Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drugs > Neurology > Flashcards

Neurology Flashcards

1
Q

Epinephrine - alpha1

Brimonidine - alpha2

A

alpha agonists

MOA: decrease aqueous synthesis via vasoconstriction

Use: Glaucoma

Adv. effects:
 Mydriasis
 Blurry vision
 Ocular hyperemia
 Foreign body sensation
 Ocular allergic reactions
 Ocular pruritis

Do not use in close-angle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Timolol
Betaxolol
Carteolol

A

Beta blockers

MOA: decrease aqeous humor synthesis

Use: Glaucoma

Adv. effects:
No pupillary or vision changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acetazolamide

A

Diuretic

MOA: decrease aqueous humor synthesis via inhibition of of carbonic anhydrase

Use: Glaucoma

Adv. effects:
No pupillary or vision changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pilocarpine

Carbachol

A

Direct cholinomimetic (M3)

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

Use: Glaucoma
Pilocarpine used in emergencies (very effective at opening meshwork into canal of Schlemm)

Adv. effects:
Miosis
Cyclospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Physostigmine

Echothiophate

A

Indirect Cholinomimetic (M3)

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

Use: Glaucoma

Adv. effects:
Miosis
Cyclospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bimatoprost

Latanoprost (PGF2a)

A

Prostaglandins

MOA: increase outflow of aqueous humor

Use: Glaucoma

Adv. effects: darkens color of iris (browning), eyelash growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Opioid analgesics

Morphine
Fentanyl
Codeine
Loperamide
Methadone
Meperidine
Dextromethorphan
Diphenoxylate
Pentazocine
A

MOA:
Agonist at opioid receptors
Open K+ channels, close Ca2+ channels –> decrease synaptic transmission
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

Use:
Pain
Couch suppression (Dextromethorphan)
Diarrhea (Loperamide, Diphenoxylate)
Acute pulmonary edema
Maintenance programs for heroin addicts (methadone)

Adv. effects:
Addiction, respiratory depression, constipation, miosis (Except meperidine –> mydriasis), additive CNS depression with other drugs.
Tolerance does not develop to miosis and constipation
Treat toxicity with naloxone or naltrexone (antagonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pentazocine

A

MOA: k-opioid receptor agonist, u-opioid receptor antagonist

Use: Analgesia for mod. to severe pain

Adv. effects:
opioid withdrawal symptoms if patient also taking full opioid antagonist (compete for opioid receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Butorphanol

A

MOA:
k-opioid receptor agonist, u-opioid receptor partial agonist; produces analgesia

Use: Severe pain. Causes less resp. distress than full opioid agonists

Adv. effects:
opioid withdrawal symptoms if patient also taking full opioid agonist (compete for opioid receptors)
overdose not easily reversed with naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tramadol

A

MOA:
very weak opioid agonist
inhibits 5-HT and norepinephrine reuptake
works on many neurotransmitters (“tram it all”)

Use: Chronic pain

Adv. effects:
similar to opioids
decreases seizure threshold
serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ethosuximide

A

MOA: Blocks thalamic T-type Ca2+ channels

Use: first line for Absence seizures

Adv. effects:
Fatigue, GI distress, Headache, Itching (urticaria), and Stevens-Johnson syndrome

“Sucks to have Silent (absence) Seizures”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Benzodiazepines

diazepam, lorazepam, midazolam

A

MOA: Increase GABAa action

Use: first line for acute status epilepticus; eclampsia seizures

Adv. effects:
Sedation, tolerance, dependence, respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phenobarbital

A

MOA: Increase GABAa action

Use: Partial (focal) seizures, Tonic-Clonic seizures

First line in neonates

Adv. effects:
Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Phenytoin

Fosphenytoin

A

MOA: Blocks Na+ channels; zero order kinetics

Use:
first line for Tonic-Clonic seizures
first line for prophylaxis of status epilepticus
partial seizures

Adv. effects:
Neuro - nystagmus, diplopia, ataxia, sedation, peripheral neuropathy
Derm - hirsutism, Stevens-Johnson syndrome, gingival hyperplasia, DRESS syndrome.
MSK - osteopenia, SLE-like syndrome
Heme - megaloblastic anemia
Reproductive - teratogenesis (fetal hydantoin syndrome)
Other - cytochrome P-450 induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Carbamezapine

A

MOA: Blocks Na+ channels

Use:
first line for trigeminal neuralgia
first line for partial seizures
tonic-clonic seizures

Adv. effects:
Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P450, SIADH, Stevens-Johnson syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Valproic acid

A

MOA:
Increase Na+ channel inactivation
Increase GABA concentration by inhibiting GABA transaminase

Use:
first line for tonic-clonic seizures
absence seizures
partial seizures
myoclonic seizures, bipolar disorder, migraine prophylaxis

Adv. effects:
neural tube defects, hepatotoxicity (rare but fatal), GI distress, pancreatitis, tremor, weight gain

Contraindicated in pregnancy***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Vigabatrin

A

MOA: Increase GABA by irreversibly inhibiting GABA transaminase

Use: partial seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Gabapentin

A

MOA: Inhibits high-voltage-activated Ca2+ channels; GABA analog

Use:
peripheral neuropathy
postherpatic neuralgia
partial seizures

Adv. effects:
Sedation, ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Topiramate

A

MOA:
Blocks Na+ channels
Increase GABA action

Use:
partial seizures
tonic-clonic seizures
migraine prevention

Adv. effects:
Sedation, mental dulling, kidney stones, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Lamotrigine

A

MOA: Blocks voltage-gated Na+ channels

Use:
partial seizures
tonic-clonic seizures
absence seizures

Adv. effects:
Stevens-Johnson syndrome (must be titrated slowly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Levetiracetam

A

MOA: unknown; may modulate GABA and glutamate release

Use:
partial seizures
tonic-clonic seizures

22
Q

Tiagabine

A

MOA: Increase GABA by inhibiting reuptake

Use: partial seizures

23
Q

Barbiturates

phenobarbital, pentobarbital, thiopental, secobarbital

A

MOA: Increase DURATION of Cl- channel opening (facilitate GABAa action)
—-> decrease neuron firing

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

Adv. effects:
respiratory / cardio depression - can be fatal
CNS depression - can be exacerbated by alcohol
dependence
induces cytochrome P450

Contraindicated in porphyria

Overdose treatment is supportive

24
Q

Benzodiazepines

diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam

A

MOA:
Increase FREQUENCY of Cl- channel opening (facilitate GABAa action)
Decrease REM sleep

Long half lives and active metabolites - except Alprazolam, Triazolam, Oxazepam, Midazolam (short acting —> higher addictive potential)

Use:
Anxiety (sedative)
Spasticity
Status epilepticus (lorazepam, diazepam)
Eclampsia
Detoxification (esp. alcohol withdrawal - DTs)
Night terrors, sleepwalking
General anesthetic (amnesia, muscle relaxation)
Hypnotic (insomnia)

Adv. effects: d
dependence
additive CNS depression w/ alcohol
less risk of resp. depression and coma than w/ barbiturates

Treat overdose with flumazenil (competitive antagonist)
- can precipitate seizures by causing acute benzo withdrawal

25
Q

Hypnotics

Zolpidem, Zaleplon, Eszopiclone

A

MOA: act via BZ1 subtype of GABA receptor

Use: Insomnia

Avd. effects:
ataxia, headaches, confusion
modest day-after psychomotor depression and few amnestic effects
less dependence risk than benzodiazepines
sleep cycle less affected than with benzo

Effects reversed by flumazenil

26
Q

Nitrous oxide (N2O)

A

inhaled anesthetic

low blood and lipid solubility —–> fast induction and low potency

27
Q

Halothane

A

inhaled anesthetic

high lipid and blood solubility ——> high potency and slow induction

28
Q

Inhaled anesthetics

Desflurane, Halothane, Enflurane, Isoflurane, Sevoflurane, Methoxyflurane, N2O

A

MOA: unknown

Effects:
Myocardial depression
Respiratory depression
Nausea / Emesis
Increase cerebral blood flow (decrease cerebral metabolic demand)
Adv. effects:
Hepatotoxicity (Halothane)
Nephrotoxicity (Methoxyflurane)
Proconvulsant (Enflurane)
Expansion of trapped gas in a body cavity (N2O)
Malignant hyperthermia
29
Q

Malignant hyperthermia

A

life threatening

Inhaled anesthetics or succinylcholine induce fever and severe muscle contractions

Susceptibility can be inherited as AD w/ variable penetrance.
Mutations in voltage-sensitive ryanodine receptor cause increase Ca2+ release from sarcoplasmic reticulum.

Treatment: Dantrolene (ryanodine receptor antagonist)

30
Q

Barbiturates (Thiopental)

A

Intravenous anesthetic
High potency, high lipid solubility, rapid entry into brain
Used for induction of anesthesia and short surgical procedures
Effect terminated by rapid distribution into tissue and fat
Decrease cerebral blood flow

31
Q

Benzodiazepines (Midazolam)

A

Intravenous anesthetic
Used for endoscopy
Used adjunctively w/ gaseous anesthetics and narcotics
May cause severe postoperative respiratory depression, decrease BP (treat overdose w/ flumazenil), anterograde amnesia

32
Q

Arylcyclohexylamines (Ketamine)

A

Intravenous anesthetic
PCP analogs that act as dissociative anesthetics
Block NMDA receptors
Cardiovascular stimulants
Cause disorientation, hallucination, bad dreams
Increase cerebral blood flow

33
Q

Propofol

A

Intravenous anesthetic
Used for sedation in ICU, rapid anesthesia induction, short procedures
Less postoperative nausea than thiopental
Potentiates GABAa

34
Q

Opioids

A

Intravenous anesthetic

Morphine, fentanyl used with other CNS depressants during general anesthesia

35
Q

Local anesthetics

Esters (Procaine, Cocaine, Tetracaine, Benzocaine)
Amides (Lidocaine, Mepivacaine, Bupivacaine) - 2 I’s in amides

A

MOA:
Block Na+ channels (bind inner portion of channel)
Most effective in rapidly firing neurons.

Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

Can be given with vasoconstrictors (like epinephrine) to enhance local action - decrease bleeding, increase anesthesia by decreasing systemic concentration.

In infected tissue - alkaline anesthetics are charged and cannot penetrate membrane effectively –> need more anesthetic

Order of nerve blockade:
small-diameter fibers > large diameter fibers
Myelinated fibers > unmyelinated fibers
small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers

Order of loss: pain, temperature, touch, pressure

Use:
Minor surgical procedures, spinal anesthesia
If allergic to esters, give amides

Adv. effects: 
CNS excitation
Severe cardiovascular toxicity (bupivacaine)
Hypertension
Hypotension
Arrythmias (cocaine)
Methemoglobinemia (benzocaine)
36
Q

Depolarizing neuromuscular blocking drugs

Succinylcholine

A

Strong ACh receptor agonist

Produces sustained depolarization and prevents muscle contraction

Reversal of blockade:
Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors
Phase II (repolarized but blocked; ACh receptors are available, but desensitized) - may be reversed with cholinesterase inhibitors

Use:
Muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

Complications include hypercalcemia, hyperkalemia, malignant hyperthermia

37
Q

Nondepolarizing neuromuscular blocking drugs

A

Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium - Competitive antagonists - compete with ACh for receptors

Reversal of blockade - neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

38
Q

Dantrolene

A

MOA:
prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor

Use:
Malignant hyperthermia
Neuroleptic malignant syndrome (toxicity of antipsychotic drugs)

39
Q

Baclofen

A

MOA:
Activates GABAb receptors at spinal cord level, including skeletal muscle relaxation

Use:
Muscle spasms (ex. acute low back pain)
40
Q

Cyclobenzapine

A

MOA:
Centrally acting skeletal muscle relaxant
Structurally related to TCA, similar anticholinergic side effects

Use: Muscle spasms

41
Q

Bromocriptine

A

Ergot

Dopamine agonist

Parkinson drug

42
Q

Pramipexole, Ropinirole

A

Non ergot

Dopamine agonist

Parkinson drug

43
Q

Amantadine

A

Increase dopamine release
Decrease dopamine reuptake

Toxicity = ataxia, livedo reticularis

Use: Parkinson

44
Q

L-dopa (levodopa)/carbidopa

A 
MOA:
Increase level of dopamine in brain
Prevent peripheral (pre-BBB) L-dopa degradation --> Increased L-DOPA entering CNS --> Increased L-DOPA available for conversion to dopamine 
Carbidopa blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase; also reduces side effects of peripheral L-dopa conversion into dopamine (nausea, vomiting)

Use: Parkinson

45
Q

Entacapone. Tolcapone

A

Act centrally (post-BBB) to inhibit breakdown of dopamine

MOA:
Prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT
Tolcapone works centrally to block conversion of dopamine to 3-OMD by inhibiting central COMT

Use: Parkinson

46
Q

Selegiline, Rasagiline

A

Act centrally (post-BBB) to inhibit breakdown of dopamine

MOA: Blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B.

Use: Parkinson

47
Q

Memantine

A

MOA:
NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

Adv. effects:
Dizziness, Confusion, Hallucinations

Use: Alzheimer’s

48
Q

Donepezil, Galantamine, Rivastigmine, Tacrine

A

MOA: AChE inhibitors

Adv. effects:
Nausea, dizziness, insomnia

Use: Alzheimer’s

49
Q

Tetrabenazine, Respirine

A

MOA:
Inhibit vesicular monoamine transport (VMAT) –> decrease dopamine vesicle packaging and release

Use: Huntington’s

50
Q

Haloperidol

A

D2 receptor agonist

Use: Huntington’s

51
Q

Riluzole

A

Treatment for ALS that modestly increase survival by decreasing glutamate excitotoxicity via an unclear mech.

“For Lou Gehrig disease, give riLOUzole”

52
Q

Triptans

A 
MOA: 
5HT 1B/1D agonists
Inhibit trigeminal nerve activation
Prevent vasoactive peptide release
Induce vasoconstriction

Use:
Acute migraine
Cluster headache attacks

Adv. effects:
Coronary vasospasm
Mild paresthesia

Contraindicated in patients with CAD or Prinzmetal angina

Drugs (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions