Neuro and Psych Drugs Flashcards
Drugs to Treat Glaucoma (classes)
- Goal is to decrease humor production, increase outflow, or open angle.
- Beta Blockers (timolol, betaxolol, carteolol)
- PGF2 Agonists (Latanaprosct)
- Diuretics (CA inhibitors) (acetazolamide)
- Alpha agonists (epinephrine, Brimonidine)
- Cholinomimetics (Pilocarpine, Carbachol, Phyostigmine, echothyophate)
Timolol, Betaxolol, Carteolol
- Beta 2 blockers prevent humor synthesis from the ciliary body
- S/E: None
Latanaprosct
- PGF2a agonist increases humor outflow
- S/E: darkens the eye
Acetazolamide
- Inhibits Cabonic Anhydrase thus decreasing humor production
- S/E: None
Epinephrine
- Constricts blood vessels and decreases humor production
- S/E: Do not use in closed angle as can worsen closure. Causes mydriasis.
Brimonidine
- Alpha 2 agonists, autoreceptor.
- S/E: Blurry vision, occular foreign body and pruritis
Pilocarpine and Carbachol
- Muscarinic agonists cause constriction of pupillary muscle and increased outflow of aquesous humor
- Drug of choice for acute angle closure glaucoma.
- S/E: Miosis and cycloplegia (Ciliary muscle spasm)
Physistigmine, Echothiophate
- AchE inhibitors (echothiophate is irreversible), leading to cholinomimetic actions.
- Constriction of ciliary muscle and opening of outflow
Opiods
- Act by stimulating mu (and other receptors) on inhibitory interneurons. Lead to stimulation of Gi receptors on pain and other neurons leading to a decrease in Ca and increase in K in the cleft, thus a decrease rate of firing.
- Decreases stimulatory hormones (Sub P, Ach, NE, 5-HT)
- Common S/E: Miosis, Constipation (occur early) respiratory depression (late). Additive CNS depression with other drugs.
- Toxicity treated with naloxone. Never give O2 because respiratory drive is based on O2 not CO2
Morphine, Fentanyl, Heroin
-Classical pain relievers
Coedine, dextromethorophan
-Used as antitussives
Loperamide, Diphenoxylate
-Antidiahrreals
Miperidine
-Decreased GI effects
Methadone
Long half life means lower abuse potential, often given to treat addicts
Butrophanol
- Partial agonist of mu and kappa. Weaker pain effect but lower abuse potiential and lower risk of respiratory depression
- If given in the context of full agonist, will act as blocker and may precipitate withdrawl
Bupronorphine
-Partial mu agonist, usually given with naloxone to treat opiod withdrawl
Tramadol
- Weak Mu agonist and also blocks NE and 5-HT uptake
- Used as a more mild analgesic
- Decreases siezure threshold. In the context of a patient with electrolyte imbalances may precipitate a siezure.
Clonidine
-Centrally acting alpha 2 agonist (auto receptor) that can be used to minimize opiate withdrawl symptoms
Generalized Siezures
- Phenytoin, Carbemezapine, Valproic Acid
- Lamotrigine, gabapentine, topirimate, levatiracetam
Status Epilepticus
- Benzodiazepines (diazepam (long), lorazepam(med))
- Phenytoin is used as prophylaxis
Partial
Carbemazapine
-All others second line
-Absence
- Ethosuximide
- Valproic acid 2nd line
Nueropathic pain
gabapentin
Migranes
Topirimate
Pregnancy and Kids
Phenobarbitol
Phenytoin
- Rate dependent block of Na channels (inactive state), reduces glutamate release
- First Line therapy for generalized siezures, also used as prophylaxis for status epilepticus
- S/E: Induction P-450 (porphyria), Folate absorption reduced (cleft lip/palate, megaloblastic anemia), gingival hyperplasia, SLE, Hirsuitism
Carbemezapine
- Rate dependent block of Na channels leading to decreased glutamate
- Use: 1st line complex. DOC partial, DOC Trigeminal Neuralgia
- S/E: P-450 Induction, Aplastic Anemia, Teratogenic, SIADH
Valproic Acid
- Many mechanisms, Inhibiti T Type Ca channels, Na Channels, GABA deaminase.
- Use: First line Generalized, Second Line Absence, Myoclonic
- S/E: Inhibit P450s, Major teratogen, GI, Hepatotoxicity, Alopecia
Phenobarbitol
- Bind GABAa and increase Duration of opening
- Use: First line in pregnancy and children (high protein binding), also can be used for other siezure disorders.
- S/E: Respiratory and CNS depression, Induce P-450
Barbituates
- Increase GABAa opening duration.
- Use: Induction of anesthesia, anxiety, but safer drugs exist.
- S/E: Deadly respiratory depression and induce P450s (do not use in porphyria)
Ethosuximide
- Blocks T type Ca channels
- DOC for absence siezures
- S/E: GI distress, stevens johnsons
Benzodiazepines
- Bind BZ1 and BZ2 sites on GABAa receptor and increase frequency. Only function in presence of GABA, therefore much greater safety threshold.
- Use: DT and Status Epilepticus, Anxiety, Insomnia, Detox, induce anesthesia
- S/E: Limited respiratory and CNS depression, concamitant use with alcohol or other drugs can lead to respiratory depression and death
Flumezanil
-Competitive antagonist of BZ sites on GABAa receptor. Can treat overdose with benzos and Z drugs
Ultra Short Benzo
-Midazolam
-Short Benzo
-Oxazapam, Triazolam
Med
Lorazepam, Tirezapam
Long
Diazepam, Chlorodiazoepoxide
Z Drugs
- Zolpidem, Zaleplon, eszoplicone
- Bind BZ1 site at GABAa
- Use: Insomina, used because of much more favorable side effect profile (shorter effects and half life, minimal amnesia)
- Flumezanil is still antidote
Gabapentine
- Inhibits V gated Ca channels, also mild analog of GABA
- Use: Neuropathic pain
Topirimate
- Block Na channels
- Migrane prophylaxis
Tiagabine, Vigabatrin, Levetiracetam
-Increase GABA, Can be used for eppilepsy?
Lamotrigine
- Blocks Na channels
- Used for Siezures,
- Improved S/E profile compared to others
Inhaled Anesthetics Pharm
- Mean Alveolar Concentration (MAC) - Potency. Lower the MAC the higher the potency
- Blood Solubility - The less soluble in blood the more rapid the onset of anesthesia and the more rapid the recovery
Halothane, etc
- Low MAC (very potent), high solubility in blood (takes a long time for induction)
- S/E: Hepatotoxicity (cummulative and may take weeks to develop), Malignant Hyperthermia (treated with dantrolene), Proconvulsant. CV depression and may cause arrythmias
N2O
- High MAC (minimally potent) Low Lipid Solubility (rapid induction and recovery)
- S/E: May cause spontaneous abortion and is contraindicated in pregnancy
Propfol
- Increase flux through GABAa
- Rapid onest and rapid recovery with minimal naseau
Thiopental
- Most commonly used Barb
- Increases duration of GABAa
- Rapidly redistributes in fat, can be quick recovery due to this, high lipid solubility means rapid induction.
Ketamine
- Inhibits NMDA receptor
- Causes dissociative amnesia (kids for breaks etc)
- Increases Cerebral blood flow and should not be used if there is possibility of cerebral bleed
Local Anisthetics
- Enters cell in the uncharged state (Basic env) and becomes charged intracellularly, then blocks Na channels. Preference for active sodium channels in rapidly firing neurons.
- Administered with epinephrine to cause vasoconstriction and keep effects local
- If local infection (acidic environment) need to administer higher dose because more stays in charged form.
- Blocks large unmyelinated neurons firts (C fibers). Pain then temperature, then touch, then pressure. Needs very high dose to block motor
- Esters have a single i and are more prone to allergies. Amides have 2 i’s and are less prone to allergies
- If gets to systemic circulation causes arryhtmias in the heart (Na channel block)
Depolarizing Muscle Block (succinylcholine)
- AchR agonists that cause muscle depolarization.
- Phase I: Comlete depolarization, all AchR occupied there is no antagoinst.
- Phase II: Most AchR blocked, some available. Can be treated with neostigmine
- S/E: Malignant Hyperthermia: RyR mutation leads to elevated intracellular calcium, sustaied contractions increased ETC and heat generation. Antitode is dantrolene (Ca channel blocker)
- Also can get hyprcalcemia and hyperkalemia
Tubocurarine (Curium suffix)
- Antagonist of AchR
- Used commonly for intubation
- Reversal by AchE inhibitor (neostigmine)
Parkison Drugs
- Caused by decreased DA in SNC, strategy is to increase.
- D1R is Gs and nigrostriatal
- D2a is Gi and nigostriatal
- D2c is Gi and Mesolimbic
Bromocriptine
- Dopamine agonist, can be used in parkinsons
- More commonly used in prolactinoma, and as a treatment for antipsychotic overdose
L-DOPA, CarbiDopa
- L-Dopa converted to dopamine by ADCC.
- Carbidopa given to prevent peripheral conversion (dopamine can’t cross BBB)
-Selegellin
- Selective MAO-B inhibitor
- Prevents the breakdown of DA
- Does not act on MAO-A so no interaction with tyramine. Also no interaction with 5-HT and NE levels
Tolcapone
- COMT inhibitor
- Prevents conversion of L-DOPA into unsusable substrate
Amantadine
-Increases release of Dopamine
Benztropine
-Antimuscarinic, used to treat positive symptoms of rigidity and tremor.
Memantine
- NMDAR antagonist, prevents excititoxicity
- Used in alzheimers
Donepazil, Galantamine, Rivastigmine
- Centerally acting AchE inhibitors
- Used in alzheimers
Huntingtons
- Decreased GABA and Ach Increased DA
- Haloperidol - antagonist of DA
- Reserpine - inhibit VMAT (prevent DA recycling and release)
Migranes
- Vasodilation of blood vessels in brain and activation of trigeminal nerve
- Sumatriptan: 5-HT analog, abortive therapy. Can cause hypertensive emergency, contraindicated in prinzmetals angina
- Ergotamine: has simliar effects and S/E as supitriptan but is less likely to cause hypertensive emergency
- Beta blockers and Topiramate can also be used. B blockers as prophylaxis
Alcohol Withdrawl
- DT begins 2-5 days post cessation
- Tx Lorazepam (long) Diazepam (med)
Anxiety
- SSRI, SNRI, Busprione
- SSRI and SNRI have more S/E
ADHD
-Methylphenydate, amphetamines
Bipolar
- Lithium, valproic Acid, Carbemezapime
- Atypical Antpsychotics
Bulimia
-SSRI
Depression
-SSRI, SNRI, TCA, Busprione, mirtazapine
OCD
-SSRI, Clomipramine
Panic Disorder
-SSRI, Venlafaxine, Benzos
PTSD
-SSRI
Schizophrenia
-Antipsychotics
Social Phobia
-SSRI
Tourettes
-Antipsychotics
Antipsychotics
- Block D2(c) Receptors for antipsychotic effect. Increase Serotonin for flat affect.
- Use: Psychosis, Mania, Tourettes
Haloperidol, Triflourperazine, Fluphenazine
- High potency typical antipsychotics with only D2 action
- Used for schizophrenia and psychosis
- S/E: Extrapyramidal (starts with parksinson like (block D2R) then moves to restlessness and more parkisonism (increase sensitivity) then to complete tardive dyskinesia (4 months) often begining with mouth and lips). Can give benztropine or other antimuscarinics in early stages and stop drug
- Neuroleptic Malignant syndrome: Rigidity, Fever, Myoglobinuria, hyperreflexia. Tx: Dantrolene (Ca channel) and Bromocriptine (D2 agonist)
- Alpha blockade, Muscarinic blockade (Coma, Convulsions, Cardiac arrythmias) also sedation, dry mouth, hypotension
- May also cause galactorrhea and reduced libido/amenorrhea
Clorpromazine, Thioridazine
- Same mechanism as strong antipsychotics, but have decreased risk for extrapyramidal and malignant neurolecptic syndrome.
- Corneal deposits for clorpromazine and retinal deposits for thioridazine
Atypical Antipsychotics
- Effects on 5-HT2R, Alpha, and H1 receptors, not completely understood mechanism
- Less risk for extrapyramidal symptoms and Neruoleptic Malignant syndrome
- Treat Negative symptoms of schizophrenia
- All will cause weight gain
-Olanzapine
-Weight gain
-Clozapine
- Weight gain and agranulocytosis
- Will not cause extrapyramidal symptoms.
Risperidone, aripiprazole
-Atypical antipsychotics
Lithium
- Similar structure to Na. Will decrease all GPCR signalling. Gq and Gs (reduce cAMP and PIP)
- Used as a mood stabilizer and for SIADH
- S/E: Nephrogenic DI, Hypothyroidism, Tremors, Siezures, Ebstiens Anomaly (RV hypoplasia)
- Eliminated Via kidneys, but reabsorption enhanced with the use of furosemide or loop diuretics
Busprione
- Partial 5-HT receptor partial agonist
- Primarily indicated for generalized anxiety.
- Minimal S/E profile
SSRI
- Prevent Seretonin Reuptake
- Depression, OCD, Bulimia, PTSD, Anxiety,
- Tox: Sexual Dysfunction
- Seretonin Syndrome: Fever, Tachychardia, confusion, myoclonus, CV collapse. Most commonly seen when there are other drugs present that increase seretonin (TCA, MAO)
Fluoxetine,
SSRI
Paroxatine
SSRI
Sertaline
SSRI
Citalopram
SSRI
Cyprophetadine
Antagonist of 5-HT2 receptor used to treat seretonin syndrome
SNRI
- Used to treat depression
- Stimluation, sedation, naseua
Duloxetine
- SNRI
- Also used in diabetic neuropathy
Venlafaxine
-SNRI also used anxiety and panic disorders
TCA
- Inhibit Seretonin and NE uptake
- Toxicity: CCC. Coma, Convulsions, Cardiac Arrythmias
- Lowers siezure threshold
- Most common cause of death is arrythmia (common cause of poisoning)
- Give NaHCO3 to alkalanize the urine and increase clearance
- Anticholinergic S/E are the most commonly reported
- Also have other alpha blocker and atropine like side effects. (Dry mouth, hypotension, confusion, hallucinations)
-Amitryptaline
-TCA also use in Fibromyalgia and neuropathic pain
-Imipramine
-TCA also used to treat enuresis
clomimpramine
-TCA also used to treat OCD
doxepin amoxepin
TCA
MAOI
- Block MAO and decrease metabolism of DA, 5HT, NE
- Used as second line in atypical depression, anxiety, hypochondriasis
- S/E: Ingestion with tyramine may precipitate hypertensive crisis (sensitized terminals)
- If given with anything that increases 5HT (St johns wort) can cause seretonin syndrome
Phenelzine
-MAOI
Trancyclopramine
MAOI
Isocarboxazide
MAOI
Selegeline
-MAOI B specific
Buproprion
- Increase NE and DA
- Used to quit smoking
- Siezure and headache
Mirtazapine
- alpha 2 antagoinst (autoR) inreases NE and 5HT
- Sedation, weight gain
- Used in anorexics and elderly
Maprotiline
-Increase NE
Trazadone
- SSRI
- Used for insominia
- Causes hypotension and priapism
Cyclobenzaprine
- Muscle relaxant that is similiar to TCA
- S/E are anticholinergic