (names, MOA, clinical use, toxicity)

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.

MOA: unknown

Effects: Myocardial depression, respiratory depression, nausea/emesis, incr cerebral blood flow (decr cerebral
metabolic demand).

Toxicity: 
Hepatotoxicity (halothane)
nephrotoxicity (methoxyflurane)
proconvulsant (enflurane), 
expansion of trapped gas in a body cavity (nitrous oxide).

Can cause malignant hyperthermia—rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.

28
Q

Intravenous anesthetics

A

“B. B. King on OPIOIDS PROPOses FOOLishly”

Barbiturates: Thiopental—high potency, high lipid solubility,
rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. Decr cerebral blood flow.

Benzodiazepines: Midazolam most common drug used for
endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decr BP (treat overdose with flumazenil), and anterograde amnesia.

Ketamine (arylcyclohexylamine): PCP analogs that act as dissociative anesthetics.
Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Incr cerebral blood flow.

Opioids: Morphine, fentanyl used with other CNS
depressants during general anesthesia.

Propofol: Used for sedation in ICU, rapid anesthesia
induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABAA.

29
Q

Local Anesthetics

A

Esters—procaine, cocaine, tetracaine.
Amides—lidocaine, mepivacaine, bupivacaine
(amIdes have 2 I’s in name).

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

Principle: Can be given with vasoconstrictors (usually epinephrine) to enhance local action - decr bleeding, incr anesthesia by decr systemic concentration.
In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively–>need more anesthetic.
Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated
fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
Order of loss: (1)pain, (2)temperature, (3) touch, (4)pressure

Clinical use: Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

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

30
Q

Depolarizing Neuromuscular blocking drugs

A

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

Succinylcholine—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)—antidote consists of cholinesterase inhibitors.

Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia.

31
Q

Nondepolarizing Neuromuscular blocking drugs

A

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

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.

32
Q

Dantrolene

A

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

Clinical use: Used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).

33
Q

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

A

Parkinson disease drugs. non-ergots are preferred.

Dopamine agonists.

34
Q

Amatadine

A

Increase dopamine.
Amantadine (may incr dopamine release); also
used as an antiviral against influenza A and rubella
Toxicity = ataxia L-dopa/carbidopa (converted to dopamine in CNS)

35
Q

Selegiline

A

MOA: Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby incr the availability of dopamine.

Clinical use: Adjunctive agent to L-dopa in treatment of Parkinson disease

Toxicity: May enhance adverse effects of L-dopa.

36
Q

Benztropine

A

Curb excess cholinergic activity

Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia

37
Q

L-dopa/carbidopa

A

MOA: Incr level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.

Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to incr the bioavailability of L-dopa in the brain and to limit peripheral side effects.

Clinical use: Parkinson disease

Toxicity: Arrhythmias from incr peripheral formation of catecholamines. Long-term use can lead to dyskinesia
following administration (“on-off” phenomenon), akinesia between doses.
38
Q

entacapone, tolcapone

A

COMT inhibitors— prevent L-dopa degradation–> incr dopamine availability

39
Q

Alzheimer drugs (memantine)

A

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
Toxicity: Dizziness, confusion, hallucinations.

40
Q

Alzheimer drugs (donepezin, galantine, rivastigmine)

A

MOA: AChE inhibitors
Toxicity: nausea, dizziness, insomnia

41
Q

Huntington drugs (tetrabenazine, reserpine)

A

Neurotransmitter changes in Huntington disease:
decr GABA, decr ACh, incr dopamine.

-Tetrabenazine and reserpine—inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.

42
Q

Huntington drugs (haloperidol)

A

Neurotransmitter changes in Huntington disease:
decr GABA, decr ACh, incr dopamine.

-Haloperidol—dopamine receptor antagonist.

43
Q

Sumatriptan

A

MOA: 5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours

Clinical use: Acute migraine, cluster headache attacks.

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

Neuro FirstAid (5 decks)

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