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STEP 1 (3) > Neurology- Pharmacology > Flashcards

Neurology- Pharmacology Flashcards

1
Q

What drug classes are used to tx glaucoma?

A

a-agonsts

BBs

diuretics (acetazolamide)

cholinomimetics

prostaglandins

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2
Q

What is the purpose of glaucoma tx?

A

decreased IOP by decreasing the amount of aqueous humor (inhibit synthesis/secretion or increase drainage)

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3
Q

What a-agonists are used to tx glaucoma?

A

epinephrine (a1)- decrease aqueous humor synthesis via vasoconstriction

brimonidine (a2)- decrease aqueous humor synthesis

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4
Q

What are some AES of using a-agonists to tx glaucoma?

A

mydriasis (a1)- dont use in closed-angle glaucoma

blurry vision, ocular hyperemia, foreign body sensation, ocular allergic rxns, ocular pruritis

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5
Q

What are some BBs used for glaucoma tx?

A

Timolol, betxaolol, and carteolol- all decrease aqueous humor synthesis

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6
Q

How do diuretics (acetazolamide) help in glaucoma tx?

A

they decrease aqueous humor synthesis via inhbition of carbonic anhydrase

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7
Q

What are some cholinomimetics used to tx glaucoma?

A

direct (pilocarpine, carbachol)

indirect (physostigmine, echothiophate)

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8
Q

How do cholinomimetics help tx glaucoma?

A

they increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

use pilocaprine is emergencies (very effective at opening meshwork into the canal of Schlemm)

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9
Q

What are some AEs of cholinomimetics?

A

miosis and cyclospams (contraction of the ciliary muscle)

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10
Q

How do prostaglandins help tx glaucoma?

A

PGs like latanoprost (PGF2a) increase outflow of aqueous humor

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11
Q

What is a major AE of latanoprost?

A

darkening of the iris color (browning)

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12
Q

What are some opiods?

A

morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan,

diphenoxylate, pentazocine

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13
Q

How do opiods work?

A

they act as agonists at opiod recepotrs (u= morphine, delta= enkepalin, kappa= dynorphin) to modulate synaptic transmission- open K+ channels, close Ca2+ channels to decrease synaptic transmission

Also inhibit the release of ACh, nor, 5-HT, glutamate, and substance P

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14
Q

What are the clinical uses of opiods?

A

pain, cough suppresion (dextromethorphan), diarrhea (loperamide, diphenoxylate), acute pulmonary edema, maintenance for heroin addicts (methadone, naloxone)

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15
Q

What are some common AEs of opiods?

A

addiction, respiratory depression, constipation, miosis, additive CNS depression with other drugs

tolerance does not develop to miosis and constipation

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16
Q

Opiod toxicity/addiction is well tx with what?

A

naloxone or naltrexone (opiod receptor antagonist)

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17
Q

What is Butorphanol?

A

k-opiod receptor agonist and u-opiod receptor partial agonist (produces analgesia) for tx of severe pain (e.g. migraine, labor)

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18
Q

What is a major advantage of Butorphanol?

A

it causes less respiratory depression than full opiod agonists

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19
Q

What are the AEs of Butorphanol?

A

can cause opiod withdrawal symptoms if pt is also taking a full opiod agonist (OD not easily reversed with naloxone)

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20
Q

What is Tramadol?

A

a very weak opiod agonist (also inhibits 5-HT and nor reuptake) for tx of chronic pain

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21
Q

What are the AEs of Tramadol?

A

decreased seizure threshold

serotonin syndrome

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22
Q

What is the first line tx for simple, partial (focal) epilepsy?

A

carbamazepine

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23
Q

What else is carbamazepine the first line tx for?

A

complex partial epilepsy

tonic-clonic, generalized epilepsy (can also use valproic acid or phenytoin first line)

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24
Q

What are the other tx options for a simple, partial (focal) epilepsy?

A

pheyntoin

valproic acid

gabapentin

phenobarbital

topiramate

vigabatrin, tiagabine, lamotrigine, levetriacetam

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25
Q

What are the other tx options for a complex, partial (focal) epilepsy?

A

same as simple (again, dont use ethosuximide or benzodiazepines)

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26
Q

What are the other tx options for a tonic clonic, partial epilepsy between the first line options (pheyntoin, valproic acid, and carbamazapine)?

A

phenobarbital

topiramide

lamotrigine

levetiracetam

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27
Q

What is the first line for absence generalized epilepsy?

A

ethosuximide

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28
Q

What is the other tx options for absence generalized epilepsy?

A

valproic acid

lamotrigine

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29
Q

What are the tx options for ACUTE status epilepticus epilepsy?

A

benzodiazepines (diazepam and lorazepam)

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30
Q

What are the tx options for prophylaxis of status epilepticus epilepsy?

A

phenytoin

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31
Q

How does Ethosuximide work?

A

blocks thalamic T-type Ca2+ channels

(Sux to have silent (absence) seizures)

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32
Q

What are the AEs of ethosuximide?

A

EFGHIJ- Ethosuximide causes fatigue, GI distress, HA, itching, and Steven-Johnson Syndrome

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33
Q

How do benzodiazepines work?

A

they increase GABAa action (also used for ecampsia seizures)

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34
Q

What are the AEs of benzodiazepines?

A

sedation, tolerance, dependence, and respiratory depression

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35
Q

How does pheyntoin work?

A

increased Na+ channel inactivation; zero-order kinetics

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36
Q

What are the AEs of phenytoin?

A

Nystagmus, diplopia

ataxia

sedation

gingival hyperplasia

hirsutism

peripheral neuropathy

megalobalstic anemia

teratotoxic (fetal hydantoin syndrome)

SLE- like syndrome

LAD

SJS

osteopenia

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37
Q

How does carbamazepine work?

A

increases Na+ channel inactivation

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38
Q

What are the AEs of carbamazepine?

A

diplopa, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia)

liver toxicity

teratogenesis

induction of CYP450

SIADH

SJS

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39
Q

carbamazepine is also first line for what?

A

trigeminal neuralgia

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40
Q

How does valproic acid work?

A

increases Na+ channel inactivation, and increases GABA concentration by inhibiting GABA transaminase

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41
Q

What are the AEs of valproic acid?

A

GI distress

rare but fatal liver toxicity

teratogenic- neural tube defects (spina bifida)

tremor

weight gain

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42
Q

What else is valproic acid used for?

A

myoclonic seizures and bipolar disorder

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43
Q

How does gabapentin work?

A

primarily inhibits Ca2+ channels (designed as a GABA analog)

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44
Q

What are the AEs of gabapentin?

A

sedation, ataxia

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45
Q

What are the other uses of gabapentin?

A

peripheral neuropathy

postherpetic neuralgia

fibromyalgia

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46
Q

How does phenobarbital work?

A

increases GABAa action

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47
Q

What are the AEs of phenobarbital?

A

sedation, tolerance

dependence

induction of CYP450

cardiorespiratory depression

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48
Q

Phenobarbital is first line in seizure tx in who?

A

neonates

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49
Q

How does Topiramate work?

A

blocks Na+ channels, increased GABA action

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50
Q

What are the AEs of Topiramate?

A

Sedation, mental dulling, kidney stones, weight loss

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51
Q

How does lamotrigine work?

A

blocks voltage-gated Na+ channels

52
Q

What are the AEs of lamotrigine?

A

SJS (titrate slowly)

53
Q

How does Levetriacetam work?

A

unknown but may modulate GABA and glutamate release

54
Q

How does Tiagabine work?

A

increased GABA by inhibiting reuptake

55
Q

How does Vigabatrin work?

A

increases GABA by irreversibly inhibiting GABA transaminase

56
Q

What are some barbiturates?

A

Phenobarbital, pentobarbital, thipental, secobarbital

57
Q

How do barbiturates work?

A

they facilitate GABAa action by increasing the duration of Cl- channel opening, thus decreasing neuron firing

58
Q

barbiturates are contraindicated in what?

A

porphyria pts.

59
Q

What are the main uses of barbiturates?

A

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

60
Q

What are the AEs of barbiturates?

A 
respiratory and CV depression (can be fatal)
CNS depression (worse with EtOH use)

dependence

induces CYP450

61
Q

How is barbiturate OD tx?

A

supportive (assist respiration and maintain BP)

62
Q

What are the main benzodiazepines?

A

diazepam, lorazepam, triazolam, temazepam, ozazepam, modazolam, alprazolam

63
Q

How do benzodiazepines work?

A

they facilitate GABAa action by icnreasing the frequency of Cl- channel opening

Also decrease REM sleep

64
Q

Metabolism of benzodiazepines

A

Most have long half-lives and active metabolites (exceptions: Alprazolam, Triazolam, Oxazepam, and Midazolam- ATOM- these have higher addiction potential due to short half-life)

65
Q

What are the clinical uses of benzodiazepines?

A

anxiety, spasticity, status epilepticus (lorazepam and diazepam)

detox (especially EtOH withdrawal-DTs)

night terrors, sleepwalking

general anesthetic (amnesia, muscle relaxation)

hypnotic (insomnia)

66
Q

What are the AEs of benzodiazepines?

A

dependence

additive CNS depression effects with alcohol

less risk of respiratory depression and coma than with barbiturates

67
Q

How should benzodiazepines OD be tx?

A

flumazenil (competitive antagonist at GABA benzodiazepine receptors)

68
Q

What are some nonbenzodiazepine hypnotics?

A

Zolpidem, Zaleplon, and esZopiclone (Gives you the ZZZs)

69
Q

How do nonbenzodiazepine hypnotics work?

A

they act via the BZ1 subtype of the GABA receptor (effects reversed by flumazenil) for tx of insomnia

70
Q

What are the AEs of nonbenzodiazepine hypnotics?

A

ataxia, HA, and confusion

71
Q

What is the DOA of nonbenzodiazepine hypnotics?

A

short duration b/c of rapid metabolism by liver enzymes. Unlike older sedative-hyponotics, these only cause modest day-after psychomotor deression and a few amnestic effects (also less dependence risk than benzodiazepines)

72
Q

What are some general principles of Anesthetics?

A

CNS drugs must be lipid soluble to cross the BBB or be actively-transported

73
Q

What is MAC= Minimal Alveolar Conc (of inhaed anesthetics)?

A

requires to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision)

74
Q

Exs of anesthetics: Nitrous oxide (N2) has lower blood and lipis solubility and this fast induction and low potency. Halothane, in constrat, has high lipid and blood solubility, and this high potency and slow induction

A
75
Q

What are some inhaled anesthetics?

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane

N2O

All mechanisms unknown

76
Q

What are the effects of inhaled anesthetics?

A

myocardial depression, respiratory depression

N/V

increased cerebral blood flow (decreased cerebral metabolic demand)

77
Q

What are the AEs of inhaled anesthetics?

A

hepatotoxicity (halothane)

nephrotoxicity (methoxyflurane)

proconvulsant (enflurane)

expansion of trapped gas in a body cavity (N2O)

malignant hyperthermia

78
Q

How do inhaled anesthetics caused malignant hyperthermia?

A

they induce fever and severe muscle contraction

79
Q

What is the tx for malignant hyperthermia?

A

dantrolene

80
Q

What are some choices for IV anesthetics?

A
  • Barbiturates
  • Benzodiazepines
  • Arylcyclohexylamines (Ketamine)
  • Opiods
  • Propofol
81
Q

Describe the use of Barbiturates as IV anethetics

A

Thiopental- high potency, high lipid solubility, and rapid entry into the brain.

Used for induction of anestehsia and short surgical procedures.

Effect terminated by rapid redistribution into tissue (skeletal tissue and fat)

decreases cerebral blood flow

82
Q

Describe the use of Benzodiazepines as IV anethetics

A

Midazolam most common drug used for endoscopy

used adjunctively with gaseos anesthetics and narcotics

may cause sever postoperative respiratory depression, decreased BP (tx with flumazenil), and/or anterograde amnesia

83
Q

Describe the use of Ketamine as IV anethetics

A

PCP analogs that at as dissociative anesthetics.

They block NMDA receptors

CV stimulants

cause disorientation, bad dreams, and hallucinations

increased cerebral BF

84
Q

Describe the use of Opiods as IV anethetics

A

Morphine, fentanyl used with other CNS depressents during general anesthesia

85
Q

Describe the use of Propofol as IV anethetics

A

Used for sedation in the ICU, rapid anesthesia induction, and short procedures

Less postoperative neausea than thiopental

Potentiates GABAa

86
Q

What are some local anesthetics?

A

Esters- procaine, cocaine, tetracaine

Amides- IIdocaine, Mepovacaine, Bupivacine

87
Q

How do local anesthetics work?

A

they block Na+ channels by binding to specific receptors on the inner portion of the cell (preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons)

tertiary amine local anesthetics penetrate membranes in their uncharged form, then bind to ion channels in their charged form

88
Q

Principles of local anesthetics

A
  • Can be given with vasoconstrictors (usually epi) to enhance local action- decreased bleeding, increases anesthesia by blocking systemic spread
  • If used in infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate the membrane so more is needed
89
Q

What is the order of nerve blockade produced by local anesthetics?

A

small diameter fibers > large diameter

Myelinated fibers > unmyelinated fibers

Overall, size factor predominates over myelination such that small myelinated fivers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers

90
Q

Which sensations are lost first with local anesthetics?

A

pain > temp > touch > pressure

91
Q

What are the clinical uses of local anesthetics?

A

minor surgical procedures, spinal anesthesia. If allergic to esters, give amides

92
Q

What are the AEs of local anesthetics?

A

CNS excitation, severe CV toxicity (Bupivacaine), HTN, hypotension, arrhythmias (cocaine), and methemoglobinemia (benzocaine)

93
Q

What are the categories of neuromuscular blocking drugs used for muscle paralysis in surgery or mechanical ventilation? (Selective for motor nicotinic receptors)

A

depolarizing or non-depolarizing

94
Q

What are some non-depolarizing NMJ blockers?

A

Tubocurarine, atracurium, pancuronium, vecuronium, rocuronium

all act as competitive antagonists that compete with ACh for binding

95
Q

How can the effects of non-depolarizing NMJ blockers be reversed?

A

Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonum, and other cholinesterase inhibitors

96
Q

What is the major depolarizing NMJ blockers

A

Succinylcholine

97
Q

How does Succinylcholine act?

A

acts as a strong ACh receptor agonists to produce sustained depolarization initially and then prevents further muscle contraction

98
Q

How are the effects of succinylcholine reversed?

A

Phase I (prolonged depolarization)- no antidote. Block potentiated by cholinesterase inhibitors

Phase II (repolarized but blocked; ACh receptors are available, but desensitized)- antidote is cholinesterase inhibitors

99
Q

What are the main AEs of Succinylcholine?

A

hypercalcemia, hyperkalemia and malignant hyperthermia

100
Q

What is Dantrolene?

A

prevents release of Ca2+ from the SR of skeletal muscle for tx of malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

101
Q

How does Baclofen work?

A

It inhibits GABAb receptors at spinal cord level, inducing skeletal muscle relaxation for tx of muscle spasms (e.g. acute low back pain)

102
Q

How does Cyclobenzaprine work?

A

centrally acting skeletal muscle relaxant, structurally related to TCAs, with similar anticholinergic side effects for tx of muscle spasms

103
Q

What causes Parkinsonism?

A

loss of dopaminergic neurons and excess cholinergic activity

104
Q

What are some strategies for tx Parkinson disease?

A
  • Dopamine agonists (increase dopamine availability, increased L-DOPA availability, prevent doapmine breakdown)
  • Decrease excess cholinergic activity
105
Q

What are the major dopamine agonists?

A

Ergot- Bromocriptine

Non-ergot (preferred)- Pramipexole, and ropinirole

106
Q

What are some drugs used to increase dopamine availability?

A

Amantadine (increase dopamine release and decrease uptake)

107
Q

What else is Amantadine used for?

A

as an antiviral against influenza A and rubella

108
Q

What are the major AEs of Amantadine?

A

ataxia and livedo reticularis

109
Q

What drugs increase L-DOPA availability?

A

agents that prevent peripheral L-DOPA degradation to increase the amount of it entering the CNS (L-DOPA is converted to dopamine). These include:

  • Levodopa/Carbidopa
  • Entacapone/tolcapone
110
Q

How does Carbidopa work?

A

it blocks peripheral conversion of L-DOPE to dopamine by inhibiting DOPA decarboxylase. It also reduces the side effects of peripheral L-DOPA conversion (e.g. N/V)

111
Q

How do Entacapone and Tolcapone work?

A

they prevent peripheral L-DOPA degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT

112
Q

How can dopamine breakdown be prevented for Parkinson tx?

A

agents act centrally to block dopamine breakdown and include:

Selegiline (blocks conversion of dopamine into 3-MT by inhibiting MAO-B)

Tolcapone (blocks converison of dopamine to DOPAC by inhibiting central COMT)

113
Q

What is an antimuscarinic used to tx Parkinson?

A

Benzotropine (improves tremor and rigidity but has little effect on bradykinesia)

114
Q

Mnemonic for tx of Parkonsin’s

A

BALSA:

Bromocriptine

Amantadine

Levodopa (with carbidopa)

Selegiline

Antimuscarinics

115
Q

Mechanism of L-Dopa (levodopa)/carbidopa?

A

They increase the levels of dopamine in the brain. Unlike dopamine, L-DOPA can cross the BBB and is converted by doap decarboxylase in the CNS to dopamine

Carbidopa, a peripheral DOPA decarboxylase inhibitor, is given with L-DOPA to increase its bioavailability in the brain and to limit side effects

116
Q

What are the AEs of L-Dopa (levodopa)/carbidopa?

A

arryhthmias from inrceased peripheral formation of catecholamines.

Long term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses

117
Q

How does Selegiline work?

A

Selectively inhibits MAO-B, which metabolizes dopamine over nor and 5-HT, thereby increasing the availabilty of dopamine (used with L-DOPA in Parkinson tx)

118
Q

What are the main drugs for Alzheimer tx?

A
  • Memantine
  • Donepezil, galantamine, rivastigmine, tacrine
119
Q

What is Memantine?

A

NMDA receptor antagonist that helps prevent excitability (mediated by calcium)

120
Q

What are the AEs of Memantine?

A

dizziness, confusion, and hallucinations

121
Q

What are Donepezil, galantamine, rivastigmine, and tacrine?

A

AChE inhibitors

122
Q

What neurotransmitter changes are seen in Huntington’s disease?

A

decreased GABA and ACh

increased dopamine

123
Q

How is Huntington’s disease tx?

A

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

Haloperidol- D2 receptor antagonist

124
Q

How do Triptans (e.g. Sumatriptan) work?

A
  • 5-HT agonists
  • Inhibit CN V activation
  • prevent vasoactive peptide release
  • induce vasoconstriction
125
Q

What are Triptans used to tx?

A

acute migraine

cluster HA attacks

126
Q

What are the AEs of triptans?

A

coronary vasospasm (contraindicated in pts with CAD or Prinzmetal angina)

mild paresthesia

STEP 1 (3) (16 decks)

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