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Pharmacology > Neurodegenerative and Movement Disorders > Flashcards

Neurodegenerative and Movement Disorders Flashcards

1
Q

Excitotoxicity:

  1. Suggested as a possible factor in?
  2. 2 types of movement disorder classifications and examples.
A

Excitotoxicity:

  1. Possible factor in ALS, dementia, stroke, and parkinsons
  2. Akinetic - Rigid (hypokinetic) movement: parkinsons and parkinsonian like disorders (atrophy, supranuclear palsy, dimentia, ALS, corticobasal ganglionic degeneration); Hyperkinetic movement disorder: chorea (huntingtons), dystonia, tremor, tics, myoclonus
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2
Q

Idiopathic Parkinsons Disease:

  1. Degenerative disorder of the CNS (primarily the ____ ___) that often impairs?
  2. Characterization?
  3. Imbalance between?
A

Idiopathic Parkinsons Disease:

  1. Primarily the basal ganglia that impairs motor skills, speech, and other functions
  2. Characterized by muscle rigidity, tremor, bradykineasia/akinesia, and postural instability
  3. Imbalance between dopaminergic and cholinergic inputs
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3
Q

Idiopathic Parkinsons Disease:

  1. Shift is caused by death of ___ neurons where?
  2. Clinical diagnosis requires 2-3 of the cardinal signs: what are these signs?
A

Idiopathic Parkinsons Disease:

  1. Death of DA neurons in the SNc
  2. Tremor (rest>action), rigiditiy (+/- cogwheeling), bradykinesia, and impaired postural effects
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4
Q

Idiopathic Parkinsons Disease:

  1. What are the two pathways? What occurs when theres degeneration?
  2. Other disorders with Parkinsonian-like symptoms?
A

Idiopathic Parkinsons Disease:

  1. Direct and indirect pathway; there is a decreased activity in the direct pathway and increased activity in the indirect
  2. Drug induced parkinsons, progressive supranuclear palsy, olivopontocerebellar syndrome, shy-drager syndrome (multiple system atrophy), and cortico-basal degeneration
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5
Q

Parkinsons medications:

  1. Levodopa meds?
  2. DA agonists?
  3. Adjunctive meds?
A

Parkinsons meds:

  1. Levodopa: sinemet and stalevo
  2. DA agonists: Ropinirole, pramipexole, pergolide, and bromocriptine
  3. Adjunctive: carbidopa, entacapone/tolcapone, selegiline/rasagiline, amantadine, and anticholinergics
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6
Q

Sinemet:

  1. Parkinsons indication?
  2. Treatment of what else?
  3. Effectiveness?
  4. Sinemet is a combination of?
A

Sinemet:

  1. Most effective and rapidly acting agent for treatment of IPD symptoms
  2. Also used for Dopa-responsive dystonia (DRD)
  3. Initially releives almost all symptoms in over 1/3 of patients
  4. Sinemet is a combination of levodopa and carbidopa
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7
Q

Sinemet:

Levadopa (L-DOPA)

  1. A ____ used to increase brain DA levels, especially in the ____. Difference from dopamine?
  2. Absorption mediated by? Competition?
  3. Converted to DA by ______. Where?
A

Sinemet:

Levadopa (L-DOPA)

  1. A prodrug to increase brain DA levels, especially in the striatum. CAN cross BBB whereas DA CANNOT
  2. Absorption mediated by saturable amino acid transporter and dietary AA can compete for transport
  3. Converted to DA by aromatic L amino acid decarboxylase (LAAD) in BOTH the CNS and PERIPHERY
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8
Q

Sinemet:

Levodopa

  1. Required cofactor?
  2. Percent that reaches brain? Why?
A

Sinemet:

Levodopa:

  1. Pyridoxal phosphate (vitamin B6) is required for decarboxylation
  2. <1% because of peripheral synthesis of DA and metabolism by COMT
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9
Q

Sinemet:

Carbidopa:

  1. MOA?
  2. Reduces side effects caused by DA in the _____ such as?
  3. Increases concentration of _____ and _____ in the ___
A

Sinemet:

Carbidopa:

  1. MOA: inhibits peripheral synthesis (impermeable at BBB) of levodopa to DA by inhibiting DOPA decarboxylase (allows 75% decrease in dose)
  2. Reduces side effects in the periphery like orthostatic hypotension and cardiac arrhythmias
  3. Increases L-DOPA and DA in the Brain
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10
Q

Sinemet:

Side effects:

  1. Levodopa can cause N/V and anorexia due to DA effects where? Antiemetics?
  2. Most common symptom?
  3. What can be reduced with the use of carbidopa?
A

Sinemet:

Side effects:

  1. N/V due to DA on area postrema. NO antiemetics bc they reduce the effects of levodopa
  2. Most common: Dyskinesias esp choreoathetosis of the face and distal extremities
  3. With carbidopa can decrease the possibility of cardiac dysrhythmias ( initially due to increased peripheral catecholamines and their activation of Beta receptors)
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11
Q

Sinemet:

Side effects:

  1. What develops in 20% of patients? Treatment?
  2. Can also cause ____ attack without warning.
A

Sinemet:

Side effects:

  1. 20%: psychosis. Contraindication to give typical antipsychotics (they increase symptoms of PD) but can give clozapine (atypical antipsychotic)
  2. Can also cause sleep attack
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12
Q

Sinemet:

Loss of effects:

  1. Time period? What changes?
  2. two patterns and description?
  3. Can try to minimize by doing what?
A

Sinemet:

Loss of effects:

  1. Less than 5 years; Increase motor fluctuations and dyskinesias
  2. Gradual (at end of dosing period) or abrupt loss (anytime)
  3. Some try to increase therapeutic effects by going on a drug holiday for 10 days (withdrawal at the hospital)
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13
Q

Catechol-O-methyl transferase (COMT) inhibitors:

  1. Drugs?
  2. Indications? When is it prescribed? Role?
A

Catechol-O-methyl transferase (COMT) inhibitors:

  1. Entacapone, Stalevo, and tolcapone
  2. Adjunct to levodopa/carbidopa; prescribed only when patient begins to experience “off” periods; role is to delay wearing off and extend “on” time
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14
Q

Catechol-O-methyl transferase (COMT) inhibitors:

  1. What is stalevo a combination of?
  2. Which of the COMT inhibitors can cross the BBB?
  3. Entacapone side effects?
  4. Tolcapone side effects? This makes it a drug of ____ ____.
A

Catechol-O-methyl transferase (COMT) inhibitors:

  1. Stalevo: levodopa/carbidopa/entacapone
  2. Tolcapone can cross the BBB
  3. Entacapone SE: N/V, diarrhea, and constipation
  4. Tolcapone can cause severe hepatotoxicity and is this a drug of last resort
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15
Q

Dopamine Agonists:

  1. Indication?
  2. Less effective than _____
  3. Advantages?
A

Dopamine Agonists:

  1. First line for treatment of symptomatic IPD, esp pts with mild to moderate symptoms
  2. Less effective than levodopa
  3. Advantages: arent converted to toxic metabolites, dont compete with proteins for uptake and transport into CNS, and lower incidence of dyskinesia and response failure with long-term use
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16
Q

Dopamine Agonists:

  1. MOA?
  2. 2 subclasses of drugs? Which is used more widely? Why?
A

Dopamine Agonists:

  1. MOA: mimic dopamine in the CNS at D2 receptors (inhibits INDIRECT pathway)
  2. Drug subclasses: ergot-derived and non-ergot derived; non-ergot derives are used more widely because ergot can cause valvular heart disease
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17
Q

Dopamine Agonists:

Non-ergot derivatives:

  1. Drugs?
  2. Indications?
  3. Non-parkinson indications?
A

Dopamine Agonists:

Non-ergot derivatives:

  1. Pramipexole, ropinirole, rotigotine, and apomorphine
  2. Monotherapy in early and late IPD and combined with levodopa in late IPD
  3. Restless leg syndrome; apomorphine: acute intermittent hypomobility (rescue therapy for freezing!)
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18
Q

Dopamine Agonists:

Non-ergot derivatives:

  1. Which drug is excreted unchanged in urine?
  2. MOA?
A

Dopamine Agonists:

Non-ergot derivatives:

  1. Pramipexole is excreted unchanged in urine
  2. MOA: D2 agonists; pramipexole and rotigotine also activate D3 receptors
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19
Q

Dopamine Agonists:

Non-ergot derivatives:

  1. Side effects?
  2. Side effects when combined with levodopa?
  3. Additional side effects of apomorphine?
A

Dopamine Agonists:

Non-ergot derivatives:

  1. SE: GI distress, daytime somnolence, “sleep attacks”, insomnia, orthostatic hypotension, constipation, and hallucinations and compulsive behaviors
  2. DA agonist + Levodopa = orthostatic hypotension, dyskinesia, and increased risk of hallucinations
  3. Apomorphine: risk of serious CV events and is only used as rescue therapy in “off” periods
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20
Q

Dopamine Agonists:

Ergot derivatives:

  1. Drug?
  2. Indications?
  3. Excretion?
A

Dopamine Agonists:

Ergot derivatives:

  1. Bromocriptine
  2. Alone in early PD with levodopa later, usually used as an adjunct to levodopa in pts with advanced PD experiencing wearing-off or on-off motor fluctuations
  3. Feces! (bile)
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21
Q

Dopamine Agonists:

Ergot derivatives:

  1. Bromocriptine MOA?
  2. Side effects?
  3. Rare SE?
  4. Avoid use in who?
A

Dopamine Agonists:

Ergot derivatives:

  1. MOA: D2 agonist, D1 antagonist
  2. SE: GI distress, confusion, hallucinations, “sleep attacks”, insomnia, orthostatic hypotension, and dyskinesia
  3. Rare: pulmonary/retroperitoneal fibrosis, cardiac valve dysfunction, raynaud like phenomenta, and erythromyalgia
  4. Avoid in frail elderly, demented, and hypotensive pts
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22
Q

MAO-B inhibitors:

  1. Drugs?
  2. Indications?
  3. MOA?
A

MAO-B inhibitors:

  1. Selegiline and rasagiline
  2. Rasagiline: first line monotherapy or adjunct; Selegeline: 2nd or 3rd line drug, usually adjunctive
  3. MOA: increases dopamine levels by selectively inhibiting MAO-B
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23
Q

MAO-B inhibitors:

  1. Enhances actions of ____ within a few weeks.
  2. Common side effects?
  3. High dose side effects?
A

MAO-B inhibitors:

  1. Enhances actions of levodopa
  2. SE: exacerbation of levodopa side effects, insomnia, and confusion
  3. High dose: “tyramine crisis” and increased risk of seizures
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24
Q

MAO-B inhibitors:

Contraindications and result of combination:

  1. Concurrent use of other ____ or ____
  2. What increases plasma levels of MAO-B inhibitors?
  3. _______ drugs may cause _____ crisis
A

MAO-B inhibitors:

Contraindications:

  1. Concurrent use of other MAOIs or SSRIs
  2. Carbamazepine and CYP1A2 inhibitors (increase plasma levels)
  3. Sympathomimetic drugs may cause hypertensive crisis
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25
Q

MAO-B inhibitors:

Contraindications:

  1. Certain muscle ____ and _____ may cause increased risk of _________. Example of drug?
  2. Given with levodopa what could occur?
  3. Contraindicated in patients with ______ impairment
A

MAO-B inhibitors:

Contraindications:

  1. Certain muscle relaxants and narcotics may cause increased risk of seizures. Tramadol
  2. Levodopa: potentiation of DA side effects and exacerbation of dyskinesia
  3. Hepatic impairment
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26
Q

Anticholinergics:

  1. Drugs?
  2. Indication?
  3. Reduces ____ but not _____.
A

Anticholinergics:

  1. Benztropine and trihexyphenidyl
  2. Adjunctive for PD, 2nd line for tremor, maybe monotherapy in early onset PD where tremor is the prominent feature
  3. Reduces tremor but not bradykinesia
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27
Q

Anticholinergics:

  1. Also used for treatment of generalized ___ and first line agents for?
  2. Blocks _____ receptors (antagonists) in ___ to compensate for loss of substantia nigra
A

Anticholinergics:

  1. Generalized dystonias and first line agents for EPS disorders related to use of antipsychotics
  2. Blocks M1 muscarinic receptors in striatum to compensate
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28
Q

Anticholinergics:

  1. CNS side effects? Worse in who?
  2. Peripheral side effects?
A

Anticholinergics:

  1. CNS: sedation, confusion, anxiety, delusions, and hallucinations especially in the elderly
  2. Peripheral: nausea, dry mouth, blurred vision, urinary retention, constipation, decreased sweating, and pupillary dilation
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29
Q

Anticholinergics:

Life threatening side effects? One of which is reported in association with?

A

Anticholinergics:

a. Angle-closure glaucoma
b. Fatal neuroleptic malignant syndrome: in association with reduction or discontinuation of trihexyphenidyl

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30
Q

Anticholinergics:

Drug interactions:

  1. What can cause increased sedative effects?
  2. ____, MAOIs, and _______ antidepressants may intensify ________ effects, severe _____ and fatal ____
  3. Anticholinergics may increase central and side effects of _____
A

Anticholinergics:

Drug interactions:

  1. Alcohol or other CNS depressants increase sedation
  2. Phenothiazines, MAOIs, and Tricyclic antidepressants may intensify anticholinergic effects, severe anhidrosis and fatal hyperthermia
  3. May increase side effects of meperidine (narcotic analgesic)
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31
Q

Amantadine:

  1. Initially developed as?
  2. Indication?
A

Amantadine:

  1. Initially an antiviral agent
  2. Useful in early IPD and dyskinesias in late IPD
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32
Q

Amantadine:

  1. Possible MOAs? (4)
  2. Side effects?
  3. Possible rare side effect?
A

Amantadine:

  1. MOA: (a) promotes DA release (b) inhibits DA reuptake (c) blockade of cholinergic receptors (d) blockade of glutamate receptors
  2. SE: mild CNS and peripheral anticholinergic side effects
  3. Rare: Livedo reticularis (mottled discoloration of skin)
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33
Q

Management of Motor symptoms:

Early wearing off:

What should be done?

A

Management of Motor Symptoms:

Early wearing off:

a. Adjust levodopa
b. add DA agonist
c. Add COMT or MAO-B inhibitor

34
Q

Management of Motor Symptoms:

Dyskinesias:

What should be done/given?

A

Management of Motor Symptoms:

Dyskinesias:

a. Decrease levodopa
b. Add or increase DA agonist
c. Add amantadine

35
Q

Management of Motor Symptoms:

Freezing:

Give or do what?

Postural instability:

Give or do what?

A

Management of Motor Symptoms:

Freezing:

“Rescue therapy” apomorphine

Postural instability:

PT, conditioning, or assitive devices

36
Q

Essential tremor:

  1. Prevalence of 6% and 50% of people with essential tremor have what pattern of inheritance?
  2. Treatment? (5 drugs)
A

Essential tremor:

  1. 50% of those with essential tremor have autosomal dominant pattern of inheritance
  2. Treat: propranolol (Beta adrenergic agonist), Primodone/Gabapentin/Clonazepam (AED), or Alprazolam (antianxiety)
37
Q

Dystonia:

  1. Movement disorder where what occurs?
  2. Therapeutic options?
A

Dystonia:

  1. Sustained muscle contractions cause twisting and repetitive movements or abnormal postures
  2. Treat: DA agonists, Anticholinergic agents (benztropine), or benzodiazepines (clonazepam or diazepam)
38
Q

Spasticity:

  1. What occurs?
  2. Condition can interfere with? Affects what part of CNS?
  3. Treatment options?
A

Spasticity:

  1. Stiff/rigid muscles with exaggerated, deep tendon reflexes
  2. Can interfere with walking, movement or speech; affects the upper motor neurons
  3. Treatment: anticholinergics (trihexylphenidyl) or benzodiazepines (clonazepam or diazepam)
39
Q

Baclofen:

  1. Indications?
  2. MOA: _____ receptor agonist. Inhibits _____ at the ___ level possibly by ____ of afferent terminals
A

Baclofen:

  1. For spasticity (associated with MS), SC injury, athetosis, hiccups, and dystonia
  2. MOA: GABAb receptor agonist. Inhibits reflexes at the spinal level possibly by hyperpolarization of afferent terminals
40
Q

Baclofen:

  1. Side effects?
  2. Rapid discontinuation can cause?
  3. Interactions?
  4. Contraindications?
A

Baclofen:

  1. SE: sedation, dizziness, and weakness
  2. Rapid discontinuation can cause withdrawal and induce seizures and acute psychosis
  3. Interactions: CNS depressant can increase sedation
  4. Contraindication: treatment of skeletal muscle spasm resulting from rheumatic disorders
41
Q

Dantrolene:

  1. Indications?
  2. The only specific and effective treatment for? Also treats?
  3. MOA?
A

Dantrolene:

  1. Indication: spasticity
  2. Only specific/effective treatment for malignant hyperthermia also treats neuroleptic malignant syndrome
  3. MOA: depresses excitation-contraction coupling in skeletal muscle by decreasing intracellular calcium release from the sarcoplasmic reticulum
42
Q

Dantrolene:

  1. Common side effects?
  2. Rare but serious side effects?
  3. Contraindications?
A

Dantrolene:

  1. SE: fatigue, weakness, diarrhea, dizziness, drowsiness, nausea, speech/visual disturbances, nervousness, depression, and lightheadedness
  2. Rare: heptatotoxicity (hepatitis)
  3. Contraindications: active liver disease, muscle spasm resulting from rheumatic disorders, and patients where spasticity is used for posture, balance, or to obtain increased function
43
Q

Dantrolene:

Interactions:

  1. _____ channel blockers can cause severe _____ ____
  2. Non-depolarizing neuromuscular blocking agents do what?
A

Dantrolene:

Interactions:

  1. Calcium channel blockers can cause severe CV collapse
  2. Nondepolarizing NMJ blocking agents potentiate neuromuscular blockade
44
Q

Dantrolene:

Interactions:

  1. What causes increased sedation?
  2. What causes additive muscle weakness?
  3. Combined oral ___ and ____ replacement therapy with ___ may enhance ____ toxicity
A

Dantrolene:

Interactions:

  1. CNS depressants cause increased sedation
  2. Benzodiazepines may cause additive muscle weakness
  3. Combined oral contraceptives and hormone replacement therapy with estrogens may enhance liver toxicity
45
Q

Botulinum toxin:

  1. Indications?
  2. MOA?
A

Botulinum toxin:

  1. For focal dystonia, upper limb spasticity, severe armpit sweating, strabismus and blepharospasam associated with dystonia or CN VII disorder, migraines, and cosmetic
  2. MOA: neurotoxin by Clostridium botulinum
46
Q

Botulinum toxin:

  1. Side effects?
  2. Rare but serious side effects?
A

Botulinum toxin:

  1. SE: pain at injection site and excessive weakness
  2. Rare: spread of toxin effect (can spread from area of injection and cause diplopia, ptosis, dysphagia, dysphonia, dysarthria, urinary incontenence and breathing difficulties) and dysphagia/breathing difficulties in the treatment of cervical dystonia
47
Q

Tizanidine:

  1. Indications? Off label fo?
  2. MOA?
  3. Difference from baclofen/benzos?
A

Tizanidine:

  1. Spasticity; off label for fibromyalgia, migraine, and as an anticonvulsant
  2. MOA: centrally acting alpha2 adrenergic agonist that reduces spasticity by increasing presynaptic inhibition of motor neurons
  3. LESS muscle weakness than baclofen or benzos
48
Q

Tizanidine:

  1. Common SE? Rare?
  2. What reduces clearance of tizanidine?
  3. Contraindications?
A

Tizanidine:

  1. SE: dry mouth, fatigue, weakness, drowsiness, and dizziness; RARE: hepatotoxicity and hypotension
  2. Oral contraceptives reduce tizanidine clearance
  3. Contraindications: CYP1A2 inhibitors (fluvoxamine or cipro), liver disease, muscle spasm from rheumatic disorders, and patients where spasticity is used to sustain posture and balance
49
Q

Huntingtons:

  1. Characterization?
  2. Degeneration of what and where?
  3. How to treat?
A

Huntingtons:

  1. Characterized by chorea, personality changes, depression, dementia, psychosis, oculomotor abnormalities, dysphagia, dysarthria, deterioration of gait and balance
  2. Degeneration of GABAergic neurons in the straitum
  3. Treatment is symptomatic
50
Q

Huntingtons:

  1. How to treat Chorea?
  2. How to treat rigidity/bradykinesia/dystonia?
A

Huntingtons:

  1. Chorea: neuroleptics (haloperidol), tentrabenzine, or benzodiazapines
  2. Rigidity/bradykinesea: decrease neuroleptics, baclofen (GABA agonist), anticholinergis, benzos, or levodopa
51
Q

Huntingtons:

  1. MOA of tentrabenzine and indication?
  2. Tentrabenzine side effects?
  3. How to treat dysphagia?
A

Huntingtons:

  1. Tetrabenzine: Inhibits VMAT2 which leads to decreased uptake of monoamines into vesicles and depletion of monoamines; for chorea and to suppress involuntary jerking and writhing movements
  2. Tetrabenzine SE: sedation, fatigue, insomnia, depression, and akathesia
  3. Dysphagia: therapy, diet change, and caloric supplements
52
Q

Huntingtons:

  1. Treat mood?
  2. Treat anxiety?
  3. Treat apathy? But only if there is minimal _____
A

Huntingtons:

  1. Mood: SSRI
  2. Anxiety: SSRI, SNRI, buspirone, or benzodiazapines
  3. Apathy: methyphenidate but only if there is minimal chorea
53
Q

Huntingtons:

  1. Treatment of TICs?
  2. Treatment of myoclonus?
  3. Treatment of restless leg syndrome?
A

Huntingtons:

  1. Tics: neuroleptics, DA depleting agents (tetrabenzine), or antihypertensives
  2. Myoclonus: anticonvulsants or benzo
  3. Restless leg: DA agonists (pramipexole, ropinirole) or gabapentin
54
Q

Dementia/Alzheimers:

  1. Characterized by?
  2. 4 pathological findings?
A

Dementia/Alzheimers:

  1. Characterized by progressive loss of memory, impaired thinking, and inability to preform routine daily tasks
  2. Path: (a) degeneration of brain tissue (b) loss of cholinergic neurons (c) neuritic plaques (d) neurofibrillary tangles
55
Q

Dementia/Alzheimers:

2 types of drug therapies?

A

Dementia/Alzheimers:

Therapy:

a. cholinesterase inhibitors
b. Memantine

56
Q

Dementia/Alzheimers:

Cholinesterase inhibitors:

  1. Drugs?
  2. Improves? But does not significantly?
  3. MOA?
A

Dementia/Alzheimers:

Cholinesterase inhibitors:

  1. Donepezil, rivastigmine, and galantamine
  2. Improves quality of life (only in 30%) but does not significantly slow progression of disease
  3. MOA: prevent breakdown of ACh by acetylcholinesterase resulting in an increased concentration of ACh in the synapse
57
Q

Dementia/Alzheimers:

Cholinesterase inhibitors:

  1. Which drug is an irreversible inhibitor?
  2. Side effects?
  3. Interactions: Drugs that block _____ receptors will _____ effects. Examples?
A

Dementia/Alzheimers:

Cholinesterase inhibitors:

  1. Rivastigmine is irreversible
  2. SE: N/V, dyspepsia, dizziness, HA, syncope, chest pain, bronchoconstriction, Afib, tremor, and restlessness
  3. Drugs that block cholinergic receptors will reduce effects: tricyclic antidepressants, antipsychotics, and first generation antihistamines
58
Q

Dementia/Alzheimers:

Memantine:

  1. Indication?
  2. MOA?
  3. SE?
  4. Interactions? (2)
A

Dementia/Alzheimers:

Memantine:

  1. Moderate to severe AD
  2. Low potency noncompetitive NMDA (glutamate) receptor antagonist
  3. SE: dizzy, HA, confusion, and constipation
  4. Interactions: synergistic with other NMDA (amantadine or ketamine) and drugs that alkalinize urine (sodium bicarb) can decrease excretion and result in accumulation
59
Q

Amyotropic Lateral Sclerosis:

  1. This is a progressive, fatal, neurodegenerative diseased caused by?
  2. Treatment?
  3. First (and only) drug approved for ALS?
A

Amyotropic Lateral Sclerosis:

  1. Caused by degeneration of UMN and LMN
  2. Treat symptomatically
  3. ALS drug: riluzole
60
Q

Amyotropic Lateral Sclerosis:

  1. MOA of Riluzole? (several)
  2. SE?
  3. Interactions: prescribed with care to patients with history of abnormal ____ function; why?
  4. Interaction: _____ promotors/inhibitors can change plasma concentrations of Riluzole
A

Amyotropic Lateral Sclerosis:

  1. MOA Riluzole: decrease release of glu via activation of transporters, blocks Na+ and Ca++ channels, inhibits PKC, and promotes NMDA antagonism
  2. SE: allergic rxn, liver probs, somnolence, weakness, N/V
  3. Care with abnormal liver function pts: increase serum aminotransferase
  4. CYP1A2 can change plasma concentrations
61
Q

Restless leg syndrome:

  1. Clinical presentation?
  2. 3 meds?
A

Restless leg syndrome:

  1. Presentation: overwhelming urge to move legs (esp when lying down), worst at night and sufferers have to pace for hours to relieve the discomfort
  2. Pramipexole, ropinirole and gabapentin enacarbil
62
Q

Restless leg syndrome:

Gabapentin enacarbil:

  1. This is a gabapentin _____.
  2. Shows affinity for? (MOA)
  3. How are the pharmokinetics different from gabapentin?
  4. Side effects?
A

Restless leg syndrome:

Gabapentin enacarbil:

  1. Gabapentin prodrug
  2. Affinity for voltage-gated Ca++ channels
  3. Extensive first pass hydrolysis (gabapentin is excreted unchanged in the urine)
  4. SE: somnolence, sedation, dizziness - dont drive (NO INTERACTIONS/CONTRAINDICATIONS)
63
Q

Multiple Sclerosis:

  1. This is a chronic, _______, _______ disease in which what is damaged?
  2. ______ treatment is important.
  3. Current therapies?
A

Multiple Sclerosis

  1. Chronic, inflammatory, autoimmune disease in which the myelin sheaths are damaged
  2. EARLY treatment
  3. Immunomodulators and immunosuppressants and corticosteroids
64
Q

Multiple Sclerosis

Interferon Beta Drugs:

  1. Indications?
  2. Reduces?
  3. MOA?
A

Multiple Sclerosis

Interferon Beta Drugs:

  1. First MS attack and relapsing/remitting MS
  2. Reduces rate of relapse, development of new lesions, and volume of lesions
  3. MOA: anti-inflammatory and improvement of BBB integrity
65
Q

Multiple Sclerosis

Interferon Beta Drugs:

  1. Administered by _____. Patients may develop what to the medication?
  2. Common side effects?
A

Multiple Sclerosis

Interferon Beta Drugs:

  1. Administered by injection. May develop neutralizing Abs to the meds
  2. SE: flu-like symptoms following injection, reaction at injection site
66
Q

Multiple Sclerosis

Interferon Beta Drugs:

  1. Rare but serious side effects?
  2. Periodic ____ testing recommended
  3. Interactions: potential with drugs associated with ____ injury
A

Multiple Sclerosis

Interferon Beta Drugs:

  1. Rare SE: increased frequency of depression/suicide, severe hepatic injury, seizures, decreased peripheral blood counts (all cells), pancytopenia, thrombocytopenia
  2. Periodic blood testing
  3. Hepatic injury
67
Q

Glatiramer acetate:

  1. Indications?
  2. MOA: non-_____ and non-_____ immunomodulator that shifts the population of ___ cells from ___-inflammatory to cells that ____ the inflammatory response. May act as a ____ to divert an autoimmune response
A

Glatiramer acetate:

  1. First MS attack and relapsing MS
  2. MOA: non-_interferon_ and non-_steroidal_ immunomodulator that shifts the population of T cells from proinflammatory to cells that suppress the inflammatory response. May act as a decoy to divert an autoimmune response to myelin
68
Q

Glatiramer acetate:

  1. Patients may develop?
  2. Common side effects?
  3. Rare side effects?
  4. Interactions?
A

Glatiramer acetate:

  1. Develop neutralizing Abs to the meds
  2. SE: injection site reactions, rash, chest pain, flushing, shortness of breath, anxiety, and increased HR
  3. Rare: lipoatrophy or necrosis at site of injection
  4. Hypersensitivity to mannitol (water diuretic)
69
Q

Natalizumab:

  1. Indication?
  2. MOA: humanized _________ ________ against the cellular _____ molecule _______. It is thought to reduce the ability of inflammatory immune cells to pass through?
A

Natalizumab:

  1. Monotherapy for MS and also Crohn’s disease
  2. MOA: humanized monoclonal antibody against the cellular adhesion molecule alpha4-integrin. Thought to reduce the ability of inflammatory immune cells to pass through the BBB
70
Q

Natalizumab:

  1. Common SE?
  2. Serious SE?
A

Natalizumab:

  1. SE: HA, fatigue, joint pain, increased infections, rash, and depression
  2. Serious: liver injury including failure that may require a transplant, increased risk of developing encephalitis and meningitis (Caused by HSV and VZV)
71
Q

Natalizumab:

  1. Black box warning?
  2. Interactions with other immune-modulating drugs may increase risk of?
  3. Should not be used during?
A

Natalizumab:

  1. Black box: may increase risk of developing PML
  2. Interaction with other immunomodulators: increased risk of PML
  3. NOT for pregnancy or when trying to get pregnant
72
Q

Fingolimod:

  1. Indications?
  2. MOA: ________ 1-phosphate receptor modulator. Works by sequestering __________ in _______ ____ preventing them from moving to the CNS. Stimulate repair process of _____ cells after injury
A

Fingolimod:

  1. First oral drug to reduce relapses and delay progression of disability
  2. MOA: sphingosine 1-phosphate receptor modulator. Sequesters lymphocytes in lymph nodes preventing them from moving to the CNS. Stimulate repair process of Glial cells after injury
73
Q

Fingolimod:

  1. Common side effects?
  2. Serious side effects?
  3. 2 black box warnings?
A

Fingolimod:

  1. SE: HA, flu, diarrhea, back pain, increase in liver transaminase, and cough
  2. Serious SE: fatal infections, bradycardia, skin cancer, macular edema
  3. Black box: hepatotoxicity and teratogenicity
74
Q

Fingolimod:

Interactions:

  1. Not recommended for people with a history/presence of?
  2. What can cause risk of rhythm disturbance?
  3. Effects of beta blockers?
A

Fingolimod:

Interactions:

  1. Not for those with heart or vascular conditions
  2. Antiarrhythmic drugs can increase risk of serious rhythm disturbances
  3. Beta blockers may have an additive effect on HR
75
Q

Fingolimod:

Interactions:

  1. What increases fingolomide exposure during concomitant use?
  2. Increased risk of infection to _____ as well as for 2 months after.
  3. Who is at risk for macular edema?
A

Fingolimod:

Interactions:

  1. Ketoconazole increases exposure
  2. Increased risk of infection to vaccines
  3. Macular edema: pts with history of uveitis and those with diabetes
76
Q

Teriflunomide:

  1. Indication?
  2. MOA: inhibits _____ synthesis and reduces the number of activated ____ in the ____ and inhibits the production of ____ ____ chemicals by ___ cells.
  3. Not recommended for what patients? Whye?
A

Teriflunomide:

  1. For relapsing MS
  2. MOA: inhibits pyrimidine synthesis. Reduces # of activated lymphocytes in the CNS and inhibits pdtn of immune messenger chemicals by T cells
  3. Not for patients with severe immunodeficiency or infections because it is an immunosuppressant and decreases WBC and platelet counts
77
Q

Teriflunomide:

  1. Common SE?
  2. Rare SE?
  3. Black box warnings?
A

Teriflunomide:

  1. SE: diarrhea, alopecia, flu, nausea, parasthesia, and abnormal liver tests
  2. Rare: acute renal failure, hypercalcemia, and peripheral neuropathy
  3. Black box: hepatotoxicity (liver failure has been reported in patients on leflunomide for RA and these drugs are similar) and severe birth defects if taken during pregnancy
78
Q

Dimethyl Fumarate:

  1. Indication?
  2. MOA?
  3. Common se?
A

Dimethyl Fumarate:

  1. First line therapy for relapsing MS
  2. MOA: inhibit immune cells and molecules and may have anti-oxidant properties
  3. SE: flushing, ab pain, diarrhea, and nausea; reduced blood cell counts
79
Q

Mitoxantrone:

  1. An immunosuppressant also used in?
  2. Indications?
  3. MOA?
A

Mitoxantrone:

  1. Also used in cancer chemo
  2. For worsening relapsing/remitting, progressive relapsing, or secondary-progressive MS
  3. MOA: inhibits or prevents the development of any uncontrolled new or abnormal growth, such as a neoplasm/tumor, and suppresses B and T cell immunity
80
Q

Mitoxantrone:

  1. Must be given how?
  2. Common SE?
  3. Severe SE?
A

Mitoxantrone:

  1. Given IV
  2. N/V, diarrhea, HA, alopecia, menstrual disorder, and amenorrhea
  3. Serious SE: cardiotoxicity, risk of developing secondary AML, neutropenia, and moderate to severe teratogenic effects

Pharmacology (24 decks)

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