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Step 1 Neurology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

alpha-agonists for Tx of Glaucoma?

MOA?

A

Epi (alpha1)- decr aqueous humor synthesis via vasoconstriction
Brimonidine (alpha2)- decr aqueous humor synthesis

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2
Q

Epi and Brimonidine: adverse effects on eye?

A

Mydriasis (epi)- do NOT use in closed-angle glaucoma,

Blurry vision, ocular hyperemia, foreign body sensation, allergic rxns, pruritus

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3
Q

BBs for Tx of Glaucoma?

MOA?

A

Timolol, Betaxolol, Carteolol

decr aqueous humor synthesis
no pupillary or vision changes

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4
Q

Diuretic for Tx of Glaucoma?

MOA?

A

Acetazolamide

decr aqueous humor synthesis via inhibition of carbonic anhydrase
no pupillary or vision changes

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5
Q

Direct Cholinomimetics for Tx of Glaucoma?

MOA?

Adverse effects to eye?

A

Pilocarpine, Carbachol
incr outflow of aqueous humor via contraction of ciliary m. and opening of trabecular meshwork
Use Pilocarpine in emergencies- very effective at opening meshwork into canal of schlemm

Miosis, Cyclospasm

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6
Q

Indirect Cholinomimetics for Tx of Glaucoma?

MOA?

Adverse effects to eye?

A

Physostigmine, Echothiophate

incr outflow of aqueous humor via contraction of ciliary m. and opening of trabecular meshwork

Miosis, Cyclospasm

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7
Q

Prostaglandins for Tx of Glaucoma?

MOA?

Adverse effects to eye?

A

Bimatoprost, Iatanoprost (PGF2alpha)

incr outflow of aqueous humor

Darkens color of Iris (browning), eyelash growth

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8
Q

Opioid Analgesics?

A

Morphine, Fentanyl, Codeine, Loperamide, Meperidine, Dextromethorphan, Diphenoxylate, Pentazocine

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9
Q

Opioid Analgesics: MOA?

A

agonists at opioid receptors to modulate synaptic transmission- open K+ channels, close Ca++ channels–> decr synaptic transm.
Inhibit release of ACh, NE, 5-HT, glutamate, substance P

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10
Q

Opioid Analgesics: clinical use?

A 
Pain, acute pulm edema, maintenance programs for heroin addicts (methadone, Buprenrphine + Naloxone),
diarrhea (Loperamide, Diphenoxylate),
cough suppression (Dextromethorphan)
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11
Q

Opioid Analgesics: ADR?

A

Addiction, resp depression, constipation, miosis (except Meperidine –> Mydriasis), additive CNS depression w other drugs
Tolerance does not develop to miosis or constipation

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12
Q

Opioid Analgesics toxicity Tx?

A

Naloxone or Naltrexone (opioid receptor antagonist)

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13
Q

Opioid receptors?

A

mu= beta-endorphin,
delta= enkephalin,
k= dynorphin
(FA pg 499)

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14
Q

k-opioid receptor agonist and mu-opioid receptor antagonist that is used for moderate-severe pain?
ADR?

A

Pentazocine

can cause opioid withdrawal Sx if pt is also taking full opioid antagonist

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15
Q

k-opioid receptor agonist and mu-opioid receptor partial agonist that produces analgesia and is used for severe pain (ie Migraine, Labor)?

A

Butorphanol

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16
Q

Butorphanol adverse effects?

A

can cause opioid withdrawal Sx if pt is also taking full opioid agonist, and OD is NOT easily reversed by Naloxone

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17
Q

Tramadol MOA?

A

Very weak opioid agonist, also inhibits 5-HT and NE reuptake

(works on multiple neurotransmitters- “Tram it all” with Tramadol)

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18
Q

Tramadol clinical use?

ADRs?

A

Chronic pain

similar to opioids; decr seizure threshold; Serotonin syndrome

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19
Q

Barbiturates?

A

Phenobarbital, Pentobarbital, Thiopental, Secobarbital

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20
Q

Barbiturates: MOA?

A

Facilitate GABA(A) action by incr duration of Cl- channel opening, thus decr neuron firing

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21
Q

Barbiturates: CI?

A

Porphyria

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22
Q

Barbiturates: clinical use?

A

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

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23
Q

Barbiturates: ADRs?

A

Resp and CV depression (can be fatal), CNS depression (worse w alcohol), dependence, drug intxns (induces cytP-450)

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24
Q

Barbiturates: OD Tx?

A

Supportive (assist resp and maintain BP)

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25
Q

Benzos?

A

Diaze-, Loraze-, Temaze-, Oxaze- pam
Triazolam, Midazolam, Alprazolam
Chlordiazepoxide

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26
Q

Benzo MOA?

A

Facilitate GABA(A) action by INCR FREQUENCY of Cl- channel opening. Decr REM sleep

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27
Q

Most Benzos have long half-lives and active metabolites.. what are the exceptions?

A

Alprazolam, Triazolam, Oxazepam, Midazolam (“ATOM”)

these are short-acting –> higher addictive potential

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28
Q

Benzos: clinical use?

A

Anxiety, spasticity, eclampsia, detox (esp alcohol withdrawal- DTs), night terrors, sleepwalking, Insomnia (hypnotic), Gen anesthetic (amnesia, m. relaxation),

status epilepticus (lorazepam, Diazepam)

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29
Q

Benzos: ADRs?

A

Dependence, additive CNS depression w. alcohol.

OD Tx: Flumazenil, can —> seizures bu causing acute benzo withdrawal

LESS risk of resp depression/coma than w Barbs

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30
Q

What are the Nonbenzodiazepine Hypnotics?

A

Zolpidem, Zaleplon, esZopiclone

“All ZZZs put you to sleep”

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31
Q

Nonbenzodiazepine Hypnotics: MOA?

A

act via the BZI subtype of the GABA receptor

Sleep cycle less affected compared to benzos and less risk of dependence
Effects reversed by Flumazenil

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32
Q

Nonbenzodiazepine Hypnotics: clinical use?

ADRs?

A

Insomnia

Ataxia, HAs, confusion. Rapidly metabolized by liver enzymes –> short duration

(Unlike other hypnotics, cause only modest day-after psychomotor depression and few amnestic effects)

33
Q

MAC of inhaled anesthetics?

A

=Minimal Alveolar Conc. required to prevent 50% of subjects from moving in response to noxious stimulus

34
Q

Anesthetics w incr solubility in lipids have ?

A

incr potency (=1/MAC)

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

35
Q

Anesthetics w decr solubility in blood –>

A

rapid induction and recovery times

36
Q

inhaled anesthetics?

A

Desflurane, Halothane, Enflurane, Isoflurane, Sevoflurane, Methoxyflurane, N2O
(MOA unknown)

37
Q

inhaled anesthetics: effects?

A

Myocardial and resp depression, N/V, incr cerebral blood flow (decr cerebral metabolic demand)

38
Q

inhaled anesthetics: ADRs?

A 
Malignant Hyperthermia 
Hepatotoxicity (Halothane)
Nephrotoxicity (Methoxyflurane)
Proconvulsant (Enflurane)
Expansion of trapped gas in a body cavity (N2O)
39
Q

Malignant Hyperthermia?

A

Rare, life threatening, inhaled anesthetics or Succinylcholine induce fever/severe m. contractions.
Susceptibility inherited AD w. variable penetrance.
Mutations in voltage-gated ryanodine receptor –> incr Ca++ release for SR

40
Q

Malignant Hyperthermia and neuroleptic malignant syndrome Tx?

A

Dantrolene (ryanodine receptor antagonist- prevents release of Ca++ from SR of skeletal m.)

41
Q

IV anesthetics?

A

THiopental (barb), Midazolam (Benzo), Ketamine, Propofol, OPioids
(“THe Mighty King Proposes foolishly to Oprah”)

42
Q

Thiopental as an IV anesthetic?

A

High potency, high lipid solubility, rapid entry into brain.
Used for induction of anesthesia and short surgical procedures.
Effect terminated by rapid redistribution into tissue/fat.
decreases cerebral blood flow

43
Q

IV anesthetic commonly used for endoscopy (used adjunctively w gaseous anesthetics and narcotics)?
ADRs?

A

Midazolam

severe post-op resp depression, decr BP (OD Tx= Flumazenil), Anterograde amnesia

44
Q

PCP analogs that act as dissociative anesthetics, Block NMDA receptors, CV stimulants?

A

Arylcyclohexylamines (Ketamine)

45
Q

Arylcyclohexylamines (Ketamine) ADRs?

A

Disorientation, hallucinations, bad dreams, increased cerebral blood flow

46
Q

IV anesthetic used for sedation in ICU, rapid anesthesia induction, short procedures. Potentiates GABA(A)
Less post-op nausea than Thiopental.

A

Propofol

47
Q

L-dopa (Levodopa)/Carbidopa: clinical use?

A

Parkinson Disease

48
Q

L-dopa (Levodopa)/Carbidopa: general MOA?

A

incr level of dopamine in brain

unlike dopamine, L-dopa can cross BBB and is cnvtd by dopa decarboxylase in the CNS to dopamine

49
Q

Carbidopa: MOA

A

peripheral DOPA decarboxylase inhibitor

Is given w L-dopa to incr bioavailability of L-dopa in the brain and to limit peripheral side effects

50
Q

L-dopa (Levodopa)/Carbidopa: ADRs?

A

Arrhythmias (from incr peripheral formation of catecholamines)
Long term use: Dyskinesia then akinesia between doses (“on-off” phenomenon)

51
Q

Selegline, Rasagiline: clinical use?

ADRs?

A

Adjunctive agent to L-dopa in Tx of Parkinson disease

may enhance ADRs of L-dopa

52
Q

Selegline, Rasagiline: MOA?

A

selectively inhibit MAO-B (metabolize dopamine) –> incr dopamine availability

53
Q

Drugs used to treat Alzheimers?

A

Memantine, Donepezil, galantamine, rivastigmine, tacrine

54
Q

Donepezil, galantamine, rivastigmine, tacrine: MOA?

ADRs?

A

AChE inhibitors (used in Tx of Alzheimers);

Nausea, dizziness, insomnia

55
Q

Memantine MOA

A

NMDA receptor antagonist

helps prevent excitotoxicity (mediated by Ca++)

56
Q

Memantine ADRs?

A

dizziness, confusion, hallucinations

57
Q

Huntington Disease Drugs?

A

Tetrabenazine and Reserpine: inhibit VMAT –> decr dopamine vesicle packaging/release (FA pg 505)

Haloperidol: D2 receptor antagonist

58
Q

Tx for ALS that modestly incr survival by decr glutamate excitotoxicity via an unclear mech?

A

Riluzole

“for Lou Gehring disease, give riLUzole”

59
Q

5-HT (1B/1D) agonists. Inhibit trigeminal n. activation; prevent vasoactive peptide release; induce vasoconstriction; Used for acute migraines/ cluster HA attacks?

A

Sumatriptan

60
Q

Sumatriptan: ADRs?

CIs?

A

Coronary vasospasm, mild paresthesia

CI in pts w/ CAD or Prinzmetal angina

61
Q

Parkinson Disease drugs?

A

Bromocriptine, Amantadine, Levodopa (w. carbidopa), Selegline (and COMT inhibitors), Antimuscarinics

62
Q

Antimuscarinic used in Tx of Parkinson Disease to curb excess cholinergic activity? effects?

A

Benzotropine- improves tremor and rigidity but has little effect on bradykinesia
(“Park your Benz”)

63
Q

Drugs used in Tx of Parkinson Disease that prevent dopamine breakdown?

A

Selegline (selectively inhibits MAO-B),

Tolcapone (inhibits central COMT)

64
Q

Drug used in Tx of Parkinson Disease to increase dopamine availability by incr release and decr reuptake?

Toxicity=?

A

Amantadine ;

Ataxia, livedo reticularis

65
Q

Drugs used in Tx of Parkinson Disease that prevent peripheral L-dopa degradation –> incr availability?

A

Levodopa, Tolcapone, Entacapone

66
Q

Drug used for muscle spasms (acute low back pain) by activating GABA(B) receptors at spinal cord level –> skeletal m. relaxation?

A

Baclofen

67
Q

Centrally acting skeletal m. relaxant used for muscle spasms?

A

Cyclobenzaprine

related to TCAs, similar anticholinergic ADRs

68
Q

Strong ACh receptor agonist –> sustained depol. and prevents m. contraction?

A

Succinylcholine (Depolarizing NM blocking drug)

69
Q

Nondepolarizing NM blocking drugs?

A

Tubocurarine, Atracurium, Mivacurium,
Pan-, Ve-, Ro- curonium
Competitive antagonists, compete w ACh for receptors

70
Q

Local anesthetics: Esters?

A

Procaine, Tetracaine, Cocaine, Benzocaine

71
Q

Local anesthetics: Amides?

A

Lidocaine, Mepivacaine, Bupivacaine

Amides have 2 i’s in name, esters have 1

72
Q

Local anesthetics: clinical use?

A

minor surgeries, spinal anesthesia

if allergic to esters give amides

73
Q

Local anesthetics: ADRs?

A

CNS excitation, HTN, hypoTN,
arrhythmias (cocaine),
severe CV toxicity (bupivacaine)

74
Q

Local anesthetics: order of nerve blockade

A

Small myelinated fibers>small unmyelinated fibers>Large myelinated fibers>Large unmyelinated fibers

Order of Loss: 1) pain, (2) temp, (3) touch, (4) pressure

75
Q

Local anesthetics: MOA?

A

Block Na+ channels

most effective in rapidly firing neurons

76
Q

Primidone is metabolized to ?

A

phenobarb

77
Q

Which two β-blockers are commonly prescribed for variceal bleeding?

A

Nadolol and propranolol

78
Q

Increased peripheral dopamine can cause N/V. Carbidopa attenuates this effect, how?

A

inhibits DOPA decarboxylase, thus reduces peripheral conversion of L-DOPA into dopamine

Step 1 Neurology (3 decks)

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