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Neuro II > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is metronidazole

A

Prodrug that is active against anaerobic bacteria and anaerobic Protozoa

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2
Q

What is the “drug class” of metronidazole

A

5-nitroimidazoles; includes tinidazole, behave similarly in mechanism, resistance and spectrum; tinidazole is better tolerated

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3
Q

What is the MOA of metronidazole

A

Relies on activation by susceptible organisms; donates electrons to metronidazole which forms a highly reactive nitro radical anion -> radical mediated DNA damage of organisms; can be recycled by losing electron; O2 can compete with metronidazole (when O2 rises, less likely to be active)

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4
Q

What organisms have developed resistance to metronidazole via increasing levels of O2

A

T. Vaginalis, G. Lamblia

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5
Q

What are the adverse effects of metronidazole

A
  • metallic taste
  • dry mouth
  • Nausea
  • HA
  • disulfiram-like effect (anti-alch medication designed to induce vomiting)
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6
Q

What are the dopamine receptor agonists

A

Apomorphine, bromocriptine, pramipexole, ropinirole

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7
Q

What are the monoamine oxidase inhibitors

A

Rasagiline and selegiline

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8
Q

What are the catechism-o-methyltransferase inhibitors

A

Entacapone and tolcapone

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9
Q

What are the anti-cholinergic drugs

A

Benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl

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10
Q

What do the dopamanergic neurons from the substantia nigra usually do

A

Inhibit GABAergic output from the striatum (caudate and putamen) (cholinergic has opposite effect)

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11
Q

What can be used to treat PD

A

Dopamine agonists or anticholinergic drugs

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12
Q

What is levodopa

A

Immediate metabolic precursor to dopamine

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13
Q

How does levodopa enter the CNS

A

L-amino acid transporter (LAT); *dopamine cannot cross BBB

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14
Q

What is the MOA of levodopa

A

Agonist at dopamine receptors

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15
Q

How do you increase the amount of levodopa available to enter the brain

A

Coadministration with a DOPA decarboxylase inhibitor (carbidopa); does NOT cross BBB

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16
Q

What are the adverse effects of levodopa

A
  • GI: in the absence of carbidopa, causes anorexia, N/V due to activation of chemoreceptor trigger zone
  • CV: postural hypotension; when taking large doses or in combo w/ nonselective MAOI/sympathomimetic, can cause HTN
  • dyskinesia; choreoathetosis
  • behavioral: depression, anxiety, agitation, insomnia, hallucinations, euphoria
  • “on-off phenomenon”: give apomorphine to relieve this
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17
Q

What is levodopa contraindicated in

A

Psychotic patients, angle closure glaucoma, history of melanoma or suspicious skin lesions, active peptic ulcer

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18
Q

What is bromocriptine

A

D2 agonist, also approved for rx of endocrine disorders; extensive first pass metabolism

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19
Q

What is pramipexole

A

D3 agonist; approved for treatment of restless leg syndrome; most excreted unchanged in urine; renal insufficiency may require dose adjustment

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20
Q

What is ropinirole

A

D2 agonist; approved for treatment of RLS

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21
Q

What are the adverse affects of dopamine agonists

A
  • GI: anorexia, N/V; constipation, dyspepsia, reflux
  • CV: postural hypotension
  • dyskinesia
  • mental disturbances
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22
Q

What are contraindications of dopamine agonists

A

Patients with psych history, recent MI, active peptic ulcer; PVD

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23
Q

What are the two forms of monoamine oxidase

A
  • MAO-A: metabolizes NE and serotonin
  • MAO-B: metabolizes phenylethylamine and benzylamine
  • dopamine and tryptamine metabolized equally by both
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24
Q

What is selegiline

A

Aka deprenyl; selective irreversible MAO-B inhibitor (inhibits A at high doses); prolongs affects of l-dopa; contraindicated in patients taking meperidine, tricyclic antidepressants, or serotonin reputable inhibitors

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25
Q

What is rasagiline

A

Irreversible MAO-B inhibitor; more potent than selegiline; used as neuroprotective agent for early symptomatic treatment of PD

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26
Q

What are catechism-o-methyltransferase inhibitors

A

COMT metabolizes l-dopa to 3-o-methyldopa, which competes w/l-dopa for transports across BBB; *tolcapone and entacapone prolong activity of l-dopa; entacapone is peripherally acting only; tolcapone may cause increase in liver enzyme levels and causes acute hepatic failure; *side effects -> orange urine, diarrhea, ab pain, sleep disturbances

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27
Q

What is apomorphine

A

Dopamine agonist at D2 receptors; injected for quick relief of off-periods of akinesia w/ dopaminergic therapy; adverse affects: nausea (treat with trimethobenzamide), drowsiness, sweating, hypotension and injection site bruising

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28
Q

What is amantadine

A

Antiviral that has a MOA in PD; can cause livedo reticularis (purplish discoloration of skin); use with caution in ppl w/ history of seizures or heart failure

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29
Q

Which anticholinergic drugs are used to treat PD

A

MAChR antagonists; improve tremor and rigidity but have no effect on bradykinesia; *benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl

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30
Q

What can be used to treat tremors

A

B1 antagonists -> metoprolol, propranolol; symptomatic tremor -> primidone (anti-epileptic); topirimate (SSR agonist), alprazolam (benzodiazepine) and botulinum toxin A

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31
Q

What can be used to treat the movement aspect of Huntington’s

A

Reserpine, tetrabenazine

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32
Q

What can be used to treat tics

A

Antipsychotics (tetrabenzaine, haloperidol, pimozide) but these cause weight gain, sedation, irritability ad phobias; alpha agonists are effective with less side effects

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33
Q

What is used to treat ALS

A

Riluzole -> inhibits glutamate release and blocks post synaptic NMDA and kainate type glutamate receptors and inhibits Na+ channels

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34
Q

What can be used to treat Wilson dz

A

Reduce serum copper; penicillamine (cheating agent that forms complex w/copper and excreted by kidney; adverse effects: nephritic syndrome, myasthenia, optic neuropathy, and blood disorders); potassium disulfide: reduces absorption of copper; Trientine:

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35
Q

What are the drug classes used to treat glaucoma

A

Beta blockers, alpha 2 agonists, prostaglandin analogs, carbonic anhydrase inhibitors, muscarinic agonists, and inhibitors of cholinesterase

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36
Q

What are the beta blockers used to treat glaucoma

A

Betaxolol, timolol, metipranolol, levobunolol, carteolol

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37
Q

What are the alpha 2 agonists used to treat glaucoma

A

Apraclonidine and brimonidine

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38
Q

What are the prostaglandin analogs used to treat glaucoma

A

Latanoprost, bimatoprost, travoprost

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39
Q

What are the carbonic anhydrase inhibitors used to treat glaucoma

A
  • topical: brinzolamide and dorzolamide

- systemic: acetazolamide and methazolamide

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40
Q

What are the muscarinic agonists used to treat glaucoma

A

Carbachol and pilocarpine

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41
Q

What are the inhibitors of cholinesterase used to treat glaucoma

A

Demecarium and echothiophate

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42
Q

What does the iris circular m do

A

Constricts pupil to cause miosis; contains M3 receptors

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43
Q

What does the iris radial muscle do

A

Dilates pupil to cause mydriasis; alpha 1 receptors

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44
Q

What does the ciliary m do

A

Accommodation and opens trabecular meshwork to improve outflow of aqueous humor; M3 receptors

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45
Q

What receptor is found on ciliary epithelium

A

Beta; causes increase in aqueous humor productions

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46
Q

Activation of what receptor decreases production of aqueous humor

A

Alpha 2

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47
Q

What does activation of the prostaglandin F2 receptor do

A

Improves uveoscleral or unconventional outflow

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48
Q

Does activation of the sympathetic or parasympathetic system increase aqueous outflow

A

Parasympathetic

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49
Q

What is a Scotoma

A

Area of vision loss or decreased visual acuity surrounded by field of normal vision; *every normal eye has a scotoma (bind spot)

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50
Q

What is the goal of treating glaucoma

A

Decrease IOP by 30% (want it less than 21 mm Hg)

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51
Q

What should you do if you want to use 2 agents to treat glaucoma

A

Administer them 10 min apart

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52
Q

What are the first line agents to use in open angle glaucoma

A

Prostaglandin analogues, beta blockers (timolol favored) and brimonidine

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53
Q

What is the second line therapy for open angle glaucoma

A

Pilocarpine, apraclonidine, topical carbonic anhydrase inhibitors

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54
Q

What is the last line therapy for open angle glaucoma

A

Carbachol, inhibitors of cholinesterase and oral carbonic anhydrase inhibitors

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55
Q

Why are beta blockers commonly used for open angle glaucoma

A

Convenience of dosing and lack of adverse effects

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56
Q

Why is timolol favored when treating open angle glaucoma

A

Lacks local anesthetic effects; available as generic; full antagonist, as effective as pilocarpine, MOA: reducing production of aqueous humor

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57
Q

What are the local adverse effects of beta blockers

A

Stinging, dry eyes, blurred vision, blepharitis, keratitis, conjunctivitis

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58
Q

What are the systemic effects of beta blockers

A

Bradycardia, bronchospasm, hyperlipidemmia, hypoglycemia (in patients on insulin), can interact with orally given verapamil (increased risk of cardiac depression and heart block)

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59
Q

What prostaglandin analog is the most effective in lowering IOP

A

Bimatoprost

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60
Q

Do prostaglandin analogs more effectively reduce IOP than beta blockers

A

Yes

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61
Q

When do you give prostaglandin analogs

A

Once daily at night

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62
Q

What are the local side effects of prostaglandin analogs

A

Corneal erosions, conjunctival hyperemia, iris hyperpigmentation *irreversible, and hypertrichosis (hyperpigmentation around eye lashes and eyelids *reversible)

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63
Q

Why is brimonidine the first line alpha 2 agonist used to treat glaucoma

A

Apraclonidine has frequent allergic reactions

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64
Q

What is the effect of alpha 2 agonists

A

Decreases rate of aqueous humor production

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65
Q

What are the adverse reactions to alpha 2 agonists

A

Dizziness, fatigue, dry mouth, bradycardia, reduced BP

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66
Q

What is the algorithm for pharmacotherapy of open angle glaucoma

A

Start w/ beta blocker, if intolerant, use class alternative, if contraindicated switch to alternative first line agent, if intolerant to prostaglandin use class alternative; if contraindications to all first class agents, use topical carbonic anhydrase inhibitors; if monotherapy fails, use combined therapy; if intolerant use surgical procedure

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67
Q

What are the goals of treatment of closed angle glaucoma

A

Rapid reduction of IOP *pilocarpine -> drug of choice before surgery

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68
Q

What is surgical or laser iridectomy

A

Produce a hole in iris which facilitates the humor outflow; used to treat closed angle glaucoma

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69
Q

What drugs are contraindicated in people with open angle glaucoma

A

Glucocorticoids, fenoldopam, topical anti muscarinic

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70
Q

What drugs are contraindicated in people with closed angle glaucoma

A

Anti muscarinic, drugs with alpha-adrenomimetic activity, tricyclic antidepressants and serotonin/NE reuptake inhibitors (because anti muscarinic actions)

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71
Q

What is the suffix for local anesthetics

A

-Caine

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72
Q

What local anesthetics are in the amide chemical class

A

All the ones with an “i” (not including the i in Caine)

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73
Q

What local anesthetic has a very short duration of action

A

Procaine

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74
Q

What local anesthetic is for surface use only

A

Benzocaine

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75
Q

What local anesthetics have a long duration of action

A

Tetracaine, ropivacaine and bupivacaine

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76
Q

Which types of local anesthetics generally have a longer duration of action

A

Amide; those with ester linkages are more prone to hydrolysis

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77
Q

What an reduce the systemic absorption of agents

A

Use of vasoconstrictors; useful for drugs with intermediate or short durations of actions

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78
Q

What is the difference between how ester type local anesthetics versus amide type local anesthetics are metabolized

A

Ester in the plasma via butyrylcholinesterase enzymes and amide in the liver and excrete in urine

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79
Q

What is the MOA of local anesthetics

A

Block voltage gated Na+ channels

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80
Q

What makes a local anesthetic more potent

A

If it is more lipophilic (tetracaine, bupivacaine, and ropivacaine)

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81
Q

What kind of nerve fibers to local anesthetics preferentially block

A

Smaller fibers; myelinated become blocked before unmyelinated; motor before sensory

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82
Q

What is infiltration anesthesia

A

Injection directly into the tissue; superficial enough to only effect skin or abdominal organs

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83
Q

What is block anesthesia

A

Injection in major nerve trunks; anesthetize region distal to block

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84
Q

What is spinal anesthesia

A

Injection into the CSF in the lumbar space; produces anesthesia over large part of body with a dose that produces negligible plasma levels

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85
Q

What is epidural anesthesia

A

Injection into epidural space; allows for continuous infusion

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86
Q

What is intravenous regional anesthesia (bier block)

A

Used for short surgical procedures on limbs; injection into vein while circulation of limb is isolated with tourniquet; large doses are used

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87
Q

what can you inject with a local anesthetic to increase its duration of action

A

Vasoconstrictor (epi) *use caution when injecting into skeletal mm can cause vasodilation and increase systemic toxicity

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88
Q

What adverse effects do local anesthetics have on the CNS

A

Sleepiness, metallic taste, nystagmus and convulsions, *giving benzodiazepine with the local anesthetic can raise seizure threshold and be preventative against systemic toxicity

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89
Q

What side effects can local anesthetics have on the CV system

A

Block cardiac sodium channels and decrease contractility and cause arteriolar dilation leading to hypotension

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90
Q

What is the most cardiotoxic local anesthetic

A

Bupivacaine b/c long duration of action

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91
Q

What is the effect of lidocaine on the heart

A

Antiarrhthmic; its side effects are mainly CNS

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92
Q

What kind of local anesthetics tend to produce allergic reactions

A

Ester type

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93
Q

What are the features of benzocaine

A

Poor solubility in water, ONLY topical, used for derm, hemorrhoids, premature ejaculation, and anesthetic lubricant (NG tube insertion)

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94
Q

What are the features of bupivacaine

A

Long duration of action; more sensory than motor block

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95
Q

What are the features of cocaine

A

Block nerve impulses and vasoconstriction; used as topical anesthetic or of UE airways

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96
Q

What are the features of dibucaine

A

Toxicity asssociated with injections so now only used topically

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97
Q

What are the features of lidocaine

A

Amide local anesthetic; alternative choice for those allergic to ester type; faster more intense longer lasting and more extensive anesthesia than same dose as procaine; used as antiarrhythmic

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98
Q

What are the features of procaine

A

Lower potency, slower onset, shorter duration of action, used for infiltration anesthesia; metabolized to para-aminobenzoic acid which inhibits action of sulfa abx

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99
Q

What are the inhaled general anesthetics

A

Desflurane, enflurane, halothane, isoflurane, nitrous oxide, sevoflurane

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100
Q

What are the IV anesthetics

A

Dexmedotomidine, diazepam, etomidate, fetanyl, fospropofol, ketamine, lorazepam, methohexital, midazolam, proposal, thiopental

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101
Q

What is monitored anesthesia care

A

Sedation-based anesthetic technique used for minor therapeutic surgical procedures; typically uses midazolam as premedication and propofol

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102
Q

What is conscious sedation

A

Used by nonanesthesiologists; can maintain patent airway and respond to verbal commands, benzodiazepines and opioids (fentanyll) are used because are reversible by receptor antagonists (flumazenil and nalaxone)

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103
Q

What is usually used for deep sedation

A

Propofol and midazolam

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104
Q

What is the MOA for general anesthetics

A

Most use GABA-a and glycine receptors to activate chloride channels;

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105
Q

What are the volatile anesthetics

A

Halothane, enflurane, isoflurane, desflurane, and sevoflurane - liquids at room temp

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106
Q

What does the rate that an inhaled anesthetic is absorbed depend on

A

Concentration of anesthetic in inspired air, ventilation rate, and solubility in air, blood, and CNS

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107
Q

What are the features of agents with low blood solubility

A

Ex: nitrous oxide and desflurane; fast onset of action

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108
Q

What drug is an example of an anesthetic with a high blood solubility

A

Halothane

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109
Q

How are inhaled anesthetics eliminated

A

In lung usually; insoluble in blood elminated more quickly

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110
Q

What is the minimal alveolar concentration

A

The dose that prevents movement in response to a surgical incision in 50% of subjects; measures potency

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111
Q

What do MAC values greater than 100% indicate

A

You must use another agent in conjunction with the one being used

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112
Q

What is the effect of inhaled anesthetics on heart rate

A

Can be mixed; halothane induces bradycardia while desflurane and isoflurane increase HR

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113
Q

Which inhaled anesthetic can cause hepatitis

A

Halothane

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114
Q

Which inhaled anesthetics are renal toxic

A

Enflurane and sevoflurane

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115
Q

How do you treat malignant hyperthermia

A

Dantrolene

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116
Q

What are the features of etomidate

A

IV anesthetic; rapid onset and fast recovery; CV stability

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117
Q

What are the features of ketamine

A

CV stimulation; increased cerebral blood flow

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118
Q

What are the features of methohexital

A

IV anesthetic that is preferred over thiopental for ambulatory procedures

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119
Q

What are the features of midazolam

A

Used in balanced anesthesia and conscious sedation; CV stability and marked amnesia; slow onset and recovery -> flumazenil reversal available

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120
Q

What are the features of propofol

A

Used for induction; can cause hypotension; useful antiemetic properties

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121
Q

What are the features of thoipental

A

Slow recovery; standard induction agent; CV depression; avoid in porphyrias

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122
Q

What are the features of fentanyl

A

IV anesthetic that has a slow onset and recovery -> naloxone reversal available; opioid used in balanced anesthesia and conscious sedation; analgesia

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123
Q

What is the MOA of propofol

A

Targets GABAa receptors; metabolized in the liver; allergic reactions in ppl allergic to eggs

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124
Q

Which IV anesthetics increase their half lives dramatically with prolonged infusions

A

Diazepam and thiopental

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125
Q

What are the CNS effects of propofol

A

Decreases cerebral blood flow which decreases ICP and IOP

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126
Q

What is fospropofol

A

Water soluble prodrug of propofol that is metabolized by alkaline phosphates to propofol and formaldehyde; onset and recovery are prolonged in comparison to propofol; itching and paresthesias are side effects

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127
Q

What is the MOA of etomidate

A

Enhances action of GABA on GABAa receptors; hypnotic but no analgesic effect; minimal CV and resp depression; less rapid recovery rate; metabolized by liver

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128
Q

What are the effects of etomidate on the CNS

A

Potent cerebral vasoconstrictor; decreases cerebral blood flow

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129
Q

What are the endocrine effects of etomidate

A

Adrenocortical suppression; cant make cortisol; limits its use as a continuous infusion

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130
Q

What is the MOA of ketamine

A

NMDA antagonist; eyes can remain open with nystagmus; lacrimation and salivation increased (premeditate with anticholinergic)

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131
Q

What are the CNS effects of ketamine

A

Increases cerebral blood flow -> not recommended for pts with intracranial pathology (increased ICP); causes hallucinations

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132
Q

What are the CV effects of ketamine

A

Increases systemic BP, HR, and CO

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133
Q

What is the only IV anesthetic that produces analgesia

A

Ketamine; also the only one to cause bronchodilation

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134
Q

What is the MOA of dexmedetomidine

A

Alpha-2 agonist; resembles physiological sleep state; decreases HR; used for short term sedation of intubated patients

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135
Q

What opioid analgesics are used in combo with IV anesthetics

A

Fentanyl, sufentanil, remifentanil, and morphine; agonist on opiate receptors

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136
Q

What barbiturates are used in combo with anesthetics

A

Thiopental and methohexital; highly lipophilic, CNS and resp depression; acts on GABAa receptors

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137
Q

What is the MOA of benzodiazepines

A

acts on GABAa receptors; used in perioperative period; antagonized by flumazenil; midazolam is the only water soluble one and is drug of choice for parenteral admin; have anticonvulsant properties

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138
Q

What agents can be given to prevent a migraine

A

Triptans and ergot alkaloids, beta blockers, tricyclic antidepressants, anticonvulsants, and calcium channel blockers

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139
Q

Which beta blockers can be used to treat migraines

A

Propranolol and timolol

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140
Q

Which tricyclic antidepressants can be used to treat migraines

A

Amitrityline and imipramine

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141
Q

Which anticonvulsants can be used to treat migraines

A

Topirimate and valproate

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142
Q

Which calcium channel blocker can be used to treat migraines

A

Verapamil

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143
Q

What does BOTOX act on

A

Motor neurons to decrease their activity; it cleaves SNAP-25 which inhibits Ach release

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144
Q

What is the definition of chronic migraine

A

Fifteen or more days each month w/ HA lasting 4 or more hours in ppl 18 or older

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145
Q

What is the physiology behind migraines

A

Calcitonin gene related peptide released from trigeminal A delta fibers which increases dural vessel vasodilation; substance P and neurokinin A are released from trigem C fibers which increases dural vessel permeability

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146
Q

What serotonin receptors do cranial vessels have

A

5HT-1B

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147
Q

What is the target of triptans

A

Serotonin 5HT1B/D agonists; causes vasoconstriction of cranial vessels and binds to 5HT1D receptors on presynaptic neurons to inhibit release of CGRP; also binds to 5HT1D receptors on trigeminal nucleus in brainstem which modulates ascending painful information

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148
Q

What is the prototype for triptans

A

Sumatriptan; can be given PO, nasal spray, or SC; SC is quickest action

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149
Q

What is sumatriptan metabolized by

A

Monoamine oxidase A

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150
Q

Which triptans have shown to be better tolerated and more efficient

A

Rizatriptan and eletriptan

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151
Q

Which triptan has the longest half life

A

Frovatriptan

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152
Q

Which triptans have the most delivery options

A

Sumatriptan and zolmitriptan

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153
Q

What triptans are contraindicated in someone taking MAOIs

A

Sumatriptan, rizatriptan, and zolmitriptan

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154
Q

What are people on SSRIs at risk for when taking triptans

A

Serotonin syndrome

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155
Q

When are triptans contraindicated

A

In people who have history of ischemic heart disease or other CV disorders and in patients with uncontrolled HTN

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156
Q

What are all triptans vasoconstrictors of

A

Coronary and renal vessels

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157
Q

What is the MOA of dihydroergotamine

A

Nonselectively binds to serotonin receptors as well as adrenergic and dopamine receptors

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158
Q

What side effects can dihydroergotamine have

A

Binding to alpha 1 receptors causes worse vasoconstriction than triptans which can lead to ischemia, vascular dz, acute coronary syndrome or vasospasm

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159
Q

What treatment for migraines is safe in all trimesters of pregnancy

A

Acetaminophen and codeine

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160
Q

When can aspirin and ibuprofen be given during pregnancy

A

First and second trimester only

161
Q

Can you give triptans to someone who is pregnant

A

No

162
Q

Can you give DHE and other ergot alkaloids to someone who is pregnant

A

No; abortion risk

163
Q

What drug combinations are useful treatments for migraines

A

Triptan plus analgesic (sumatriptan and naproxen = treximet)

164
Q

When is valproate given to someone with migraines

A

When triptans fail as a treatment; works by increasing GABA levels; *contraindicated in pregnant women (decreases IQ scores in offspring)

165
Q

What are the features of verapamil in terms of migraine treatment

A

First choice for migraine prevention; good side effect profile; normalizes vessel tone

166
Q

What is propranolol or timolol contraindicated in

A

Patients with asthma

167
Q

Where is the binding site for sodium channel blocker AED’s

A

Interior side of the channel; can only bind if the activation gate is open (open state or fast inactivated state) *state and use dependent

168
Q

Which sodium blocker AED’s prolong fast inactivation state of Na channel

A

Carbamazepine, oxcarbazepine, lamotrigine, phenytoin, rufinamide, topirimate, valproic acid, zonisamide and Lacosamide

169
Q

Which Na channel blocker AED’s enhance the slow inactivation of Na channels

A

Lacosamide; more efficient when stimulus is prolonged; can act in inactivated closed state

170
Q

What are the AED’s that are AMPA receptor antagonists

A

Topirimate and perampanel

171
Q

Which AED is an NMDA receptor antagonist

A

Felbamate

172
Q

What is the MOA of tiagabine

A

Inhibits GAT-1 (reuptake of GABA)

173
Q

What are the AED’s that inhibit the catabolism of GABA

A

Vigabatrin and valproic acid (inhibit GABA-T)

174
Q

What is the MOA of benzodiazepines

A

Binds to allosteric site which causes increased GABA binding which increases the frequency of Cl- channel opening

175
Q

What is the MOA of barbiturates

A

Binds to allosteric site and increases duration of Cl- channel opening; *GABA independent which makes it more lethal than BZD

176
Q

What are the multiple functions of topiramate

A

GABAa agonist (increases frequency of GABAa receptor activation), fast inactivation of Nav channels and AMPA antagonist

177
Q

What are T-type calcium channels

A

Mediate 3 hz spike and wave activity in the thalamus which is a hallmark of petit mal seizures

178
Q

What is ethosuximide

A

Only used for petit mal seizures; antagonist of t type calcium channels

179
Q

What are the antagonists of t type calcium channels

A

Ethosuximide, valproic acid, and zonisamide

180
Q

Which AED contains sulfa

A

Zonisamide *allergy

181
Q

What does levetiracetam target

A

SV2A - synaptic vesicle protein; doesn’t allow glutamate to be packaged

182
Q

What inhibits the alpha2gamma subunit of the P/Q type calcium channel

A

Gabapentin and pregabalin

183
Q

Which AED targets potassium channels

A

Retigabine

184
Q

What drugs would you use to treat partial onset seizures

A

Lamotrigine, oxcarbazepine, perampanel, primodone, lacosamide

185
Q

What drugs would you use to treat generalized onset absence seizures

A

Ethosuximide, clonazepam, valproic acid

186
Q

What drug would you use to treat generalized onset myoclonic seizures

A

Clonazepam

187
Q

What drugs would you use to treat generalized onset tonic/clonic seizures

A

Primidone or phenytoin

188
Q

What are the broad spectrum AED’s

A

Carbamazepine, phenobarbital, topiramate, valproic acid

189
Q

What drugs do you use to treat Lennox gastaut

A

Rufinamide, topiramate, clobazam, clonazepam, lamotrigine, felbamate

190
Q

What do you use to treat status epilepticus

A

Lorazepam, diazepam, phenobarbital, phenytoin, valproic acid, levetiracetam

191
Q

What is the main side effect to AED medication

A

Suicidal behavior

192
Q

What are the toxic effects of phenytoin

A

Zero order drug; gingival hyperplasia, hypothyroidism, CV risk (hypotension and arrhythmia), hypocalcemia, vit d deficiency, osteoporosis

193
Q

What other drugs is osteopenia/osteoporosis associated with as a side effect

A

Carbamazepine, phenobarbital, valproic acid; induce vitamin D CYP450 which reduces vitamin D levels -> cant absorb calcium -> activates PTH to demineralize bone

194
Q

What are the toxicities associated with carbamazepine

A

Leukopenia, neutropenia, and thrombocytopenia; hypocalcemia; also induces self metabolism (potential loss of efficacy and recurrence of seizures)

195
Q

What is oxcarbazepine

A

Analogue of carbamazepine with fewer side effects

196
Q

What are the toxicities of phenobarbital

A

CNS depressant

197
Q

What are the side effects of vigabatrin

A

Progressive, permanent, bilateral, concentric vision loss; discontinue after 3 months if no response; prescribable only via REMs program

198
Q

What effect can AED inducers have on anticoagulants

A

Increases metabolism of warfarin -> increased risk of thrombosis

199
Q

What effect can AED induces have on antiviral

A

Can increase metabolism of HIV medications -> risk of HIV replication

200
Q

What drug reactions do valproic acid and lamotrigine have

A

Inhibit conjugation of drugs by glucoronosyltransferases causing accumulation of the parent drug (when used together)

201
Q

What drug reactions do phenytoin, carbamazepine, and phenobarbital have

A

Induce conjugation of drugs by glucoronosyltranferase; causes reduction of parent drug

202
Q

How do newer AED’s minimized drug interactions

A

Rental clearance; levetiracetam, topiramate, oxcarbazepine, gabapentin, pregabalin, vigabatrin; **renal insufficiency requires dose adjustment

203
Q

What is the initial therapy for status epilepticus

A
  • In first IV: lorazepam; alternative: diazepam; wait 1 min for response then give lorazepam PRN
  • IF NO IV ACCESS, midazolam
  • In second IV: fosphenytoin OR phenytoin OR valproic acid OR levetiracetam
204
Q

What are the legal requirements of things that need to appear on a prescription

A
  • Name/Address of prescriber
  • Name/Address of patient
  • Date prescription was written
  • Name and strength and dosage form of medication
  • Directions for use
  • Quantity to be dispensed
  • number of refills allowed
  • Prescribers signature
  • Prescribers DEA # (2 letter 7 digit)
205
Q

What is the life span of a prescription for a non controlled legend

A

12 months or number of refills; no legal limit on refills or quantity dispensed; (in MO, limit new script of opioids to 7 day supply); partial filling possible

206
Q

What is the life span of controlled/scheduled legends

A

6 months or number of refills; *exception is C-V which has a life span of 12 months

207
Q

What is the limit of refills for controlled/scheduled legends

A

For C-II: NO REFILLS
For CIII-IV: 5 refills over 6 months
For CV: no limit

208
Q

What is the limit of quantity dispensed for controlled/scheduled legends

A

90 days for CIII-V; 30 days for C-II (up to 90 days with documentation of medical reason)

209
Q

Is partial filling for scheduled/controlled legends allowed

A

Only for CIII-V until full quantity and all refills dispensed or expiration; ONLY possible for C-II if pharmacist doesn’t have full quantity or on long term hospice care

210
Q

When can physicians fax/electronically/call in scripts

A

Original prescription or refills for all legend drugs except C-II (only during emergency); faxed prescriptions musts be manually signed

211
Q

What are the rules on prescription transfers

A

CII cannot be transferred; CIII-V can only be transferred once; nursing home orders not transferable

212
Q

What cannot be changed on a controlled substance prescription

A

Patients name, drug name, prescribers name, prescribers signature

213
Q

What is an “emergency” for dispense of controlled substances

A

-immediate administration necessary, no appropriate alternative available, not reasonably possible for prescriber to have a written prescription to pharmacist (have 72 hours to deliver the script)

214
Q

What are the rules about self prescribing and prescribing drugs to family

A

In MO, cannot self prescribe controlled substances but can non-controlled; can prescribe all legend drugs to family

215
Q

What are the worrisome signs which may indicate HA of pathological origin (secondary HA)

A

Worst HA, onset of HA after 50, atypical HA for patient, HA w/ fever, abrupt onset, subacute w/ progressive worsening over time, drowsiness, confusion, memory impairment, weakness, ataxia, loss of coordination, paresthesias, abnormal medical/neuro exam

216
Q

What is recommended if any of the worrisome signs are seen

A

CT and/or LP

217
Q

What are the primary HA disorders

A

Common migraine (without aura), classic migraine (with aura), chronic migraine, tension HA, cluster HA

218
Q

What are the features of common migraine

A

Moderate to severe intensity, inhibits daily activities (aggravated by activity), age of onset peaks btw 35-40 y/o; more common in females; 14 or fewer per month; duration of 4-72 hours, unilateral or bilateral; throbbing, sharp pressure; prodrome: mood changes, food cravings, sluggishness, yawning; post drone: fatigue, fog; retreat to dark quiet room; NO AURA

219
Q

What is analgesia

A

Relief of pain without loss of consciousness

220
Q

What is the difference between opium and opioid

A

Opium: natural; opioid: natural plus synthetic morphine

221
Q

What are opioid agonists

A
  • natural opium alkaloids: morphine and codeine
  • semisynthetic opiates: hydromorphone and oxymorphone
  • synthetic opioids: pethidine, tramadol, methadone, fentanyl, alfentanil, remifentanil
222
Q

What are the opioid agonist antagonists

A

Pentazocine

223
Q

What opioid is a partial mu receptor agonist

A

Buprenorphine

224
Q

What opioid is a mu receptor antagonist

A

Naltrexone and naloxone

225
Q

What are narcotic analgesics used in hospital settings for

A

MI, sickle cell crisis, post op, trauma, cancer, kidney stones, back pain, general anesthesia, palliative care, epidural, antitussive, antidiarrheal

226
Q

What is the MOA of narcotic analgesics

A

Bind to presynaptic mu receptor an inhibits calcium influx (decreases NT release); also binds to postsynaptic mu receptor and increases K+ effluent to decrease postsynpatic response to excitatory NT

227
Q

What are the effects of morphine, methadone, and fentanyl

A

Analgesia, relief of anxiety, sedation, slowed GI transit; used for severe pain or adjunct to anesthesia, pulmonary edema (morphine), resp depression, constipation, addiction, convulsions

228
Q

What is meperidine

A

Strong mu agonist with anticholinergic effects

229
Q

What are the effects of codeine and hydrocodone

A

Less effacious than morphine; used for moderate pain

230
Q

What are the effects of buprenorphine

A

Partial mu agonist; reduces craving for alcohol; used for moderate pain; long duration of action

231
Q

What are the effects of nalbuphine

A

Mu antagonist and k agonist; similar to buprenorphine; used for moderate pain

232
Q

What are the antitussives

A

Dextromethorphan, codein, and levopropoxyphene; partial mu agonists; reduces cough reflex; not analgesic (except for codeine)

233
Q

What analgesic can cause serotonin syndrome

A

Tramadol

234
Q

Which endogenous opioid has the greatest affinity for mu receptors

A

Endorphins > enkephalins > dynorphins

235
Q

Which endogenous opioids have the greatest affinity for delta receptor

A

Enkephalins > endorphins and dynorphins

236
Q

What are the adverse effects of opioids

A

Acute: resp depression, N/V, itching, urticaria, constipation, urinary retention, delirium, sedation, myoclonus, seizures
Chronic: hypogonadism, immunosuppression, increased feeding, increased GH, withdrawal effects, tolerance/dependence, abuse, hyperalgesia, impairment while driving

237
Q

What are the contraindications for morphine

A

Acute respiratory depression, renal failure, chemical toxicity, raise ICP, biliary colic

238
Q

What population of individuals are commonly mistakenly overdosed on opioids

A

Obese ppl, elderly, infants, those w/ renal failure (morphine and pethidine toxicity), hepatic failure

239
Q

Input from which systems is required for balance

A

2 of the 3: visual, labyrinthine (judges acceleration and position), and proprioceptive (judges posture)

240
Q

What is disequilibrium

A

Can be caused by vertigo but usually nonvertiginous ; dysfunction of cerebellum, dorsal columns, basal ganglia

241
Q

What is presyncope

A

Lightheaded ness caused by orthostasis, arrhythmia, hyperventilation, and aggravated by increased temp, prolonged standing and large meals

242
Q

What is a sensory cause of disequilibrium

A

Prioprioreceptive deficit, visual impairments, compensated vestibular disorders; worse in the dark *romberg sign

243
Q

What are the motor causes of disequilibrium

A

Mechanical (arthritis), peripheral or central (motor function), cerebellar, NO Romberg sign

244
Q

What are the cerebellar causes of disequilibrium

A

No Romberg sign; cannot stand with feet together with eyes open or closed

245
Q

What are the characteristic of peripheral disorders of equilibrium

A

Intense vertigo, brief nystagmus that can be fatigued, fixed direction of horizontal nystagmus, intense N/V, possible hearing loss, never neuro symptoms

246
Q

What are the characteristics of central disorders of equilibrium

A

Mild vertigo, persistent nystagmus that cannot be fatigued, direction of nystagmus is not fixed (can be vertical), no latency of nystagmus, mild N/V, rarely causes hearing loss, usually has neuro symptoms

247
Q

What are the peripheral causes of vertigo

A

Benign positional vertigo, vestibular neuronitis, Menieres dz, drug induced ototoxicity

248
Q

What is benign positional vertigo

A

Brief episodes of vertigo triggered by change in head position; spontaneous recovery usually; thought to be due to debris floating in endo lymph (mostly in posterior canal)

249
Q

What does the Dix hallpike maneuver diagnose (specifically)

A

BPV of posterior or anterior canals; posterior is provoked by affected ear down (reverse for anterior canal)

250
Q

What does the supine roll test diagnose

A

BPV of horizontal canals

251
Q

What meds can be given for BPV

A

Vestibular suppressants (meclizine, scopolamine, Valium), antiemetic, anxiolytics

252
Q

What is vestibular neuronitis

A

Spontaneous attack of vertigo that does not involve hearing loss or tinnitus and resolves spontaneously; vertigo, nausea, and vomiting lasting up to 2 weeks; not positional

253
Q

What is meniere’s dz

A

More prominent in young females; due to an increase in volume of labyrinthine endolymph b/c of poor absorption (endolymph hydrops); recurrent episodes of spontaneous vertigo lasting more than 20 min (typically hours); *low frequency hearing loss, tinnitus and aural fullness

254
Q

What is mal de debarquement

A

Illusion of movement as aftereffect of travel; duration less than a day; failure of brain to adapt once motion has stopped; RX: meclizine, scopolamine, benzo

255
Q

What drugs can induce peripheral disorders of equilibrium

A

Alcohol, salicylates, anti-epileptics, quinine, abx (aminoglycosides), diuretics, chemo

256
Q

What is a vestibular migraine

A

Central disorder of equilibrium; at least 5 episodes of severe vestibular symptoms lasting 5 min to 72 hours; current or previous history of migraine; one or more migraine features w/ at least half of episodes; unaccounted for by other dx

257
Q

What are the features of vascular causes of central disorder of equilibrium

A

More common in elderly; abrupt onset; ischemia of labyrinth or brainstem; vertigo assoc with neuro symptoms (diploid, dysarthria, hiccups); repeated episodes of isolated vertigo w/o other neuro sx should always suggest non-neuro cause

258
Q

What metabolic disturbances can cause central disorders of equilibrium

A

Deficiencies of B1 and 12, E, and Cu; hypothyroid (affects cerebellum), Wilson dz (low serum ceruloplasmin)

259
Q

What toxins can cause central disorders of equilibrium

A

Heavy metals, CO, glue, organic solvent, NO2; ethanol (cerebellar vermis), meds -> DPH, anticonvulsants, 5-FU

260
Q

What is a neoplastic cause of central disorders of equilibrium

A

CPA tumor *hearing loss and absent corneal reflex 1st symptom and sign

261
Q

What is a paraneoplastic cause of central disorders of disequilibrium

A

Paraneoplastic cerebellar degeneration; usually from breast, lung or ovary CA; abs to purkinje cells

262
Q

What is friedrichs ataxia

A

AR; onset before 20, gait ataxia involving all 4 limbs, dysarthria, impaired proprioception in legs, weakness, absent reflexes in legs

263
Q

What is ataxia telangiectasia

A

AR (chrom 11); pancerebellar degeneration involving nystagmus, dysarthria and gait ataxia beginning in infancy; loss of proprioception and areflexia; immunodeficiency

264
Q

What does vit B12 deficiency cause

A

Degeneration of posterior columns and lateral corticospinal tracts; caused by surgery, drugs (PPI and metformin), NO2, fish tapeworm); insidious onset, vague fatigue, babinski sign, Romberg sign, increased homocysteine and methylmalonic acid

265
Q

What can cause copper deficiency

A

Malabsorption or excessive zinc intake; similar to B12 deficiency; decreased serum ceruloplasmin and urine copper

266
Q

What are the characteristics of classic migraine

A

Aura that usually lasts 15-30 min; commonly visual symptoms

267
Q

What is the definition of chronic migraine

A

History of HA 15 or more days per month, lasting 4 hours or longer for at least 3 months

268
Q

What are the characteristics of tension-type HA

A

Mild to moderate intensity; may inhibit bu doesn’t prohibit daily activity; variable age of onset; more common in females; episodic type: last several hours; chronic: waxes and wanes all day; bifrontal or bioccipital; dull squeezing pressure; *no prodrome or aura; behavior not affected

269
Q

What are the characteristics of cluster HA

A

Severe pain; prohibits daily activity; age of onset 20-50; more common in MALES; associated with sleep apnea; episodic type: 1 or more attacks a day for 6-8 wks; chronic: several attacks per week w/o remission; last 30 min-2 hours; *always unilateral (usually orbitotemporal); prodrome: mild burning in ispilateral canthus or nares; packing, rocking behavior changes; associated w/ ptosis, miosis, conjunctival injection, lacrimation, stuffed or runny nose

270
Q

What are contraindications to triptan use

A

Ischemic heart dz, PVD, Raynauds, HTN, renal/hepatic impairment, MAOI’s

271
Q

Which triptan has the longest half life and fewest side effects

A

Naratriptan; don’t use if hepatic or renal impairment

272
Q

What is the only FDA approved treatment for chronic migraine

A

Botox injection; repeated every 3 months; minimal side effects

273
Q

What are acute treatments for cluster HA

A

DHE, lidocaine, narcotics, oxygen by mask, sumatriptan

274
Q

What are preventative treatments for cluster HA

A

Calcium channel blockers, anticonvulsants, lithium, indomethacin, prednisone, ergotamine tartrate

275
Q

What can be used to treat trigem neuralgia

A

Carbamazepine or oxcarbamazepine

276
Q

What are trigeminal autonomic cephalgias

A

Group of HA disorders characterized by unilateral trigem neuralgia in assoc w/ ipsilateral cranial autonomic features (cluster HA, paroxysmal hemicarnia, hemicrania continua, SUNCT and SUNA syndrome)

277
Q

What is SUNCT syndrome

A

Shortlasting, unilateral HA attacks w/ conjunctival injection and tearing; burning stabbing electrical HA in periorbital area lasting seconds to minutes; onset over 50 in men; **rx w/ lamotrigine

278
Q

What is paroxysmal hemicrania

A

Similar to cluster HA but shorter duration and increased frequency ***rx: w/ indomethacin

279
Q

What are the different types of MS

A
  • Relapsing remitting
  • secondary progressive: begin in relapsing remitting category
  • primary progressive
  • benign
280
Q

Do women or men have a more favorable course with MS

A

Women

281
Q

Does early or late onset of MS have a more favorable course

A

Early

282
Q

What is the geographic risk associated w/ MS

A

More prevalent in temperate climates; risk determined before age 14

283
Q

What studies are used to diagnose MS

A

MRI of head, C and T spine, multimodality evoked potentials, lumbar puncture for CSF analysis

284
Q

Which drugs are used for MS maintenance (decrease frequency and severity of exacerabations and slow progression)

A

-mab’s and IFN; *used for relapsing form, not primary progressive

285
Q

What drug is approved to treat primary progressive MS

A

Ocrevus

286
Q

What medications are used to treat acute exacerbation of MS

A

Corticosteroids (methylprednisolone), ACTH

287
Q

What is a clinically isolated syndrome

A

Either: monofocal (single neurological sign caused by single lesion) or multifocal (acute disseminated encephalomyelitis - more than one sign or symptoms by lesions in more than one place)

288
Q

What type of CIS is associated with a high vs low risk of developing MS

A
  • When CIS patients have multiple lesions on MRI, have 60-80% chance of developing MS *high risk
  • When do not have multiple lesions, 20% chance -> low risk
289
Q

What is Devic’s dz

A

Neuromyelitis optica; aquaphorin abs; tx w/ steroids or plasmapheresis followed by immunosuppression

290
Q

What is epilepsy

A

2 or more unprovoked seizures

291
Q

What types of seizures are most likely to show positive findings on a single EEG

A

Petit mal

292
Q

What is the most likely way to get positive results on an EEG for all 3 types of epilepsy

A

3 sleep deprived EEGS

293
Q

What is the most important information in making a diagnosis of epilepsy

A

History

294
Q

What are simple partial seizures

A

Focal motor or sensory activity, no loss of consciousness, lasts seconds, no post-ictal state

295
Q

What are complex partial seizures

A

Nonresponsive staring, possible preceding aura, automatisms, loss of consciousness, lasts 1-3 min, post-ictal state

296
Q

What are secondary generalized seizures

A

B/l tonic-clonic activity, LOC, 1-3 min, post-ictal state

297
Q

What are absence seizures

A

Nonresponsive staring, rapid blinking, chewing, clonic hand motions, LOC, lasts 10-30 sec, no post-ictal state

298
Q

What are tonic clonic seizures

A

B/l extension followed by symmetrical jerking of extremities, LOC, lasts 1-3 min, post-ictal state

299
Q

What are atonic seizures

A

Sudden loss of muscle tone, head drops or patient collapses, LOC, variable duration, post-ictal state

300
Q

What are myoclonic seizures

A

Brief, rapid symmetrical jerking of extremities , LOC, lasts less than a few seconds, minimal post-ictal state

301
Q

Which antiepileptic drugs are used to treat partial seizures

A

Lamotrigine, topiramate, leviteracetam, zonisamide, perampanel, valproic acid

302
Q

What combination of AED’s has been show to be synergistic in treatment of epilepsy

A

Valproic acid and lamotrigine

303
Q

What supplement should be given to all women of child bearing age on AED

A

Folic acid; AED’s are folate depleting

304
Q

What features can decipher btw syncope and seizure

A

Syncope: pallor, sweating, lightheaded ness, positionally related, slow onset, brief unconsciousness
Seizure: urinary or bowel incontinence, tongue injury, tonic/clonic movement, postictal state

305
Q

What is transient global amnesia

A

Sudden, temporary, isolated loss of memory; no other neuro signs; usually resolves after few hours; doesn’t recur

306
Q

What does consciousness require

A

Arousal (level of alter ness; ability to interact w/ environment) and awareness (sum of cognitive mental functions)

307
Q

What is delirium

A

*hallucinations (usually visual)

308
Q

What is obtundation

A

Need stimuli to arouse

309
Q

What is stupor

A

Arouses only to noxious stimuli

310
Q

What is coma

A

Unarousable, unresponsive, unaware

311
Q

What can cause HTN that would lead to a coma

A

Pheochromocytoma, drugs, increased ICP, PRES

312
Q

What can cause hypotension that would lead to a coma

A

Addison’s, sepsis, drugs (beta blockers, ca channel blocker, TCA), progression to brain death

313
Q

What can cause hyperthermia that can lead to coma a

A

Infection, heat stroke, drugs (amphetamines, salicylates), serotonin syndrome, central pontine hemorrhage

314
Q

What can cause hypothermia that leads to a coma

A

Hypothyroidism, hypoglycemia, exposure, drugs (opioids, sedatives, barb)

315
Q

What are the essential things you must do in your neuro exam for stupor and coma

A

Pupillary responses, corneal reflex, extraocular movements, cough/gag reflex, motor responses, respiratory patter *in order

316
Q

What is the sympathetic path of the pupillary response

A

Hypothalamus -> lower cervical cord -> sympathetic chain -> superior cervical ganglion -> CN V -> long ciliary n to dilator (muellers m)

317
Q

What is the parasympathetic path of the pupillary response

A

Upper midbrain (Edinger wesetfall) -> CNIII -> ciliary ganglion -> short ciliary n (constrictor)

318
Q

What does absent or unequal pupillary responses indicate

A

Brainstem lesion

319
Q

What is anisocoria

A

One abnormal pupil; if the abnormal pupil is the large pupil, it should fail to constrict to light; if the abnormal pupil is the small pupil, it will fail to dilate in the dark

320
Q

What do pinpoint pupils indicate

A

Pontine lesion, opiates, pilocarpine

321
Q

What is a mid position and unreactive pupil indicative of

A

Sympathetic and parasympathetic dysfunction (midbrain)

322
Q

What can cause pupils to be dilated fixed and unequal

A

Glutethimide, hypothermia, anoxia, ischemia

323
Q

What do frontal gaze centers vs pontine gaze centers do

A

Frontal: deviate eyes to opposite side
Pontine: deviate eyes to same side

324
Q

What do conjugate roving eye movements suggest

A

Brainstem intact; dysconjugate implies brainstem lesion

325
Q

With a hemispheric lesion, which way do the eyes conjugately move with a destructive vs irritative cause

A

Destructive: toward lesion
Irritative: away from lesion

326
Q

What kind of conjugate deviation will you see in a brainstem lesion

A

Always destructive: away from lesion

327
Q

What are the different types of nystagmus and the lesions associated with them

A
  • Ping-pong: bihemispheric, midbrain
  • Convergence (slow abduction with rapid jerk back): mesencephalon
  • retractory: mesencephalon
  • bobbing (rapid down, slow up): pons
  • dipping (slow down, rapid up): bihemispheric
328
Q

What is the oculocephalic maneuver

A

Doll’s eye; tests mid-pons

329
Q

What does the caloric reflex test

A

Aka oculovestibular; lower pons

330
Q

What lesion would cause flaccid reflex

A

Pontomedullary or metabolic

331
Q

What lesion would cause Cheynes-stokes

A

B/l hemispheres or diencephalon

332
Q

What lesion causes central neurogenic hyperventilation

A

Midbrain

333
Q

What causes apneustic breathing

A

Long inspiration followed by apnea; lesion to mid/low pons; seen in anoxia hypoglycemia and meningitis

334
Q

What causes ataxic respiratory pattern

A

Medullary respiratory center

335
Q

What is a central transtentorial herniation

A

Through the foramen magnum; early coma, small pupils, normal EOM, posturing, resp arrest and death

336
Q

What are the signs of a subtentorial mass

A

Brainstem dysfunction preceding coma (usually oculovestibular), CN palsy, bizarre respiratory partners

337
Q

What are the signs of diffuse/metabolic causes of coma

A

Confusion and stupor preceded motor signs; motor signs symmetric; pupillary reactions preserved; myoclonus and seizures; acid-based imbalance usually seen

338
Q

What is psychiatric unresponsiveness

A

Pupils reactive or dilated (cycloplegics), lids actively close, oculocephalic reflexes unpredictable, oculovestibular reflexes physiologic; motor tone is inconsistent or normal; eupnea or hyperventilation usual, no path reflexes, normal EEG

339
Q

What is brain death

A

Irreversible (cause of coma must be known; must r/o sedative intox, hypothermia, and neuromuscular blockade), complete cessation of brain function including respirations but not heartbeat(no reflexes), persistent

340
Q

Explain the apnea test

A

Oxygenate to get oxygen > 200 mm HG, disconnect ventilators, catheter 100% O2, observe chest wall for movement, if no respiratory movements for 8 min and arterial blood gas CO2 >60 mm Hg = brain death

341
Q

What are the rules for “persistence” of brain death

A

Six hours w/ confirmatory EEG, 12 hours with confirmatory EEG, 24 hours for anoxic brain injury w/o a confirmatory EEG

342
Q

What are the initial steps of managing a comatose patient

A

Insure patent airways, insure breathing and adequate oxygen, insure adequate circulation; history, EKG, glucose, adjust body temp, control agitation

343
Q

What diagnostic testing should you order for a comatose patient

A

Non contrast head CT and LP

344
Q

What can you do to reduce elevated intracranial pressure

A

Elevate head of bed, intubate and hyperventilate to PCO2 of 20 mm Hg

345
Q

What is the classic triad of acute progenitor meningitis

A

Fever, HA, nuchal rigidity

346
Q

What is the standard empiric treatment for acute pyogenic meningitis

A

Cefotaxime or ceftriaxone + vancomycin; add ampicillin for adults over 50

347
Q

What do you give to someone who had a beta lactam allergy that has acute pyogenic meningitis

A

Vancomycin + moxifloxacin; add TMP/SMX if they are over 50

348
Q

What do you give to an immunocompromised patient who has acute pyogenic meningitis

A

Vancomycin + ampicillin + cefepime or meropenem

349
Q

What class of drugs are cefotaxime, ceftazidime, and ceftriaxone

A

Cephalosporins 3rd gen

350
Q

What class of abx is vancomycin

A

Glycopeptide

351
Q

What class of abx is ampicillin

A

Aminopenicillin

352
Q

What kind of abx is trimethoprim/sulfamethoxazole (TMP/SMX)

A

Benzylpyrimidine/sulfonamide

353
Q

What kind of abx is cefepime

A

Cephalosporin 4th gen

354
Q

What kind of abx is meropenem

A

Carbapenem

355
Q

What kind of abx is moxifloxacin

A

Fluoroquinolone

356
Q

What is the CSF content of a brain abscess

A

High WBC, increased protein, normal glucose

357
Q

What is the empiric therapy of brain abscesses with unknown source

A

Vancomycin + ceftriaxone or cefotaxime + metronidazole

358
Q

What does penicillin G treat

A

Aerobic and anaerobic streptococci

359
Q

What does ceftriaxone treat

A

Aerobic streptococci, and many enterobacteriaceae

360
Q

When would you use ceftazidime, cefepime, or meropenem to treat a brain abscess

A

When they complicate a neurosurgical procedure; also covers cases of Pseudomonas

361
Q

When would you discontinue vancomycin for treatment of a brain abscess

A

If culture comes back and there is no MRSA; substitute with nafcillin or oxacillin

362
Q

What bacteria are the causes of subdural empyema

A

Aerobic and anaerobic strep, staph, enterobactereae and anaerobic bacteria

363
Q

What organisms are responsible for subdural empyema after neurosurgical procedures or head trauma

A

Staph and gram negative bacilli

364
Q

What is the treatment for community acquired subdural empyema

A

Cefotaxime or ceftriaxone + vancomycin + metronidazole

365
Q

What is the treatment for hospital acquired subdural empyema (pseudomonas or MRSA)

A

Meropenem + vancomycin

366
Q

What is subacute sclerosing panencephalitis characterized by

A

Neurofibrillary tangles, inflammation of white and grey matter; cognitive decline, spasticity of limbs, seizures

367
Q

Which kind of vaccines offer protection that is greater and longer lasting

A

Live

368
Q

What Ig’s are produced as a result of live vaccines

A

IgA and IgG; killed is only IgG

369
Q

Does measles vaccine have the ability to revert to virulence

A

No; but polio does in small percentage

370
Q

What kinds of vaccines are available for polio

A
  • inactivated: killed vaccine; only one used in USA

- live attenuated oral vax; can revert to virulence

371
Q

What is the treatment for fungal meningoencephalitis

A

Induction phase: amphotericin B and flucytosine

Consolidation phase: fluconazole

372
Q

What is the only way amphotericin B can be administered

A

IV or directly into CSF

373
Q

What are the adverse effects of amphotericin B

A

Renal toxicity, acute febrile reaction, anemia

374
Q

Why must flucytosine be given in combination with another drug

A

Rapid resistance develops if given alone; MOA: inhibits DNA and RNA synthesis

375
Q

What are the adverse effects of flucytosine

A

Conversion to 5-FU outside of fungal cell leading to bone marrow depression, N/V/D

376
Q

What is the MOA of fluconazole

A

Inhibits ergosterol synthesis by inhibiting fungal P450 enzymes; very good CSF penetration; adverse effects: limited *widest therapeutic index

377
Q

What classes of drugs cannot be used to treat neuro infections

A

1st generation cephalosporins (cefazolin), aminoglycosides, tetracyclines (-cycline), macrolides, clindamycin

378
Q

What abx are part of the aminoglycosides

A

Streptomycin, gentamicin, tobramycin, amikacin, neomycin, paromomycin, kanamycin, netilmiccin

379
Q

What abx are part of the macrolides

A

Erythromycin, clarithromycin, azithromycin, fidaxomicin

380
Q

Which abx class is ototoxic

A

Aminoglycosides

381
Q

What is the DEA number comprised of

A

2 letters (2nd letter is first letter in last name) and 7 digits

382
Q

What is methysergide

A

Used to treat cluster HA * causes retroperitoneal fibrosis

383
Q

What does a primary verses secondary hemorrhage in the brain look like

A

Primary: dark purple
Secondary: lighter pink

384
Q

What worsens a stroke outcome

A

Glucose, hypotension, fever

385
Q

What can mimic stroke

A

Post ictal state, hyper/hypoglycemia and hepatic disturbances

386
Q

What drug does neuromyelitis optic not respond to

A

Rituxumab

387
Q

How do you trigger a seizure in someone who has absence seizures

A

Make them hyperventilate

388
Q

What does mesotemporal sclerosis cause

A

Seizures

389
Q

What is zolmitriptan

A

Prodrug

390
Q

What does carbidopa do

A

Inhibits decarboxylase that metabolizes dopa

391
Q

What is one side effect that adding carbidopa wont help eliminate

A

Anxiety

392
Q

What is selegiline

A

MOA-B inhibitor; decreases breakdown of dopamine

393
Q

What are ropinirole and pramipexole

A

D2 and D3 (respectively) agonists; treat RLS (side effects are impulse control disorders)

394
Q

What is apomorphine

A

*injectable

395
Q

When would you give DA agonists versus start therapy on l-dopa

A

< 65 y/o

396
Q

What drug has a side effect of purple skin

A

Amantadine *livedo reticularis

397
Q

How do you treat meniere’s dz

A

Lorazepam, sodium restriction, diuretics, surgery

398
Q

What is PRES

A

Confusion, vision loss, reversible

Neuro II (3 decks)

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