Drogas De Mod4

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Phenytoin

Back 1

First line TC and SE prophylaxis, IB antiarrhythmic
Used in simple and complex focal
MOA: increases Na+ inactivation, inhibits glutamate relase from pre-synaptic neuron

Use fosphenytoin for parenteral use

Toxicity: nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of P450. Chronic use = gingival hyperplasia in kids, peripheral neuropathy, hirsuitism, megaloblastic anemia via decreased folate absorption, teratogenic (fetal hydantoin syndrome), S-J

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Carbamezepine

Back 2

First line for simple, complex and TC, trigeminal neuralgia

MOA: Na+ channel inactivation

Toxicity: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of P450, SIADH, J-J

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Lamotrigine

Back 3

Used in simple, complex, TC

MOA: Blocks voltage-gated Na+ channels

Toxicity: S-J

Front 4

Gabapentin

Back 4

Used in simple, complex, TC, peripheral neuropathy, postherpetic neuralgia, migrane prophylaxis, bipolar disorder

MOA: GABA analog, inhibits high-voltage-activated Ca++ channels

Toxicity: Sedation, ataxia

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Topiramate

Back 5

Used in simple, complex, TC, migrane prevention

MOA: blocks Na+ channels, increased GABA

Toxicity: sedation, mental dulling, kidney stones, weight loss

Front 6

Phenobarbital

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Used in simple, complex, TC
First line in children

MOA: Increse GABA

Toxicity: sedation, tolerance, dependence, induction of P450

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Valproic acid

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First line in TC, used in simple, complex, absence, myoclonic seizures

MOA: Na+ channel inactivation, increases GABA concentration

Toxicity: GI distress, hepatotoxicity, neural tube defects in fetus (spina bifida), tremor, weight gain

Monitor: LFT, pregnancy

Front 8

Ethosuximide

Back 8

First line in absence

MOA: Blocks thalamic T-type Ca++ channels

Toxicity: GI distress, fatigue, headache, urticaria, S-J (EFGH)

Front 9

Benzodiazepines (diazepam or lorazepam)

Back 9

First line for acute SE, used for seizures of eclampsia after MgSO4, anxiety, spasticity, detox (alcohol DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

MOA: increased GABA action by increasing frequency of Cl- channel opening. Decreases REM sleep. MOst have long half-lives and active metabolites except for triazolam, oxazepam and midazolam (have higher addictive potential)

Toxicity: Dependence, additive CNS depression effects with alcohol. Benzos, barbs and EtOH all bind to GABA receptor, so risk of respiratory depression and coma

Antidote: flumazenil (competitive antagonist at GABA benzodiazepine receptor)

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Tiagabine

Back 10

Used in simple and complex

MOA: inhibits GABA reuptake

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Vigabatrin

Back 11

Used in simple and complex

MOA: Irreversibly inhibits GABA transaminase, so more GABA

Front 12

Levetiracetam

Back 12

Used in simple, complex and TC

MOA: Unknown (modulate GABA and glutamate release?)

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Barbituates
(Phenobarbital, pentobarbital, thipental, secobarbital)

Back 13

Used as sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

MOA: Facilitate GABA action by increasing duration of Cl- channel opening, so decreases neuron firing.

Toxicity: Contraindicated in porphyria
Respiratory and cardiovascular depression can be fatal. CNS depression (worse with EtOH), dependence, induces P450.

Antidote: none, assist respiration and maintain BP

Front 14

What's the difference between the effect of barbs and benzos?

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Barbidurates increases duration of Cl- channel openning (decrease neuron firing) and Frenzodiazepines increases frequenccy of Cl- opening

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Hypnotics
Zolpidem, zaleplon, eszopiclone

Back 15

Used in insomnia

MOA: BZI subtype of GABA receptor

Toxicity: ataxia, headaches, confusion, modest day-after psychomotor depression and few amnestic effects.

Antidote: Flumazenil

Short duration of action bc of rapid liver metabolism.

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Inhaled anesthetics
Haloethane, enflurane, isoflurane, sevoflurane, methoxyfulurane, NO

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MOA unknown

Effects: myocardial and respiratory depression, nausea/vomitting, increased cerebral blood flow with decreased cerebral demand

Good anesthetics: analgesia, seation, amnesia, abolishes noxious reflexes (autonomic and airway), muscle relaxation

Haloethane = smells good, decrease CO and BP
hepatotoxicity, arrhythmias with Ep, significant cardiac depression, slow emergence

Methoxyflurane = nephrotoxic

Enflurane = proconvulsant

All (except N2O)= malignant hyperthermia (inherited)

N2O= fast uptake and elimination (low solubility in blood), small hemodynamic effects, not very potent (low solubility in fat), no muscle relaxation, supports combustion, expands trapped gas in body cavity

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Opioids (morphine, fentanyl)

Back 17

Used wtih other CNS depressants during general anesthesia

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Thiopental

Back 18

IV anesthetic with high potency/lipid solubility, rapid entry into brain. Used for induction of anesthesia and short procedures.
Effect terminated by rapid redistribution into tissue and fat.
Decreases cerebral blood flow

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MIdazolam

Back 19

IV benzo anesthetic. Most common drug for endoscopy, used with gaseous anesthetic and narcotics

Toxicity: severe post-op respiratory depression, decreased BP (flumazenil as antidote) and amnesia

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Arylcycloamines (Ketamine)

Back 20

PCP analogs that block NMDA R.

Toxicity: Cardiovascular stimulant, cause disorientation, hallucination, and bad dreams. Increases cerebral blood flow.

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Propofol

Back 21

IV anesthetic that it used for sedation in ICU, rapid anesthesia induction, and short procedures. Less post-op nausea than thiopental

MOA: Potentiates GABA

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Ester anesthetics

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Procaine, cocaine, tetracaine

Front 23

Amide anesthetics

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Lidocaine, mepivacain, buivicaine

Tertiary amine penetrate membrane in uncharged form, then bind to ion channel in charged form

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Local anesthetics

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MOA: block inner part of Na+ channels, preferentially to activated channels (rapidly firing neurons).

Ep enhances action and decreases bleeding, increases anesthesia by decreasing systemic concentration

Small diameter fibers myelinated > small unmyelinated > large diameter myelinated > large unmyelinated (size more important)

Lose: 1) Pain 2) Temperature 3) touch 4) Pressure

Use: minor surgery or spinal. If allergic to esthers give amines

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

Front 25

What happens in infected tissue with local anesthetics?

Back 25

Infected tissue is acidic, so this reacts wtih anesthetics and makes them alkaline and charged. They cannot penetrate the membrane effectively so more anesthetic is needed.

Front 26

Succinylcholine

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Strong Ach receptor agonist (motor selective); produces sustained depolarization and prevents muscle contraction
Used for muscle paralysis in surgery or mechanical ventilation.

Phase I: prolonged depolarization, potentiated by cholinesterase inhibitors. No antidote
Phase II: repolarized but blocked; Ach receptors available but desensitized. Antidote: cholinesterase inhibitor

Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

Front 27

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

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Nondepolarizing neuromuscular drugs.
Competitive antagonists for ACh receptors

Reversal: neostigmine (cholinesterase inhibitor), edrophonium

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Dantrolene

Back 28

Prevents Ca++ release from SR of skeletal muscle

Used for malignant hyperthermia (in inhalation anesthetics (not seen with N20) and succinylcholine)

Used for neuroleptic malignant syndrome (with anti-psychotic drugs)

Front 29

Bromocritpine, pramipexole, ropinirole, (last 2 are non-ergots and preferred)

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Dopamine agonists used in Parkinson's

Front 30

Amantadine

Back 30

Increases dopamine release
Antiviral against Influenza A and rubella

Toxicity: ataxia

Front 31

L-dopa/carbidopa

Back 31

Converted to dopamine in CNS. L-dopa can cross BBB but dopamine cannot. Is converted to dopamine via dopa decarboxylase.

Carbidopa = peripheral decarboxylase inhibitor. Increases availability in the brain and limits peripheral side effects

Toxicity: arrhythmias from increased peripheral formation of catecholamines. Long term --> dyskinesias after administration, akinesia between doses

Front 32

Selegiline

Back 32

Prevents dopamine breakdown, selective MAO type B inhibitor. MAO-B preferentially metabolizes dopamine over NE and 5-HT, so it increases dopamine.

Use: adjunctive to L-dopa in PD

Toxicity: enhances toxicity of L-dopa

Front 33

Entacapone, tolcapone,

Back 33

Prevent L-dopa degradation by inhibiting COMT, increases dopamine availability

Front 34

Benztropine

Back 34

Anti-muscarinic that improves tremor and rigidity but has little effect on bradykinesis in PD

Front 35

Memantine

Back 35

MOA: NMDA R antagonist, helps prevent excitotoxicity mediated by Ca++

Toxicity: dizziness, confusion, hallucinations

Uses: Alzheimer's

Front 36

Donepezil, galantamine, rivastigmine

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MOA: Acetylcholinesterase inhibitors- ACh is decreased in Alzheimer's

Toxicity: Nausea, dizziness, insomnia

Use: Alzheimer's

Front 37

Tetrabenzine and reserpine

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Inhibit VMAT (limits dopamine packaging and release)

Use: Huntingtons (increased dopamine seen in HD)

Front 38

Haloperidol

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Dopamine receptor antagonist

Use: HD (increased Dopamine seen in HD)

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Sumatriptan

Back 39

5-HT(1B/1D) agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release. Induces vasoconstriction. Half life <2 hours

Use: acute migrane, cluster headache attacks

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

"A SUMo wrestler TRIPs ANd falls on your HEAD"

Front 40

Methylphenidate, dextoamphetamine, methamphetamine

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CNS stimulant that increase catecholamines at synaptic cleft, especially NE and dopamine

Use: ADHD, narcolepsy, appetite control

Intoxication: Euphoria, grandiosity, pupillary dilation, proplonged wakefulness and attention, hypertension, tachycardia, anorexia, paranoia, fever. Severe: cardiac arrest, seizrue.

Withdrawal: Anhedonia, increased appetite, hypersomnolence, existential crisis

Front 41

Haloperidol, trifluoperazine, fluphenazine (high potency), thioridazine, chlorpromazine (haloperadol + azines) (low potency)

Back 41

MOA: Block D2 receptors (increased cAMP)

Use: Schizophrenia (+ symptoms), psychosis, acute mania, Tourette's

Side effects: High potency have extrapyramidal symptoms
Low potency have anticholinergice, antihistamine, and alpha-1 blockade effects)

Toxicity: highly lipid soluble and stored in body fat; thus very slow to be removed from body
EPS (dyskinesias)
Endocrine side effects (dopamine R antagonism, hyperprolactinemia, galactorrhea)
Blocking muscarinic (dry mouth, constipation), alpha-1 (hypotension), and histamine (sedation)
Chlorpromazine = corneal deposits
Thioridazine = reTinal deposits
Haloperidol = NMS (FEVER), tardive diskinesia

EPS side effects: 4 hour acute dystonia (muscle spasm, stiffness, oculogyric crisis), 4 day akathisia (restlessness), 4 week bradykinesia (PD), 4 month tardive dyskinesia

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Neuroleptic malignant syndrome

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Rigidity, myoglobinuria, autonomic instability, hyperpyrexia.

Tx: dantrolene, D2 agonists (bromocriptine)

Fever
Encephalopathy
Vitals unstable
Elevated enzymes
Rigidity of muscles

Front 43

Tardive dyskinesia

Back 43

Stereotypical oral-facial movements as a result of long-term antipsychotic use. Often irreversible

Front 44

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

Back 44

MOA: affect 5-HT2, dopamine, alpha and H1 receptors

Use: schizophrenia (+ and - symptoms), bipolar, OCD, anxiety disorder, depression, mania, Tourette's

Toxicity: Fewer EPS and anticholinergic SEs than traditional antipsychotics!
Olanzapine/clozapine = weight gain
Cloxapine = agranulocytosis (weekly WBC monitor) and seizure
Ziprasidone = QT interval

Front 45

Lithium

Back 45

MOA: inhibits PIP cascase

Use: Mood stabilizer for bipolar disorder, blocks relapse and acute manic events.
SIADH

Toxicity: Tremor, sedation, edema heart blck, hypothyroidism, polyuria (ADH antagonist, so causes nephrogentic DI), teratogenesis (Ebstein anomaly and malformation of great vessels).

Narrow therapeutic window, monitor serum levels.

Excreted by kidneys; most reabsorbed at proximal convoluted tubules following Na+ reabsorption

LMNOP: litium side effects = movement (tremor), Nephrogenic DI, hypOthyroidism, Pregnancy problems

Front 46

Buspirone

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MOA: Stimulates 5-HT1A receptors

Use: Generalized anxiety disorders. No sedation, addiction or tolerance. Takes 1-2 weeks for effect

No alcohol interaction

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Fluoxetine, paroxetine, sertraline, citalopram

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SSRI

Use: depression, GAD, panic disorder, OCD, bulimia, social phobia, PTSD

4-8 for effect

Toxicity: GI distress, sexual dysfunction (anorgasm and decreased libido)

Serotonin syndrome = hyperthermia, confusions, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures. Tx: cyproheptadine (5-HT2 receptor antagonist)

Front 48

Venlafaxine, duloxetine

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Inhibit serotonin and NE reuptake (SNRI)

Use: depression.
Venlafaxine: GAD and panic disorders
Duloxetine: diabetic peripheral neuropathy (has greater effect on NE)

Toxicity: increased BP, stimulant, sedation, nausea

Front 49

Amitriptyline, nortiptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

Back 49

TCA, block reuptake of NE and 5-HT

Use; Depression, bedwetting (imipramine), OCD, fibromyalgia

Toxicity: sedation, alpha-1 effects (postural hypertension), anticholinergic effects (tachycardia, urinary retention, dry mouth), Tertiary TCA have more anticholinergic effects than secondary.
Desipramine = less sedating and higher seizure threhold

Tri C: Convlusions, Coma, Cardiotoxicity
Respiratory depression, hyperpyrexia.
Confusion and hallucinations in the elderly, so use nortriptyline
Tx: NaHCO3 for cardiovascular toxicity

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Tranylcypromine, phenelzine, isocarboxazid, selegline (B)

Back 50

MOA: MAO-i (increase NE, 5-HT, dopamine)

Use: atypical depression, anxiety, hypochondriasis

Toxicity: htn crisis with eating tyramine, CNS stimulation.
Contraindicated wtih SSRIs, TCAs, St. John's Wort, meperidine, dextromethorphan (to prevent serotonin syndrome)

Front 51

Buprorpion

Back 51

Increases NE and dopamine, unknown mechanism

Use: depression and smoking cessation

Toxicity: stimulant (tachycardia and insomnia), headache, seizure in bulimic patients. No sexual SEs

Front 52

Mirtazapine

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Alpha-2 antagonist (increases release of NE and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist.

Toxicity: sedation (could be used for depressed patients with insomnia), increased appetite, weight gain (used for depressed patients who are elderly or anorexic), dry mouth

Front 53

Maprotiline

Back 53

Blocks NE reuptake

Use: depression

Toxicity: sedation, orthostatic hypotension

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Trazodone

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MOA: Inhibits serotonin reuptake

Use: Insomnia - high doses neede for antidepressant effects

Toxicity: sedation, nausea, priapism, postural hypotension