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USLME Pharmacology > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

1
Q

Glaucoma is due to increased intraocular pressure and drugs are aimed at decreasing this pressure either inhibiting aqueous humor synthesis or stimulating its drainage. List the mechanism of action of a-agonists like epinephrine (a1) and brimonidine (a2) on glaucoma and side effects if any.

A

epinephrine decreases aqueous humor synthesis via vasoconstriction.

brimonidine also decreases aqueous humor synthesis

side effects for epinephrine: mydriasis (a1) therefore do not use in closed-angle glaucoma.

side effects of brimonidine are blurry vision, ocular hyperemia, foreign body sensation, ocular allergic rxn, ocular pruritis.

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2
Q

Glaucoma is due to increased intraocular pressure and drugs are aimed at decreasing this pressure either inhibiting aqueous humor synthesis or stimulating its drainage. What do beta blockers like timolol, betaxolol, and carteolol do?

A

timolol, betaxolol, carteolol decrease aqueous humor synthesis

no pupillary or vision changes.

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3
Q

Glaucoma is due to increased intraocular pressure and drugs are aimed at decreasing this pressure either inhibiting aqueous humor synthesis or stimulating its drainage. What does acetazolamide do?

A

acetazolomide is a carbonic anhydrase inhibitor that decreases reabsorption of HCO3- alkalinizing the urine and creating a metabolic acidosis state.

In the eyes, acetazolomide decreases aqueous humor synthesis via inhibition of carbonic anhydrase.

No pupillary or vision changes

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4
Q

Glaucoma is due to increased intraocular pressure and drugs are aimed at decreasing this pressure either inhibiting aqueous humor synthesis or stimulating its drainage. What who direct cholinomimetics do (pilocarpine, carbachol) and indirect cholinomimetics (physostigmine, echothiopate)

A

Pilocarpine, carbachol, physostigmine, and echothiopate will contract ciliary muscle and open trabecular meshwork to increase outflow of aqueous humor.

side effects: miosis and cyclospasm due to contraction of ciliary muscle (no accomodation)

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5
Q

Which drug do you use in emergent glaucoma situation?

A

pilocarpine b/c very effective at opening meshwork into canal of schlemm

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6
Q

Glaucoma is due to increased intraocular pressure and drugs are aimed at decreasing this pressure either inhibiting aqueous humor synthesis or stimulating its drainage.How is latanoprost used for glaucoma?

A

Latanoprost is a PGF2alpha (prostaglandin) that increases outflow of aqueous humor.

A side effect is it darkens color of iris (browning)

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7
Q

List the 9 opioid analgesics

A
  • morphine
  • fentanyl
  • codeine
  • loperamide
  • methadone
  • meperidine
  • dextromethorphan
  • diphenoxylate
  • pentazocine
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8
Q

How do opioids work?

A

act as agonists at opioid receptors (m = morphine, delta = enkephalin, k = dynorphin) to modulate synaptic transmission

  • open K+ channels
  • close Ca+ channels
  • decrease synaptic transmission
  • inhibit release of ACh, NE, 5-HT, glutamate, substance P
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9
Q

What are the clinical uses of opioids?

A

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

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10
Q

What are some side effects of opioids?

A 
addiction
resp depression
constipation
miosis (pinpoint pupils)
additive CNS depression w/ other drugs

*toxicity treated with naloxone/naltrexone

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11
Q

Which 2 side effects of opioids that the patients will not develop tolerance to?

A

tolerance does not develop to miosis and constipation.

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12
Q

What is butorphanol? What is it used for? toxicity?

A

Butorphanol is a k-opioid receptor agonist and m-opiod receptor partial agonist; produces analgesia used for severe pain (e.g. migraine, labor). IT causes less resp depression that full opioid analgesics

Toxicity: can cause opioid withdrawal symptoms if pts is also taking full opioid agonist (competitive for opioid receptors)
*overdose is not as easily reversed with naloxone

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13
Q

What is tramadol? What is it used for? Side effects?

A

Tramadol is a VERY WEAK opioid agonist that also inhibits 5-HT and NE reuptake (works on multiple NTs).

Tramadol is used for chronic pain.

Side effects are similar to other opioids, but more likelihood of seizures and potential for 5-HT syndrome.

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14
Q

What is the DOC for absence seizures? Explain moa and side effects

A

Ethosuximide is DOC for absence seizures. It blocks thalamic T-type Ca2+ channels.

Side effects (EFGHIJ): Ethosuximide causes Fatigue, GI distress, Headache, Itching, stevens-Johnson syndrome

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15
Q

What’s the first line treatment for someone with acute status epilepticus? What drug is often given after?

A

IV benzos (diazepam) followed by phenytoin

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16
Q

What’s the first line drug for partial seizures either simple or complex and for trigeminal neuralgia? List side effects

A

carbamazepine that increases Na+ channel inactivation.

Side effects: diplopia, ataxia, BLOOD DYSCRASIAS (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of P-450, SIADH, Stevens Johnson syndrome

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17
Q

List the 3 drugs that can be used for tonic-clonic generalized seizures?

A
  • phenytoin
  • carbamazepine
  • valproic acid

All increase Na+ channel inactivation. Valproic acid also increases GABA concentration by inhibiting GABA transaminase

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18
Q

List the side effects of phenytoin.

A

Phenytoin is an antiepileptic that is 1st line for ppx of status epilepticus and also for tonic-clonic seizures.

Side effects: nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia (b/c BLOCKS ABSORPTION OF FOLATE), teratogenesis –> fetal hydantoin syndrome, SLE-like syndrome, induction of CYP450, LAD, steven johnson, osteopenia

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19
Q

Valproic acid increases Na+ channel inactivation and increases GABA by inhibiting GABA transaminase is used for absence seizures, tonic clonic and partial seizures, as well as for mycolonic seizures and bipolar disorder What are some side effects?

A
  • GI distress
  • fatal hepatotoxicity (measure LFTs)
  • neural tube defects/contraindicated in pregnancy
  • tremor
  • weight gain
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20
Q

Gabapentin can be used for partial seizures and for peripheral neuropathy and postherpetic neuragia. It primarily inhibits voltage-activated Ca2+ channels; designed as GABA analog. What are 2 main side effects

A
  • sedation

- ataxia

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21
Q

Phenobarbital increases duration of Cl- channel opening to increase GABA-A action. It can lead to sedation, tolerance, induction of cytochrome P450, cardiresp depression. It is 1st line for seizures in what pop?

A

neonates and pregnant women.

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22
Q

Topiramate blocks Na+ channels, and increases GABA action can be used for MIGRAINE prevention and for partial and tonic clonic seizures. What are some side effects?

A
  • sedation
  • mental dulling
  • KIDNEY STONES
  • weight loss
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23
Q

Lamotrigine is one of 3 options of absence seizures (not first line though b/c ethosuximide is; the other is valproic acid) works by blocking voltage-gated Na+ channels. It can also be used for partial and tonic clonic seiures. It must be titrated slowly to prevent?

A

Steven johnson syndrome

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24
Q

Levetiracetam is an anti-epileptic with unknown mech although it’s believed that it may? It’s not used first-line but can be used for partial and tonic clonic seizures.

A

modulate GABA and glutamate release

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25
Q

Tiagabine is not first-line, but is used for partial seizures. What is its mech of action?

A

Tiagabine increases GABA by inhibiting reuptake

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26
Q

Vigabatrin is used for partial seizures. What is mech of action?

A

Increases GABA by irreversibly inhibiting GABA transaminase

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27
Q

List the 3 drugs used for absence seizures and their MOA, which is first line?

A
  • ethosuximide: blocks thalamic T-type Ca2+ channels ***first-line
  • valproic acid: increases inactivation of Na+ channels; increases GABA concentration by inhibiting GABA transaminase
  • lamotrigine: blocks voltage-gated Na+ channels
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28
Q

List the 4 barbiturates.

A
  • phenobarbital
  • pentobarbital
  • thiopental
  • secobarbital
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29
Q

What’s the MOA of barbiturates

A

facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuronal firing

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30
Q

Barbiturates are contraindicated in what medical condition

A

porphyria

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31
Q

What are the clinical uses and toxicity assoc with barbiturates?

A

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

toxicity: respiratory and cardio depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cyp450)

overdose treatment is supportive

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32
Q

List the benzodiazpines and separate them into long-acting and short-acting. What’s the significance of it being long or short acting?

A

Long half-lives: diazepam, lorazepam, temazepam, chlordiazepoxide

Short half-lives: alprazolam, triazolam, oxazepam, midazolam

shorter acting = higher addictive potential
longer acting = for alcohol withdrawal

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33
Q

What’s the mech of action of benzos?

A

facilitate GABA-A action by increasing frequency of Cl- channel openings.

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34
Q

What’s the effect of benzos on REM sleep?

A

decrease REM sleep

35
Q

What are the clinical uses of benzos?

A

clinical uses: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detox (esp. alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

36
Q

List side effects assoc with benzos and how to treat?

A

dependence, additive CNS depression effects with alcohol. Less risk of resp depression and coma than with barbs.

Treat overdose with flumazenil (competitive antagonist at GABA benzo receptor)

37
Q

List the 3 nonbenzo hypnotics

A
  • zolpidem
  • zaleplon
  • eszopiclone
38
Q

List the mech of action of nonbenzo hypnotics (zolpidem, zaleplon, eszopiclone). What is it used for?

A

Zolpidem, Zaleplon, Eszopiclone act via the BZ1 subtype of the GABA receptor used for Insomnia.

39
Q

Flumazenil can reverse benzo overdose Can it reverse the nonbenzo hypnotics (zolpidem, zaleplon, escopiclone)?

A

Flumazenil can also reverse nonbenzo hynotics b/c they act via BZ-1 subtype of the GABA receptors.

40
Q

What are the side effects of nonbenzo hypnotics (zolpidem, zaleplon, escopiclone)?

A
  • ataxia, headache, confusion
  • short duration of action b/c of rapid metabolism by liver enzymes
  • only modest psychomotor depression and few amnestic effects
41
Q

List the anti-epileptic drugs that can cause steven-johnson syndrome

A
  • phenytoin -increases Na+ channel inactivation
  • lamotrigine -blocks Na+ channel
  • ethosuximide -blocks thalamic T-type Ca2+ channels
  • carbamazepine -increases Na+ channel inactivation
42
Q

What must CNS drugs be to have CNS effects?

A

1) lipid soluble so can cross BBB

2) actively transported

43
Q

In terms of anesthetics, drugs that have decrease solubility in blood have slower or faster induction and recovery times? How does that relate to blood:gas partition coefficient.

A

decrease solubility in blood = faster induction and faster recovery times

lower blood:gas partition means decrease solubility in blood and more in gas form = faster induction and faster recovery times

44
Q

How can one assess anesthetic’s solubility in blood in terms of partial pressure?

A

anesthetic that has decreased solubility in blood (faster induction and recovery time) will saturate faster leading to fast rise in partial pressure.

45
Q

How does one evaluate potency of anesthetics?

A

Drugs with increase solubility in lipids have greater potency.

Potency = 1/MAC
MAC = minimum concentration to prevent 50% of subjects from moving in response to noxious stimuli  (lower this concentration is, stronger the anesthetic)
46
Q

N2O has low blood and lipid solubility. Comment on potency and onset time and recovery time.

A

low blood solubility = faster onset time and faster recovery
low lipid solubility = lower potency = more concentration is needed to prevent reaction to noxious stimuli in 50% of pop.

47
Q

List the 7 inhaled anesthetics. Inhaled anesthetics mechanism is unknown. What are some effects of inhaled anesthetics.

A
  • halothane
  • enflurane
  • isoflurane
  • sevoflurane
  • methoxyflurane
  • N2O
  • desflurane

*cause mycocardial depression, resp depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand)

48
Q

List the 7 inhaled anesthetics and their specific side effects if any.

A
  • halothane: hepatotoxicity
  • enflurane: pro-convulsant (seizures are self-limited)
  • isoflurane
  • sevoflurane
  • methoxyflurane: nephrotoxicity
  • N2O: expansion of trapped gas in a body cavity
  • desflurane: airway irritability
49
Q

All inhaled anesthetics except N2O can cause malignant hyperthermia What is it? And chances of getting it are increased when used with? Treatment?

A

Malignant hyperthermia: rare, life-threatening hereditary condition (A/D of skeletal muscles due to ryanodine receptor-mediated increase in free Ca2+) in which inhaled anesthetics (esp. halothane) w/ succinylcholine can induce fever and severe muscle contractions.

Treatment: dantrolene: inhibits ryanodine receptor Ca2+ release channels –> decrease extracellular Ca2+ –> improves muscle rigidity.

50
Q

List the 5 groups of IV anesthetics.

A
  • barbiturates (thiopental)
  • benzodiazepam (midazolam)
  • arylcyclohexylamines (ketamine)
  • opioids
  • propofol
51
Q

Of inhaled anesthetics, compare potency and induction time of halothane and enflurane.

A

Enflurance is less potent (less lipid soluble) but produces more rapid induction than halothane so it is also less blood soluble)

52
Q

In IV anesthetics, thiopental is high potency/high lipophilicity, rapid entry into brain. What is it used for? How are its effects terminated? What is its effect on cerebral blood flow?

A

Thiopental is used for induction of anesthesia and SHORT surgical procedures.

Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat.

It decreases cerebral blood flow.

53
Q

What’s the most common iv anesthetic used for endoscopy? What is it used with? Side effects? Treatment of side effects?

A

Midazolam (benzo) is used for endoscopy w/ gaseous anesthetics and narcotics; may cause severe postop respiratory depression, hypotension, and anterograde amnesia.

Treat with flumanzenil

54
Q

How are arylcyclohexylamines (ketamine) used as iv anesthetics? What does it do to cerebral blood flow?

A

PCP analogs that act as dissociative anesthetics that block NMDA receptors. Cardiovascular stimulants. Can cause disorientation, hallucinations, bad dreams, increase cerebral blood flow.

55
Q

When are opioids used as iv anesthetics?

A

morphine, fentanyl used with other CNS depressants during general anesthesia.

56
Q

How is propofol used as an iv anesthetic?

A

used for sedation in ICU
rapid anesthesia induction, short procedures
less postop nausea than thiopental
potentiates GABA-A

57
Q

Inhaled anesthetics (e.g. halothane, enflurane), IV anesthetics (propofol, fentanyl, midazolam), and local anesthetics. There are 2 groups. List them in their respective groups

A

esters (1 i): procaine, cocaine, tetracaine

amides: (2 i’s): lidocaine, mepivacaine, bupivacaine

58
Q

What is the MOA of local anesthetics (both esters and amides)

A
  • block Na+ channels by binding to specific receptors on INNER portion of channel.
  • preferentially bind to activated Na+ channels so most effective in rapidly firing neurons
59
Q

Local anesthetics can be given with vasoconstrictors (usu. epinephrine) to?

A

enhance local action = decrease bleeding, increase anesthesia by decreasing systemic concentration

60
Q

If someone with an infected tissue needs local anesthetics, will you need to increase or decrease dose? Why?

A

Infected tissue is acidic. Alkaline anesthetics are charged and cannot penetrate membrane effectively so will need more anesthetic

61
Q

Explain the order of nerve blockade when giving local anesthetics

A

size matters most (small > large) then myelination (myelinated > unmyelinated)

nerve blockade will occur first in small myelinated > small unmyelinated > large myelinated > large unmyelinated

62
Q

List the order of loss (pressure, temp, touch, pain) when given a local anesthetic

A

lose pain first!

Pain –> temperature –> touch –> pressure

63
Q

What are some toxicities associated w/ local anesthetic use? Be specific if possible.

A 
CNS excitation
severe cardiovascular toxicity (bupivacaine
HTN/hypotension
arrhytmias (cocaine)
methemoglobinemia (benzocaine)
64
Q

Which local anesthetic can cause methemoglobinemia?

A

benzocaine

65
Q

Which local anesthetic can cause severe cardiovascular toxicity?

A

bupivacaine

66
Q

When are local anesthetics used?

A

minor surgical procedures

spinal anesthesia

67
Q

Neuromuscular blocking drugs are needed to create muscle paralysis in surgery or mechanical ventilation. These drugs are selective for motor nicotinic receptors. List the one depolarizing agent, and its mech of action. Explain how blockade can be reversed.

A

succinylcholine -strong ACh receptor agonist that produces sustained depolarization and prevents muscle contraction

reversal of blockade:

  • phase 1 (prolonged depolarization): NO ANTIDOTE; do train of 4 responses, will see that the lines are even (pg 499)
  • phase 2 (repolarized but blocked; Ach receptors are available but desensitized): antidote is achase inhibitors (like physostigmine/neostigmine), will see changes on train of 4 responses with ticks going down.
68
Q

What are some side effects of succinylcholine. List 3.

A
  • hypercalcemia
  • hyperkalemia
  • malignant hyperthermia (esp when given with inhaled anesthetics to someone with the disorder)
69
Q

Neuromuscular blocking drugs are needed to create muscle paralysis in surgery or mechanical ventilation. These drugs are selective for motor nicotinic receptors. List the 6 nondepolarizing ones and the mech of action. How can you reverse the blockade?

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium = competitive antagonists that compete with ACh for receptors.

Can give neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium and other cholinesterase inhibitors.

70
Q

What’s the mech of action of dantrolene? Clinical uses?

A

MOA: prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle used for malignant hyperthermia, neuroleptic malignant syndrome

71
Q

What is baclofen? What is it used for?

A

Baclofen is a GABA-B agonist at spinal cord level to induce skeletal muscle relaxation used in muscle spasms (acute LBP)

72
Q

What is cyclobenzaprine? What is it used for? It’s similar in structure to what other drug which explains a lot of its side effects?

A

centrally acting skeletal muscle relaxant used for muscle spasms. It’s structurally related to TCAs so has similar anti-cholinergic side effects

73
Q

Parkinsons is due to loss of dopaminergic neurons and excess cholinergic activity characterized by essential tremors, rigidity, bradykinesia, postural instability, and shuffling gait. There are 5 different strategies to treat parkinson’s. List them broadly.

A
  1. dopamine agonists
  2. increase dopamine availability
  3. increase L-DOPA availability
  4. prevent dopamine breakdown
  5. curb excess cholinergic activity (2nd line b/c can improve tremors but not rigidity or bradykinesia)

think BALSA

  • bromocriptine -dopamine agonist
  • amantadine -increase dopamine availability
  • Levodopa w/ carbidopa to increase L-DOPA
  • Selegiline to prevent DA breakdown as MAO-B inhibitor
  • anticholinergics
74
Q

Of the dopamine agonists to treat parkinsonins, there is an ergot and a non-ergot group. List the drugs within and state which is preferred.

A

ergot - bromocriptine

non-ergot (preferred) -pramipexole, ropinirole

75
Q

Amantadine can be used to increase dopamine availability in the treatment of parkinsons by increasing dopamine release and decreasing dopamine reuptake. It is also used as an antiviral against influenza but not often used due to resistance. What are 2 toxities assoc with amantadine?

A
  • ataxia

- livedo reticularis (mottled skin with lace-like purplish appearance)

76
Q

How can levodopa/carbidopa increase L-DOPA availability in the treatment of parkinsons? What are side effects?

A
  • unlike dopamine, levodopa (l-dopa) can cross BBB and is converted by dopa decarboxylase in the CNS to dopamine
  • carbidopa is a peripheral DOPA decarboxylase inhibitor is given w/ L-dopa to increase bioavailability of L-dopa in the brain and to limit peripheral side effects.

side effects: arrhythmias from increase peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon: phases of immobility and incapacity associated with depression alternate with jubilant thaws), akinesia btw doses

77
Q

What are entacapone and tolcapone?

A

they can increase L-dopa availability in treatment of parkinsons by preventing peripheral L-dopa degradation to 3-O-methyldopa by inhibiting COMT.

78
Q

List the 2 drugs that can prevent dopamine breakdown centrally (post-BBB).

A
  • selegiline -blocks conversion of dopamine into DOPAC

- tolcapone -blocks conversion of dopamine to 3-methoxytyramine

79
Q

What’s the anti-muscarinic used to curb excess cholinergic activity in someone with parkinsons?

A

benztropine -antimuscarinic that improves tremor, but has little effect on bradykinesia and rigidity.

80
Q

How can memantine help with alzheimer’s disease? What are some side effects?

A

Memantine is a NMDA receptor antagonist that helps prevent excitotoxicity (mediated by Ca2+)

Side effects: dizziness, confusion, hallucinations

81
Q

Donepezil, galantamine, rivastigmine, tacrine can be used to treat Alzheimer’s disease. What is their mech o action? Side effects?

A

MOA: AChE inhibitors
Toxicity: Nausea, dizziness, insomnia

82
Q

Huntington disease is a trinucleuotide repeat (CAG) that affects the caudate. There will be decreased GABA, decreased ACh, increased dopamine. List some treatments.

A
  • tetrabenzine and reserpine: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
  • haloperidol: anti-psychotic -D2 receptor antagonist
83
Q

Sumatriptan is a 5-HT1B/1D agonist that inhibits trigeminal nerve activation, prevent vasoactive peptide release and induce vasoconstriction. What are the 2 uses of sumatriptain? Toxicity? COntraindications

A

used for acute migraines, cluster headache attacks

-toxicity: coronary vasopasm so contraindicated in patients with CAD or Prinzmetal angina), mild paresthesia

USLME Pharmacology (15 decks)

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