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Neurology 2 > Neuro Pharm 2 > Flashcards

Neuro Pharm 2 Flashcards

1
Q

Neurons in the hypothalamus that mediate very rapid transition between the sleep and awake cycles
Input from the suprachiasmatic nucleus, amygdala, dorsomedial hypothalamis
these neurons also act on the NPY neurons of the arcuate nucleus of the hypothalamus to increase food intake
These are significantly decreased in narcolepsy

A

Orexin

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2
Q

Rx works by increasing the length of time that the Cl-channel GABA-A neurons stay open (still need GABA)

A

Barbituates

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3
Q

Rx that has an allosteric leftward shift on the GABA-A neurons
Category X, CI: Liver dz, COPD, depression, glaucoma, other CNS Rx
3 kinds:
1-
2-
3-

A

Benzodiazepines
1- Sedation/ Amnesia

2- Anxiolysis

3- Myorelaxation/ Anti-convulsant

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4
Q

IV rapid acting Benz antagonist

A

Flumazenil

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5
Q

Benz Agonist

Most widely prescribed hypnotic, reduced dose for women, withdraw Rx slowly

A

Zolpidem

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6
Q

Benz agonist

Ald. Dehydrogenase, variability in Asians

A

Zaleplon

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7
Q

Melatonin Receptor Agonist
MT-1: attenuates Suprachiasmatic nucleus activity
MT-2: circadian rhythms
MT-3: not involved in sleep

A

Ramelteon

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8
Q

1st gen anti-hist AEs

A

xerostomia, blurred vision, urinary retention, increased occular pressure, rapid tolerance

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9
Q

Only antidepressant approved to tx insomnia
anti-H1 at low dose
SNRI

A

Doxepin

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10
Q

Antidepressant off-label for insomnia

a2 antagonism

A

Mirtazapine

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11
Q

Antidepressant off-label for insomnia

5-HTRI

A

Trazodone

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12
Q

TOC for migraines during pregnancy

A

Acetominophen

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13
Q

produce selective carotid vasoconstriction (via 5HT1B) and pre-synaptic inhibition of the trigeminovascular inflammatory responses of migraines (via 5HT1D/5HT1F – calcium entry)

A

Triptans

Sumatriptan

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14
Q

Routes and AE of triptans

A

Nasal route – faster

SC- fastest & most effective but w/ most AEs: CNS – dizziness, drowsiness, fatigue

May cause coronary or peripheral vasospasm, contraindicated w/ heart disease, uncontrolled HTN, ischemic bowel disease

Do not use w/ MAOIs or Ergots

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15
Q

Long Acting Triptan

A

Frovatriptan

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16
Q

Intermediate Acting Triptan

A

Naratriptan

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17
Q

Alkaloids derived from a mold

In moderate doses: causes contraction of smooth muscle fibers (used to control hemorrhage & promote uterine contractions (also used to treat migraine headaches)

In large doses, ergotamine paralyzes motor nerve endings of the SNS

Acute/Chronic AE: mental disorientation, convulsions, muscle cramps, dry gangrene

Generally less effective, may work in pts unresponsive to first-line drugs

Contraindicated in pts with vasospastic predisposing conditions
Hepatic metabolism, renal elimination

Complex agonist on multiple receptors (5HT), peripheral alpha, decreased amine uptake

Beta blockers, DA can potentiate vasoconstrictive effect
Strong CYP3A4 can increase ergot persistence
Triptans, 24 h rule
Teratogenic

A

Ergotamine

Duhydroergotamine

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18
Q

May be given for migraines in later trimesters
Last resort, respiratory depression, bradycardia, histamine, QT prolongation, constipation, N/V
*high AUS

A

Opiates: hydrocodone, oxycodone, codeine

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19
Q

Antiemetic for migraines

D2, cholinergic, and alpha adrenergic blockade

A

Prochlorperzine

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20
Q

Antiemetic for migraines

D2 central blockade & prokinetic

A

Metoclopromide

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21
Q

Antiemetic for migraines

anticholinergic

A

Chlorpromazine

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22
Q

Prophylaxis of migraines

Decreases reuptake of 5HT and NE + strong anti-cholinergic effect

A

Amitriptyline

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23
Q

Prophylaxis of migraines

Sodium channel blocker, increases GABA, Cat X, hepatotoxic, sedation, nausea, increase weight, highly protein bound

A

Valproic acid

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24
Q

Decreases arterial dilation and decreases NE induced lipolysis, fatigue, exercise intolerance, problems with asthma & diabetes, AV block
Only drug approved for migraines in children

A

propanolol

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25
Q

Blocks sodium, glutamate

Increases GABA

A

Topiramate

26
Q

No vascular or systemic effects, decreases the incidence of headache, high placebo rate, not recommended for episodic headaches

A

Botox

27
Q

Non-enzymatically activated pro-drug (DNA methylating agent)
Resistance via upregulation of MGMT activity

A

Temozolimide

28
Q

alkylating agents; cross-resistance w/ other alkylating agents is uncommon
-lipophilic, non-ionized at physiologic pH

AE: myelosuppression, pulmonary fibrosis, endocrine problems (increase prolactin, hypothyroidism), encephalopathy/seizures

A

Carmustine and Lomustine

29
Q

theory: Myer-Overton?

A

the more lipid-soluble the drug, the more potent it is (but in reality, making a drug more lipid soluble will not always enhance its potency)

30
Q

minimum alveolar concentration: vol % of the atmosphere that is the anesthetic needed to anesthetize 50% pts

Increasing the oil:gas partition can lower the drug’s MAC

A

minimum alveolar concentration

31
Q

allows you to lower how much of the anesthetic to add to the mixture
Incomplete anesthetic – useful as an additive
Not as lipid soluble so it rapidly reaches saturation in the blood
Does not block reflex response to increasing N2O
No significant CV effects alone but causes depression w/ an opiod agent
Produces analgesia

Reflexes are maintained if this is used alone
Teratogen in animal models
Increased risk of spontaneous abortion; sporadic neuro px in infants due to myelin sheath degredation upon chronic exposure (N2O is an inhibitor of B12 synthestase)
All medical facilities now have expensive N2O scavenging air-handling systems
Special Problems:
1- Second gas effect: High volume of N2O and relative insolubility, rapid uptake of anesthetic accompanying agent
2- Diffusional hypoxia – administer O2 immediately post-anesthetic phase
3- N2O solubility: can accumulate in other airspaces of body: middle ear, pneumothorax, bowel surgery

A

Nitrous Oxide

32
Q

Potentiate GABA and glycine inhibitory signaling, reinforce 2 pore potassium channel activity & inhibit glutamatergic signaling

  • Do not produce analgesia
  • Produce a lack of reflexes
A

Volatile Gases

33
Q

Older volatile gas with hepatic and heart toxicity

A

Halothane

34
Q

Volatile Gases A/w seizures

A

Halothane, Enflurane

35
Q

Newer Volatile Gases: Newer agent, equilibrates much faster to reach the brain more quickly

A

Desflurane and Sevoflurane

36
Q

Increase in cardiac output and HR of an anesthetized patient

Also act on NMDA receptors for glutamate
Inhibits glutamate by occluding the channel
Increases cerebral blood flow and intracranial pressure
Also cardio stimulatory (increase HR, MAP, CO) no effect on RR
Produces analgesia
Preserves protective reflexes
Bronchodilatory actions
Selective neuronal depression
Dissociative anesthetic

A

Ketamine

37
Q

Barbituate

Increases heart rate; depresses RR, CBF

A

Thiopental

38
Q

Short Acting Hypnotic
depresses RR, CBF increases heart rate
Reinforce GABA and inhibit Glutamate by blocking binding to receptor
Also act on NMDA receptors for glutamate
Anti-emetic
Propofol Infusion syndrome: fatal CV and organ systems failure – bad press

A

Propofol

39
Q

Short Acting Hypnotic
Reinforce GABA
No effect on heart or vasculature (good for cardiac pt)
depresses RR, CBF
Inhibition of steroidgenesis (not used in the ICU) drop in cortisol seen with one dose

A

Etomidate

40
Q

Systemic Toxicity of local agents

A

Minor toxicity: ringing in ears, metallic taste, numbness of lips and tongue
Seizures: administer diazepam, protect airway, succinylcholine in severe rxn

41
Q

*Separate into long and short-acting

A

lower pkA will have a faster onset

42
Q

Recall agents producing methemoglobulinemia:

A

prilocaine & benzocaine

43
Q

= lidocaine and prilocaine, advance of skin graft collection, onset within 1 hour

A

EMLA

44
Q

= Lidocaine and oxymetazoline – analgesia and vasoconstriction for suturing lacerations

A

LET

45
Q

Local anesthetic
Metabolism mostly in the liver but affected by CV, pregnancy, liver, BBs
Urinary metabolite elimination

A

Amide

46
Q

Local anethetic
Can be metabolized in any structure except CSF by non-specific esterase enzymes (can have genetically low capacity)
Urinary metabolite

A

Ester

47
Q

Amide

More potent, cardio toxic, prolonged activity; inadvertent trauma to tongue/mouth

A

Bupivacaine

48
Q

Amide

Reduced CV activity; greater margin of safety

A

Ropivacaine

49
Q

: first line tx for glaucoma; mechanism is unclear, thought to increase aqueous outflow via uveoscleral outflow pathway; undergo in situ hydrolysis after penetrating the cornea (blurred vision, burning/stinging, itching, chronically slow & permanent brown pigmentation of iris, eyelid skin, eye lashes, also increases growth & length
Brand name, very expensive

A

Prostaglandin: Latanoprost

50
Q

tx for glaucoma : decrease aqueous humor production, decrease cAMP, can be detected in systemic circulation (don’t use in pt w/ low heart rate or asthma)

A

Timolol maleate

51
Q

reduces fluid transport to decrease IOP; blurred vision, lacrimation, photophobia, xerophthalmia; sulfonamides : allergic rxns (will inhibit aqueous production?)

A

Carbonic Anhydrase Inhibitors
Dorzolamide
Brinzolamide

52
Q

intravitreal use of VEGF inhibitors a/w atertial thromboembolic events

A

Aflibercept
Pegaptanib
Ranibizumab
Bevacizumab

53
Q

IV nonthermal laser activator; free radicals damage vessles

A

Verteporfin

54
Q

ACheE Inhibitors: more potent, longer acting miotics + adverse effects more common; not used w/ closed angle glaucoma

A

Echothiophate

55
Q

Partial vs. generalized

Partial: simple vs. complex

A

simple - no loss of consciousness

complex: loss of consciousness

56
Q

Promote inactivated sodium channel state (partial and secondary generalized)
Binds proteins
One of the few zero order drugs; metabolism varies based on the dose
CNS effects: nystagmus, headache, ataxia, drowsiness not common at tx levels
Gingival hyperplasia, hirsutism, derm

A

Phenytoin

57
Q

Promote inactivated sodium channel state (partial and secondary generalized)
Inhibition of voltage gated calcium channels for T-type calcium currents (absence seizures)
Increases GABA, decreases sodium
Binds proteins
CNS related to the infusion rate; heme: thrombocytopenia
Greatest risk of teratogenicity
DOC: tonic/clonic, absence/ myoclonic/ atonic

A

Valproate

58
Q

Promote inactivated sodium channel state (partial and secondary generalized)
CNS effects especially during initial tx: sedation, dizziness/ drowsiness
Heme: risk of agranulocytosis/ anaplastic anemia
Xerostomia, N/V
Needs to get increased over time to maintain serum concentrations due to CYP induction
DOC: partial/ secondary generalized seizures

A

Carbamezepine

59
Q

2 anti-convulsants that act on the sodium channel and are weak carbonic anhydrase inhibitors (can cause lactic acidosis)

A

Topiramate & Zonisamide

60
Q

First response for a pt w/ an acute prolonged epileptic crisis

A

Lorazepam (benzodiazepines) – instant effect that you follow up by loading in IV at a slower rate: Diazepam (giving it rectally, it does avoid first pass metabolism, but not as rapid as IV push)

61
Q

Inhibition of voltage gated calcium channels for T-type calcium currents (absence seizures)

A

Ethosuximide

62
Q

Decreases NMDA, increases GABA
Decreases alpha-2 delta-1 subunit of calcium
SOB on exertion and weakness? Tachycardic w/ pale skin  anemia

A

Felbamate

Neurology 2 (7 decks)

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