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Neuro/Psych > Exam 3 > Flashcards

Exam 3 Flashcards

Seizures, opioids, non-cancer pain relief, multiple sclerosis

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1
Q

Drug class of clobazam

A

Benzodiazepine

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2
Q

Clobazam use

A

Adjunctive treatment of seizures associated with Lennox Gastsult syndrome in patients 2 years of age and older

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3
Q

Clobazam schedule

A

4

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4
Q

Clobazam dispensing requirement

A

Review med guide with every patient or caregiver

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5
Q

Ethosuximibe use

A

First line for absence seizures

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6
Q

Therapeutic level for ethosuximibe

A

40-100 mg/L (note: one of the few new AEDs that requires monitoring)

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7
Q

Ezogabine use

A

Adjunctive agent for partial seizures

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8
Q

Side effects of ezogabine

A

Dizziness, somnolence, urinary retention

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9
Q

Severe side effect of ezogabine

A

QT prolongation within 3 hours of administration

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10
Q

Ezogabine dispensing requirement

A

REMS for urinary retention, medication guide is available

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11
Q

Felbamate use

A

Reserved for patients not responding to other AEDs

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12
Q

Felbamate side effects

A

Aplastic anemia and acute liver failure

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13
Q

Felbamate dispensing requirement

A

Patient or guardian must sign consent form

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14
Q

Gabapentin use

A

Second line for partial seizures +/- generalizations (also largely used off label)

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15
Q

Off label use for gabapentin

A

Neuropathic pain, migraines, bipolar disorder

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16
Q

Important counseling point for how to take gabapentin

A

Do not discontinue abruptly, can cause withdrawal seizures even if not using the medication as AED

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17
Q

Why might gabapentin be adjusted in kidney disease?

A

Renal elimination, can accumulate and cause additional somnolence

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18
Q

Lacosamide use

A

adjunctive treatment of partial seizures

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19
Q

Lacosamide schedule

A

5

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20
Q

Lacosamide side effect

A

PR internval prolongation

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21
Q

Lacosamide dispensing requirement

A

Medication guide must be dispensed with each prescription

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22
Q

Important point about lamotrigine that pharmacists should look out for

A

LOTS of drug interactions

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23
Q

What is one common drug interaction with lamotrigine, what is the effect, and should this combination be avoided?

A

Valproic acid can increase lamotrigine serum concentrations by 200% (can be used together but need to start lamotrigine doses lower)

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24
Q

Lamotrigine side effect (SEVERE!) and how can we prevent?

A

Rash due to SJS, start low and go slow especially when given with valproic acid

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25
Q

Levetiracetam absorption and elimination

A

Completely absorbed after oral administration, renally eliminated

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26
Q

Important pearl about levetiracetam

A

No induction/inhibition hepatic interactions

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27
Q

T or F: oxcarbazepine is a prodrug of carbamazpine

A

False (but structurally related

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28
Q

Oxcarbazepine use

A

Potential 1st line agent for primary generalized convulsions

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29
Q

What makes oxcarbazepine different from carbamazepine? What makes them similar?

A

No auto-induction, less potent inducer than carbamazepine, possible cross-sensitivity for SJS rash between the two

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30
Q

Oxcarbazepine side effect

A

Hyponatremia

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31
Q

T or F: the dose of oxcarbazepine and carbamazepine are 1:1 (if F, how would you convert?)

A

False (CBZ dose per day * 1.5 = OXC dose per day)

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32
Q

Rufinamide use

A

Adjunctive treatment of generalized seizures of Lennox-Gastaut syndrome

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33
Q

Rufinamide side effect

A

QT shortening, Contraindicated in patients with familial short QT syndrome

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34
Q

Tigabine use

A

2nd line agent for partial seizures in patients who failed initial therapy

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35
Q

Important pearl about tigabine

A

No inhibition or induction of hepatic enzymes, but CYP3A4 substrate

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36
Q

Topiramate use in seizures

A

First line for partial seizures

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37
Q

Other common use for topiramate

A

migraine prophylaxis

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38
Q

Topiramate side effects (2 big ones)

A

CNS effects (psychomotor slowing, somnolence, irritability, slurred speech, confusion), kidney stones 2-4x normal

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39
Q

Vigabatrin use

A

Adjunctive for patients with really complex seizures

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40
Q

Vigabatrin dispensing requirement

A

REMS: causes permanent vision loss in infants, children, and adults (Blind as a BAT (vigaBATrin)); DO NOT CRUSH OR CUT; Prescribers and pharmacies must be registered with the program

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41
Q

Zonisamide side effect

A

SJS (d/c immediately)

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42
Q

Advantage of zonisamide

A

Long half-life, once daily dosing (others are normally 2-4!)

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43
Q

Role of CBD in seizures

A

major nonpsychoactive component of marijuana, expected to have anti-seizure properties, Potential alternative for refractory epilepsy in adults and children who do not respond to current medications, Epilepsy is one of 23 approved indications for medical marijuana in PA

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44
Q

Metabolism (enzymes) of medical marijuana

A

Metabolized by CYP3A4 and CYP2C19

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45
Q

Potential DDIs with medical marijuana

A

Induced by carbamazepine and phenytoin, Inhibited by ketoconazole

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46
Q

What important safety factor must we look out for with AED use?

A

Patients on AED have twice the risk of suicidal behavior

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47
Q

Common effect of epilepsy

A

Sexual dysfunction (caused by many different medications used to treat seizures as well!)

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48
Q

Important note about hormonal contraceptives with AEDs

A

Need at least 50mcg of ethinyl estradiol (decreases effectiveness)

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49
Q

What AED medication should usually be avoided in pregnancy?

A

Avoid valproic acid monotherapy or polytherapy in the first trimester

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50
Q

What supplement is important for pregnancy?

A

Folic acid

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51
Q

What is status epilepticus?

A

Neurologic emergency that can be associated with brain damage and death

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52
Q

Operational definition of SE

A

> 5 minutes of continuous seizure or >2 discrete seizures between which there is incomplete recovery of consciousness

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53
Q

Conceptual definition of SE

A

Condition resulting from either the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms that lead to abnormally prolonged seizures

Can have long term consequences, including neuronal death, neuronal injury, alteration of neuronal networks

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54
Q

2 types of SE and what they look like

A

Generalized SE: Characterized by repeated primary or secondary seizures that involve both hemispheres of the brain, Associated with persistent postictal state

Nonconvulsive SE: Fluctuating or continuous twilight state that produces altered consciousness and/or behavior

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55
Q

Common causes of SE

A

Structural lesion (stroke, anoxia, trauma, CNS tumor, hemorrhage) and no structural lesion (withdrawal of AED, alcohol withdrawal, CNS infection)

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56
Q

T or F: elderly patients have a higher mortality associated with SE than children

A

True

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57
Q

Variables in the mortality of SE

A
  • Time between onset and treatment
  • Duration of seizure
  • Presence of structural damage
  • Patient characteristics: older age, medical comorbidity, high initial APACHE-II scores
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58
Q

Complications of SE

A
  • Rhabdomyolysis
  • Lactic acidosis
  • Aspiration pneumonitis
  • Neurogenic pulmonary edema
  • Respiratory failure
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59
Q

First steps in treating SE (before you even start)

A
  • Assess vital signs
  • Establish an adequate and protected airway
  • Administer oxygen
  • Obtain arterial blood gas
  • Obtain blood sugar
  • Perform an EEG if possible
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60
Q

Non-AED therapy for SE

A

Oxygen, correct electrolytes, cooling blanket, central IV line, if Wernicke’s encephalopathy (due to alcohol, if you don’t know just give it, it won’t hurt them) give thiamine, dextrose if hypoglycemic (if you don’t know, just give it, it won’t hurt them)

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61
Q

Treating SE: time 0 (3 distinct medications)

A
  • If Wernicke’s encephalopathy is possible (occurs in alcoholics), give IV thiamine
  • If hypoglycemia cannot be ruled out, give dextrose IV
  • 1st line agents: benzodiazepines
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62
Q

What are the types of benzodiazepines that are used for SE and considerations for route of administration?

A

o Lorazepam considered first line
o Also can use diazepam, midazolam
o Give doses as IV (midazolam must be continuous infusion), IM route not preferred due to delay, can also give diazepam as rectal gel, also have intranasal diazepam (in patients as young as 6 years, weight-based dosing, can give 2 doses per episode) and midazolam (can give 2 doses per episode)

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63
Q

How do benzodiazepines work to stop seizure?

A

enhancement of GABA actions by helping GABA bind more tightly to the GABA receptor

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64
Q

Benzodiazepine side effects

A

hypotension, vasodilation, amnesia, drowsiness, headache, confusion

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65
Q

Treating SE: time 10-30 min (when benzo doesn’t work or seizure recurs)

A

2nd line agents: phenytoin IV or fosphenytoin

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66
Q

Important administration pearl for fosphenytoin (especially useful in SE emergency)

A

Can be given IM and if no central line is present, less hemodynamic effect

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67
Q

Treating SE: time 60 min

A

Additional bolus of phenytoin or fosphenyotin

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68
Q

Treating SE: time 90 min

A

3rd line agents: phenobarbital or valproic acid (most common this one)

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69
Q

Treating SE: refractory (list 3 possible medications and associated ADE)

A
  • Continuous infusion of midazolam
  • Continuous infusion of pentobarbital (associated with hypotension, may need pressor support) – not really used
  • Propofol (may cause hypotension, bradycardia, hypertriglyceridemia)
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70
Q

Advantages of using newer AED (side effects, monitoring, dosing, DDI)

A
  • Lower ADE rates
  • Little or no need for serum monitoring
  • QD or BID dosing
  • Fewer drug interactions
  • Pregnancy category C (not D!)
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71
Q

Important safety consideration for AED

A

Monitor patients for emergence or worsening of suicidal thoughts or behavior or depression

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72
Q

Phenytoin MOA

A

inhibition of voltage-dependent sodium channels

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73
Q

Phenytoin use

A

First line for primary generalized convulsive and partial seizures

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74
Q

Important point about dispensing phenytoin

A

Differences exist between different salt products (cannot substitute products!!)

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75
Q

How do tube feedings affect phenytoin?

A

Tube feedings decrease absorption (separate by 2 hours)

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76
Q

Phenytoin oral bioavailability

A

100%

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77
Q

How does protein binding affect phenytoin? Similarly, how does protein binding of phenytoin affect other drugs?

A

90% bound to albumin, free phenytoin is the part that causes therapeutic effect (therefore, less albumin, more free drug, more effect), low albumin levels caused by renal failure, malnutrition, burn patients

Drug interactions possible due to drug displacement from albumin (warfarin, valproate)

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78
Q

Volume of distribution consideration for phenytoin

A

Obesity increases volume of distribution, use adjusted body weight instead

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79
Q

Metabolism of phenytoin (what enzymes and kinetics?)

A

Extensive hepatic metabolism by CYP2C9/19

Zero order kinetics, metabolism saturates at doses used clinically (at saturation, small increases in dose can result in high serum concentrations)

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80
Q

Phenytoin elimination route

A

Renal

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81
Q

Loading dose for phenytoin

A

15-20 mg/kg IV at rate of <50mg/min

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82
Q

Why is there a rate limit for phenytoin administration?

A

Slow IV to avoid venous irritation, pain, thrombophlebitis, administration related hypotension and arrhythmias

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83
Q

Maintenance dose for phenytoin

A

300 mg/day (5-6mg/kg/day) in 1-3 divided doses

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84
Q

Concentration dependent ADE of phenytoin

A

lethargy, fatigue, in-coordination, blurred vision, dizziness, ataxia, nystagmus

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85
Q

Concentration independent ADE of phenytoin (think of the example pictures from lecture)

A

hypertrichosis, gingival hypertrophy, thickening of facial features, osteomalacia, folate deficiency, hypersensitivity reactions

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86
Q

Monitoring for phenytoin

A

BP, vital signs, plasma phenytoin, CBC, LFTs

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87
Q

Therapeutic range for phenytoin (and what do we measure?)

A

Total 10-20 mg/L; free 1-2 mg/L

Trough levels for therapeutic range

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88
Q

When should you obtain trough to test if dose is correct for patient?

A

Obtain 2-3 weeks after initiation or change of dose, Obtain trough about 30 minutes before next dose (lowest level)

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89
Q

Dose increases for phenytoin based off trough levels

A

If <7, increase by 100mg/day
If 7-12, increase by 50mg/day
If >12, increase by 30mg/day

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90
Q

If trough is subtherapeutic, but not zero, how should you fix this (and what is the calculation?)

A

Extra LD (if someone already has drug in the body, and drug level comes back low, don’t need to totally reload the dose, just need to give a little more) to achieve desired serum levels; then use table if normal renal function to change maintenance dose

IV dose (mg/kg)=(Cdesired-Cactual)*0.7
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91
Q

Correction for hypoalbuminemia

A

Ccorrected= Cobserved/(0.2(Alb+0.1))

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92
Q

Correction for renal failure

A

Ccorrected= Cobserved/(0.1(Alb+0.1))

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93
Q

T or F: fosphenytoin is a prodrug of phenytoin

A

True

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94
Q

How is fosphenytoin dosed and what is the loading dose?

A

Dosed by phenytoin equivalents (PE)

Loading dose: 10-20 mg/kg PE

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95
Q

Major benefit of fosphenytoin over phenytoin

A

Less infusion site reactions, can also give IM for those without IV access

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96
Q

Carbamazepine MOA

A

inhibition of voltage-dependent sodium channels, interaction with voltage-gated calcium and potassium channels

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97
Q

Carbamazepine use

A

First line for partial and primary generalized convulsive seizures who are not in an emergent situation

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98
Q

What pregnancy category is carbamazepine?

A

D

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99
Q

Difference in absorption of various formulations of carbamazepine

A

Erratic from IR tablets due to low water solubility, SR formulations minimize fluctuations

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100
Q

Describe the metabolism of carbamazepine (which enzyme and what makes this drug special)

A

Hepatic metabolism via CYP3A4, induces hepatic enzymes, auto-induction of its own metabolism

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101
Q

Describe how auto-induction of carbamazepine might affect dosing

A

Max auto-induction 2-4 weeks after initiation, Re-adjust dose at 3-4 weeks due to auto-induction

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102
Q

Starting dose, weekly increase, and target dose for carbamazepine

A

o Starting dose: 200 mg BID PO
o Weekly increase: 200 mg/day
o Usual dose: 800-1200 mg/day given in 2-4 divided doses (max 1600-2400 mg/day)

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103
Q

Important counseling point about carbamazepine ER capsules

A

ER capsules may be opened and sprinkled on food

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104
Q

Concentration dependent ADE of carbamazepine

A

nystagmus, ataxia, blurred vision, diplopia, vomiting, sedation, dizziness

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105
Q

Concentration independent ADE of carbamazepine

A

leukopenia, hypersensitivity

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106
Q

Carbamazepine FDA alert (what is it for, who does it affect, how does it affect them)

A

Screening of patients for Human leukocyte antigen (HLA) B*1052 allele, Present in patients with Asian ancestry

Strong correlation with allele and serious dermatologic reactions with carbamazepine (SJS, toxic epidermal necrolysis)

Patients who are positive should NOT be treated with carbamazepine

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107
Q

Carbamazepine monitoring

A

CBC with platelet count, serum iron at baseline and periodically, serum level

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108
Q

Therapeutic range for carbamazepine

A

4-12 mg/L

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109
Q

Valproic acid MOA

A

potentiate postsynaptic GABA responses, have a direct membrane stabilizing effect, affect potassium channels

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110
Q

Valproic acid use

A

First line for primary generalized seizures such as myoclonic, atonic, and absence seizures, can be used as monotherapy or adjunctive therapy for partial seizures, useful in patients with mixed seizure disorder

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111
Q

Important dispensing point about valproic acid

A

DO NOT substitute between dosage forms

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112
Q

DDI with valproic acid

A

Lots of CYP interactions

 Increases carbamazepine
 Increases lamotrigine
 Increases free phenytoin
 Increases phenobarbital
 Aspirin increases valproic acid
 Carbamazepine, phenytoin, and phenobarbital decrease valproic acid

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113
Q

Loading dose for valproic acid

A

15-20 mg/kg IV

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114
Q

Starting dose, weekly increase, and target dose for valproic acid

A

 Initial: 10-15 mg/kg/day in 2-3 divided doses
 Weekly increase 10 mg/kg/day
 Target: 30-60 mg/kg/day in 2-3 divided doses

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115
Q

Dose dependent ADE for valproic acid

A

GI complaints (take with food), alopecia, thrombocytopenia, platelet dysfunction

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116
Q

Dose independent ADE for valproic acid

A

hepatotoxicity

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117
Q

Monitoring for valproic acid

A

baseline and periodically LFTs, CBC with platelets, serum valproate levels

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118
Q

Therapeutic range for valproic acid

A

50-100 mg/L total

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119
Q

Phenobarbital MOA

A

elevate seizure threshold by interaction with GABA receptors to facilitate intrinsic chloride channel function, blockade of high voltage calcium channels

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120
Q

Phenobarbital use

A

Drug of choice for neonatal seizures but is reserved in other situations for patients who have failed therapy with other AEDs, may be useful given IV in refractory SE

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121
Q

Loading dose for phenobarbital

A

15-20 mg/kg IV

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122
Q

How should we administer the loading dose of phenobarbital?

A

Avoid rapid administration due to hypotension, Use caution in hemodynamically unstable patients

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123
Q

Maintenance dose for phenobarbital

A

50-100 mg 2-3 times daily (1-3 g/kg/day in 1-2 doses)

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124
Q

Concentration dependent ADE for phenobarbital

A

sedation, respiratory depression, hypotension

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125
Q

Concentration independent ADE for phenobarbital

A

hypersensitivity reactions, hyperactivity, altered concentration, altered learning, depression

126
Q

Therapeutic level for phenobarbital

A

15-40 mg/L

127
Q

When is MS usually diagnosed? Who is at greater risk?

A

Diagnosed between 15 and 45 years old, women are greater risk than men

128
Q

T or F: there are both genetic factors and environmental factors that play into the etiology of MS

A

True

129
Q

Describe the pathophysiology of MS

A

Auto-reactive T lymphocytes are activated, cross into CNS, and attack myelin (Damage to myelin and underlying axon, damage to grey and white matter caused by inflammation involving activation of T cells)

T cells differentiate into T helper cells that induce pro-inflammatory response in which cytokines further activate B cells and macrophages

Immune system attacks the myelin sheath of neurons (Forms scar tissue (sclerosis), disrupted signals lead to neurological effects)

130
Q

Why might MS diagnosis be delayed?

A

vague, transient symptoms may lead to delay in diagnosis

131
Q

Primary symptoms of MS

A

Visual complaints, gait problems, paresthesia, pain, spasticity, weakness, ataxia, speech difficulty, psychological changes, cognitive changes, fatigue, bowel/bladder dysfunction, tremor, heat sensitivity

132
Q

Describe the importance of heat sensitivity in MS

A

Many people with MS have worsening symptoms with increased body temperature, cooling may help (cooling vests), but very cold temperatures may cause spasticity

133
Q

Secondary symptoms of MS

A

Recurrent UTI, urinary calculi, decubiti, muscle contractures, respiratory infections, poor nutrition

134
Q

Tertiary symptoms of MS

A

Financial problems, personal/social problems, vocational problems, emotional problems

135
Q

Four subtypes of MS (what are they and what are they defined by?)

A

Relapsing-remitting MS (RRMS): Clearly defined relapses with full recovery or with residual deficit following recovery

Secondary progressive MS (SPMS): Disease progression with or without occasional relapses, minor remissions, or plateau

Primary progressive MS (PPMS): Progressive from onset with occasional plateau and temporary improvements

Progressive relapsing MS (PRMS): Progressive from onset with acute relapses, with or without full recovery, and continuous progression between relapses

136
Q

Factors for a favorable prognosis of MS

A

<40 yo, female, optic or sensory symptoms (as opposed to motor or cerebellar), low attack frequency early in disease, relapsing/remitting

137
Q

Criteria for MS diagnosis (what does this include that was different from before?)

A

McDonald Criteria, includes MRI

138
Q

CSF evaluation for MS

A

CNS synthesis of IgG is increased, whereas serum IgG is normal

Electrophoretic studies show oligoclonal bands, present in >90% of patients with clinically definite MS

After initial symptoms, CSF only positive in 30% of patients so analysis reserved for situations where need help to define more definitive diagnosis of MS

> 50x10^6 mononuclear cells in CSF indicated a diagnosis other than MS

139
Q

What is the instrument used in the clinical evaluation of MS?

A

Expanded Disability Status Scale (EDSS)

140
Q

Goals of MS treatment

A

Reduce the number of relapses, slow the rate of disability, reduce the number of brain lesions and the rate of brain atrophy

141
Q

When should we start treating MS?

A

Start therapy immediately after diagnosis, shown to reduce second attacks, but does not suppress disease completely

142
Q

What are the three categories of treatment of MS?

A

Acute attacks, disease-modifying therapy, symptomatic therapy

143
Q

Goal of treating acute attacks of MS, how would you treat, and effect of treatment?

A

Shorten duration and perhaps severity

If functional decline: IV high dose corticosteroids 3-5 days (Methylpred 500-1000 mg/day)

May decrease edema in area of demyelination, may shorten duration of exacerbation and delay repeat attacks after optic neuritis, has not been shown to affect progression of disease

144
Q

Goal of disease-modifying therapy and the four different algorithms for treatment

A

Goals are to decrease frequency and severity of exacerbations, diminish the progression of lesions seen on the brain and spine MRIs, and slow progression of disability over time

Safety (“tried and true”) approach: injection with interferon beta-1a, interferon beta-1b, or glatiramer

“Convenience” approach: oral therapy with dimethyl fumarate, teriflunomide, or fingolimod

“Efficacy” approach: infusion monotherapy with natalizumab or ocrelizumab

Stem cell transplantation: Eliminate and replace pathogenic immune system to achieve long-term remission, only small studies to date

145
Q

Goal of symptomatic therapy for MS

A

Improve quality of life (gait difficulties, spasticity, fatigue, tremor, bowel and bladder symptoms, major depression, sensory symptoms, sexual dysfunction)

146
Q

Treatment for gait difficulties (MOA, CI, ADE, DDI)

A

Dalfampridine (Ampyra)

CNS potassium blocker indicated to improve walking in patients with MS

Tablets should be take whole

CI: seizures, renal impairment

ADE: UTI, insomnia, dizziness, HA, nausea

DDI: metformin

147
Q

Treatment for spasticity in MS (goal, non-pharm, 1st-3rd line treatments, ADE and MOA for 1st and 2nd line)

A

Reduce muscle tone to a degree that function is improved

Non-pharm: physiotherapy, structured exercise, transcranial magnetic stimulation, electromagnetic therapy

1st line: Baclofen
* GABA analog
* ADE: somnolence, confusion, motor weakness, must not be d/c abruptly (hallucinations and seizures)

2nd line: Tizanidine
* Centrally acting alpha-adrenergic agonist
* ADE: sedation, dizziness, dry mouth, hypotension, hepatotoxicity

3rd line: Clonazepam and Dantrium sodium less effective but alternative options

148
Q

Non-pharm and pharm treatments for fatigue in MS

A

Non-pharm: aerobic exercise

Amantadine
* Caution with renal insufficiency

Modafinil
* CNS stimulant
* Can reduce hormonal contraception

149
Q

Treatment for tremor in MS

A

Propranolol or primidone

150
Q

Treatment for hyperreflexic bladder, hyporeflexic bladder, and overflow incontinence in MS

A

Hyperreflexic bladder (inability to store urine)
* Oxybutynin, tolterodine

Hyporeflexic bladder (failure to empty)
* Self-cath, risk of UTIs

Overflow incontinence
* Alpha blockers (terazosin, doxazosin, tamsulosin)

151
Q

Treatment of constipation in MS

A
  • Increase fiber and hydration
  • Laxative or enemas
152
Q

Treatment of depression in MS

A

 SSRI
 With concurrent pain, can use duloxetine
 With fatigue, use fluoxetine or bupropion

153
Q

Treatment of chronic pain in MS

A

carbamazepine

154
Q

Treatment of burning sensations in MS

A

TCAs, carbamazepine, gabapentin

155
Q

Treatment of neuropathic pain in MS

A

SNRIs, TCAs, gabapentin, pregabalin

156
Q

Treatment of sexual dysfunction in MS

A

Sildenafil, tadalafil, vardenafil

157
Q

Explain the relationship between vitamin D and MS

A

Increasing vitamin D levels may decrease severity of symptoms

Consider obtaining vitamin D level or providing supplementation to every patient with MS

158
Q

Teriflunomide brand and route

A

Aubagio, oral

159
Q

Teriflunomide ADE

A

Hepatotoxicity, pregnancy category X, dose related alopecia, diarrhea, nausea, flu, abnormal LFTs, paresthesia

Less common: lowered WBC, increased BP, severe liver damage, SJS, interstitial lung disease, acute renal failure

160
Q

Teriflunomide monitoring

A

Undergoes enterohepatic circulation, so plasma levels are detectable for up to 2 years (can speed up with cholestyramine or activated charcoal)

Check LFTs before start, every month for 6 months

Check CBC before start, monitor for infection

Monitor renal fxn, electrolytes, BP

Many drug interactions (warfarin, CYP2C8, CYP1A2)

161
Q

Dimethyl fumarate brand and route

A

Tecfidera, oral

162
Q

Dimethyl fumarate ADE

A

Flushing (common, sensation of heat, itching, red blush), GI (N/D, upper GI pain)

Highest in first month, decreases after, taking with food may reduce GI ADE, flushing may be lessened with ASA given 30 min before dose

163
Q

Dimethyl fumarate monitoring

A

Baseline CBC with lymphocyte, then Q6months

May cause lymphopenia, interrupt therapy if lymphocyte count less than 0.5x10^9 for more than 6 months

164
Q

Monomethyl fumarate brand and route

A

Bafiertam, oral

165
Q

Diroxemil fumarate brand and route

A

Vumerity, oral

166
Q

Diroxemil fumarate ADE

A

Lower rates of GI ADE compared to dimethyl fumarate

167
Q

T or F: diroxemil fumarate can be taken at the same time as dimethyl fumarate

A

False. Converts to same active metabolite as dimethyl fumarate, should not take concurrently but can be started day after ending the other

168
Q

Fingolimod brand and route

A

Gilenva, oral

169
Q

Fingolimod ADE and CI

A

Increased risk of life-threatening infections and tumor development

HA, diarrhea, back pain, elevated LFTs, cough

Less common: bradyarrhythmia and AV block

CI: recent hx of MI, stroke, TIA, HF, heart block, QTc >500, use with antiarrhythmics (amio or sotalol)

Pregnancy category C

170
Q

Fingolimod monitoring

A

Before: CBC, LFTs, ECG, opthalmalogic exam, varicella serology and zoster vaccination if antibody negative

Avoid live attenuated vaccines

Eye exams every 3-4 months

171
Q

Siponimod brand and route

A

Mayzent, oral

172
Q

Siponimod ADE

A

CI: CYP2C93/3 genotype, recent MI, unstable angina, advanced HF, AV block

HA, HTN, increased transaminase

Dose-dependent decreased lymphocyte counts, infections, macular edema, bradyarrhythmia, liver toxicity

May cause fetal harm, avoid in pregnancy

173
Q

Siponimod monitoring

A

Test for CYP2C9 genotype, CBC, LFT, varicella antibodies, ophthalmic, ECG

First dose: monitor for bradycardia and arrhythmias

Monitor LFT and BP during treatment

174
Q

Ozanimod brand and route

A

Zeposia, oral

175
Q

Cladribine brand and route

A

Mavenclad, oral

176
Q

Cladribine ADE and CI

A

URIs, HA, lymphocytopenia

CI: patients with malignancy or active chronic infection

CI in pregnancy, breastfeeding, and for women and men or reproductive potential unless effective contraception for 6 months after last dose

177
Q

Cladribine monitoring

A

Screen for infections, malignancy, pregnancy, baseline MRI

Lymphocyte counts before, during, and after treatment

178
Q

Interferon beta-1a brand and route

A

Avonex, Rebif, injectable

179
Q

Interferon beta-1a ADE and CI

A

Injection site redness and swelling, flu-like symptoms (can take NSAIDs, acetaminophen, steroids)

CI: severe depression, risk of suicide

Counsel on appropriate contraception

180
Q

Interferon beta-1a monitoring

A

Baseline CBCs, platelets, LFTs at 1 month, Q3months x 1 year, then Q6months

181
Q

Interferon beta-1b brand and route

A

Betaseron, Extavia, injectable

182
Q

Peginerfon beta-1a brand and route

A

Plegridy, injectable

183
Q

Glatiramer acetate brand and route

A

Copoxone, Glatopa, injectable

184
Q

Glatiramer acetate ADE

A

SQ injection, mild pain and pruritus at site

Transient chest tightness, flushing, dyspnea  if pt has no CAD, self-limited and benign

NO flu-like sx or depression

Pregnancy category B

185
Q

Glatiramer acetate monitoring

A

No lab monitoring required

186
Q

Ofatumumab brand and route

A

Kesimpta, injectable

187
Q

Ofatumumab ADE and CI

A

URI, HA, injection-related reactions, serious infections

CI: active HBV infection

Females should use effective form of contraception during treatment and 6 months after stopping

188
Q

Ofatumumab monitoring

A

HBV and quantitative serum immunoglobulins screening are required

Live vaccines not recommended

189
Q

Alemtuzumab brand and route

A

Lemtrada, infusion

190
Q

Alemtuzumab use

A

Reserve for patients with inadequate response to two or more MS therapies (safety profile)

191
Q

Alemtuzumab premedication

A

Premedicate with corticosteroids, administer antivirals for herpetic prophylaxis

192
Q

Alemtuzumab black box

A

Black Box: causes serious and sometimes fatal autoimmune conditions such as immune thrombocytopenia, infusion reactions, and increased risk of malignancies including thyroid cancer, melanoma, and lymphoproliferative disorders

193
Q

Mitoxantrone brand and route

A

Novantrone, infusion

194
Q

Mitoxantrone ADE

A

Nausea, alopecia, leukopenia

May impart blue-green color to urine, bluish color to sclera

195
Q

Mitoxantrone monitoring

A

Ejection fraction (required before each dose), signs of CHF

196
Q

Natalizumab brand and route

A

Tysabri, infusion

197
Q

Natalizumab black box

A

Black Box: Reports of progressive multifocal leukoencephalopathy (PML)  potentially lethal CNS infection caused by JCV, risk increases with number of infusions and also when used with other DMDs

198
Q

Natalizumab use

A

Can be used as monotherapy but only in patients who have not responded to or do not tolerate others

199
Q

Natalizumab ADE

A

Infusion reaction (rash, drowsiness, fever, chills, nauseas, flushing, decreased BP, SoB), HA, fatigue, UTI, depression, joint pain, abdominal pain

200
Q

Natalizumab monitoring

A

JCV antibody every 3-6 months

201
Q

Ocrelizumab brand and route

A

Ocrevus, infusion

202
Q

Ocrelizumab premedication

A

Premedicate with methylpred and antihistamine

203
Q

Ocrelizumab ADE

A

Infusion reactions and infections (upper and lower resp tract, skin infections)

204
Q

Ocrelizumab monitoring

A

Hepatitis B screening before each dose

205
Q

Rituxumab brand and route

A

Rituxan, infusion

206
Q

Definition of pain

A

ill-defined, unpleasant sensation, evoked by an external or internal noxious stimulus

207
Q

2 components of pain perception

A

o Nociceptive component
o Affective component

208
Q

Two pain pathways

A

ascending and descending

209
Q

What is transduction in the ascending pain pathway?

A

stimulation of nerve fibers known as nociceptors

210
Q

What is conduction in the ascending pain pathway?

A

nociceptor activation leads to the conversion of a chemical signal into an electrical signal through voltage-gated sodium channels which produce generation of action potentials that are conducted along A-delta and C fibers to the dorsal horn of the spinal cord

211
Q

What is the difference between the A-delta fiber and the C fiber?

A
  • C fiber – slow conducting (aching, poorly localized, unmyelinated, small diameter)
  • A-delta fiber – fast conducting (sharp, well-localized, myelinated, large diameter)
212
Q

What is transmission in the ascending pain pathway?

A

nociceptive pain fibers synapse in various layers of the dorsal horn and convert the electrical signals back into chemical signal by releasing excitatory neurotransmitters such as glutamate and substance P. Pain signals reach the brain through a host of ascending spinal cord pathways. The thalamus acts as a relay station within the brain as these pathways ascend and pass the impulses to higher cortical structures

213
Q

What is modulation in the descending pathway?

A

transmission can be facilitated by glutamate or substance P to make signals stronger, or the signal can be inhibited by descending pathways that consist of endogenous opioids (enkephalins and Beta-endorphins), GABA, norepinephrine, or serotonin

214
Q

How do endogenous opioids exert inhibitory effects?

A

Endogenous opioids exert inhibitory effect on pain transmission through substantia gelatinosa

Sensory A-beta fibers stimulate release of met-enkephalin from interneurons of substantia gelatinosa and block pain transmission

215
Q

How do exogenous opioids work?

A

Agonist (fentanyl, morphine, etc.) binding –> conformational changes in the GPCR (inhibition of adenyl cyclase, stimulation of K+ current, inhibition of voltage-gated calcium channels) –> decreased release of neurotransmitter (substance P, neurokinin A, neurokinin B, glutamate) –> hyperpolarization and relieves pain

216
Q

Opioid classes and receptor type

A

Class –> Receptor type
Endorphins –> Mu
Enkephalins –> Delta
Dynorphins –> Kappa

217
Q

Opioid receptor coupling and effects

A

Major opioid receptors are coupled to their effectors via G proteins
* Affect ion channel gating
* Modulate intracellular calcium disposition
* Alter protein phosphorylation

218
Q

What are the two well established direct G-protein coupled actions on neurons and what is the effect?

A

Closure of voltage gated Ca+ channels –> on presynaptic nerve terminals, reduction and inhibition of neurotransmitter release

Opening of K+ channels –> inhibition of postsynaptic neurons

219
Q

What is tolerance

A

With frequently repeated therapeutic doses of morphine, there is a gradual loss of effectiveness, larger dose must be administered

220
Q

How does the body maintain normal sensitivty of recetors

A

Maintenance of normal sensitivity of receptors requires reactivation by endocytosis and recycling
 Endogenous ligands result in this endocytosis followed by resensitization
 Morphine fails to induce endocytosis
 In contrast, methadone does induce receptor endocytosis

221
Q

Structure activity relationship of endogenous opioids

A

the relationship between chemical structure and pharmacological activity for a series of compounds

222
Q

What are the two regions of endogenous opioids

A

Message region: confers recognition at opioid receptors –> common sequence is Tyr – Gly – Gly – Phe

Address sequence: substype selectivity (mu, kappa, delta)

223
Q

Metabolism steps for fentanyl

A

Fentanyl –> dealkylation (phase I rxn) –> norfentanyl

224
Q

Biological activity of norfentanyl

A

Norfentanyl has no significant biological activity at the mu opioid receptor, “nor”= loss of functional group

225
Q

Metabolism steps for codeine

A

Two pathways

Codeine –> N-demethylation –> Norcodeine (inactive)

Codeine –> O-demethylation –> morphine (active)

Morphine either then undergoes phase I demethylation to become normorphine or phase II reactions to become other morphine substrates

226
Q

Metabolism steps for methadone

A

Two pathways

Methadone –> reduction –> methadol –> dealkylation –> normethadol –> dealkylation –> dinormethadol (active)

Methadone –> alkylation –> normethadone –> dealkylation –> dinormethadone –> reduction –> dinormethadol (active)

227
Q

Explain the difference between methadone, buprenorphine, and naltrexone for medication assisted treatment (MAT) for opioids addiction

A

 Methadone (full agonist)  fully replacing the effect of whichever opioid the person is addicted to
 Buprenorphine (partial agonist)  partially replacing the effect of whichever opioid the person is addicted to
 Naltrexone (antagonist)  block the effects of opioids

228
Q

What dose of morphine is associated with acute morphine poisoning?

A

> 50 mg, lethal dose is 250 mg

229
Q

How to treat acute morphine poisoning?

A

Positive pressure respiration, IV fluids, gastric lavage, naloxone

230
Q

How does naloxone work? How do we administer it?

A

Mu, kappa, and delta antagonist
Can reverse opioid overdose

If first dose does not work, can administer 2nd
Takes 2-5 minutes to take effect

Stays in system for one hour
* Shorter half-life than heroin
* Can go back into overdose after the hour

231
Q

What is pain?

A

unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

232
Q

What is chronic pain?

A

pain lasting >12 weeks or >3 months

233
Q

Describe the 3 different types of pain syndrome (include the definition and descriptors)

A

Somatic Pain: Pain arising from damage to muscle, bone, or skin; well localized; Sharp, intense, throbbing, localized

Visceral Pain: Pain arising from damage to organs; not well localized, can be referred; Gnawing, cramping, squeezing, diffuse, distant

Neuropathic pain: Pain arising from a lesion or disease of the somatosensory nervous system; Shooting, burning, numb, tingling, enhanced sensitivity to heat/cool

234
Q

What are the parts of pain assessment?

A

P: precipitating/palliating
Q: quality (what kind of pain?)
R: region/radiating
S: severity
T: timing/temporal
U: utilization (what have you tried?)
V: values

235
Q

What is osteoarthritis? Where is it most common?

A

 Common degenerative disorder of the joints leading to hypertrophic bone changes
 Most common in hands, knees, hips, and spine (asymmetric)

236
Q

Symptoms of osteoarthritis

A

persistent joint pain, stiffness, locomotor restriction

237
Q

Treatment algorithm for osteoarthritis

A
  • Non-pharm (regular exercise, bracing, splinting)
  • Topical NSAID –> systemic NSAID
  • Consider opioids, but monitor for dependence
  • Intraarticular injections
  • Surgery
238
Q

What is diabetic neuropathy?

A

 Nerve damage caused by poorly controlled diabetes that leads to numbness in extremities
 Most common microvascular complication of diabetes

239
Q

What are the symptoms of diabetic neuropathy?

A

unprompted numbness, tingling, burning, shooting (symmetrical)

240
Q

What are the risk factors of diabetic neuropathy?

A

poor blood sugar control, longer duration of diabetes, kidney disease, obesity, cigarette smoking

241
Q

What is the treatment algorithm for diabetic neuropathy? Include which agents are first and second line.

A
  1. Non-pharm (optimize glycemic control)
  2. 1st line: antidepressants (duloxetine) and anticonvulsants (pregabalin and gabapentin)
  3. 2nd line: antidepressants (venlafaxine and amitriptyline), topical (lidocaine patch and capsaicin), opioid (tramadol and tapentadol)
242
Q

What is fibromyalgia?

A

Widespread soft tissue pain affecting muscles, ligaments, tendons with no obvious objective abnormalities

243
Q

What are the symptoms of fibromyalgia?

A

diffuse musculoskeletal pain present for >3 months, often accompanied by fatigue, headache, cognitive disturbance, and sleep disturbance

244
Q

Treatment algorithm for fibromyalgia

A
  1. Non-pharm
  2. Pharm –> target bothersome symptoms

For sleep disturbances, use amitriptyline, cyclobenzaprine, pregabalin, gabapentin

For depression/anxiety, use duloxetine, milnacipran, amitriptyline, pregabalin

245
Q

What is post herpetic neuralgia

A

Pain in a dermatomal distribution caused by nerve damage secondary to an inflammatory response induced by viral replication (herpes zoster) within a nerve sustained for at least 90 days after acute herpes zoster

246
Q

What are the symptoms of postherpetic neuralgia

A

burning, shock-like pain, may be associated with allodynia (pain from stimuli which are not normally painful) or hyperalgesia (abnormally heightened sensitivity to pain)

247
Q

What are the risk factors of post herpetic neuralgia?

A

immunosuppression, advanced age, female, underlying diabetes

248
Q

Treatment algorithm for post herpetic neuralgia

A

1st line: gabapentin, pregabalin, lidocaine patch, capsaicin cream
2nd line: TCAs
3rd line: opioids (not preferred)

249
Q

What is acetaminophen used for? How is it used?

A

OA

max dose 3000mg OTC, 4000mg Rx

250
Q

What are NSAIDs used for and how are they used?

A

OA

Topical or systemic Q6-12H

Diclofenac gel: 2-4g, 4x/day, max 32 g/day

251
Q

Which NSAID is hardest on the GI tract? Which can be used?

A

Ketorolac, use celecoxib/ibuprofen

252
Q

Which NSAID should be used with CV risk factors? Which should be avoided?

A

Use naproxen, avoid celecoxib/diclofenac

253
Q

Which NSAID should be used with renal risk factors?

A

Use celecoxib/diclofenac, avoid naproxen (opposite CV risk factors)

254
Q

What is the order of NSAIDs from most COX-2 selective to most COX-1 selective?

A

My Crazy Dad Is Not In the Kitchen

Meloxican, celecoxib, diclofenac, ibuprofen, naproxen, indomethacin, ketorolac

255
Q

What are topicals used for?

A

Neuropathic, OA

256
Q

Which topical is used for diabetic neuropathy? How long do they take to work?

A

capsaicin patches and cream, helpful for pain that responds to heat, see relief in 2-4 weeks

257
Q

Which topical is used for post herpetic neuralgia?

A

Lidocaine patches

258
Q

What type of pain are antidepressants used for?

A

Neuropathic pain

259
Q

Which antidepressants are used for diabetic neuropathy? For fibromyalgia? For post herpetic neuralgia?

A

Diabetic: venlafaxine, duloxetine, amitriptyline, nortriptyline, desipramine

Fibromyalgia: duloxetine, milnacipran, amitriptyline

Post herpetic neuralgia: amitriptyline, nortriptyline, desipramine

260
Q

How long does it take to see results from antidepressants for pain?

A

4 weeks

261
Q

What pain syndromes are anticonvulsants used for?

A

Neuropathic pain

262
Q

What type of anticonvulsants are gabapentin and pregabalin?

A

Calcium channel blockers

263
Q

How long does it take to see pain improvement with anticonvulsants?

A

1-2 weeks (shorter for pregabalin)

264
Q

Advantages of pregabalin over gabapentin

A

Faster onset, higher bioavailability, dose can be titrated more rapidly, BID dosing

265
Q

Disadvantages of pregabalin

A

Higher risk of peripheral edema, schedule IV, more expensive, dose reduction for renal impairment (gabapentin needs this too)

266
Q

What type of pain are skeletal muscle relaxants used for? How are they used?

A

Muscle spasms, TID PRN

267
Q

What is the role of opioids in non-cancer pain?

A

LAST line, use lowest effective dose

268
Q

6 A’s for monitoring of opioid use

A

analgesia, affect, activities, adjuncts, ADE, aberrant behavior

269
Q

What is a seizure? How are they triggered?

A

Seizure: disorder viewed as a symptom of disturbed electrical activity in the brain

Disruption of homeostasis of neurons and their stability, which may trigger hyperexcitability

270
Q

Describe the occurrence of first seizure in terms of likelihood based on age

A

Bimodal distribution of first seizure occurrence (either infants or elderly usually)

271
Q

What is epilepsy?

A

chronic disorder of recurrent, unprovoked seizures

272
Q

List characteristics for increased seizure risk

A

Genetic mutations

Patients with cerebral palsy, head injury, strokes

Factors that may precipitate seizures
 Hyperventilation, sleep deprivation, stress, hormonal changes, puberty, menses, photo-stimulation

Medications
 Sub-therapeutic anti-epileptic drug (AED) levels
 Withdrawal of CNS depressants
 Antibiotics (penicillin, cephalosporins, ciprofloxacin, carbapenems)
 Bupropion
 SSRIs (if serotonin syndrome develops)
 Theophylline
 Meperidine (especially with renal dysfunction)
 Overdose (Effexor, TCAs, salicylates, tramadol)

273
Q

What are seizures in terms of pathophysiology?

A

Seizures result from excessive excitation of a large population of cortical neurons

Normal membrane conductance and inhibitory synaptic currents break down

274
Q

Mechanisms that contribute to hyperexcitability

A

 Alterations in the distribution number, type, and biophysical properties of ion channels in the neuronal membranes
 Biochemical modifications of receptors
 Modulation of second messaging systems and gene expression
 Changes in extracellular ion concentrations
 Alterations in neurotransmitter uptake and metabolism
 Modifications in the ratio and function of inhibitory circuits

275
Q

Mechanisms of control of abnormal neuronal activity (how do the AEDs work?)

A

Elevating the threshold of neurons to electrical or chemical stimuli
* Involves stabilization of neuronal membranes

Limiting the propagation of the seizure discharge from the origin
* Depression of synaptic transmission and reduction of nerve conductance

276
Q

How are seizures classified? (what is looked at clinically?)

A

EEG and symptoms

277
Q

What is a partial (focal) seizure? How does it manifest?

A

Begin in one hemisphere and result in asymmetric motor manifestation

Can manifest as changes in motor function, sensory, or somatosensory symptoms, or automatisms (brief set of unconscious behaviors like lip smacking or finger rubbing)

278
Q

What are the 3 types of partial seizure?

A

Simple partial: WITHOUT loss or change of consciousness

Complex partial: WITH loss or change of consciousness

Secondary: partial onset which evolves into generalized tonic-clonic seizure

279
Q

What is a generalized seizure? How does it manifest?

A

Clinical manifestations that indicate involvement in both hemispheres

Bilaterally symmetrical without local onset

Loss of consciousness

280
Q

What are the 6 types of generalized seizures?

A

Absence, myoclonic, clonic, tonic, tonic-clonic, atonic

281
Q

Describe absence seizures

A

Sudden onset, interruption of ongoing activities, blank stare, possibly brief upward rotation of the eyes

Commonly occurs in young children

282
Q

Describe myoclonic seizures

A

Brief shock-like contractions of the face, trunk, and extremities

283
Q

Describe clonic seizures

A

Contraction of muscles into a rigid position

284
Q

Describe tonic-clonic seizures

A

Sudden sharp contractions followed by a period of rigidity

Patients may moan, cry, lose sphincter control, bite the tongue, develop cyanosis

285
Q

Describe atonic seizures

A

Sudden loss of muscle tone

Head drop, dropping of a limb, slumping to the ground

Patients often wear protective head gear

286
Q

What are idiopathic seizures?

A

no identifiable cause

287
Q

What are secondary seizures caused by?

A

Infections, fever, intracranial events, toxins, metabolic

288
Q

What are febrile seizures? Who are they most common in?

A

Occurs primarily in children between 6 months and 6 years

Seizures develop as the temperature is increasing rapidly but may develop as the fever is declining

Can occur during both viral and bacterial infections

Majority have the seizure on the first day of illness, often first sign child is sick

289
Q

T or F: only high temperatures lead to febrile seizures

A

False

290
Q

T or F: febrile seizures require daily AED

A

False

291
Q

T or F: usually children who have a febrile seizure will not have another

A

False, children with febrile seizures are at risk for developing recurrent febrile seizures

292
Q

What is the most important cause of symptomatic epilepsy in people 15-24 years old?

A

TBI (traumatic brain injury)

293
Q

T or F: the less severe the injury, the longer the patient is at risk for late seizures

A

False. More severe the injury, longer the patient is at risk for late seizures

Mild TBI at risk for 5 years, moderate for 10 years, severe for 20+ years

294
Q

What is the difference between early seizures after TBI and late seizures after TBI?

A

Early seizures (within 7 days of TBI): Acute symptomatic events with a low likelihood of recurrence, prophylaxis with antiepileptic drugs is used to prevent early post-traumatic seizures (has been shown to reduce number of early seizures)

Late seizures: represent epilepsy

295
Q

T or F: AED are always initiated after the 1st seizure

A

False, started after the 2nd seizure, not usually initiated after 1st seizure unless:
 Abnormalities on EEG
 Remote symptomatic cause
 Abnormal neurologic examination

296
Q

T or F: we should always try to use multiple AED for patients with epilepsy

A

False, monotherapy is preferred, but we often need multiple AED

297
Q

How often should drug levels of AED be checked? Why is this useful? What might cause them to flucutate?

A

Drug levels should be checked at least yearly (in patients not having seizures, not undergoing medication changes)

Useful to…
* Establish individual therapeutic concentration when a patient is in remission
* Assist in the diagnosis of clinical AED toxicity
* Assess compliance
* Guide dose adjustments

But drug concentrations may fluctuate in compliant patients
* Lab errors
* Generic substitution
* Drug interactions
* Variable pill potency (where was the medication stored?)

298
Q

T or F: AED are lifelong medications

A

False, discontinuation may be considered after 2-4 year seizure-free interval

299
Q

How should AED be discontinued?

A

Gradual tapering (25% monthly, can be tapered faster for ADE)

If on more than one, stop the medication that is less appropriate for the seizure type or the agent responsible for the ADE

300
Q

What can happen if AED are abruptly discontinued? What are factors that increase this risk?

A

Withdrawal seizures

Factors that increase the risk of seizure recurrence
* History of high frequency seizures
* Repeated SE episodes
* Combination of seizure types
* Development of abnormal mental functioning
* Identifiable brain disease
* Abnormal neurologic examination
* Seizure onset after the first decade
* Poor initial response to treatment
* Combination therapy
* Selected epilepsy syndromes
* Abnormal EEG
* Family history of epilepsy

301
Q

Why is it important to dose adjust AED in the elderly? (think of ADME)

A

Drug interactions (CYP3A4)

Hypoalbuminemia is common in elderly
* Many drugs are bound, more free, active drug

Body mass changes during aging (affects drug distribution)

Declining renal or hepatic function

Pharmacodynamic response can change and become more sensitive to neurocognitive ADEs

302
Q

Why is it important to dose adjust AED in infants? (think of ADME)

A

Increase in total body water to fat ratio

Decrease in serum albumin

Decreased renal and hepatic function

Past 2-3 years of age, children may have greater hepatic activity than adults, may require higher doses

303
Q

Role of estrogen in seizures

A

seizure-activating effect

304
Q

Role of progesterone in seizures

A

seizure-protecting effect

305
Q

When are women at highest risk for seizures?

A

Just before and during menstruation

At ovulation (Related to progesterone withdrawal, Changes to estrogen : progesterone ratio)

Peri-menopausal period can be associated with worsening seizure (fluctuations of sex hormones)

306
Q

How is hormonal contraceptive affected by AED? If we use hormonal contraceptive in these patients, what should we use?

A

Enzyme induction of oral contraceptive metabolism by AEDs

Associated with decreased estrogen and progesterone levels

Suggest alternative form of contraception

Often recommend contraceptive with at least 50 mcg of estrogen

307
Q

Relationship between pregnancy and seizures

A

25% of women have increased seizures during pregnancy

308
Q

Relationship between AED and pregnancy

A

Congenital malformation occurs in infants born to women with epilepsy
* 90% of pregnancies have successful outcomes
* Congenital heart malformations, orofacial clefs, spina bifida, neural tube defect
* Thought to be due to folate insufficiency associated with AEDs
* Many teratogenic effects can be prevented with adequate folate intake

Pregnancy category D (phenytoin, carbamazepine, valproic acid, phenobarbital)

309
Q

Which AED are inducers?

A

carbamazepine, phenytoin, phenobarbital

310
Q

Which AED are inhibitors?

A

Valproic acid

311
Q

Which AED are both inducers and inhibitors?

A

Felbamate, oxcarbazepine, topiramate

Neuro/Psych (1 decks)

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