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Pharm-CNS Flashcards

1
Q

What is the purpose of glaucoma drugs/how do they accomplish them?

A

Decr. IOP by decr. amount of aqueous humor (inhibit synth/secretion or incr. drainage)

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2
Q

What type of drug is epinephrine when used for glaucoma? Mechanism? Side effects? CIs?

A

alpha 1 agonist

Decr. aqueous humor secretion by vasoconstriction

Mydriasis; don’t use in closed angle glaucoma

Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, cular pruritus

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3
Q

What type of drug is brimonidine? mechanism? Side effects?

A

alpha 2 agonist

Decr. aq. humor synth

lurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, cular pruritus

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4
Q

What type drug are timolol (1), betaxolol (2), and carteolol (3)? What is their mechanism in treating glaucoma? Sx?

A

Beta blockers (3)

decr. aque humor synth

No pupillary or vision changes

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5
Q

What kind of drug is acetazolamide? What is its mech. in treating glaucoma? Sx?

A

Diuretic

Decr. aq humor synth via inhibition of carb. anhydrase

No pupillary or vision changes

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6
Q

What kind of drugs are pilocarpine (1) and carbachol (2)? What is their mech of treating glaucoma? Sx? Which should be used in emergencies? Why?

A

Direct cholinomimetics (2)

Incr. outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular mesh

Miosis and cyclospasm

Use 1 in emergencies-very effective at opening meshwork into canal of schlemm

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7
Q

What kind of drugs are physostigmine and echothiophate? What is their mech in treating glauc? Sx?

A

InDirect cholinomimetics (2)

Incr. outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular mesh

Miosis and cyclospasm

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8
Q

What kind of drug is latanoprost? Mech of treating glauc? Sx?

A

Prostaglandin (PGF2alpha)

Incr. outflow of aq humr

Darkens color of iris (browning)

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9
Q

What kind of drugs are dextromethorpan (1), loperamide/diphenoxylate (2), methadone/buprenorphine + naloxone (3), morphine, fentanyl, codein, meperidine, pentazocine? What is their mechanism? What is their clinical use overall? Of 1? 2? 3? What is their toxicity? How is toxicity treated? Mech? Which sx does tolerance develop to?

A

Opioid analgesics (11)

Agonists at opioid receptors (mu=morphine, delta=enkephalin, kappa=dynorphin) to modulate synaptic transmission (open k+ channels, close Ca channels) leading to decr. synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, and substance P

1=cough suppresion (1)
2=diarrhea (2)
3=maintenance programs for heroin addicts (3)

pain, acute PE

Addiction, resp. depression, constipation, miosis, additive CNS depression w/ other drugs.

Tolerance does not develop to constipation and miosis

Naloxone or naltrexone (opiod receptor antag)

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10
Q

What is the mechanism f butorphanol? Clinical use? Why is it beneficial compared to peers? Toxicity?

A

Kappa opioid receptor agonist and mu opioid receptor partial agonist; produces analgesia

Severe pain (migraine/labor).

Causes less resp. depression than full agonist

Can cause opioid withdrawal symptoms if pt. is also taking full agonist
Overdose not easily reversed w/ naloxone

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11
Q

What is the mechanism of tramadol? Clinical use? Toxicity?

A

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

Chronic pain

Similar to opioids. Decreases seizure threshhold. Serotonin syndrome.

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12
Q

What is the mechanism of ethosuximide? Which seizures is it used to treat? Sides effects?

A

Blocks thalamic T type Ca channels

Absence (first line)

EFGHIJ

Ethosuximide
Fatigue
GI Distress
Headache
Itching (urticaria)
Stevens-Johnson syndrome
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13
Q

What seizures are benzos used to treat? What is their mechanism? Side effects?

A 
Status epilepticus (acute 1st line)
Eclampsia

Incr. GABA-A action

Sedation, tolerance, dependence, resp. depression

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14
Q

What seizures is phenytoin used to treat? What is their mechanism? Side effects?

A

Simple, complex, tonic clonic (first line), status epilepticus (prophylaxis first line)

Incr. Na channel inactivation; zero order kinetics

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, periph neuro, megaloblastic anemia, teratogenesis, SLE like syndrome, induction of cytochrome p450, SIADH, SJS

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15
Q

What seizures is carbamazepine used to treat? What is their mechanism? Side effects?

A

Simple, complex, tonic clonic (all first line)
1st line for trigeminal neuralgia

Incr. Na channel inactivation

Diplopia, ataxia, blood dyscrasias, liver toxicity, teratogenesis, induction of p450, SIADH, SJS

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16
Q

What seizures is valproic acid used to treat? What is their mechanism? Side effects?

A

Simple, complex, tonic clonic (first line), absence, myoclonic seizures, BPD

Incr. na channel inactivation
Incr. GABA conc. by inhibiting GABA transaminase

GI, distress, rare but fatal hepatotoxicity, neural tube defects, tremor, weight gain, CI in pregnancy

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17
Q

What seizures are gabapentin used to treat? What is their mechanism? Side effects?

A

Simple, complex
periph neuro
postherpetic neuralgia

Primarily inhibits high voltage gated Ca channels: GABA analog

Sedation, ataxia

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18
Q

What seizures is phenobarbital used to treat? What is their mechanism? Side effects?

A

Simple, complex, tonic clonic
1st line in neonates

Incr. GABA-A action

Sedation, tolerance, dependence, induction of P450, cardioresp depress

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19
Q

What seizures is topiramate used to treat? What is their mechanism? Side effects?

A

simple, complex, tonic clonic
Migraine prevention

Blocks Na channels
Incr. GABA action

Sedation, mental dulling, kidney stones, weight loss

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20
Q

What seizures is lamotrigine used to treat? What is their mechanism? Side effects?

A

Simple, complex, tonic clonic, absence

Blocks voltage gated Na channels

SJS

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21
Q

What seizures is levetiracetam used to treat? What is their mechanism?

A

simple, complex, tonic clonic

unknown; may modulate GABA and glutamate release

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22
Q

What seizures is tiagabine used to treat? What is their mechanism?

A

simple, complex

Iincr. GABA by inhibit uptake

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23
Q

What seizures is vigabatrin used to treat? What is their mechanism?

A

simple, complex

Incr. GABA by irreversibly inhib GABA transaminase

24
Q

What is SJS?

A

Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital)

Skin lesions progress to epidermal necrosis and sloughing

25
Q

What drug is first line for simple seizures? complex? Tonic clonic? Absence? Status epilepticus acute? SE prophylaxis? Trigeminal neuralgia? In neonates?

A 
Simple=carbamazepine
complex=carbamazepine
tonic clonic=phenytoin, carbamazepine, valproic acid
absence=ethosuximide
Status Epilepticus acute=benzos
SE proph=phenytoin
26
Q

What type of drug are phenobarbital, pentobarbital, thiopental (1), and secobarbital? Mechanism? Clinical use? For 1 only? Toxicity? CI?

A

Barbituates (4)

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

Sedative for anxiety, seizures, insomnia, induction of anesthesia (1)

Resp. and CV depression
CNS depression (worse with alcohol)
Dependence
Induces P450
Overdose treatment is support

Not in porphyria

27
Q

What type of drugs are diazepam (1), lorazepam (2), temazepam, chlordiazepoxide? Mechanism? Clinical use? Of 1/2? Toxicity? Treatment for overdose?

A

Long acting benzos=less abuse potential

Facilitate GABA-A action by incr. freq. of Cl- opening.
Decr. REM sleep

Anxiety, spasticity, Status epilepticus (1/2), detoxification (DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relax), hypnotic (insomnia)

Dependence, additive CNS depression effects with alcohol, less risk of resp depression than with barbituates.

Flumazenil for overdose (comp antag)

28
Q

What kind of drug are alprazolam, triazolam, oxazepam, and midazolam? mechanism? Clinical use? Sx? Treatment for overdose?

A

short acting benzos=less abuse potential

Facilitate GABA-A action by incr. freq. of Cl- opening.
Decr. REM sleep

Anxiety, spasticity, detoxification (DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relax), hypnotic (insomnia)

Dependence, additive CNS depression effects with alcohol, less risk of resp depression than with barbituates.

Flumazenil for overdose (comp antag)

29
Q

What kind of drugs are zolpidem, zaleplon, and eszopiclone? Mechanism? Clinical use? Toxicity?

A

All ZZZs put you to sleep

Act via the BZ1 subtype of GABA receptor (flumenazil reversal)

Insomnia

Ataxia, headaches, confusion.
Only modest day after psychomotor depression
Decr. dependence risk than benzos
Rapid metabolism (short acting)

30
Q

What is the result of a general anesthetic that has decr. solubility in blood? Incr. solubility in lipids? What does a drug need to act in brain? What is MAC? What is nitrous oxide (N2O) concerning these principles? What is halothane concerning these principles?

A

Decr. blood solubility=rapid induction and recover
Incr. lipid solubility=Incr. potency=1/MAC

Be lipid soluble or be actively transported to reach brain

MAC=minimal alveolar conc. required to prevent 50% of subjects from moving in response to noxious stimulus

N2O has decr. blood and lipid solubility=low potency and fast induction

Halothane has incr. lipid and blood solubility=High potency and slow induction

31
Q

What type of drugs are halothane (1), enflurane (2), isoflurane, sevoflurane, methoxyflurane, and N2O (3)? Mechanism? Effects? Toxicity of 1? Of 2? Of 3? Of all but 3?

A

Inhaled anesthetics

Mechanism unknown

Myocardial depression
respiratory depression
nausea/emesis
Incr. cerebral blood flow (decr. cerebral metabolic demand)

1-hepatotoxicity
2-proconvulsant
3-nephrotoxicity

All but 3=malignant hyperthermia: life threatening hereditary condition in which inhaled anesthetics with succinylcholine induce fever and severe muscle contractions

32
Q

What type of drugs are barbituates, benzos, ketamine, opioids, and propofol?

A

IV anesthetics

33
Q

What type of drug is thiopental? What is lipid solubility of thiopental? What is it used for? Blood solubility? What does it do to cerebral blood flow?

A

barbituate

High potency/lipid solubility
High blood solubility/rapid induction and recovery

Induction of anesthesia and short surgical procedures

Decr. cerebral blood flow

34
Q

What type of drug is Midazolam? What is it used for? What is it used with? Toxicity?

A

Benzo

Endoscopy
Gaseous anesthetics and narcotics

Severe post op resp depression
Decr. BP
Anterograde amnesia

35
Q

What kind of drug is ketamine? Mechanism? Clinical use? Toxicity? CBF?

A

Arylcyclohexylamines=PCP like

Block NMDA receptors

Dissociative anesthetics

CV stim
disorientation
hallucination
bad dreams

incr. CBF

36
Q

What type of drug are morphine and fentanyl? How are they used as anesthetics?

A

Opioids (2)

Used with other CNS depressants during general anesthesia

37
Q

What is the mechanism of propafol? Clinical use?

A

Potentiates GABA-A

Sedation in ICU
Rapid anesthesia induction
short procedures

Less post op nausea

38
Q

What type of drug are procaine, cocaine, and tetracaine (1-3)? Lidocaine, mepivicaine, bupivacaine (4-6)? What are they given with? Why? What must be done in infected tissue? What is the order of nerve blockade? Order of functional nerve loss? Clinical use? Toxicity?

A

1-3=Ester local anesthetic
4-6=amide anesthetic (2 I’s)

Blocks Na channels by binding specific receptors on iner portion of channel.
Preferentially binds to activated Na channels, so most effective in rapidly firing neurons
Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

Given with vasoconstrictors (epi) to enhance local action (it won’t dilute away)
In infected tissue (acidic), must use more
small myel >small unmyel > large myeli =n > large unmyel

Pain > temp > touch > pressure

Minor surgical procedures
Spinal anesthesia
If allergic to esters, give amide

CNS excitation, severe CV toxicity (6), hypertension, hypotension, arrythmias (2), methemoglobinemia (benzocaine)

39
Q

What kind of drug is succinylcholine? mechanism? Clinical use? Complications?

A

Depolarizing NM blocking drug; strong ACh receptor agonist

Produces sustained depolarization and prevents muscle contraction.

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

Hypercalcemia, hyperkalemia, malignant hyperthermia

40
Q

What kind of drugs are tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium? How are they reversed?

A

Non depolarizing NM blocking drug

Competitive antag at ACh receptor

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

Reversal-Neostigmine (with atropine to prevent musc effects), edrophonium, and other cholinesterase inhib.

41
Q

What is the mechanism of dantrolene? Clinical use?

A

Prevents release of Ca from the SR of skel muscle

Malignant hyperthermia and NMS

42
Q

What is the mechanism of baclofen? Clinical use?

A

Inhibits GABA-B receptors at spinal cord level, inducing skel muscle relaxation

Muscle spasms

43
Q

What is the mechanism of cyclobenzaprine? Clinical use?

A

Centrally acting skel muscle relaxant. Structurally related to TCAs, similar anticholinergic side effects.

Muscle spasms.

44
Q

What are some ways to treat parkinsons (classes of drugs)?

A

Incr. dopamine decr. ACh

Dopamine agonist
Incr. dopamine availability (amantadine)
Incr. L-DOPA availability (prevent degradation in periphery)
Prevent dopamine breakdown
Curb excess cholinergic activity (benztropine)

45
Q

What are 3 dopamine agonists? Classes? Which class is preferred?

A 
Ergot-bromocriptine
Non ergot (preferred)-pramipexole, ropinirole
46
Q

What is the mechanism of amantadine? Toxicity?

A

Incr. DA release and decr. reuptake

Ataxia
livedo reticularis

47
Q

What is the mechanism of carbidopa? Actions?

A

Blocks periph conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase

More L-DOPA in CNS
Reduces side effects of periph dopamine (N/V)

48
Q

What is the mechanism of selegiline? Clinical use? Toxicity?

A

Selectively inhibits MAO-B, which preferentially metabolizes DA over NE and 5-HT.
DA isn’t converted to 3-MT and thus more is available in brain

Adjunctive agent to L-dopa i treatment of park disease

49
Q

What is the mechanism of entacapone? What are the other mechanism of tolcapone (1)?

A

Prevent peripheral Ldopa degradation to 3-O-methyldopa by inhibiting COMT

1-blocks conversion of dopamine to DOPAC by inhibiting CENTRAL COMT

50
Q

What is the mechanism of benztropine? Action?

A

Antimuscarinic

Improves tremor and rigidity, not bradykinesia

51
Q

What is the mechanism of L-DOPA? Clinical use? Toxicity?

A

Incr. level of DA in brain. It can cross BBB and is converted by Dopa decarboxylase in the CNS to DA. Used with carbidopa.

parkinsons

Arrhythmias from periph formation of catecholamines
Long term use can lead to dyskinesia following administration, akinesia b/w doses.

52
Q

What is the mechanism of memantine? Clinical use? Toxicity?

A

NMDA receptor antag; helps prevent excitotoxicity

Alzheimers

Dizziness
confusion
hallucinations

53
Q

What is the mechanism of donepezil, galantamine, rivastigmine? use? Toxicity?

A

AChE inhibitors

Alzheimers

Nausea, dizziness, insomnia

54
Q

What is the mechanism for tetrabenazine and reserpine? For haloperidol? Use?

A

Inhibit vesicular monoamine transporter (VMAT)
Limit DA vesicle packaging and release

D2 receptor antagonist

Huntingtons

55
Q

What is the mechanism of sumatriptan? clinical use? Toxicity? CI?

A

5-HT-1B/1D agonist
Inhibit CNV activation
Prevent vasoactive peptide release
Induce vasoconstriction

Acute migraine
Cluster headaches

coronary vasospasm (CI in CAD or prinzmetal angina)
Mild paresthesia

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