Neuro Flashcards

1
Q

Epinephrine (alpha1), Brimonidine (alpha 2)

[Effect in Glaucoma]

A

> Epinephrine: vasoconstriction – dec. aqueous humor synth; can cause mydriasis via alpha1 (not for closed-angle glaucoma).
Brimonidine: dec. aqueous humor synth

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2
Q

Timolol, Betaxolol, Carteolol (B-blockers)

[Effect in Glaucoma]

A

Dec. aqueous humor synth by the ciliary epithelium.

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3
Q

Acetazolamide (diuretic)

[Effect in Glaucoma]

A

Inhibit carbonic anhydrase – dec. aqueous humor synth.

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4
Q

Pilocarpine, Carbachol (direct cholinomimetics).
Physostigmine, Echothiophate (indirect).
[Effect in Glaucoma, SE]

A

Contracts ciliary muscle (M3) and opening of trabecular meshwork – Inc. aqueous humor outflow.
*Pilocarpine for emergencies: effective in opening canal of Schlemm.
SE: mitosis, cyclospasm.

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5
Q

Latanoprost (PGF2a)

[Effect in Glaucoma, SE]

A

Inc. outflow of aqueous humor (by inc. uveoscleral outflow).

SE: darkens iris color (browning)

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6
Q
Opioid analgesics
Drug names (4)
A

Morphine, Fentanyl, Codeine
Loperamide, Methadone, Meperidine
Dextromethorphan, Diphenoxylate Pentazocine

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7
Q

Opioid analgesics

MOA

A

> Agonists at opioid receptors – open K channels, close Ca channels – dec. synaptic transmission.
Inhibits release of neurotransmitters (ACh, NE, 5HT, glutamate, substance P).
[Mu - morphine, Delta - enkephalin, Kappa - dynorphin]

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8
Q

Opioid analgesics

Use

A
Pain.
Cough suppression (dextromethorphan).
Diarrhea (loperamide, diphenoxylate).
Acute pulmo edema.
Maintenance for heroin addicts.(methadone, buprenorphine + naloxone)
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9
Q

Opioid analgesics

Toxicity

A
Addiction, Respi depression, constipation.
Pinpoint pupils (miosis).
Tx: Naloxone, Naltrexone (opioid receptor antagonist).
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10
Q

Butorphanol

[use]

A

Kappa receptor agonist; partial agonist to Mu-receptor.
For severe pain (migraine, labor).
*Don’t give w/ full opioid agonist – withdrawal sx due to competition for receptors; overdose not easily reversed w/ naloxone

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11
Q

Tramadol

[use, SE]

A

Weak opioid agonist; also inhibits 5HT and NE reuptake.
For chronic pain.
SE: Serotonin syndrome.

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12
Q

Ethosuxamide

[Seizure type, MOA, SE]

A

Absence seizures.
>MOA: Blocks thalamic T-type Ca channels – inhibits the transient depolarizations necessary to make spike-wave patterns seen in Absence (maintains rhythmic discharge in thalamic neurons).
>SE: Fatigue, GI distress, Headache, Itching, SJS.

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13
Q

Diazepam, Lorazepam

[Seizure type, MOA]

A

Status epilepticus; Eclampsia seizures.

MOA: Inc. GABA-A action by inc. frequency of Cl- channel opening.

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14
Q

Phenytoin

[Seizure types, MOA, SE]

A

Tonic-clonic (1st line), Status epilepticus (prophylaxis); partial seizures.
>MOA: Inc. Na channel inactivation (dec. propagation)
>SE: gingival hyperplasia, megaloblastic anemia, teratogenesis, SJS, osteopenia

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15
Q

Carbamazepine

[Seizure types, MOA, SE]

A

1st line: Partial seizures, Tonic-clonic.
1st line: trigeminal neuralgia.
>MOA: Inc. Na channel inactivation.
>SE: blood dyscrasias (agranulocytosis, aplastic anemia), teratogenesis, liver toxicity

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16
Q

Valproic acid

[Seizure types, MOA, SE]

A

Tonic-clonic (1st line), absence, Partial seizures.
>MOA: Inc. Na channel inactivation; Inhibits GABA transaminase (inc. GABA conc.).
>SE: Neural tube defects, CI in preg

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17
Q

Gabapentin

[Seizure types, MOA]

A

Partial seizures.
>MOA: inhibits voltage-activated Ca channels (GABA analog).
*Also for peripheral neuropathy, postherpetic neuralgia

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18
Q

Phenobarbital

[Seizure types, MOA]

A

Partial seizures, Tonic-clonic.
MOA: inc. GABA-A action by inc. duration of Cl- channel opening.
*1st line in neonates

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19
Q

Lamotrigine

[Seizure types, MOA, SE]

A

Partial seizures; Tonic-clonic, Absence.
MOA: Blocks voltage-gated Na channels.
SE: SJS (titrate slowly).

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20
Q

Topiramate

[Seizure types, MOA]

A

Partial seizures, Tonic-clonic.
MOA: Blocks Na channels, Inc. GABA action.
*Also for migraine prevention

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21
Q

Tiagabine

[Seizure types, MOA]

A

Partial seizures.

MOA: Inhibits GABA reuptake.

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22
Q

Barbiturates

[Drug names, use]

A

Phenobarbital, Pentobarbital, Thiopental, Secobarbital.
Sedative for anxiety, seizures, insomnia.
Induction of anesthesia (thiopental).

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23
Q

Barbiturates

[MOA, toxicity]

A

> MOA: Inc. duration of Cl channel opening – inc. GABA-A action – dec. neuron firing.
SE: respi and cardiovascular depression; CNS depression, dependence.

24
Q

Benzodiazepines

[Drug names, use]

A

> Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam.
For anxiety, Status epilepticus (lorazepam, diazepam), detoxification (alcohol-w/d DT), general anesthetic, night terrors, hypnotic.

25
Q

Benzodiazepines

[MOA, toxicity]

A

> MOA: GABA-A receptor; Inc. frequency of Cl channel opening – inc. GABA-A action.
SE: dependence, additive CNS depression w/ alcohol; less risk of respi depression vs barbiturates.
*Tx overdose: flumazenil (competetive antagonist)

26
Q

Non-BZ hypnotics

[Drugs, MOA, use]

A

Zolpidem, Zaleplon, Eszopiclone.
Acts on BZ1 subtype of GABA receptor.
For insomnia (short-term tx).
*Effects reversed by flumazenil

27
Q

Inhaled anesthetics

[Drug, effects]

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane; N2O.
>Effects: myocardial depression, respi depression, inc. cerebral blood flow (dec. cerebral metabolic demand).

28
Q

Inhaled anesthetics

Toxicity

A

Hepatotoxic (halothane); Nephrotoxic (methoxyflurane); Proconvulsant (enflurane).
Expansion of trapped gas in body cavity (N2O).
*Malignant hyperthermia: life-threatening, hereditary; inhaled anesthetics (except N2O) and succinylcholine induce fever, muscle contractions; Tx is Dantrolene.

29
Q

Why is thiopental (as an IV barbiturate) most commonly used for induction of anesthesia and short surgical procedures?

A

Has high potency, high lipid solubility, and rapid entry into brain.
Rapid redistribution into tissues terminates effects.

30
Q

Which benzodiazepine is most commonly used for endoscopy? What are possible side effects?

A

Midazolam, used adjunctively w/ gas anesthetics and narcotics.
May cause severe post-op respi depression and dec. BP (tx overdose w/ flumazenil).
Possible anterograde amnesia

31
Q

Ketamine

[use, MOA, SE]

A

PCP analog.
>Blocks NMDA receptors. Cardiovascular stimulants.
>Starting and maintaining anesthesia – induces a trance-like state; provides pain relief, sedation, memory loss; inc. cerebral blood flow.
>SE: disorientation, hallucination, bad dreams

32
Q

Propofol

[use, MOA]

A

Used for sedation in ICU, rapid anesthesia induction, short procedures.
Less post-op nausea vs thiopental.
Potentiates GABA-A.

33
Q
Local anesthetics (-caine)
[Names (Esters, Amides), uses]
A

> Esters: Procaine, Cocaine, Tetracaine
Amides: Lidocaine, Mepivacaine, Bupivacaine.
For minor surgeries, spinal anesthesia.

34
Q

Local anesthetics.

How do you enhance local action?

A

To enhance local action, can give w/ vasoconstrictors (Epi) – dec. bleeding; dec. systemic concentration to inc. local anesthesia.

35
Q

Local anesthetics.

How do you use a local anesthetic in tissue that’s infected (acidic)?

A

In infected (acidic) tissues, need more anesthetic because alkaline anesthetics are charged and can’t penetrate membrane effectively.

36
Q

Local anesthetics.

Order of nerve blockade (diameter, myelination)

A
  • Small diameter > large diameter (predominates).
  • Myelinated > nonmyelinated.
  • Small myelinated > small unmyelinated > large myelinated > large unmyelinated
37
Q

Local anesthetics.

Order of loss (sensations)

A

1) pain
2) temp
3) touch
4) pressure

38
Q

Local anesthetics

MOA

A

Binds to receptors on inner portion of Na channels – blocks Na channels.
Preferential for activated Na channels – effective in rapidly firing neurons.

39
Q

Local anesthetics

Toxicity

A

Severe cardiovascular toxicity (bupivacaine).
Arrhythmias (cocaine).
Methemoglobinemia (benzocaine)

40
Q

Succinylcholine

[MOA, clinical use, SE]

A

Neuromuscular blocker; muscle paralysis in surgery or mech vent; selective for motor N-receptors.
>Succinylcholine: strong ACh receptor agonist – sustained depol, prevents muscle contraction.
>SE: hyperCa, hyperK, malignant hyperthermia

41
Q

Reversal of blockade made by Succinylcholine

A

> Phase I: prolonged depol – SCh has longer duration than ACh, keeps membrane above threshold and prevents repol; no antidote; potentiated by cholinesterase inhibitors.
Phase II: repolarized but blocked – SCh persists in cleft at high conc.; ACh receptors available but desensitized – antidote is cholinesterase inhibitors.

42
Q

Tubocurarine, atracurium, mivacurium, pancuronium, etc.

How to reverse blockade?

A

> Nondepolarizing neuromuscular blockers (vs. depolarizing Succinylcholine).
Compete w/ ACh for receptors.
Reversal of blockade: neostigmine (give w/ atropine), edrophonium, other cholinesterase inhibitors.

43
Q

Dantrolene

[MOA, use]

A

> Prevents Ca release from SR of skeletal muscle.

>For malignant hyperthermia, neuroleptic malignant syndrome.

44
Q

Baclofen

[MOA, use}

A

> Stimulates GABA-B receptors at spinal cord level – induces skeletal muscle relaxation.
For muscle spasms (acute low back pain).

45
Q

Cyclobenzaprine

[MOA, use]

A

> Centrally acting muscle relaxant. >Structurally related to TCAs w/ similar anticholinergic side effects.
For muscle spasms.

46
Q

Dopamine agonists

Names (ergot, non-ergot)

A

> Ergot: Bromocriptine.

>Non-ergot (preferred): Pramipexole, Ropinirole

47
Q

Drug that inc. dopamine availability

A

Amantadine
>inc. dopamine release, dec. dopamine reuptake
>Toxicity: ataxia, livedo reticularis

48
Q

Drugs that inc. L-DOPA availability

A
Prevent peripheral (pre-BBB) L-DOPA degradation -- inc. central L-DOPA for conversion to dopamine in CNS.
>Levodopa (L-DOPA)/carbidopa: carbidopa blocks peripheral conversion to dopamine by inhibiting DOPA decarboxylase.
>Entacapone, tolcapone: prevent peripheral degradation to 3-OMD by inhibiting COMT
49
Q

Drugs that prevent dopamine breakdown

A
Act centrally (post-BBB) to block dopamine breakdown -- inc. available dopamine.
>Selegiline: blocks conversion of dopamine into 3-MT by inhibiting MAO-B.
>Tolcapone: blocks conversion into DOPAC by inhibiting central COMT
50
Q

L-dopa/Carbidopa

[MOA, use]

A

For Parkinson dse; inc. dopamine in brain
>L-dopa can cross BBB (vs dopamine) – central DOPA decarboxylase converts L-dopa in to dopamine.
>Carbidopa is a peripheral DOPA decarboxylase inhibitor – inc. bioavailability of L-dopa in brain, limits peripheral SE.

51
Q

L-dopa/Carbidopa

[Side effects, “On-off phenomenon”]

A

Arrhythmias from inc. peripheral catechs.

>”On-off” phenomenon: long-term use can lead to dyskinesia ff. admin, akinesia b/w doses.

52
Q

Selegiline

[MOA, use]

A

> Inhibits MOA-B (preferentially metabolizes dopamine over NE, 5HT) – inc. dopamine bioavailability.
For Parkinson dse (adjunct to L-dopa).

53
Q

Entacapone, tolcapone

A

Inhibits COMT – prevents PERIPHERAL L-dopa degradation to 3-OMD.
*Tolcapone also blocks CENTRAL dopamine conversion to DOPAC by inhibiting COMT.

54
Q

Alzheimer dse drugs: Memantine; Donepezil, Galantamine, Rivastigmine, Tacrine

A

> Memantine: NMDA receptor antagonist – prevents excitotoxicty (mediated by Ca).
Donepezil, Galantamine, Rivastigmine, Tacrine: AChE inhibitors.

55
Q

Tx for Huntington dse: Tetrabenazine, Reserpine; Haloperidol

A

> Huntington: Dec. GABA, Dec. ACh, Inc. dopamine.
Tetrabenazine, Reserpine: inhibit VMAT; limit dopamine vesicle packaging and release.
Haloperidol: D2 receptor antagonist

56
Q

Sumatriptan

[MOA, SE/CI]

A

5HT-1B/1D agonist.
>For acute migraine, cluster headache attacks (abortive).
>Inhibits trigeminal nerve activation; Prevents vasoactive peptide release; Induces vasoconstriction.
>SE: coronary vasospasm – CI in CAD, Prinzmetal angina.

57
Q

GABA-A receptor vs. GABA-B receptor

A

> GABA-A: chloride channel – Cl entry inhibits depolarizing/firing – inhibits neurons.
GABA-B: transmembrane protein linked to K channels via G-proteins – K channels remain open longer and hyperpolarize neuron at end of AP – block voltage-gated Na channels from opening, block depolarization.