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Neurology Block > Pharm 2 - Insomnia, Migraine, Brain Tumors, Anesthetics, Ocular, Epilepsy, Vertigo > Flashcards

Pharm 2 - Insomnia, Migraine, Brain Tumors, Anesthetics, Ocular, Epilepsy, Vertigo Flashcards

1
Q

Mediator of sleep and awake states

A

Orexin

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2
Q

Drug classes for insomnia

A

Benzodiazepines (BNZ), BNZ receptor agonists (BRAs), Melatonin receptor agonists, tricyclic antidepressants, 1st gen anti-histamines

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3
Q

MOA of BNZ and BRAs

A

Binding to GABA-A receptor (but at different locations) - GABA channel open longer - more inhibitory action - more CNS depression; BRAs have ceiling effect at high doses

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4
Q

Goals of insomnia drug pharmacokinetics

A

Rapid onset time and sufficient durability as to not wake up in the middle of the night but not too long as to have “morning after” symptoms

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5
Q

Benzodiazepine drugs

A

Estazolam, flurazepam, quazepam, temazepam, triazolam

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6
Q

Pregnancy category for BNZ

A

Category X!

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7
Q

Side effects of BNZs

A

Contraindicated with COPD, driving, depression, other CNS drugs, and glaucoma

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8
Q

BNZ with least CYP interaction

A

Temazepam

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9
Q

BNZ receptor agonists

A

Zolpidem, zaleplon, eszopiclone

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10
Q

Zolpidem

A

Most widely prescribed hynotic, only drug approved for “middle of the night” awakening (short acting/less durable)

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11
Q

Role of melatonin on sleep

A

Works on suprachiasmatic nucleus and sleep-wake switch

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12
Q

Antidepressants for insomnia

A

Doxepin, mirtazapine, trazodone

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13
Q

Side effect of antidepressants

A

Suicidal ideations

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14
Q

First generation anti-histamines

A

Diphenhydramine and doxylamine; cross the BBB

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15
Q

Drug offenders of insomnia

A

TCA, MAOI, SSRIs, Venlafaxine, Bupriopion, Levodopa, Felbamate, Beta-Blockers, Decongestants, Antibiotics, Asthma meds, Stimulants

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16
Q

NSAIDS MOA for migraine Tx

A

Inhibiting inflammatory stimuli, thus decreasing MAPK and decreasing CGRP synthesis

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17
Q

Triptans MOA for migraine Tx

A

Selective carotid vasoconstriction and presynaptic inhibition of trigeminovascular inflammatory response

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18
Q

NSAIDS for migraine

A

Ketoprofen, fenoprofen, nabumetone, ibuprofen, naproxen

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19
Q

NSAIDS in pregnancy

A

Cat C; but avoid in late pregnancy bc of PDA and prolonged labor

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20
Q

NSAID combinations

A

Combined with butalbital (for sedative effects via GABA) and caffeine (for caffeine withdrawal headaches)

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21
Q

Serotonin agonists “triptans”

A

Almotriptan, Eletriptan, Frovatriptan, Naratriptan, Rizatriptan, Sumatriptan, Zolmitriptan

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22
Q

Triptans with fastest onset

A

Sumatriptan - given sub-Q

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23
Q

Triptans most durable (also long onset)

A

Naratriptan and frovatriptan

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24
Q

Contraindications of triptans

A

Don’t take with other vasoconstricting drugs or ergots; don’t combine with SSRIs or SNRIs (serotonin syndrome)

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25
Q

Ergots

A

Dihydroergotamine, ergotamine

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26
Q

Location of ergot receptors

A

CNS and periphery (unlike triptans)

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27
Q

Ergot use in pregnancy

A

NO!…Cat X

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28
Q

Migraine drug to use during pregnancy

A

Acetaminophen; opioids maybe in later trimesters

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29
Q

Tx of menstrual migraine

A

NSAIDS 2-3 days before period until it ends

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30
Q

Migraine and oral contraceptives

A

Multiplicative risk when taking OC and having migraine w/ aura

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31
Q

Antiemetics used in migraine

A

Metoclopramide, prochlorperazine, promethazine, chlorpromazine

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32
Q

MOA of antiemetics

A

All block D2 centrally except promethazine (cholinergic blockade)

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33
Q

Management of brain metastases

A

Antitumoral agents (chemo generally not indicated) and steroids (for brain edema) and anticonvulsants (for seizures). Definitive Tx with surgery or radiation

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34
Q

Mechanisms of resistance in brain tumors

A

Inability to pass BBB, overexpression of P-gp, and gene-related effects from astrocytes (don’t forget also the usual mechanisms from regular tumors too)

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35
Q

Uses for Temozolomide

A

Astrocytoma, GBM, malignant glioma, malignant melanoma

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36
Q

MOA of Temozolomide

A

Pro-drug yielding DNA methylator

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37
Q

Mechanism of resistance to TMZ

A

Repair with methyl guanine methyl transferase

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38
Q

Nitrosourea drugs

A

Carmustine (BCNU) and lomustine (CCNU)

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39
Q

MOA of nitrosoureas

A

Alkylating agents; CARmustine also CARbamylates proteins

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40
Q

Side effects of nitrosoureas

A

Myelosuppression, pulmonary toxicity, endocrine dysfunction

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41
Q

Inhaled Anesthetics

A

Gases: nitrous oxide, Liquids: halothane, enflurane, isoflurane, desflurane, sevoflurane

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42
Q

Conscious sedation

A

Maintain protective reflexes, airway maintained, response to external stimuli

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43
Q

Levels of sedation

A

Analgesia, anxiolysis, conscious sedation, deep sedation, general anesthesia

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44
Q

Advantage of inhalation and IV route

A

Immediate control over dose and duration of action

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45
Q

Minimum Alveolar Concentration

A

Minimum amount of drug required to render half of the patients unconscious

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46
Q

Correlation of MAC and lipid solubility

A

Higher partition coefficient (more lipid soluble) means lower MAC (more potent)

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47
Q

Agents containing halogens

A

Isoflurane, desflurane, sevoflurane (fluorine makes it less volatile)

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48
Q

Incomplete anesthetic

A

Nitrous oxide; MAC 105% - does not work completely, so don’t use alone!

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49
Q

Inhalation agents with faster equilibrium in blood

A

Sevoflurane and desflurane

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50
Q

Ventilation rate and arterial tension

A

More delivery to blood with greater ventilation; more pronounced for nitrous oxide

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51
Q

Respiratory effect of inhaled agents

A

Increased respiration rate and decreased tidal volume

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52
Q

CV effects of inhaled agents

A

Decreased blood pressure and cardiac output

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53
Q

Inhaled agent with no CV effects

A

Nitrous oxide

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54
Q

Inhaled agent with analgesic effects

A

Nitrous oxide

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55
Q

Inhaled agents with muscle relaxant properties

A

Enflurane and isoflurane

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56
Q

Inhaled agents causing hepatic toxicity and arrhythmias

A

Halothane

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57
Q

Inhaled agent that causes seizures

A

Enflurane

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58
Q

Toxicity of nitrous oxide

A

Teratogen, myelin sheath degeneration, B12 deficiency

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59
Q

Problems with nitrous oxide

A

Second gas effect, diffusional hypoxia, solubility

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60
Q

Targets of IV agents

A

Mostly reinforces GABA and glycine inhibitory effects; propofol and ketamine work on NMDA receptors for glutamate

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61
Q

MOA of propofol

A

Acts like GABA itself and also blocks binding of glutamate

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62
Q

MOA of ketamine

A

Physically blocks ion channel

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63
Q

Drug distribution of IV agents

A

Instant effect - goes to high flow organs first (brain, heart, liver, kidneys) then to skeletal muscle/skin and then accumulates in adipose tissue

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64
Q

Redistribution of IV agents

A

Drug passes BBB by going down concentration gradient into the brain and then leaves BBB when gradient inverts

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65
Q

IV agent with longest half life….shortest?

A

Longest - diazepam; shortest - etomidate

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66
Q

IV agent with increased cerebral blood flow

A

Ketamine

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67
Q

IV agent with increased ICP

A

Ketamine again

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68
Q

IV agent without respiratory depression

A

Ketamine a third time

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69
Q

IV agent with cardiostimulatory effect

A

Thiopental, propofol, but mainly ketamine

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70
Q

Best drug to use during surgery if there is nausea and vomiting as an adverse effect

A

Propofol (anti-emetic)

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71
Q

IV agent that inhibits steroidogensis

A

Etomidate

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72
Q

More special properties of ketamine

A

Preserves reflexes, bronchodilatory action, analgesia, hallucinations (like angel-dust)

73
Q

Propofol Infusion Syndrome

A

Metabolic acidosis, rhabdomyolysis, arrhythmias, MI, renal failure, heptaomegaly

74
Q

BNZ used for anesthesia

A

Diazepam, lorazepam, midazolam

75
Q

Properties of BNZ in anesthesia

A

No analgesic properties, but functions as an anticonvulsant and amnesic

76
Q

CV effects of opioids

A

Bradycardia, hypotension, reflex HTN

77
Q

Anesthetics and response to CO2

A

Decreased responsiveness (less ventilation to increased CO2)

78
Q

Neurolept-analgesia

A

State of indifference and pain relief but still responsive; can be transitioned into anesthesia with nitrous oxide

79
Q

Neurolept-analgesia combination

A

Droperidol and fentanyl

80
Q

Ultrafast acting opioid

A

Remifentanil (need analgesia coverage when finished)

81
Q

Long vs short acting opioid

A

Morphine good for long-lasting relief; fentanyl is short acting (less nausea and vomiting unlike morphine)

82
Q

Mechanism of malignant hyperthemia

A

Release of calcium from sarcoplasmic reticulum; succinylcholine thought to be involved

83
Q

Antidote for malignant hyperthemia

A

Dantrolene - repackages calcium back into SR; don’t take with calcium channel blockers

84
Q

Naturally occurring toxins

A

Erythroxylum coca, gymnodinium breve, puffer fish, snake/spider venom

85
Q

The ideal local anesthetic

A

Lipophilic AND hydrophilic; low toxicity, short onset, reversible

86
Q

MOA of local anesthetics

A

Passes through neuronal membrane and blocks voltage-gated sodium channels

87
Q

Differential blockade

A

Certain nerves are more susceptible to blockade than others; this depends on fiber diameter, myelination, position, and nerve activity

88
Q

Fiber sensitivity to anesthetic

A

Small myelinated and non myelinated most sensitive; large myelinated A alpha fibers least sensitive

89
Q

When are local agents most effective

A

When nerve is more spontaneously active

90
Q

Ideal pH in extraneural and neural spaces

A

Extraneural pH should be basic (relative to pKa); neural pH should be acidic (relative to pKa). You want uncharged molecule to cross membrane but you want a charged molecule to bind to Na channel

91
Q

Local anesthetic in area of inflammation

A

IT WAS SUPER INEFFECTIVE

92
Q

Anatomical aspects of nerve block

A

Block begins proximal to distal and outside to inside; recover also proximal to distal

93
Q

Nomenclature of amides and esters

A

____i____caine = amide; _____caine = ester; just remember amIde has the I in it; exception is articaine which is considered an ester despite it’s spelling

94
Q

Metabolism of amide agents

A

Hepatic

95
Q

Metabolism of ester agents

A

Any other tissue - shorter duration of action because of this

96
Q

Systemic toxicities of local agents

A

Ringing in ears, metallic taste, numbness in lips and tongue (stop drug immediately); can also have seizures

97
Q

Role of vasoconstrictors in nerve blockade

A

Vasoconstrictor will increase the duration and intensity of the blockade; phentolamine will vasodilate and promote removal of the anesthetic

98
Q

Additives to local anesthetics

A

Epinephrine or levonordrefin - can lead to situational anxiety

99
Q

Sulfite allergy

A

Allergic to esters give amides

100
Q

How many mg/mL in a 2% solution?

A

Let’s arbitrarily say there’s 100 mL; so 2% = 2 g/100 mL = 2000 mg / 100 mL = 20 mg/mL at a density of 1 g/mL

101
Q

How many ug/mL epinephrine at 1:100,000 solution?

A

1:100,000 = 1 g / 100,000 mL = 10 ug/mL

102
Q

Local anesthetics that cause methemoglobinemia

A

Prilocaine and benzocaine (a lesser extent)

103
Q

Prolonged drug action in bupivacaine

A

Good for postoperative analgesia, more cardiotoxic

104
Q

Articaine

A

Penetration into bone; good for dental work

105
Q

Topical anesthetic for mouth, pharynx, larynx, trachea, esophagus, and urethra

A

Benzocaine, dyclonine

106
Q

Topical anesthetic for skin ONLY

A

Dibucaine, pramoxine

107
Q

Epidural/spinal anesthesia

A

Distribution depends on baricity and pt orientation; works on nerve fibers exiting the cord not the spinal cord itself

108
Q

Drug sequence regimen

A

BNZ night before surgery for anxiety; shortly before surgery - sedative/amnesic, drugs to neutralize acidity/dry secretions

109
Q

Other drugs for anxiety

A

Phenothiazines, 1st gen antihistamines

110
Q

Benefits of H1 antagonists

A

Sedation, cholinergic antagonism, and anti-emetic effect

111
Q

Prophylaxis for allergic reaction

A

Treat with H1 and H2 blockers

112
Q

Problem with delayed awakening

A

Residual anesthetics and ancillary drugs - give opiate or BNZ antagonists; physostigmine can reverse anticholinergic effects

113
Q

Postoperative nausea and vomiting

A

Propofol rarely causes it but nitrous oxide is associated with it

114
Q

Glycemic control for surgery

A

Stop oral hypoglycemics and cut down on insulin

115
Q

Anaphylaxis support

A

Stop drug, discontinue anesthesia, give O2, give epi, expand intravascular volume

116
Q

Effect of opiates on the eye

A

Pinpoint pupils

117
Q

Use of esterases for the eye

A

Good for local activation of prodrugs - dipevefrin and latanoprost

118
Q

Effects of muscarinic antagonists

A

Loss of accomodation (cycloplegia) and adaptation (mydraisis) - pupils enlarge and can worsen glaucoma

119
Q

Muscarinic antagonists

A

Atropine, homotropine, tropicamide, cyclopentolate, scopolamine

120
Q

Adverse effects of muscarinic antagonists

A

Increased intraocular pressure, transient stings

121
Q

Two mechanisms to treat glaucoma

A

Decreased production of aqueous humor; increased outflow of humor

122
Q

Firstline Rx for glaucoma

A

Prostaglandin analogs - Latanoprost, Travoprost, Bimatoprost (“Bi, Lata, Travo” = “Bye, Later Trevor (Sweatman)”

123
Q

Beta blockers for glaucoma

A

Timolol maleate, levobunolol, metipranolol, carteolol

124
Q

Carbonic anhydrase inhibitors to treat glaucoma

A

Dorzolamide, Brinzolamide, Acetazolamide (zolamides)

125
Q

Effects of PGF2a analogs

A

Acutely - blurred vision, stinging, itching

Chronically - brown pigmentation of iris, eyelid, eyelashes

126
Q

Drug that produces eye lash thickening

A

Bimatoprost

127
Q

MOA of beta blockers in glaucoma

A

Inhibits production of aqueous humor

128
Q

MOA of CA inhibitors in glaucoma

A

Less bicarb = less fluid transport = decreased IOP

129
Q

Adverse effects of CA inhibitors

A

Allergic reaction to sulfonamides, agranulocytosis, aplastic anemia, SJS/TEN, fulminant hepatic necrosis, taste disturbances (early)

130
Q

MOA of muscarinic agonists and AchE inhibitors for glaucoma

A

Increased aqueous humor flow

131
Q

Contraindication of muscarinic agonists/AchE inhibitors

A

Not used when constriction not wanted

132
Q

Contraindication of AchE inhibitors

A

Not used in closed angle glaucoma (increased IOP)

133
Q

Muscarinic agonists/AChE inhibitors

A

Carbachol, pilocarpine, acetylcholine, achothiophate

134
Q

MOA of sympathomimetics

A

Work on alpha receptors to increase outflow of aqueous humor

135
Q

Sympathomimetic drugs

A

Dipivefrin, phenylephrine, apraclonidine, brimonidine, naphazoline, tetrahydrozoline

136
Q

Rx for macular degeneration

A

Aflibercept, pegaptanib, ranibizumab, bevacizumab, verteporfin

137
Q

VEGF inhibitors

A

Ranibizumab, bevacizumab (the mAbs), aflibercept (intercepts), pegaptanib (antagonist)…it kinda rhymes

138
Q

Generates free radicals when activated by a laser

A

Verteporfin - obviously avoid direct sunlight

139
Q

3 MOA of anti-epileptics

A

Inhibition of voltage gated sodium channels, activation of GABA-mediated inhibition, inhibition of voltage gated calcium channels

140
Q

GABA enhancement

A

Vigabatrin and valproate will stall the metabolism of GABA; gabapentin works presynaptically to promote GABA release; BNZ and barbituates bind to GABA receptors itself promoting Cl- influx

141
Q

Calcium channel blocker AEDs

A

Ethosuximide and zonisamideq

142
Q

Problem with AEDs

A

Suicidal ideation

143
Q

AEDs that inactivate Na channels (still depolarized/open but stabilizes inactive conformation)

A

Carbamazepine, phenytoin, topiramate, lamotrigine, valproate, zonisamide

144
Q

Hepatically eliminated AEDs

A

Half-life decreases as there is more hepatic metabolism so upward adjustment of drugs necessary; all are hepatically eliminated except for Gabapentin and Pregabalin

145
Q

Issues with topiramate and zonisamide

A

Weak CA inhibitors - decreased bicarb, formation of renal stones

146
Q

Abrupt termination of AEDs

A

Don’t do it - can cause status epilepticus

147
Q

Pharmacokinetics of phenytoin

A

Zero ordered metabolism - half life varies with dose

148
Q

Prodrug of phenytoin

A

Fosphenytoin

149
Q

Adverse effects of phenytoin

A

CNS EFFECTS (Nystagmus, headaches, ataxia), GINGIVAL HYPERPLASIA, SJS/TEN/DRESS, HYPERTRICHOSIS/HIRSUTISM

150
Q

Adverse effects of carbamazepine

A

Agranulocytosis/aplastic anemia, dizziness, drowsiness, ataxia, DERM EFFECTS RARE (but also has SJS/TEN), n/v, dry mouth

151
Q

HLA-B 1502 screening

A

Worry about with Asians using carbamazepine, phenytoin, fosphenytoin, lamotrigine - can cause SJS/TEN

152
Q

Adverse effects of valproic acid

A

Thrombocytopenia, derm effects rare, n/d

153
Q

Other black box warnings

A

Felbamate - aplastic anemia, myelosuppression, hepatic dz; lamotrigine - serious rash (TEN/SJS)

154
Q

AED most associated with teratogenicity

A

Valproate

155
Q

Birth defects seen with phenytoin and carbamazepine

A

Fetal hydantoin syndrome - upturned nose, mild midfacial hypoplasia, long upper lip w/ thin vermilion border, distal digital hypoplasia

156
Q

Regimen for partial seizures

A

Lamotrigine, carbamazepine, levetiracetam, oxcarbazepine

157
Q

Regimen for primary generalized tonic-clonic seizures

A

Valproate, lamotrigine, levetiracetam

158
Q

Regimen for absence seizures

A

Ethosuximide, valproate

159
Q

Regimen for atypical absence, myoclonic, atonic seizures

A

Valproate, lamotrigine, levetiracetam (same as for primary generalized tonic-clonic)

160
Q

Rx for status epilepticus

A

BNZ initially and followed with AED

161
Q

Use of phenobarbital/benzodiazepine in seizures

A

Issues with dependence/withdrawal/tolerance, dose-related sedation, but good for rapid IV administration

162
Q

Drug causes of irreversible hearing loss

A

Aminoglycosides, loop diuretics, chemo drugs

163
Q

MOA of toxicity of aminoglycosides and cisplatin

A

AG - both caspase-dependent and independent; CP - only caspase dependent

164
Q

MOA of diuretic toxicity

A

Same - block Na/K/2Cl transporter and upsets fluid balance in endolymph

165
Q

Rx for vertigo

A

Meclizine, diphenhydramine, scopolamine, promethazine, diazepam (except for dizepam all work to block H1 and M1 receptors)

166
Q

Adverse effects of H1 and M1 blockers

A

Produce dizziness/drowsiness; diphenhydramine and promethazine are CYP2D6 inhibitors

167
Q

Centers involved in emesis

A

Lateral reticular formation, chemoreceptor trigger zone (in area postrema), solitary tract nucleus, cerebral cortex, vestibular center

168
Q

Receptors in chemoreceptor trigger zone

A

5-HT, dopamine, opioids

169
Q

Receptors in solitary tract nucleus

A

5-HT, enkephalin, histamine, Ach

170
Q

Serotonin antagonists for antiemesis

A

Dolasetron, granisetron, ondansetron, palonosetron (“setrons”)

171
Q

Adverse effect of serotonin antagonists

A

CYP interactions, QT prolongation

172
Q

D2 receptor antagonists for antiemesis

A

Prochlorperazine, chlorpromazine

173
Q

Adverse effect of D2 receptor antagonists

A

Don’t give with antipsychotics (CNS effects), QT prolongation, Torsades

174
Q

Substance P/Neurokinin-1 receptor antagonist

A

Aprepitant, fosaprepitant (works on solitary tract)

175
Q

Metabolism of Sub P/NK1 receptor antagonists

A

Hepatic - CYP3A4 inhibitors

176
Q

Cannabinoid receptor agonists

A

Dronabinol, THC

177
Q

Adverse effects of cannabinoid receptor agonists

A

Gets you HIGH, Schedule III (weakly reinforcing and slow onset - not too addictive)

178
Q

Antiemetic regimen for chemotherapy

A

Serotonin antagonist, NK-1 antagonist, corticosteroid

Neurology Block (6 decks)

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