Intro to Prescription Writing and Antiepileptic Pharm Flashcards Preview

Neuroscience II Exam III - Pharm and Clinical Medicine > Intro to Prescription Writing and Antiepileptic Pharm > Flashcards

Flashcards in Intro to Prescription Writing and Antiepileptic Pharm Deck (50)
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1
Q

In terms of prescription writing, what aspects does a designation as a scheduled/controlled substance impact?

A

Dispense quantity
Refills allowed
Prescription lifespan

2
Q

9 legal requirements of prescriptions

A
  1. Name/address of prescriber
  2. Name/address of patient
  3. Date prescription was written
  4. Name, strength, dosage
  5. Directions for use
  6. Quantity to be dispensed
  7. Number of refills allowed
  8. Prescriber’s signature
  9. Prescriber’s DEA number (controlled drugs only)
3
Q

Lifespan of non-controlled legend drug prescriptions

A

12 months, or number of refills (whichever occurs first)

4
Q

Lifespan of controlled/scheduled legend drug prescriptions

A

6 months or number of refills (exception is C-V which has lifespan of 12 months)

5
Q

Legal limit on number of refills for controlled/scheduled legend drugs

A

C-II = None

C-III or C-IV = 5 refills over 6 months

C-V = no limit on refills

6
Q

Legal limit on quantity dispensed for controlled/scheduled legend drugs

A

C-II = 30 day supply (up to 90 days with documented medical reason)

C-III and C-IV = 90 day supply

7
Q

Partial filling for C-II is not permitted except under what circumstances?

A

Pharmacist does not have full quantity

Long-term care/hospice

8
Q

Law on prescription transfers of scheduled drugs

A

Not allowed for C-II

C-III through C-V can be transferred only once

9
Q

What can NEVER be changed/added on a controlled substance prescription?

A

Patient’s name
Drug name
Prescriber’s name
Prescriber’s signature

10
Q

Definition of “emergency” for controlled drugs

A

Immediate administration is necessary for proper tx of intended user and no appropriate alternative tx is available

note that 72 hours are allowed for delivery of Rx to the dispensing pharmacy and quantity is limited to amount needed during emergency time period

11
Q

Laws on self-prescribing and prescribing to family

A

Self-prescribing of controlled substances is illegal in most states; self-prescribing of non-controlled substances is legal but discouraged

Physicians may prescribe all legend drugs for a family member as long as same records are maintained as for any other patient

12
Q

One way that anti-epileptic drugs (AEDs) target epileptic-transmitter systems is by suppressing excitatory (glutamate) tranmission.

This may be done by suppressing voltage-gated ____ channels, or by suppressing ligand-gated ______ and _____ channels

A

Na+; AMPA; NMDA

13
Q

AED’s that work by suppressing activation of voltage-gated Na+ channels bind at the _______ side of the channel pore, thus the ______ gate must be open for the drug to work

A

Interior; activation

[note that voltage-gated sodium channels can be affected during open state or during fast-inactivated state]

14
Q

What is the explanation for the fact that voltage-gated Na+ channel blockers act preferentially on neurons involved in seizure activity?

A

The probability of Na(v) blockade is proportional to the frequency of Na(v) chanel opening and dose — epileptic seizures involve neurons firing at higher frequency than normal so they are more likely to attract the drug

15
Q

Which of the Na(v) blockers can do its job irrespective of open-close of channels — meaning it can both prolong fast inactivation and enhance slow inactivation of Na(v) channels?

A

Lacosamide

[whereas other AED Na(v) blockers just prolong fast inactivation state of Na(v) ion channels]

16
Q

What are the AEDs that act on voltage-gated Na+ channels to enhance fast inactivation?

A
Carbamazepine
Oxcarbazepine
Lamotrigine
Phenytoin
Rufinamide
Topiramate
Valproic acid
Lacosamide
Zonisamide
17
Q

AEDs that are AMPA receptor antagonists

A

Topiramate

Perampanel

18
Q

AED that is an NMDA receptor antagonist

A

Felbamate

19
Q

AEDs that affect pre-synaptic GABA-ergic transmission and their MOAs

A

Vigabatrin inhibits GABA metabolism by GABA-T

Valproic acid promotes formation of GABA via activation of glutamic acid decarboxylase; also inhibits GABA metabolism by SSD

Tiagabine inhibits GABA reuptake by GAT-1

20
Q

AED that affects post-synaptic GABA-ergic transmission by binding to a distinct allosteric site that potentiates GABA binding so that Cl- channels open with greater frequency

A

Benzodiazepines (lorazepam, diazepam, clonazepam)

21
Q

AED that affects post-synaptic GABA-ergic transmission by binding to a distinct site on the receptor and increasing the duration of Cl- channel opening

A

Barbiturates (phenobarbital, primidone)

22
Q

Which has higher lethality, benzodiazepines or barbiturates?

A

Barbiturates — because high doses are GABA-independent

23
Q

MOAs of Topiramate

A

GABA-A agonist — increases frequency of GABA-A receptor activation

Fast inactivation of Na(v) channels

AMPA receptor antagonist

24
Q

Hallmark of absence (petit mal) seizures

A

T-type Ca++ channels mediate 3 Hz spike and wave activity in the thalamus

25
Q

What drug is ONLY used for absence seizures because it only limits excitation at T-type Ca++ channels?

A

Ethosuximide

26
Q

Other than ethosuximide, what are 2 other drugs used that antagonize T-type Ca++ channels?

A

Valproic acid

Zonisamide

27
Q

All MOAs of valproic acid

A

T-type Ca2++ channel antagonist

Fast inactivation of Na(v) channels

GABA-T inhibitor

28
Q

All MOAs of zonisamide

A

T-type Ca++ channel antagonist

Fast inactivation of Na(v) channels

29
Q

Which AED has the MOA involving inhibition of synaptic vesicle 2A protein in presynaptic neuron?

A

Levetiracetam (and other -acetams)

30
Q

Which AEDs have the MOA of inhibiting alpha-2-delta subunit of P/Q-type Ca2+ channels on presynaptic neuron?

A

Gabapentin

Pregabalin

31
Q

AED indications for partial onset seizures, both simple and complex

A
Lamotrigine
Oxcarbazepine
Perampanel
Primidone
Lacosamide
32
Q

AED indications for generalized onset absence seizures

A

Ethosuximide
Clonazepam
Valproic acid

33
Q

AED indications for generalized onset myoclonic seizures

A

Clonazepam

34
Q

AED indications for generalized onset tonic/clonic seizures

A

Primidone

Phenytoin

35
Q

AED indications for broad-spectrum seizures (minus absence)

A

Carbamazepine
Phenobarbital
Topiramate
Valproic acid

36
Q

AED indications for Lennox-Gastaut seizures (adj. therapies)

A
Rufinamide
Topiramate
Clobazepam
Clonazepam
Lamotrigine
Felbamate
37
Q

AED indications for status epilepticus

A
Lorazepam
Diazepam
Phenobarbital
Phenytoin
Valproic acid
Levetiracetam
38
Q

Broad warning/risk of ALL AEDs

A

Abrupt withdrawal may precipitate status epilepticus

Suicidal behavior and ideation

39
Q

What are some known issues with Phenytoin?

A

Zero-order (saturable) pharmacokinetics

Required serum-drug level monitoring (10-20 mcg/mL)

Well known inducer of CYP450 enzymes

Select toxicities: gingival hyperplasia, hypothyroidism, CV risk, hypocalcemia—>osteoporosis

40
Q

Osteopenia/osteoporosis are associated with what AEDs due to their induction of CYP450-dependent vitamin D catabolism?

A

Phenytoin
Carbamazepine
Phenobarbital
Valproic acid

41
Q

Issues with Carbamazepine

A

Serum drug level monitoring (4-12 mcg/mL)

Known inducer of CYP450 enzymes, also induces auto-induction (self-metabolism)

Toxicities: leukopenia/neutropenia/thrombocytopenia, hypocalcemia —>osteoporosis

42
Q

Carbamazepine induces its own metabolism at certain serum levels, resulting in potential loss of efficacy and recurrence of seizures. What other drug does this occur with, though to a lesser extent?

A

Lamotrigine

43
Q

Analogue of carbamazepine with fewer CNS/hematological side effects due to formation of an alternative active metabolite; also a less-potent CYP450 inducer

A

Oxcarbazepine

44
Q

Issues with phenobarbital

A

C-IV agent— can’t prescribe as often/as many refills

Serum drug level monitoring (10-40 mcg/mL) — coma, respiratory depression, fatality risk at high concentrations

Known inducer of CYP450

Toxicities: CNS depressant, hypocalcemia —> osteoporosis

45
Q

Issues with vigabatrin

A

Toxicities — progressive, permanent, bilateral, concentric vision loss

Only prescribable via REMS program

46
Q

Drug-drug interactions associated with hepatic CYP450 induction by carbamazepine, phenytoin, phenobarbital, and valproate

A

Oral contraceptives — risk of unplanned pregnancy

Anticoagulants — risk of arterial/venous thrombosis

Antivirals — risk of HIV replication

47
Q

Valproic acid + lamotrigine interaction

A

Inhibits conjugation of drugs by UGT causing accumulation of parent drug

48
Q

Non-CYP450 drug interactions with phenytoin, carbamazepine, and phenobarbital

A

Induce conjugation of drugs by UGT, causing reduction of parent drug

49
Q

Renal insufficiency requires dose adjustments of what AEDs?

A
Levetiracetam
Topiramate
Oxcarbazepine
Gabapentin
Pregabalin
Vigabatrin
50
Q

Initial therapy protocol for convulsive status epilepticus in adults

A

In first IV: Lorazepam (alternative is diazepam)

In second IV: Fosphenytoin, phenytoin, valproic acid, or levetiracetam

If no IV access: midazolam