Neuro Drugs Flashcards by Ashley Bolin

Alpha agonists used to treat Glaucoma

Epinephrine (alpha 1) - decreased aqueous humor synthesis via vasoconstriction
Brimonidine (alpha 2) - decreased aqueous humor synthesis

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S/E of Epinephrine

Mydriasis (alpha 1) –> don’t use in acute closed angle glaucoma

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Mechanism of beta blockers in Glaucoma

Decrease aqueous humor synthesis

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Acetazolamide mechanism in Glaucoma

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase

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Direct cholinomimetics used for glaucoma

Pilocarpine, Carbachol

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Latanoprost (mechanism, use and S/E)

Mech - increases outflow of aqueous humor (a prostaglandin PGF2alpha)
Use - Glaucoma
S/E - Darkens color of iris (browning)

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Uses of opioids

Pain
Cough suppression
Diarrhea (loperamide, diphenoxylate)
Acute pulmonary edema
Maintenance programs for heroin addicts

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Butorphanol

a. Mechanism
b. Use
c. Toxicity

a. K opioid agonist and mu opioid partial agonist –> produces anesthesia
b. Severe pain (less resp depression that full agonists)
c. Can cause opioid withdrawal symptoms if patient is also taking full agonist

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Tramadol

a. Mechanism
b. Use
c. Toxicity

a. Very weak opioid agonist; also inhibits 5-HT and NE reuptake (tram it all = multiple receptors)
b. Chronic pain
c. Decreases seizure threshold, serotonin syndrome

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Ethosuximide

a. Mechanism
b. Use
c. Toxicity (EFGHIJ)

a. Blocks thalamic T type Ca channels
b. Absence seizures
c. Fatigue, GI distress, Headache, Itching, stevens Johnson syndrome

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1st line for acute status epilepticus

Benzodiazepines

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Phenytoin

a. Mechanism
b. Use
c. Toxicity

a. Increases Na channel inactivation; zero order kinetics
b. Prophylaxis of status epilepticus, treatment of simple, complex, tonic-clonic seizures
c. Gingival hyperplasia, hirsutism, megaloblastic anemia, fetal hydantoin syndrome, SLE like syndrome, p-450 induction, Stevens johnson, osteopenia, nystagmus, diplopia, ataxia, sedation

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Carbamazepine

a. Mechanism
b. Use
c. Toxicity

a. Increases Na channel inactivation
b. Trigeminal neuralgia, simple/complex/tonic-clonic seizures
c. Liver toxicity, Stevens johnson, p-450 inducer, teratogen, SIADH, aplastic anemia, agranulocytosis

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Valproic acid

a. Mechanism
b. Use
c. Toxicity

a. Increased Na channel inactivation by increasing GABA concentration
b. All seizures, bipolar disorder
c. Hepatotoxic, teratogen

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Gabapentin

a. Mechanism
b. Use
c. Toxicity

a. Inhibits high voltage activated Ca channels (GABA analog)
b. Simple or complex seizures, peripheral neuropathy or postherpetic neuralgia
c. Sedation, ataxia

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Phenobarbital

a. Mechanism
b. Use
c. Toxicity

a. Increases GABAa action
b. First line in neonates; simple/complex/tonic-clonic seizures
c. P450 inducer, tolerance, sedation, cardiorespiratory depression

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Treatment for absence seizure

Ethosuximide, Valproic acid, Lamotrigine

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Mechanism of barbiturates

Facilitate GABAa action by increasing DURATION of Cl channel opening –> decreased neuronal firing

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Mechanism of benzodiazepines

Facilitate GABAa action by increased frequency of Cl channel opening

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Which BDZs have short half life? (ATOM)

Alprazolam
Triazolam
Oxazepam
Midazolam

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NonBDZ hypnotics

Zolpidem
Zaleplon
EsZopiclone

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Difference between BDZs and Zolpidem/Zaleplon/Eszopiclone

Less potential for tolerance and addiction
No anticonvulsant properties
No muscle relaxing effects
Not used for anesthesia

What affects speed of induction and recovery times?

Decreased solubility in blood = rapid induction and recovery time

What determines anesthetic potency?

Inversely proportional to minimal alveolar concentration

Drugs with increased solubility in lipids

NO vs. Halothane as anesthetics

NO has low blood and lipid solubility --> fast induction and fast recovery, low potency Halothane has high blood and lipid solubility --> slow induction/recovery and high potency

Which drugs cause malignant hyperthermia (fever and severe muscle contractions)?

``` Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurance, N2O) Succinylcholine (neuromusclar blocking drug) ```

Which anesthetics can be used for brain surgery?

Barbiturates are good because they cause decreased cerebral blood flow

Ketamine mechanism

Blocks NMDA receptors --> act as dissociative anesthetics | Cardiovascular stimulants, cause disorientation, bad dreams, hallucination

Mechanism of local anesthetics

Block Na channels by binding receptors on INNER portion of channel (preferentially bind activated Na channels; tertiary amines penetrate membrane in uncharged form and then bind to ion channels as charged form)

Why do you need more local anesthetic in infected tissues?

Infected tissues are acidic and alkaline anesthetics are charged/cannot penetrate membrane effectively

What can you give with local anesthetics to enhance action?

Epinephrine (vasoconstrictor)

Order of nerve blockade

Small myelinated > small unmyelinated > large myelinated > large unmyelinated

Order of loss of sensations with local anesthetic

Pain > temp > touch > pressure

What are the local anesthetics?

Esters - Procaine, Cocaine, Tetracaine | Amides - Lidocaine, Mepivicaine, Bupivacaine (two Is in name)

What is succinylcholine?

Depolarization neuromuscular blocking drug --> Ach receptor agonist that produces sustained depolarization and inhibits muscle contraction

What are the non depolarizing neuromuscular blockers?

Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium --> competitive antagonists of Ach nicotinic muscular receptors

Baclofen mechanism and use

Inhibits GABAb receptors at spinal cord level --> skeletal muscle relaxation (used for muscle spasms)

Cyclobenzaprine mechansim and use

Centrally acting skeletal muscle relaxant used for muscle spasms (Has similar anticholinergic side effects)

Dopamine agonists used for Parkinsons

Ergot - Bromocriptine | Non-ergot (preferred) - Pramipexole, Ropinirole

Mechanism of Amantadine

Causes increased dopamine release and decreased dopamine reuptake

Mechanism of Carbidopa

Prevents peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase (reduces peripheral S/E)

Mechanism of Entacapone, Tolcapone

Prevent peripheral L-DOPA degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT (Tolcapone also inhibits central COMT but causes hepatotoxicity)

Drugs that prevent dopamine breakdown

Selegiline - inhibits MAOb (dopamine not converted to 3-MT) | Tolcapone - blocks conversion of dopamine to DOPAC by inhibiting central COMT

Benztropine mechanism

Antimuscarinic that improves tremor in Parkinson patients

S/E of L-dopa

Arrhythmias from increased conversion to catecholamines

Donepezil

AchE inhibitor used for Alzheimers

Galantamine

AchE inhibitor used for Alzheimers

Rivastigmine

AchE inhibitor used for Alzheimers

Tacrine

AchE inhibitor used for Alzheimers

Neurotranmistter changes in Huntingtons

Increased dopamine | Decreased GABA, Ach

Treatment for Huntingtons

Tetrabenazine and Reserpine - inhibit VMAT to limit dopamine vesicle packaging and release Haloperidol - D2 receptor antagonist

Triptans a. Mechanism b. Use c. Toxicity

a. 5-HT1b/1d agonists --> induce vasoconstriction, prevent vasoactive peptide release, inhibit trigeminal nerve activation b. migraine, cluster headache attacks c. Coronary vasospasm (C/I in patients with Prinzmetal angina and CAD), Mild paresthesia

When are triptans C/I?

In patients with prinzmetal angina and CAD, pregnancy