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PT 2 > Block 7 - L5-L6 > Flashcards

Block 7 - L5-L6 Flashcards

1
Q

What is an epileptic seizure?

A

Sudden change in behavior that is the consequence of electrical hypersynchronization of neuronal networks involving the cortex

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2
Q

What percent of the population experience a single seizure? What percent of that group develop epilepsy?

A

10%

1/3

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3
Q

What age groups have epilepsy?

A

Bimodal distribution - young and old

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4
Q

The majority of seizures are ___ (focal vs. generalized).

A

Focal

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5
Q

What is the criteria for diagnosis of epilepsy?

A

2+ unprovoked seizures more than 24 hours apart

OR

1 seizure + increased risk for further seizures

OR

Diagnosis of an epilepsy syndrome

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6
Q

What are the general classifications of seizures?

A
  1. Focal onset vs. Generalized onset
  2. Within focal - aware vs. impaired awareness
  3. Within generalized - motor (eg. tonic-clonic) vs. non-motor (absence)
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7
Q

What are the major underlying features of the pathophysiology of seizures?

A
  1. Altered intrinsic membrane properties (ionic conductance of Na+ and Ca2+ channels)
  2. Altered synaptic function (reduced inhibition - less GABA, increased excitation - more glutamate)
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8
Q

Which anti-epileptic drugs work on Na+ channels? (8)

A
  1. Carbamazepine
  2. Lacosamide
  3. Lamotrigine
  4. Oxcarbazepine
  5. Phenytoin
  6. Topiramate
  7. Valproate
  8. Zonisamide
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9
Q

Which anti-epileptic drugs work on Ca2+ channels? (4)

A
  1. Ethosuximide
  2. Gabapentin
  3. Valproate
  4. Zonisamide
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10
Q

Which anti-epileptic drugs work on GABA (A) receptors? (7)

A
  1. Benzodiazepines
  2. Phenobarbital
  3. Lamotrigine (?)
  4. Tiagabine
  5. Topiramate
  6. Valproate
  7. Vigabatrin
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11
Q

Which anti-epileptic drug works on glutamate receptors? (1)

A
  1. Topiramate
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12
Q

Discuss the generalities of the pharmacokinetics of anti-epileptic drugs.

  1. Distribution
  2. Absorption
  3. Plasma proteins
  4. Clearance
A
  1. Must enter the CNS, distributed into TBW
  2. Good absorption
  3. Most are not highly bound to plasma proteins
  4. Mostly cleared through the liver
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13
Q

Most anti-epileptics follow a linear dosing. Describe what happens with phenytoin and carbamazepine.

A

Both are non-linear.

Phenytoin - saturable system in which increased doses leads to decreased clearance

Carbamazepine - eventually begins to self-metabolize (autoinduction) - cannot increase concentration by increasing dose

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14
Q

Which anti-epileptics are P450 inducers?

A
  1. Phenytoin
  2. Carbamazepine
  3. Phenobarbital
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15
Q

Which anti-epileptics are P450 inhibitors?

A
  1. Valproate
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16
Q

Which anti-epileptics should not be given to a patient with liver disease?

A
  1. Phenytoin
  2. Carbamazepine
  3. Valproate
  4. Ethosuximide
  5. Benzodiazepines
  6. Tiagabine
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17
Q

Which anti-epileptics should not be given to a patient with renal disease/will necessitate a dose reduction?

A
  1. Gabapentin
  2. Topiramate
  3. Levetiracetam
  4. Oxcarbazepine
  5. Vigabatrin
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18
Q

After a second unprovoked seizure, epilepsy is diagnosed and medications are prescribed. What is involved in selecting an anti-epileptic?

A
  1. Efficacy
  2. Safety/tolerability
  3. Ease of use
  4. Comorbidity
  5. MOA
  6. Cost
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19
Q

What drug is specific for absence seizures only?

A

Ethosuximide

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20
Q

What drug is specific for myoclonic seizures only?

A

Levetiracetam

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21
Q

What drugs are specific for infantile spasms only?

A

Vigabatrin (especially in the presence of tuberous sclerosis), ACTH, steroids

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22
Q

What are the 5 first line treatment options for focal onset seizures?

A
  1. Oxcarbazepine
  2. Lacosamide
  3. Carbamazepine
  4. Lamotrigine*
  5. Levetiracetam*
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23
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Oxcarbazepine.

A

MOA: Na+ channels
AE: skin rash, hyponatremia
Drug interactions: moderate potential
Contraindications: renal disease, penchant for rashes, combining with other Na+ blocking AEDs
Teratogenicity: category C (cleft lip, palate)

Note - advantageous due to extended release formulation

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24
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Lacosamide.

A 
MOA: Na+ channels
AE: dizziness, headache, N/V, diplopia, fatigue, sedation
Drug interactions: low/no potential
Contraindications: none
Teratogenicity: category C

Note - can be used with another drug of a different MOA for greater efficacy/tolerability

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25
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Carbamazepine.

A

MOA: Na+ channels
AE: SJS and toxic epidermal necrolysis (especially with HLA-B1502 - Asian descent), hyponatremia
Drug interactions: high potential
Contraindications: hepatic disease, generalized myoclonic, atonic, and absence seizures (may exacerbate)
Teratogenicity: category D (congenital birth defects)

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26
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Lamotrigine.

A

MOA: Na+ channels and something else (?)
AE: skin rash, SJS, toxic epidermal necrolysis, hypersensitivity syndrome
Drug interactions: moderate potential
Contraindications:
Teratogenicity: category C (but may be the lowest)

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27
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Levetiracetam.

A

MOA: Na+ channels
AE: behavioral or psychiatric disturbances
Drug interactions: low/no potential
Contraindications: renal disease
Teratogenicity: category C (but may be the lowest)

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28
Q

What are the 3 first line treatment options for idiopathic generalized seizures with onset in adolescence (males)?

A
  1. Valproate
  2. Levetiracetam
  3. Lamotrigine
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29
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Valproate.

A

MOA: GABA potentiation, Na+ and Ca2+ channels
AE: skin rash
Drug interactions: moderate potential
Contraindications: hepatic disease, urea cycle disorder
Teratogenicity: Category X (highest)

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30
Q

What are the 2 first line treatment options for idiopathic generalized seizures with onset in adolescence (females)?

A
  1. Lamotrigine
  2. Levetiracetam

+ folic acid

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31
Q

What are the 3 first line treatment options for generalized onset, non-motor childhood absence seizures?

A
  1. Ethosuximide

2. Valproate

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32
Q

Discuss the MOA, AE, drug interactions, contraindications, and teratogenicity of Ethosuximide.

A 
MOA: blocking T-type Ca2+ channels
AE: aplastic anemia, thrombocytopenia, agranulocytosis, SLE, suicidal ideation
Drug interactions: low/no potential
Contraindications: hepatic disease
Teratogenicity: Category C
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33
Q

What factors are important when considering discontinuing anti-epileptic drugs?

A
  1. Natural history of epilepsy
  2. Probability that patient will remain seizure-free
  3. Duration of seizure-free interval before withdrawal
  4. Risk factors for recurrence
  5. Consequences of recurrence
  6. Risks of long-term AED therapy
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34
Q

What is SUDEP?

A

Sudden Unexpected Death in Epilepsy - leading cause of mortality in patients with chronic refractory epilepsy

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35
Q

What is PNES?

A

Psychogenic Non-epileptic Seizures - sudden changes in behavior that resemble epileptic seizures but are not associated with typical EEG or other diagnostic changes

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36
Q

Which anti-epileptic medications have a high potential for drug-drug interaction? (6)

A
  1. Phenytoin
  2. Carbamazepine**
  3. Valproate
  4. Phenobarbital
  5. Primidone
  6. Felbamate
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37
Q

Which anti-epileptics have significant cognitive effects? (4)

A
  1. Phenobarbital
  2. Primidone
  3. Benzodiazepines
  4. Topiramate
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38
Q

What are the idiosyncratic reactions seen in the “classic” anti-epileptic drugs (Carbamazepine, Ethosuximide, Phenobarbital, Phenytoin, Valproate)?

A
  1. Agranulocytosis
  2. Aplastic anemia
  3. Dermatitis/rash
  4. SJS
  5. Hypersensitivity
  6. Hepatic failure
  7. Pancreatitis

Ethosuximide (not 6-7)
Phenobarbital (not 2, 7)
Others - all

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39
Q

What is the main reaction seen in the “newer” anti-epileptic drugs (Gabapentin, Lamotrigine, Topiramate, Tiagabine, Oxcarbazepine, Levetiracetam, Zonisamide)?

A
  1. Dermatitis and rash

Lamotrigine - also SJS, hypersensitivity, hepatic failure
Topiramate - also hepatic failure
Zonisamide - also agranulocytosis, aplastic anemia, SJS

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40
Q

What is the black box warning on Carbamazepine?

A

Aplastic anemia

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41
Q

What is the black box warning on Lamotrigine?

A

SJS, toxic epidermal necrolysis, hypersensitivity syndrome

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42
Q

What is the black box warning on Valproate?

A

Hepatotoxicity, pancreatitis, Teratogenicity

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43
Q

What is first line treatment of status epilepticus?

A

IV Lorazepam

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44
Q

Which anti-epileptic medication is Category X teratogenicity?

A

Valproate

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45
Q

What is the major indication for Phenytoin?

A

Status epilepticus

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46
Q

What are the key AE of phenytoin?

A
  1. Gingival hyperplasia, hirsutism, coarse facial features
  2. Osteomalacia
  3. Category D (birth defects)
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47
Q

What is the major contraindication for phenytoin?

A

Generalized myoclonic and absence seizures (may exacerbate)

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48
Q

What is the major indication for phenobarbital?

A

Status epilepticus

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49
Q

What are the key AE of phenobarbital?

A
  1. Sedation, decreased concentration, mood changes (depression)
  2. Dupuytren’s contractures, plantar fibromatosis, frozen shoulder [long term use]
  3. Category D (cardiac malformations)
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50
Q

Which drug can be given for juvenile myoclonic epilepsy?

A

Valproate

51
Q

What is indicated for Lennox-Gastaut syndrome?

A

Lamotrigine

52
Q

How can the skin rash be avoided in Lamotrigine?

A

Slow titration of dose

53
Q

Lamotrigine is synergistic when combined with ___.

A

Valproate

54
Q

What are the key AE of topiramate?

A

Cognitive slowing, renal stones, Category D (cleft lip/palate)

55
Q

What are the keyAE of tiagabine?

A

Dose-related episodes of non-convulsive status epilepticus or encepahlopathy

56
Q

What is the contraindication of tiagabine?

A

May exacerbate absence and myoclonic seizures

57
Q

Which drug has no known significant pharmacokinetic interactions?

A

Levetiracetam

58
Q

What is the major indication for Levetiracetam?

A

Generalized myoclonic seizures

59
Q

What is a key AE of Zonisamide?

A

Kidney stones

60
Q

Zonisamide cannot be used with a ___ allergy.

A

Sulfa

61
Q

What is the black box warning of Vigabatrin?

A

Permanent bilateral concentric visual field constriction; requires regular visual field testing

62
Q

What is the contraindication of Vigabatrin?

A

May exacerbate absence and myoclonic seizures

63
Q

How is serotonin produced?

A 
1. L-tryptophan = aa precursor
[Tryptophan hydroxylase]
2. 5-hydroxy-L-tryptophan = OTC
[5-hydroxytryptophan decarboxylase]
3. Serotonin
[Monoamine oxidase]
4. 5-hydroxyindoleacetic acid (inactive metabolite, excreted)
64
Q

What is the rate limiting enzyme in the production of serotonin?

A

Tryptophan hydroxylase

65
Q

List the 7 serotonin receptor families.

A

5-HT__

1A, 1B, 2A, 2B, 2C, 3, 4

66
Q

Which serotonin receptors are pre-synaptic (cell body vs. nerve terminal)?

A

1A (cell body) and 1B (nerve terminal)

67
Q

How do pre-synaptic serotonin receptors function?

A

As auto-receptors to provide negative feedback

68
Q

What is the general function of 1A and 1B receptors?

A

Pre-synaptic: inhibitory (decrease neuronal activity/NT release (A vs. B)

Post-synaptic: inhibitory (reduce membrane excitability) - coupled to G-alpha-i

69
Q

What is the general function of 2 A, B, C receptors?

A

Coupled to G-alpha-q, activate IP3/DAG to increase Ca2+ release, causing excitation in the post-synaptic membrane

70
Q

What is the general function of 5-HT3 receptors?

A

Activate ligand-gated ion channels (fast excitatory response)

71
Q

What is the general function of 5-HT4 receptors?

A

Coupled to G-alpha-s, lead to increase cAMP and excitatory response

72
Q

What is the primary location and function of 5-HT1A receptor families and the effect manipulated?

A

Location: cortex and hypothalamus

Effect: mood, cognitive function, neuroendocrine function (activating 1A receptors leads to inhibition of inhibitory GABAergic neurons and thus activation)

Location: raphe nuclei

Effect: inhibition of 5-HT release

73
Q

What is the primary location and function of 5-HT1D receptor families and the effect manipulated?

A

Location: cerebral vascular smooth muscle, nerve terminal

Effect: vasoconstriction and inhibition of NT release

74
Q

What is the primary location and function of 5-HT2A/C receptor families and the effect manipulated?

A

Location: striatum and frontal cortex

Effect: hallucination and inhibition of DA release

75
Q

What is the primary location and function of 5-HT3 receptor families and the effect manipulated?

A

Location: enteric chromaffin cells, area postrema, emetic center

Effect: gut motility, nausea/vomiting

76
Q

What is the primary location and function of 5-HT4 receptor families and the effect manipulated?

A

Location: myenteric plexus

Effect: gut motility

77
Q

What is the primary location and function of 5-HT transporters and the effect manipulated?

A

Location: 5-HT nerve terminals
Effect: removal of 5-HT from synapse

78
Q

Describe the mechanism by which SSRIs are thought to act to improve mood.

A

SSRIs block the 5-HT transporters, increasing 5-HT post-synaptic receptor activation; takes 2-4 weeks for full effect due to the autoreceptor activation

79
Q

What are the indications for SSRIs?

A

Depression, PTSD, OCD

80
Q

What are the AE of SSRIs?

A

Sexual dysfunction and insomnia

81
Q

What is the contraindication of SSRIs and why?

A

MAO inhibitor - can cause serotonin syndrome

82
Q

What is the MOA of 5-HT1A agonists?

A

Unknown; likely due to activation of post-synaptic receptors in cortical regions

83
Q

What are the indications of 5-HT1A agonists?

A

GAD

Off-label: w/SSRI for major depression

84
Q

What are the AE of 5-HT1A agonists?

A

Increased anxiety during initial treatment, drowsiness, nausea

85
Q

What is the MOA of SARIs (serotonin antagonist-reuptake inhibitors)?

A

5-HT 2A/2C antagonist + SSSRI - blocks side effects associated with SSRI

86
Q

What are the indications of SARIs?

A

Anxiety, depression (with SSRI)

Off-label - insomnia

87
Q

What are the AE of SARIs?

A

Drowsiness, black box warning - increased suicidality in young adults at start of treatment

88
Q

What are the contraindications of SARIs?

A

MAO inhibitors

89
Q

___ contain 90% of the body’s serotonin.

A

Eterochromaffin cells

90
Q

What is the MOA of 5-HT3 receptor anatgonists? Give an example of a drug.

A

Blocks 5-HT3 receptor; odansetron

91
Q

What is the indication for odansetron?

A

Chemo-induced emesis

92
Q

What are the AE of odanestron?

A

None

93
Q

What is the MOA of 5-HT4 receptor agonists? Give an example of a drug.

A

Stimulates release of Ach in the myenteric plexus, which promotes peristalsis; metoclopramide

94
Q

What is metoclopramide indicated for?

A

Gastroparesis

95
Q

What are the AE of metoclopramide?

A

Arrhythmia (QT prolongation)

96
Q

Describe how 5-HT1D receptor agonists are thought to prevent migraines; give an example of a drug.

A

Migraines may be related to vasodilatory neuropeptide release from trigeminal nerve fibers that surround cerebral blood vessels. These drugs inhibit release of nociceptive and inflammatory NT from the trigeminal nerve axons. They also promote cerebrovascular vasoconstriction by decreasing cAMP and PKA-mediated inhibition of MLCK

Sumatriptan (triptans)

97
Q

What is the indication for sumatriptan?

A

Prophylaxis for migraines

98
Q

What are the AE/contraindications of sumatriptan?

A

Coronary vasoconstriction; patients with CAD

99
Q

Activation of the D1 (D1, D5) receptor family has what effect?

A

Increased cAMP - increases excitability

100
Q

Activation of the D2 (D2, D3, D4) receptor family has what effect?

A

Decreased cAMP
Increased K+ currents
Decreased Ca2+ currents

Decreases excitability

101
Q

What is the goal of pharmacological therapy in Parkinson’s disease?

A

Re-establish dopaminergic tone in the striatum through increased dopamine production, decreased dopamine metabolism, and suppression of the indirect pathway through D2/D3 receptor activation

102
Q

What is the indication of L-DOPA?

A

Parkinson’s Disease

103
Q

What is the MOA of L-DOPA?

A

Increases dopamine release in the nigrostriatal pathway

104
Q

What are the AE of L-DOPA?

A

Dyskinesias and motor fluctuations with long term use

Arrhythmia, nausea, anxiety, hallucinations

105
Q

What is the indication of Carbidopa?

A

Concurrent treatment with L-DOPA ti reduce peripheral dopamine formation

106
Q

What is the MOA of Carbidopa?

A

Inhibits AADC in peripheral tissue (which cannot cross the BBB)

107
Q

What are the AE of Carbidopa?

A

Augmentation of side effects of L-DOPA in the CNS

108
Q

What is the MOA of Selegiline?

A

Selective inhibition of MAO-B (no dietary restrictions at low doses)

109
Q

What are the indications of Selegiline?

A

Parkinson’s disease (lower doses), depression (higher doses)

110
Q

What are the AE of Selegiline?

A

Hypotension (dizziness), dry mouth, hypertensive crisis, serotonin syndrome

111
Q

What are the contraindications of Selegiline?

A

Concomitant use of indirect acting sympathomimetics or drugs that increase 5-HT NT

112
Q

What is the indication of Tolcapone?

A

More advanced Parkinson’s disease

113
Q

What is the MOA of Tolcapone?

A

Inhibition of COMT; prolongs and increases the effect of L-DOPA, reduces the fluctuations

114
Q

What are the AE of Tolcapone?

A

Dyskinesia, hallucinations, nausea

115
Q

What are the contraindications of Tolcapone?

A

Liver failure

116
Q

What is the indication of Pramipexole and Rapinirole?

A

Monotherapy in early Parkinson’s or adjunt to L-DOPA

117
Q

What is the MOA of Pramipexole and Rapinirole?

A

D3 and D2 receptor agonists - post-synaptic activation in basal ganglia; may be neuroprotective (antioxidant, etc.)

118
Q

What are the AE of Parmipexole and Rapinirole?

A

GI distress, postural hypotension, arrhythmia, dyskinesias, mental disturbances (hallucinations, delusions)

119
Q

What are the dopamine agonists used to treat Parkinson’s?

A

L-DOPA, Pramipexole and Ropinirole

120
Q

What is the MOA of Donepezil, Rivastigmine, and Galantamine?

A

Orally active acetylcholinesterase inhibitors that cross the BBB (modest efficacy)

121
Q

What are the AE of Donepezil, Rivastigmine, and Galantamine?

A

N/V, peripheral cholinomimetic effects

122
Q

What is the MOA of Memantine?

A

Use-dependent binding and non-competitive blockade of NMDA receptors

123
Q

How does Memantine compare to AchE inhibitors?

A

Less toxic, but less efficacious

PT 2 (15 decks)

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