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Pharmacology > Neuro drugs > Flashcards

Neuro drugs Flashcards

1
Q

What classes of drugs can be used to treat glaucoma?

A

alpha-agonists, beta-blockers, diuretics, cholinomimetics, prostaglandin

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2
Q

Alpha-agonists for glaucoma

A

Epinephrine (alpha1), Brimonidine (alpha2)

Mechanism: both decrease aqueous humor synthesis (epinephrine via vasoconstriction)

Side effects: mydriasis (epinephrine) blurry vision, ocular hyperemia, foreign body sensation, allergic rxn, ocular pruritis

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3
Q

When is epinephrine contraindicated for use in glaucoma?

A

Do NOT use with closed-angle glaucoma! Will make it worse

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4
Q

Beta-blockers for glaucoma

A

Timolol, betaxolol, carteolol

mechanism: decrease aqueous humor synthesis

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5
Q

diuretics for glaucoma

A

Acetazolamide

Mechanism: decrease aqueous humor synthesis via inhibition of carbonic anhydrase

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6
Q

cholinomimetics for glaucoma

A

Direct: pilocarpine, carbachol
Indirect: physostigmine, echothiophate

Mechanism: increase outflow of aqueous humor via ciliary muscle contraction and opening trabecular meswork

side effects: miosis and cyclospams (contraction of ciliary muscle)

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7
Q

What is the best drug to use in glaucoma emergency?

A

Pilocarpine - very effective at opening meshwork into canal of Schlemm

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8
Q

Prostaglandin for glaucoma

A

Latanoprost (PGF2alpha)

Mechanism: increase outflow of aqueous humor

Side effects: darkening of iris

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9
Q

What is the mechanism of opioid analgesics?

A

Agonists at opioid receptors (mu=morphine, delta= enkephalin, kappa= dynorphin) -> open K+ channels and close Ca2+ channels -> decrease synaptic transmission

Inhibit release of ACh, NE, 5-HT, glutamate, substance P

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10
Q

What are examples of opioid analgesics and what is their clinical use?

A

morphine, codeine, fentanyl, meperidine, pentazocine

Pain, cough suppression - dextromethorphan
diarrhea - loperamide, diphenoxylate
acute PE
maintenance for heroin addicts (methadone, buprenorphine + naloxone)

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11
Q

What are the toxicities of opioid analgesics?

A

addiction, respiratory depression, constipation, miosis, additive CNS depression. Do NOT develop tolerance to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid antagonist)

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12
Q

Butorphanol

A

mechanism: kappa-opioid receptor agonist and mu-opioid receptor partial antagonist

Use: severe pain (migraine, labor); causes less respiratory depression than full opioid agonists

Toxicity: can cause opioid withdrawal symptoms if patient also taking full opioid agonist (acts as competition), overdose not easily reversed with naloxone

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13
Q

Tramadol

A

Mechanism: very weak opioid agonist; also inhibits 5-HT and NE reuptake

Use: chronic pain

Toxicity: similar to opioids, decreases seizure threshold, serotonin syndrome

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14
Q

What is first line for simple partial seizures?

A

Carbamazepine

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15
Q

What is first line for complex partial seizures?

A

Carbamazepine

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16
Q

What is first line for tonic-clonic seizures?

A

Phenytoin, carbamazepine or valproic acid

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17
Q

What is first line for absence seizures?

A

Ethosuximide

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18
Q

What is first line for status epilepticus? What is used for prophylaxis for status epilepticus

A

acute: Benzodiazepines (diazepam, lorazepam)
prophylaxis: Phenytoin

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19
Q

Ethosuximide

A

Uses: 1st line for absence seizures

Mechanism: blocks thalamic T-type Ca2+ channels

Side effects: GI, fatigue, HA, urticaria, Stevens-Johnson syndrome

Notes: “Sux to have Silent Seizures”

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20
Q

Benzodiazepines

A

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

Uses: Anxiety, spasticity, acute status epilepticus (diazepam, lorazepam), detoxification (especially alcohol - DTs), night terrors, sleep walking, general anesthesia

Mechanism: increases action of GABA-A by increasing FREQUENCY of Cl- channel opening. Decreases REM sleep.

(Note: alprazolam, triazolam, oxazepam and midazolam are short acting -> higher addiction potential)

Side effects: Sedation, tolerance, dependence, respiratory depression (less risk of respiratory depression than barbituates) *Treat overdose with flumazenil (competitive antagonist)

Notes: Also used for eclampsia seizures, but 1st line is MgSO4

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21
Q

Phenytoin

A

Uses: 1st line for tonic-clonic seizures, prophylaxis for status epilepticus, also used for partial seizures

Mechanism: increase Na+ channel inactivation, 0-order kinetics!!

Side effects: nystagmus, diplopia, ataxia, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, TERATOGEN, SLE-like syndrome, induces P450, LAD, Stevens-Johnson, osteopenia

Notes: Fosphenytoin for IV

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22
Q

Carbamazepine

A

Uses: a first line drug for partial seizures and tonic-clonic seizures

Mechanism: increases Na+ channel inactivation

Side effects: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), hepatotoxicity, induction of P450, SIADH, Steven-Johnson syndrome, CONTRAINDICATED IN PREGNANCY- teratogenesis,

Notes: 1st line for trigeminal neuralgia

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23
Q

Valproic acid

A

Uses: one of the 1st line drugs for tonic-clonic seizures, also used for partial seizures and absence seizures

Mechanism: increases Na+ channel inactivation, increases GABA by inhibiting GABA transaminase

Side effects: GI distress, rare but fatal hepatotoxicity (measure LFTs), tremor, weight gain, CONTRAINDICATED IN PREGNANCY - neural tube defects

Notes: also used for myoclonic seizures, bipolar disorder

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24
Q

Gabapentin

A

Uses: simple and complex partial seizures

Mechanism: inhibits high-voltage-activated Ca2+ channels; GABA analog

Side effects: sedation, ataxia

Notes: also used for peripheral neuropathy, postherpetic neuralgia

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25
Q

Phenobarbital

A

Uses: simple and complex partial seizures and tonic-clonic seizures

Mechanism: increases GABA-A action

Side effects: sedation, tolerance, dependence, induces P450, cardiorespiratory depression

Notes: 1st line in neonates*

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26
Q

Topiramate

A

Uses: simple and complex partial seizures and tonic-clonic seizures

Mechanism: Blocks Na+ channels, increases GABA action

Side effects: sedation, mental dulling, kidney stones, weight loss

Notes: also used for migraine prevention

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27
Q

Lamotrigine

A

Uses: All seizures, except status epilepticus

Mechanism: Blocks voltage-gaited Na+ channels

Side effects: Sevens-Johnson syndrome

Notes: must titrate slowly!

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28
Q

Levetiracetam

A

Uses: simple and complex partial seizures and tonic-clonic seizures

Mechanism: unknown, may modulate GABA, glutamate release

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29
Q

Tiagabine

A

Uses: simple and complex partial seizures

Mechanism: increase GABA by inhibiting reuptake

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30
Q

Vigabatrin

A

Uses: simple and complex partial seizures

Mechanism: increase GABA by inhibiting GABA transaminase

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31
Q

Barbituates

A

(-barbital/-pental) phenobarbital, pentobarbital, thiopental, secobarbital

Mechanism: increases DURATION of Cl- channel opening -> decreases neuron firing Note: contraindicated in porphyria

Clinical use: sedative for anxiety, seizures, insomnia, anesthesia (thiopental)

Toxicity: cardiorespiratory depression, CNS depression (exacerbated by EtOH use), dependence, induces P450

Overdose treatment is supportive

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32
Q

Nonbenzodiazepine hypnotics

A

Zolpidem, zaleplon, eszopiclone

Mechanism: act via BZ1 subtype of GABA receptor. Reversed by flumazenil

Uses: insomnia “All ZZZs put you to sleep”

Toxicity: ataxia, HA, confusion. Short acting due to rapid liver metabolism. Modest day-after psychomotor depression and few amnestic effects, lower dependence risk than benzos

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33
Q

What is the MAC?

A

Minimal alveolar concentration of inhaled anesthetic required to prevent 50% of patients from moving in response to noxious stimuli

potency is proportional to 1/MAC –> potency increases with lower MAC

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34
Q

What are examples of inhaled anesthetics, what are there effects and toxicity?

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O

Effects: myocardial and respiratory depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand)

Toxicity: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas (N2O)

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35
Q

What drugs can cause malignant hyperthermia and what is the treatment?

A

Inhaled anesthetics (except N2O) and succinylcholine induce fever and severe muscle contractions. Treat with dantrolene

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36
Q

What barbituate is used for IV anesthesia?

A

Thiopental - high potency and high lipid solubility, rapid brain entry

Used for induction of anesthesia and short procedures

Effects terminated by rapid redistribution. Decreases cerebral blood flow

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37
Q

Which benzo is commonly used for IV anesthesia

A

Midazolam most common for endoscopy, used with gas anesthetics and narcotics. May cause anterograde amnesia and severe post-op respiratory depression -> give flumazenil for OD

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38
Q

How are arylcylcohexylamines (ketamine) used for IV anesthesia?

A

PCP analogs act as dissociative anesthetics

Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, bad dreams. Increases cerebral blood flow

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39
Q

What is used for sedation in ICU, rapid anesthesia induction, short procedures and causes less post-op nausea than thiopental?

A

Propofol. potentiates GABA-A

40
Q

What are examples of local anesthetics and what is their mechanism, use and toxicity?

A

Esters - procaine, cocaine, tetracaine
Amide: Lidocaine, mepivacaine, bupivacaine, (amides have 2 i’s)

Mechanism: Bind activated Na+ channels (most effective in rapidly firing neurons) on inner portion of channel

Use: minor surgical procedures, spinal anesthesia. Give amides if allergic to esters

Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, hypotension, arrhythmias (cocaine), methemoglobinemia (benzocaine)

41
Q

Succinylcholine

A

Depolarizing neuromuscular blocking drug

Mechanism: strong ACh agonist- produces sustained depolariziation to prevent muscle contraction

Reversal of blockade:
Phase I (prolonged depolarization)- no antidote
Phase II (repolarized but blocked, ACh receptors available but desensitized)- give AChE inhibitors

Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

42
Q

Nondepolarizing neuromuscular blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

Mechanism: competitive antagonist for ACh receptors

Reversal of blockade with neostigmine (must be given with atropine to prevent muscarinic side effects), edrophonium and other AChE inhibitors

43
Q

Dantrolene

A

Prevents Ca2+ release from sarcoplasmic reticulum

Used to treat malignant hyperthermia and neuroleptic malignant syndrome (toxicity of antipsychotics)

44
Q

Baclofen

A

Mechanism: inhibits GABA-B receptors at spinal cord level, induces muscle relaxation

Use: muscle spasms (acute back pain)

45
Q

Cyclobenzaprine

A

Mechanism: centrally acting skeletal muscle relaxant. Similar to TCA structurally and similar anticholinergic side effects

Use: muscle spasms

46
Q

Dopamine agonists to treat Parkinson disease

A

Ergot - Bromocriptine

Non-ergot (preferred) - pramipexole, ropinirole

47
Q

Amantadine

A

Increases dopamine release and decreases reuptake

Used for Parkinson disease and as antiviral against influenza A and rubella

Toxicity: ataxia, livedo reticularis

48
Q

Levodopa (L-dopa)/carbidopa

A

Mechanism: Carbidopa blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase. Is given with L-dopa to increase bioavailability of L-dopa in brain and limit peripheral side effects (nausea)

Use: Parkinson disease

Toxicity: arrhythmias from increase peripheral formation of catecholamines. Long-term use can lead to dyskinesia after administration and akinesia between doses “on-off” phenomenon

49
Q

Entacapone, tolcapone

A

Prevent peripheral L-dopa degradation to 3-O-methyldopa by inhibiting COMT (tolcapone acts both peripherally and centrally, entacapone only peripherally)

Use: Parkinson disease

50
Q

Selegiline

A

Mechanism: selectively inhibits MAO-B which metabolizes dopamine over NE and 5-HT -> increase dopamine availability

Use: Adjunctive to L-dopa in treating Parkinson disease

Toxicity: may enhance adverse effects of L-dopa

51
Q

Memantine

A

Mechanism: NMDA receptor antagonist; prevents excitotoxicity mediated by calcium

Use: Alzheimer disease

Toxicity: dizziness, confusion, hallucinations

52
Q

What AChE inhibitors are used to treat Alzheimer’s?

A

Donepezil, galantamine, rivastigmine, tacrine

Toxicity: nausea, dizziness, insomnia

53
Q

What drugs are used to treat Huntington disease?

A

[NOTE: NT changes in Huntington: decreased GABA and ACh and increased dopamine]

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

Haloperidol - D2 receptor antagonist

54
Q

Triptans

A

Sumatriptan

Mechanism: 5-HT(1B/1D) agonist. Inhibits trigeminal nerve activation; prevent vasoactive peptide release; induce vasoconstriction

Use: acute migraine and cluster headaches

Toxicity: coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina)

55
Q

What is a sensitive indicator of alcohol use? What should the AST and ALT values be?

A

Indicator: serum gamma-glutamyltransferase (GGT)

AST =2xALT

56
Q

What are the symptoms and treatment of opioid intoxication?

A

Symptoms: euphoria, respiratory and CNS depression, decreased gag reflex, pinpoint pupils, seizures (OD)

Treatment: naloxone, naltrexone

57
Q

What are the symptoms and treatment of opioid withdrawal?

A

Sweating, dilated pupils, piloerection, “flu-like” symptoms

Treatment: methadone, buprenorphine, tincture of opium for newborns with opioid withdrawal

58
Q

What are treatments for cocaine intoxication?

A

alpha-blockers, benzodiazepines (beta-blockers NOT recommended)

59
Q

What is used to treat nicotine withdrawal?

A

nicotine patch, gum etc; bupriopion/varenicline

60
Q

What is used to treat PCP intoxication?

A

symptoms: impulsivity, fever, psychomotor agitation, vertical and horizontal nystagmus

Treatment: benzodiazepines, rapid-acting antipsychotic

61
Q

What is the pharmaceutical form of marijuana?

A

Dronabinol

62
Q

What is the treatment for heroine addiction?

A

Methadone - long acting oral opiate used for heroine detox or long-term maintenance

Naloxone + buprenorphine - antagonist+ partial agonist. Naloxone not orally bioavailable -> withdrawal symptoms only if injected (lower abuse potential)

Naltrexone - long-acting opioid antagonist for relapse prevention once detoxified

63
Q

What are treatments for alcoholism?

A

Disulfiram (condition to abstain, inhibits acetalaldehyde dehydrogenase), acamprosate, naltrexone, supportive care

64
Q

What are complications of alcoholism?

A

alcoholic cirrhosis, hepatitis, pancreatitis, peripheral neuropathy, testicular atrophy,

Wernicke-Korsakoff - B1 deficiency- damage to mammillary bodies; Wernicke encephalopathy (confusion, ophthalmoplegia, ataxia) may progress to Korsakoff psychosis (irreversible memory loss, confabulation, personality change)

Mallory-Weiss syndrome - partial thickness tear at gastroesophageal jxn - hematemesis, often misdiagnosed as ruptured esophageal varices

65
Q

How does delirium tremens present and what is the treatment?

A

alcohol withdrawal syndrome peaking 2-4 days after last drink

Autonomic hyperactivity - tachycardia, tremors, anxiety, seizures

Treatment: benzodiazepines

Treat alcoholic hallucinosis (visual hallucinations 12-48 hrs after last drink with long-acting benzodiazepines (chlordiazepoxide, lorazepam, diazepam)

66
Q

What are examples of CNS stimulants? What is the mechanism and clinical use?

A

Methylphenidate, dextroamphetamine, methamphetamine

mechanism: increases catecholamines in the synaptic cleft, especially NE and dopamine

clinical use: ADHD, narcolepsy, appetite control

Toxicity: sympathomimetic side effects (HTN, arrhythmia, psychosis), risk of dependency

67
Q

What are examples of typical antipsychotics? What is the mechanism and clinical use?

A

Haloperidol, trifluoperazine, fluphenazine, chlorpromazine (haloperidol + “azines”)

Mechanism: block dopamine D2 receptors (increase cAMP)

Clinical use: Schizophrenia (positive symptoms), psychosis, acute mania, Tourette syndrome

68
Q

Which antipsychotics are high potency and what are their side effects?

A

Trifluoperazine, Fluphenazine, Haloperidol

Neurologic side effects - Huntington disease, delirium, EPS symptoms

69
Q

Which antipsychotics are low potency and what are their main side effects?

A

Chlorpromazine, Thioridazine

Non-neuro side effects; Anticholinergic (dry mouth, constipation), antihistamine (sedation) and alpha1-blockade effects (hypotension)

Chlorpromazine - corneal deposits
Thioridazine - reTinal deposits

70
Q

What contributes to toxicity of antipsychotics?

A

highly lipid soluble -> stored in fat and slow to be removed from body

71
Q

What are endocrine side effects of antipsychotics?

A

dopamine receptor antagonism -> hyperprolactinemia -> galactorrhea

72
Q

What cardiac toxicity do antipsychotics have?

A

QT prolongation

73
Q

What are EPS side effects and how are they treated?

A

Caused by high potency antipsychotics (haloperiodol, fluphenazine)

Evolution of EPS side effects: 4 hr acute dystonia (muscle spams, stiffness), 4 day akathesia (restlessness), 4 wk bradykinesia (parkinsonism), 4 mo tardive dyskinesia (oral-facial movements)

Treatment: benztropine or diphenydramine

74
Q

What are the symptoms of neuroleptic malignant syndrome (NMS) and how is it treated?

A

Toxicity of neuroleptic agents

Symptoms: fever, encephalopathy, unstable vitals, increased enzymes, rigidity of muscles
Myoglobinuria

Treatment: dantrolene, D2 agonists (bromocriptine)

75
Q

What are examples of atypical antipsychotics, what are their mechanism and clinical uses?

A

Olanapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone (It’s atypical for old closets to quietly risper from A to Z)

Mechanism: varied effects on 5HT2, dopamine, alpha and H1 receptors

Clinical use: Schizophrenia - positive and negative symptoms. Bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome

76
Q

What is the toxicity of atypical antipsychotics?

A

Fewer EPS and anticholinerigic effects than traditional antipsychotics

All can prolong QT interval

Olanzapine/clozapine - can cause weight gain

Clozapine may cause agranulocytosis -> WATCH WBC count weekly!! and seizure

Risperidone may increase prolactin -> (lactation and gynecomastia) -> decrease GnRH, LH and FSH -> irregular menstruation and fertility problems

77
Q

What is the use and toxicity of lithium?

A

Clinical use: mood stabilizer for bipolar; blocks relapse and acute manic events. Also SIADH

Toxicity:
Tremor
Hypothyroidism
Nephrogenic diabetes insipidus (polyuria)
Teratogen - causes Ebstein anomaly ( septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart)

Narrow therapeutic window - close monitoring of serum levels

Almost exclusive renal excretion - most reabsorbed at PCT with sodium

78
Q

What can increase side effects in patients taking lithium

A

Thiazides -> increases lithium toxicity since lithium is excreted by kidneys and reabsorbed at PCT with sodium

79
Q

Buspirone

A

Mechanism: stimulates 5HT1A receptors

Use: Generalized anxiety disorder, depression

*Does not cause sedation, addiction or tolerance, takes 1-2 weeks for effect, does not interact w/ EtOH (unlike barbiturates and benzodiazepines)

80
Q

Selective serotonin reuptake inhibitors (SSRIs) - what are examples, the mechanism and clinical use?

A

Fluoxetine, paroxetine, sertraline, citalopram

Mechanism: 5HT specific reuptake inhibitors -> more 5HT at synaptic cleft

*usually takes 4-8 weeks to have an effect

Clinical use: depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD

81
Q

What is the toxicity of SSRIs?

A

Fluoxetine, paroxetine, sertraline, citalopram

Fewer side effects than TCAs.
GI distress, SIADH, sexual dysfunction

*Serotonin syndrome with any drug that increases 5HT (MAOIs, SNRIs, TCAs)

82
Q

What is Serotonin syndrome and how is it treated?

A

Drug toxicity of increased 5HT (SSRIs combined with MAOIs, SNRIs, TCAs)

hyperthermia, confusion, myoclonus, cardiovascular instability, flushing, diarrhea, seizures

Treatment: cyproheptadine (5HT2 receptor antagonist)

83
Q

Serotonin NE reuptake inhibitors (SNRIs)

A

Venlafaxine, duloxetine

Mechanism: inhibit 5HT and NE reuptake

Clinical use: Depression
Venlafaxine - also generalized anxiety disorder, panic disorder, PTSD
Duloxetine - also for diabetic peripheral neuropathy

Toxicity: increased BP, stimulant effects, sedation, nausea

84
Q

Tricyclic antidepressants (TCAs) - what are examples, the mechanism and clinical use?

A

Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

Mechanism: block reuptake of NE and 5HT

Clinical use: major depression, OCD (clomipramine), peripheral neuropathy, chronic pain, migraine prophylaxis

85
Q

TCA toxicity

A

Sedation, alpha1-blocking effects (postural hypotension), anticholinergic effects (tachycardia, urinary retention, dry mouth)

Tertiary TCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline).

Can prolong QT interval

Tri-Cs: Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly from anticholinergic effects -> use nortriptyline

NaHCO3 sodium bicarb to prevent arrhythmia

86
Q

MAOIs

A

Tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B inhibitor, metabolizes dopamine preferentially over 5HT)

Mechanism: MAO inhibition -> increase levels of amine NTs (NE, 5HT, dopamine)

Clinical use: atypical depression, anxiety

Toxicity: HTN crisis (usually with ingestion of tyramine found in wine and cheese)
CNS stimulation

87
Q

What drugs are contraindicated with MAOIs?

A

SSRIs, TCAs, St. John’s wort, meperidine, dextromethorphan -> can cause serotonin syndrome

88
Q

What are examples of atypical antidepressants?

A

Bupropion, mirtazapine, trazodone

89
Q

Bupropion

A

Uses: depression and smoking cessation

Mechanism: increases NE and dopamine

Toxicity: stimulant effects (tachycardia, insomnia), HA, seizures in anorexic/bulimic patients. *No sexual side effects!

90
Q

Mirtazapine

A

Uses: depression

Mechanism: alpha2-antagonist -> increases release of NE and 5HT and potent 5HT2/3 receptor antagonist

Toxicity: sedation, increased appetite, weight gain, dry mouth

91
Q

Trazodone

A

Uses: insomnia, high dose needed for depression treatment

Mechanism: blocks 5HT2 and alpha1 receptors

Toxicity sedation, nausea, PRIAPISM (TrazoBONE), postural hypotension

92
Q

What is the treatment of generalized anxiety disorder?

A

short term: benzodiazepines; long term: SSRIs (peroxitine, sertraline), buspirone, venlafaxine

93
Q

Pentazocine

A

partial opioid agonist and weak antagonist to mu opioid receptor

Use: analgesia without abuse potential

Toxicity - can precipitate withdrawal in patient on morphine

94
Q

What is used to prevent vasospasm due to subarachnoid hemorrhage?

A

Nimodipine (Ca2+ channel blocker)

95
Q

What side effects from organophosphates can occur after atropine is given. How can this be prevented?

A

Muscle paralysis due to excessive nicotinic activation by increased ACh levels from organophosphate (irreversibly binds AChE). Atropine only affects muscarinic receptors

Give Pralidoxime which “restores” AChE if given early and can therefore increase breakdown of ACh at muscarinic and nicotinic receptors

96
Q

Clonidine - mechanism, use and toxicitiy

A

Mechanism: alpha2-agonist (decreases sympathetic outflow)

Use: ADHD, Tourette syndrome, HTN urgency (doesn’t decrease renal perfusion)

97
Q

Modafinil

A

Mechanism: non-amphetamine stimulant, unknown exact mechanism but most likely increases dopaminergic signaling

Use: 1st line for narcolepsy

Much better tolerated than amphetamine stimulants and lower risk of dependence

Pharmacology (19 decks)

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