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USMLE Step I Pharmacology > Neurology Pharmacology > Flashcards

Neurology Pharmacology Flashcards

(165 cards)

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1
Q

glaucoma drugs–mechanism

A
  • decrease IOP by decreasing amount of aqueous humor
    • inhibit synthesis synthesis/secretion of aqueous humor OR increase drainage
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2
Q

what are the 5 categories of glaucoma drugs?

A
  • alpha agonists
  • beta blockers
  • diuretics
  • cholinomimetrics (M3)
  • prostaglandin
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3
Q

name the alpha agonist glaucoma drugs

A
  • epinephrine (alpha 1)
  • brimonidine (alpha 2)
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4
Q

alpha agonist (glaucoma drugs)–mechanism

A
  • decrease aqueous humor synthesis via vasoconstriction
  • decrease aqeous humor synthesis
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5
Q

alpha agonist (glaucoma drugs)–toxicity

A
  • mydriasis (alpha 1)
  • blurry vision
  • ocular hyperemia
  • foreign body sensation
  • ocular allergic rxns
  • ocular pruritus
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6
Q

what is a contraindication for using epinephrine for glaucoma?

A
  • patients with closed angle glaucoma
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7
Q

name the beta blocker glaucoma drugs

A
  • timolol
  • betaxolol
  • carteolol
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8
Q

beta blocker (glaucoma drugs)–mechanism

A
  • decrease aqueous humor synthesis
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9
Q

beta blocker (glaucoma drugs)–toxicity

A
  • no pupillary or vision changes
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10
Q

name the diuretics glaucoma drugs

A
  • acetazolamide
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11
Q

diuretics (glaucoma drug)–mechanism

A
  • decrease aqueous humor synthesis by inhibition of carbonic anhydrase
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12
Q

diuretics (glaucoma drug)–toxicity

A
  • no pupillary or vision changes
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13
Q

name the 2 categories of cholinomimetics glaucoma drugs and their corresponding drugs

A
  • direct
    • pilocarpine
    • carbachol
  • indirect
    • physostigmine
    • echothiophate
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14
Q

cholinomimetics–mechanism

A
  • increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
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15
Q

when should pilocarpine be used and why?

A
  • pilocarpine is a cholinomimetic glaucoma drug
    • use in emergencies
    • very effective at opening meshwork into the canal of Schlemm
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16
Q

cholinomimetics–toxicity

A
  • miosis–contraction of pupillary sphincter muscles
  • cyclospasm–contraction of ciliary muscle
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17
Q

name the prostaglandin glaucoma drugs

A
  • bimatoprost
  • latanoprost (PGF 2 alpha)
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18
Q

prostaglandin (glaucoma drugs)–mechanism

A
  • increase outflow of aqueous humor
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19
Q

prostaglandin (glaucoma drugs)–toxicity

A
  • darkens color of iris (browning)
  • eyelash growth
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20
Q

name the opioid analgesics

A
  • morphine
  • fentanyl
  • codeine
  • loperamide
  • methadone
  • meperidine
  • dextromethorphan
  • diphenoxylate
  • pentazocine
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21
Q

opioid analgesics–mechanism

A
  • acts as agonists at opioid receptors to modulate synaptic transmission–open K + channels and close Ca2+ channels –> dec synaptic transmission
    • opioid receptors:
      • µ = beta endorphin
      • delta = enkephalin
      • kappa = dynorphin
  • inhibit release of ACh, norepinephrine, 5-HT, glutamine, substance P
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22
Q

opioid analgesics–use

A
  • pain
  • cough suppression (dextromethorphan)
  • diarrhea (loperamide, diphenoxylate)
  • acute pulmonary edema
  • maintenance programs for heroin addicts (methadone, buprenorphine + naloxone)
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23
Q

opioid analgesics–toxicity

A
  • addiction
  • respiratory depression
  • constipation
  • miosis
    • except meperidine which causes mydriasis
  • additive CNS depression with other drugs
  • tolerance does not develop to miosis and constipation
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24
Q

opioid analgesics–antidote

A
  • naloxone
  • naltrexone
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25
pentazocine--mechanism
* kappa-opioid receptor agonist * µ-opioid receptor antagonist
26
pentazocine--use
* analgesia for moderate to severe pain
27
pentazocine--toxicity
* can cause opiod withdrawal symptoms if patient is also taking full opioid antagonist * b/c competition for opioid receptors
28
butorphanol--mechanism
* kappa opiod receptor agonist * µ opioid receptor partial agonist * produces analgesia
29
butorphanol--use
* severe pain * migraine * labor * causes less respiratory depression than full opioid agonists
30
butorphanol--toxicity
* can cause opioid withdrawal symptoms if patient is also taking full opioid agonist * competition for opioid receptors
31
butorphanol--antidote
* overdose not easily reversed with naloxone
32
tramadol--mechanism
* very weak opioid agonist * inhibits 5-HT and norepinephrine reuptake * works on multiple neurotransmitters * "**tram it all**" in with **tramadol**
33
tramadol--use
* chronic pain
34
tramadol--toxicity
* similar to opioids * decreases seizure threshold * serotonin syndrome
35
etho**sux**imide--use
* _first line_ for generalized absence (petit mal) seizures * **S**ucks to have **S**ilent (absence) **S**eizures
36
ethosuximide--side effects
* DI * fatigue * headache * urticaria * Stevens-Johnson syndrome * **EFGHIJ**--**E**thosuximide causes **f**atigue, **G**I distress, **H**eadache, **I**tching, and Stevens **J**ohnson syndrome
37
ethosuximide--mechanism
* blocks thalamic T type Ca2+ channels
38
name the benzodiazepines
* diazepam * lorazepam * midazolam
39
benzodiazepines--use
* generalized static epilepticus * _first line for acute_ * also for eclampsia seizures * first line for eclampsia seizures is MgSO4
40
benzodiazepines--mechanism
* increase GABAA action
41
benzodiazepines--side effects
* sedation * tolerance * dependence * respiratory depression
42
phenobarbital--use
* simple partial (focal) seizures * complex partial (focal) seizures * generalized tonic clonic seizures (grand mal) * first line in neonates
43
phenobarbital--mechanism
* increase GABAA action
44
phenobarbital--side effects
* sedation * tolerance * dependence * induction of cytochrome P 450 * cardiorespiratory depression
45
phenytoin, fosphenytoin--use
* simple partial (focal) seizures * complex partial (focal) seizures * _first line_ generalized tonic clonic (grand mal) seizures * generalized static epilepticus * _first line for prophylaxis_
46
phenytoin, fosphenytoin--mechanism
* blocks Na+ channels * zero order kinetics
47
phenytoin, fosphenytoin--side effects
* neurologic * nystagmus * diplopia * ataxia * sedation * peripheral neuropathy * dermatologic * hersutism * Stevens Johnson syndrome * gingival hyperplasia * DRESS syndrome * musculoskeletal * osteopenia * SLE-like syndrome * hematologic * megaloblastic anemia * reproductive * teratogenesis--fetal hydantoin syndrome * other * cytochrome P 450 induction
48
carbamazepine--use
* _first line_ for simple partial (focal) seizures * _first line_ for complex partial (focal) seizures * generalized tonic clonic (grand mal) seizures * first line for trigeminal neuralgia
49
carbamazepine--mechanism
* blocks Na+ channels
50
carbamazepine--side effects
* diplopia * ataxia * blood dyscrasias * agranulocytosis * aplastic anemia * liver toxicity * teratogenesis * induction of cytochrome P-450 * SIADH * Stevens Johnson Syndrome
51
valproic acid--use
* simple partial (focal) seizures * complex partial (focal) seizures * _first line_ for generalized tonic clonic (grand mal) seizures * generalized absence seizures * also used for myoclonic seizures, bipolar disorder, migraine prophylaxis
52
valproic acid--mechanism
* increase Na+ channel inactivation * increase GABA concentration by inhibiting GABA transaminase
53
valproic acid--side effects
* GI distress * rare but fetal hepatotoxicity (measure LFTs) * pancreatitis * neural tube defects * tremor * weight gain
54
what is a contraindication for valproic acid?
* pregnancy
55
vigabatrin--use
* simple partial (focal) seizures * complex partial (focal) seizures
56
vigabatrin--mechanism
* increase GABA by irreversibly inhibiting GABA transaminase
57
gabapentin--use
* simple partial (focal) seizures * complex partial (focal) seizures * also used for peripheral neuropathy, postherpetic neuralgia
58
gabapentin--mechanism
* primarily inhibits high voltage activated Ca2+ channels * designed as a GABA analog
59
gabapentin--side effects
* sedation * ataxia
60
topiramate--use
* simple partial (focal) seizures * complex partial (focal) seizures * generalized tonic clonic (grand mal) seizures * also used for migraine prevention
61
lamotrigine--use
* simple partial (focal) seizures * complex partial (focal) seizures * generalized tonic clonic (grand mal) seizures * generalized absence (petit mal) seizures
62
lamotrigine--mechanism
* blocks voltage gated Na+ channels
63
lamotrigine--side effects
* Stevens Johnson syndrome * must be titrated slowly
64
levetiracetam--use
* simple partial (focal) seizures * complex partial (focal) seizures * generalized tonic clonic (grand mal) seizures
65
levetiracetam--mechanism
* unknown * may modulate GABA and glutamate release
66
tiagabine--use
* simple partial (focal) seizures * complex partial (focal) seizures
67
tiagabine--mechanism
* increase GABA by inhibiting reuptake
68
name the barbiturates
* phenobarbital * pentobarbital * thiopental * secobarbital
69
barbiturates--mechanism
* facilitate GABAA action by increasing **duration** of Cl- channel opening * so decreases neuron firing * barbi**durat**es increase **durat**ion
70
what is a contraindication for barbiturate use?
* porphyria
71
barbiturates--use
* sedative for anxiety * seizures * insomnia * induction of anesthesia (thiopental)
72
barbiturates--toxicity
* respiratory and cardiovascular depression--can be fatal * CNS depression--can be exacerbated by alcohol use * dependence * drug interactions--induces cytochrome P-450
73
barbiturates--antidote
* overdose treatment is supportive * assist respiration * maintain BP
74
name the benzodiazepines
* diazepam * lorazepam * triazolam * temazepam * oxazepam * midazolam * chlordiazepoxide * alprazolam
75
benzodiazepines--mechanism
* facilitate GABAA action by in **frequency** of Cl- channel opening * **"fre**nzodiazepines increase **fre**quency" * benzos, barbs, and alcohol all bind the GABAA receptor, which is a ligand gated Cl- channel * decrease REM sleep * most have long half lives and acive metabolites * exceptions: **ATOM**: **A**lprazolam, **T**riazolam, **O**xazepam, **M**idazolam--short acting * higher addictive potential
76
benzodiazepines--use
* anxiety * spasticity * status epilepticus (lorazepam and diazepam) * eclampsia * detoxification--especially alcohol withdrawal (DTs) * night terrors * sleepwalking * general anesthetic--amnesia, muscle relaxation * hypnotic--insomnia
77
benzodiazepines--toxicity
* dependence * additive CNS depression effects with alcohol * less risk of respiratory depression and coma than with barbiturates
78
benzodiazepines--antidone
* treat overdose with flumazenil--competitive antagonist at GABA benzodiazepine receptor * can precipitate seizures by causing acute benzodiazepine withdrawal
79
name the non-benzodiazepine hypnotics
* **Z**olpidem * **Z**alepon * es**Z**opiclone * "All **ZZZ**s put you to sleep"
80
non-benzodiazepine hypnotics--mechanism
* act via the BZ1 subtype of the GABA receptor * sleep cycle less affected as compared with benzodiazepine hypnotics
81
non-benzodiazepine hypnotics--antidote
* flumazenil
82
non-benzodiazepine hypnotics--use
* insomnia
83
non-benzodiazepine hypnotics--toxicity
* ataxia * headaches * confusion * decreased dependence risk than benzodiazepines
84
why do non-benzodiazepine hypnotics have a short duration?
* b/c of rapid metabolism by liver enzymes
85
how are non-benzodiazepine hypnotics different than older sedative hypnotics?
* they have only modest day-after psychomotor depression * have few amnestic effects
86
what is important about CNS drugs?
* must be lipid soluble (cross the blood brain barrier) OR be actively transported
87
what is true about anesthetics with decreased solubility in blood?
* rapid induction * rapid recovery times
88
what is true about anesthetics with increased solubility in lipids?
* increased potency = 1/MAC * **MAC** = **M**inimal **A**lveolar **C**oncentration (of inhaled anesthetic) required ot prevent 50% of subjects from moving in response to noxious stimulus (ie. skin incision) * examples: * nitrous oxide (N2O) has dec blood and lipid solubility, and thus fast induction and low potency * halothan has increased lipid and blood solubility, and thus high potency and slow induction
89
name the inhaled anesthetics
* desflurane * halothane * enflurane * isoflurane * secoflurane * methoxyflurane * N2O
90
inhaled anesthetics--mechanism
* mechanism unknown
91
inhaled anesthetics--side effects
* myocardial depression * respiratory depression * nausea/emesis * increased cerebral blood flow * decreased cerebral metabolic demand
92
inhaled anesthetics--toxicity
* hepatotoxicity (halothane) * nephrotoxicity (methoxyflurane) * proconvulsant (enflurane) * expansion of trapped gas in a body cavity (N2O) * malignant hyperthermia
93
explain malignant hyperthermia
* rare, life threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions * susceptibility inherited as autosomal dominant with variable penetrance * mutations in voltage sensitive ryanodine receptor cause increased Ca2+ release from sarcoplasmic reticulum * treatment: dantrolene--ryanodine receptor antagonist
94
name the intravenous anesthetics
* barbiturates * **TH**iopental * benzodiazepines * **M**idazolam * arylcyclohexylamines * **K**etamine * **Propofol** * **Op**ioids * "**Th**e **Mi**ghty **K**ing **Propo**ses **Fool**ishly to **Op**rah."
95
barbiturates (thiopental) as IV anesthetic--mechanism
* high potency * high lipid solubility * rapid entry into brain * effect terminated by rapid reditribution into tissue and fat
96
barbiturates (thiopental) as IV anesthetic--use
* used for induction of anesthesia * short surgical procedures
97
barbiturates (thiopental) as IV anesthetic--toxicity
* decreased cerebral blood flow
98
benzodiazepines (midazolam) as IV anesthetic--use
* used for endoscopy * used adjunctively with gaseous anesthetics and narcotics
99
benzodiazepines (midazolam) as IV anesthetic--toxicity
* may cause severe post op respiratory depression * decrease BP * treat overdose with flumazenil * anterograde amnesia
100
arylcyclohexylamines (ketamine) as IV anesthetic--mechanism
* PCP analogs that act as dissociative anesthetics * block NMDA receptors * cardiovascular stimulants
101
arylcyclohexylamines (ketamine) as IV anesthetic--toxicity
* disorientation * hallucination * bad dreams * increased cerebral blood flow
102
propofol as IV anesthetic--use
* sedation in ICU * rapid anesthesia * short procedures
103
propofol as IV anesthetic--mechanism
* potentiates GABAA
104
benefits of using propofol as IV anesthetic
* less post op nausea than thiopental
105
opioids as IV anesthetic--use
* morphine, fentanyl used with other CNS depressants during general anesthesia
106
name the local anesthetics that are esters
* procaine * cocaine * tetracaine * benzocaine
107
name the local anesthetics that are amides
* l**I**doca**I**ne * mep**I**vaca**I**ne * bup**I**vaca**I**ne * am**I**des have **2 I**'s
108
local anesthetics--mechanism
* block Na+ channels by binding to specific receptors on inner portion of channel * tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form
109
where are local anesthetics most effective?
rapidly firing neurons
110
why would local anesthetics be administered with vasoconstrictors, particularly epinephrine?
* to enhance local action * causes decreased bleeding, increased anesthesia by decreasing systemic concentration
111
alkaline anesthetics in infected (acidic) tissue
* in infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively * you would need more anesthetic
112
what is the order of the nerve blockade with local anesthetics?
* small diameter fibers \> large diameter fibers * myelinated fibers \> unmyelinated fibers * overall size factor predominates over myelination, so: * small myelinated fibers \> small unmyelinated fibers \> large myelinated fibers \> large unmyelinated fibers
113
what is the order of loss with local anesthetics?
1. pain 2. temperature 3. touch 4. pressure
114
local anesthetics--use
* minor surgical procedures * spinal anesthesia * if allergic to esters, give amides
115
local anesthetics--toxicity
* CNS excitation * severe cardiovascular toxicity (bupivacaine) * hypertension * hypotension * arrhythmias (cocaine) * methemoglobinemia (benzocaine)
116
neuromuscular blocking drugs--use
* muscle paralysis in surgery * mechanical ventilation
117
neuromuscular blocking drugs--mechanism
* selective for motor (vs autonomic) nicotinic receptors
118
name the depolarizing neuromuscular blocking drugs
* succinylcholine
119
succinylcholine--mechanism
* (depolarizing neuromuscular blocking drug) * strong ACh receptor agonist * produces sustained depolarization * prevents muscle contraction
120
depolarizing neuromuscular blocking drugs--reversal of blockade
* phase I--prolonged depolarization * no antidote * block potentiated by cholinesterase inhibitors * phase 2--repolarized but blocked; ACh receptors are available but desensitized * may be reversed with cholinesterase inhibitors
121
depolarizing neuromuscular blocking drugs--complications
* hypercalcemia * hyperkalemia * malignant hyperthermia
122
name the nondepolarizing neuromuscular blocking drugs
* tubocurarine * atracurium * mivacurium * pancoronium * vecuronium * rocuronium
123
nondepolarizing neuromuscular blocking drugs--mechanism
* competitive antagonists * compete with ACh for receptors
124
nondepolarizing neuromuscular blocking drugs--reversal of blockade
* neostigmine--must be given with atropine to prevent muscarinic effects such as bradycardia * endrophonium * other cholinesterase inhibitors
125
dantrolene--mechanism
* prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor
126
dantrolene--use
* malignant hyperthermia * neuroleptic malignant syndrome--a toxicity of antipsychotic drugs
127
baclofen--mechanism
* activates GABAB receptors at spinal cord level * which induces skeletal muscle relaxation
128
baclofen--use
* muscle spasms * ie. acute low back pain
129
cyclobenzaprine--mechanism
* centrally acting skeletal muscle relaxant * structurally related to TCAs * similar anticholinergic side effects
130
cyclobenzaprine--use
* muscle spasms
131
what is the cause of Parkinson disease?
* loss of dopiminergic neurons * excess cholinergic activity
132
what are the 5 Parkinson disease drugs?
* **B**romocriptine * **A**mantidine * **L**evodopa (with carbidopa) * **S**elegiline (and COMT inhibitors) * **A**ntimuscarinics * **"BALSA"**
133
what are 5 strategies used for Parkinson disease drugs?
1. dopamine agonists 2. increase dopamine availability 3. increase L-dopa availability 4. prevent dopamine breakdown 5. curb excess cholinergic activity
134
name the Parkinson disease drugs that are dopamine agonists
* Ergot--**B**romocriptine * Non-Ergot (preferred)--pramipexole, ropinirole
135
Parkinson disease drugs that increase dopamine availability
* **A**mantidine * increase dopamine release and decrease dopamine reuptake
136
amantidine--toxicity
* (Parkinson disease drug that inc dopamine availability) * ataxia * livedo reticularis
137
name the Parkinson disease drugs that increase L-DOPA availability
* **L**evodopa/cardidopa * Entacarpone * tolcapone
138
Parkinson disease drugs that increase L-DOPA availability--mechanism
* agents prevent peripheral (pre-BBB) L-dopa degradation --\> increase L-DOPA entering CNS --\> increase central L-DOPA availabilie for conversion to dopamine
139
Entacapone, Tolcapone--mechanism
* (Parkinson disease drugs that increase L-DOPA availability) * prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT
140
name the Parkinson disease drugs that prevent dopamine breakdown
* agents act centrally (post BBB) to inhibit breakdown of dopamine * Selegiline * Tolcapone
141
Selegiline--mechanism
* (Parkinson disease drugs that prevent dopamine breakdown) * blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B
142
Tolcapone--mechanism
* (Parkinson disease drugs that prevent dopamine breakdown) * blocks conversion of dopamine to 3-OMD by inhibiting central COMT
143
name the Parkinson disease drugs that curb excess cholinergic activity and what is the mechanism?
* **Benz**tropine * **A**ntimuscarinic * improves tremor and rigidity but has little effect on bradykinesia in **Park**inson disease * "**Park** your Mercedes **Benz**"
144
Levodopa (L-dopa)/Carbidopa--mechanism
* increase level of dopamine in the brain * converted by dopa decarboxylase in the CNS to dopamine
145
how is L-dopa (levodopa)/carbidopa different than dopamine?
* L-dopa can cross blood brain barrier and is converted by dopa decarboxylase in the CNS to dopamine
146
why is carbidopa administered with L-dopa?
* carbidopa is a peripheral DOPA decarboxylase inhibitor * given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects (like nausea and vomiting)
147
L-dopa (levodopa)/Carbidopa--use
Parkinson disease
148
L-dopa (levodopa)/Carbidopa--toxicity
* arrhythmias from increase peripheral formation of catecholamines
149
L-dopa (levodopa)/Carbidopa--what can come about as a result of long term use?
* dyskinesia following administration ("on off" phenomenon * akinesia b/w doses
150
selegiline, rasagiline--mechanism
* selectively inhibit MAO-B (metabolize dopamine) --\> increase dopamine availability
151
selegiline, rasagiline--use
* adjunctive agent to L-dopa in treatment of Parkinson disease
152
name the 5 Alzheimer drugs
* Memantine * Donepezil * galantamine * rivastigmine * tacrine
153
Memantine--mechanism
* (Alzheimer drug) * NMDA receptor antagonist * helps prevent excitotoxicity * mediated by Ca2+
154
memantine--toxicity
* (Alzheimer drug) * dizziness * confusion * hallucination
155
donepezil, galantamine, rivastigmine, tacrine--mechanism
* (Alzheimer drug) * AChE inhibitors
156
donepezil, galantamine, rivastigmine, tacrine--toxicity
* (Alzheimer drug) * nausea * dizziness * insomnia
157
name the 3 drugs that can be used to treat Huntington disease
* tetrabenazine * reserpine * Haloperidol
158
Tetrabenazine and reserpine--mechanism
* (Huntington dz drug) * inhibit vesicular monoamine transporter (VMAT) --\> dec dopamine vesicle packaging and release
159
Haloperidol--mechanism
* (Huntington dz drug) * D2 receptor antagonist
160
riluzole--mechanism and use
* tx for ALS * modestly increases survival by decreasing glutamate excitotoxicity via an unclear mechanism * "For **Lou** Gehrig dz, give ri**lou**zole"
161
name the Triptan and what is the mechanism?
* **Sum**a**trip**t**an** * 5-HT1B/1D agonists * inhibit trigeminal nerve activation * prevent vasoactive peptide release * induce vasoconstriction * "A **SUM**o wrestler **TRIP**s **AN**d falls on your **head**"
162
sumatriptan--use
* (Triptan) * acute migrain * cluster **head**ache attacks * "A **SUM**o wrestler **TRIP**s **AN**d falls on your **head**​"
163
sumatriptan--toxicity
* (Triptan) * coronary vasospasm * mild paresthesia
164
what is a contraindication of sumatriptan?
* patients with CAD or Prinzmetal angina
165

USMLE Step I Pharmacology (17 decks)

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