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Pharmacology II > Exam 2 - Neurology Meds (Part 2) > Flashcards

Exam 2 - Neurology Meds (Part 2) Flashcards

1
Q

PARKINSONS DISEASE

A

PARKINSONS DISEASE

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2
Q

What drugs can cause Parkinson’s disease?

A 
Antipsychotics
Dopamine antagonists
Methyldopa
Reserpine
MPTP (made by scientist)
Hydrogen sulfide
Methanol
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3
Q

Pathophysiology of Parkinson’s disease

A

PARKINSONS DISEASE -
Depletion of dopamine neurons from substantia nigra, less activity on D1 and D2.

D1 - striatum sends out less GABA, which means GPi sends out more GABA.

D2 - has some dopaminergic activity; GABA is decreased, more glutamate stimulates GPi to release more GABA from GPi. More GABA means more inhibitory transmitters on Thalamus. Less movement on motor cortex.

Less dopamine leads to overactivity of acetylcholine.

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4
Q

Huntington’s Disease

A
  • Involuntary motion and corea

- Don’t have enough inhibitory D2 action, which leads to overactivity and more movement initiated at the Thalamus.

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5
Q

How do you treat Huntington’s disease?

A

Tetrabenazine

  • Depletes catelcholamines (Serotonin, NE, dopamine) to inhibit the involuntary movements.
  • ADR: Can cause hypotension, depression, suicide.
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6
Q

Patient with an acute dystonic reaction from dopamine blocker, how do you treat condition?

A

You know they have too much Ach (flexed), so you use an anticholinergic:

  • Benadryl
  • Cogentin

Want to restore balance between Ach and dopamine.

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7
Q

If we have too little dopamine in CNS, how can we fix that problem?

A

Inhibit metabolic enzymes so dopamine can stay longer and have more activity.

OR

Provide patient with more precursor dopamine (L-DOPA) to help them produce more dopamine.

  • Levodopa
  • Carbodopa
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8
Q

How do you diagnose Parkinson’s disease?

A
  • Clinical diagnosis
  • Can also use levodopa or apomorphine (precursors to dopamine)
  • If s/s decrease, can help to confirm dx.
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9
Q

What are non-pharmacologic options for Parkinson’s patients?

A
  • Education and support
  • Exercise and speech therapy
  • Surgical: thalamotomy or deep brain stimulation
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10
Q

What types of drugs are neuroprotective and used to slow progression of PD?

A
  • MAO-B inhibitors

- Dopamine agonists

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11
Q

What drugs are used for symptomatic treatment of PD?

A
  • Anticholinergics
  • MAO-B inhibitors
  • COMT inhibitors
  • Dopamine agonists, like ergot and non-ergot derivatives
  • Dopamine precursors
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12
Q

What’s an advantage to neuroprotective drugs affect on dopamine metabolism?

  • Dopamine agonists
  • MAO-B inhibitors
A

Dopamine is metabolized by MAO-B enzymes, which yields dopamine and H2O2 as products.

H2O2 turns into free radicals and can damage cells/denature proteins. With more oxidative stress, neurons can be damaged and cause progression of disease.

Inhibiting enzyme = less free radical damage and dopamine stays around with longer duration of action.

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13
Q

When treating PD, how can you avoid oxidative stress from MAO-B enzyme?

A

If you keep giving precursor drugs that stimulate MAO-B, it can lead to progression of disease!!! BAD.

+ If you inhibit MAO-B enzyme, you can have less oxidative stress and excitatory toxicity. Dopamine neurons can work for longer.

+ Dopamine agonists can be used to replace normal dopamine to delay dyskinesia caused by oxidative stress.

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14
Q

What drugs, specifically, inhibit MAO-B?

A
  • Selegiline

- Rasagiline

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15
Q

Selegiline

A

MAO-B inhibitor

  • Delays need for levodopa
  • Initial effects are not sustained
  • Amphetamine derivative; is metabolized into amphetamine. False positive drug screen.

ADR
-Agitation, insomnia, hallucinations, orthostatic hypotension

-Hypotension - when standing, body sends out catecholamines to regulate BP. When you go to stand, you don’t have the reserves for extra to compensate as well for sitting-standing.

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16
Q

Rasagiline

A

MAO-B inhibitor

  • Not metabolized into an amphetamine
  • Fewer side effects

Rasagilline preferred over Selegiline.

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17
Q

When prescribing a patient Selegiline or Rasagiline; what is a risk?

A

Serotonin Syndrome
-By decreasing MAO-B, they can increase activity of other catecholamines, like dopamine.

Too much in synapse = serotonin syndrome.

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18
Q

When is it most appropriate to use MAO-B inhibitors?

A
  • Mild PD, early on in treatment
  • Don’t prescribe with tramadol, methodone, amphetamines, ephedra, dextromethorpan, MAO-inhibitors, or cyclobenzaprine…
  • Will INCREASE risk of Serotonin Syndrome!!!!!
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19
Q

When prescribing MAO-inhibitors, what dietary restrictions should patient be placed on?

A

Tyramine

  • Broken down into serotonin and NE
  • If you inhibit MAO-B, you can get too high activity: increases Serotonin Toxicity risk.

High amounts in aged cheeses, meats, fava beans, red wine, dark chocolate, beer

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20
Q

If a patient on a MAO-B inhibitor ingests foods high in Tyrosine, what S/S may they experience?

A

Serotonin Syndrome

  • Increased BP, tachycardia, hallucinations
  • Good education point
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21
Q

In early, uncomplicated PD, how do you manage symptoms?

A

Anticholinergics - blocks Ach in XS to restore balance and limit side effects.

  • Benztropin (Cogentin)
  • Trihexyphenidyl (Artane)
  • Diphenhydramine (Benadryl)

-Good for patients with tremor, but little hypokinesia.
-If they have cognitive impairment, DO NOT GIVE anticholinergic –
Will cause altered mental toxicity!!

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22
Q

Patient diagnosed with PD; main features are a tremor with no cognitive impairment. What drug would you use to treat?

A

-Benztropin (Cogentin)

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23
Q

Amantidine (Symmetrel)

A

Unclear MOA

  • Amphetamine-like activity to increase release of dopamine.
  • Anticholinergic effects
  • MDMA antagonist affects

-Used in mild PD and in in ICU for patients with prolonged coma to reset CNS and wake them up.

  • Renal elimination - adjust dose!!
  • Can cause SEIZURES if drug level is too high!!
  • Tolerance develops over time, will see decreased release of effect. :(
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24
Q

Dopamine Agonists

A
  • First line therapy; delay treatment with L-DOPA.
  • Goal: Keep patients off L-DOPA as long as possible to prevent the wearing of neurons.
  • Can add to L-DOPA, but need to reduce the dose or you might see toxicity
  • Slow progression of disease by replacing dopamine
  • Drugs can work on D1, D2, and D3.

ADR
-Somnolence, confusion, hallucinations, punding, orthostatic hypotension, dyskinesia, peripheral edema

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25
Q

Ergot and non-ergot derivatives

A

Dopamine Agonists

  • Ergots are based off of fungus.
  • Non-ergots do NOT share chemical structure with those.
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26
Q

Punding

A

A human activity characterized by compulsive fascination with and performance of repetitive, mechanical tasks, such as assembling and disassembling, collecting, or sorting household objects.

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27
Q

What is a unique side effect to ergot derivatives?

A

Causes retroperitoneal fibrosis and mitral valve regurgitation.

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28
Q

Ergot Derivatives

A

Ergot Derivatives

  • Bromocriptine (Parlodel)
  • LSD
  • Causes vasoconstriction, bc it binds to dopamine and serotonin receptors. Especially on fingers and toes.
  • Can cause tissue necrosis and gangrene.
  • CAT X: Do not give in pregnancy.
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29
Q

What are the non-ergot derivatives?

A

Non-Ergot Derivatives

  • Pramipexole (Mirapex)
  • Ropinirole (Requip)
  • Rotigotine (Neupro)
  • Apomorphine (Apokyn)
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30
Q

Which non-ergot derivative requires renal dosing?

A

Pramipexole (Mirapex)

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31
Q

Which non-ergot derivative is a transdermal product?

A

Rotigotine (Neupro)

-Rotate the application site

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32
Q

What non-ergot derivative is used for restless leg syndrome?

A

-Ropinirole (Requip)

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33
Q

Apomorphine (Apokyn)

A
  • Dopamine receptor agonist (non-ergot derivative)
  • Used for provocative testing; can give it to pt to see if they have a response to confirm dx of PD.
  • Late stage disease, maybe used long-term.
  • Subcutaneous
  • Titrate to see response; response = improvement of symptoms.
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34
Q

What do Dopamine Agonists typically cause?

A

N/V – To prevent N/V, use Zofran and Phenergan to treat, normally. Do NOT use with apomorphine.

  • Zofran: blocks 5HT3
  • Phenergan: blocks dopamine receptors
  • Monitor BP Q20mins.
  • Will have stimulatory actions on neurons
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35
Q

Why don’t you mix Apomorphine (Apokyn) with 5HT3 antagonists (Zofran)?

A
  • QT prolongation

- Hypotension

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36
Q

Gold standard for PD?

A

Levodopa/Carbidopa (Sinemet)

Levodopa

  • Active component, precursor to dopamine
  • Crosses BBB, gets converted to dopamine by L-AAD in striatum.
  • Normal activity follows

Carbidopa

  • Does not cross BBB
  • Inhibits peripheral breakdown of Levodopa and reduces side effects.
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37
Q

Why isn’t Levodopa administered alone?

A

Drug, given by itself, will not get to BBB.

Can be metabolized by catecholamines and aminotransferase.

When given alone also causes N/V, arrythmias, hypotension.

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38
Q

If patient isn’t having good activity of Levodopa/Carbidopa, what do you do?

A
  • Absorbed in duodenum
  • Diet high in protein will inhibit absorption, because amino acids will compete for absorption
  • Space out time drug is given from meal times.
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39
Q

Levodopa/Carbidopa (Sinemet) Pharmacokinetics

A
  • Crosses BBB
  • Saturable diffusion - when overloaded with drug, transporters are saturated and may take time to cross over.
  • Half-life increased when you add enzyme inhibitors (entacopone).
  • Give drug frequently or in XR preps.
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40
Q

Half-life of Levodopa

A
  • 1 hr by itself
  • 1.5hrs when combined with Carbidopa
  • 2-2.5hrs when combined with Entacapone
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41
Q

Levodopa/Carbidopa (Sinemet)

- Place in therapy?

A
  • Can be used as an initial therapy, but normally used when other drugs fail.
  • Stresses out neurons and produces reactive oxygen species!!
  • Most effective treatment for symptomatic treatment of PD.
  • All patients require treatment.

ADR
-N/V, dyskinesia, hallucinations, insomnia, somnolence, depression, orthostatic hypotension.

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42
Q

What are the given forms of Levodopa/Carbidopa?

A

Sinemet

  • Given TID
  • Titrate to how well they can tolerate it based on their symptoms and SE

Sinemet CR
-Extended release, change dose every 3 days until they have good symptom release and limited SE.

Parcopa

  • Oral disintegrating tablet
  • Good for more progressive patients that have difficulty swallowing pill.
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43
Q

If you have a PD patient that has difficulty swallowing, what medication is apropriate?

A

Parcopa

  • Oral disintegrating tablet
  • More progressive patients that have difficulty swallowing pill.
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44
Q

Why is there a controversy between the initial choice of therapy for PD?

A
  • Dopamine metabolism creates free radicals
  • Dyskinesias are common with levodopa; too much dopamine can enhance huntington effect.
  • Levodopa reduces mortality in PD
  • Use of dopamine agonists and MAO-BIs for short term neuroprotection, before switching to L-DOPA.
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45
Q

What enhances affects of dopamine produced?

A

COMT inhibitors

  • Tolcapone (Tasmar)
  • Entacapone (Comtan)
  • Inhibits COMT to increase half-life of L-DOPA
  • Prolongs effects of dopamine and increases half-life.
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46
Q

If your PD patient is on COMT inhibitors and you are prescribing them Levodopa/Carbidopa (L-DOPA); what do you need to do?

A
  • Decrease the L-DOPA dose by 25%. Dopamine lasts longer
  • Increased side effects.
  • Taper off dose, so there’s no sudden changes in dopamine levels.
  • Do NOT give COMT inhibitors to patient in combination with MAO-inhibitors!!!!!!!!!!!!!!!!!
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47
Q

COMT Inhibitors ADR

A
  • Overactivity of L-DOPA

- Urine discoloration can be brown or orange.

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48
Q

Tolcapone (Tasmar)

A
  • COMT inhibitor; not used.

- Black-boxed warning for hepatotoxicity (increases AST/ALT).

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49
Q

Entacapone (Comtan)

A
  • Dosed along with carbidopa/levodopa

- Go to COMT inhibitor

50
Q

Stalevo

A

Combination of Carbidopa, Levodopa, AND Entacapone

51
Q

Early diagnosis of PD, no cognitive impairment. Tx:

A

Rasagilline

  • MAO-B inhibitor
  • Neuroprotective
52
Q

Early diagnosis of PD, with tremor. No cognitive impairment. Tx:

A

Anticholinergic

-Not used on older patients, bc it can worsen dementia (CNS effects).

53
Q

If you have an elderly patient with PD and signs of tremor - What could you give them?

A
  • Do not give older patients anticholinergics, because of the CNS effects
  • Could give them Carbidopa/Levidopa
54
Q

Early diagnosis of PD, with tremor. Treated with anticholinergics to no avail. Tx:

A

Carbidopa/Levidopa

-Used b/c anticholinergic wasn’t useful

55
Q

Patient with PD showing signs of bradykinesia and rigidity. Tx:

A

Dopamine agonists

  • Ergot
  • Non-ergot

Carbidopa/Levodopa

56
Q

Levodopa Honeymoon

A

Pt on mono/polytherapy - Sinemet is most effective, patients start to feel much better.

But it does put oxidative stress on the heart, so eventually the honeymoon phase is going to go away. Disease progresses on.

57
Q

Late (Complicated) PD

A

Motor fluctuations

  • Drug wears off
  • Delayed onset of drug
  • On-ff mix
  • Freezing refractory symptoms, such as catatonia. Dopamine is depleted.

Dyskinesias
-Related to peak dose

Dysarthria/Dysphagia

  • Consider apomorphine, surgery, levodopa oral solution in G tubes to adminster med.
  • Most progressive form of disease
58
Q

Motor complications of PD/TX

A
  • Early PD, drug will hit peak and degrade off.
  • Response threshold is where the symptoms get better.
  • Drug not near dyskinesia threshold.
  • Moderate PD, duration of response is decreased. Threshold for response goes up.
  • Advanced PD, short-duration response, reaches above the dyskinesia threshold, and has a narrow therapeutic window.
59
Q

If action of drug is “wearing off” too soon, what can you do to increase duration of action?

A

Wearing off, due to loss of presynpatic neurons

  • Add entacopone
  • Add dopamine antagonist
  • Administer Sinemet more frequently, 6-8x a day.
  • Oral solution can aid absorption
  • Add MAO-B inhibitor
  • Switch to Sinemet CR
  • Apomorphine injections
  • Duodenal levodopa infusions
60
Q

If patient has an “off dystonia” - inhibited movements from drug wearing off too early, what can you do?

A
  • Add bedtime dose of Sinemet CR
  • Add DA antagonists
  • Add Rotigotine
  • Take Sinemet when waking
  • Add Botulinum Toxin - paralytic to prevent Ach release from neuron, inject to spastic muscles to release.
61
Q

If patient has “unpredictable on-off”?

A

-Add dopamine agonist or try a different one
-Add MAO-inhibitor or COMT-inhibitor
-Protein redistribution - avoid AA intake when giving drug
-Sinemet oral solution
-Apomorphine injections
Continuous duodenal levodopa infusion

62
Q

If patient has “delayed on” or delayed onset of action, how do you fix?

A
  • Reduce protein in diet, increase fiber, add laxative
  • Discontinue anticholinergic
  • Take Sinemet 1hr before or 2hr after meals.
  • Add dopamine agonist
  • Use Parcopa
  • Add domperidone
  • Intermittent subq apomorphine
  • Avoid Sinemet
63
Q

If patient is experiencing dyskinesia’s during peak dose or has a peak dose “on”, how do you fix?

A
  • Lower the Sinemet dose
  • D/C agents that potentiate levodopa (enzyme inhibitors).

Add dopamine agonist or amantidine, clozapine, or propranolol

64
Q

If patient has a biphasic dyskinesia, how do you fix?

A
  • Shorten the dosing interval to produce over-lapping of effects
  • Normalizes levels
  • Add DA agonist
  • Switch to CR
65
Q

MULTIPLE SCLEROSIS

A

MULTIPLE SCLEROSIS

66
Q

What are the main tx for MS?

A
  1. treatment of exacerbation to shorten duration and severity
  2. disease modifying therapy DMTs - diminish progressive disability over time
  3. Sympatomatic therapy - maintains QOL
67
Q

How do you treat a typical MS exacerbation?

A

Treat with corticosteroids, like IV methylprednisolone:

  • Limits edema at area of demyelination
  • Take within 2 weeks onset; improvement around 3-5 days
  • Taper off if given for over 1 week to AVOID adrenal insufficiency.

ADR:
-Sleep disturbance, poor glycemic control, mood changes

68
Q

For patients with severe MS exacerbation, what else could you do?

A

Plasma exchange; will decrease amount of inflammatory factors in the blood to decrease severity.

69
Q

Disease Modifying Therapy

A
  • First generation decreases relapse rate and white matter lesions.
  • Don’t take effect immediately, 1-2yrs for efficacy to be noted. Make sure using symptomatic management apropriately.

-Second generation is used for progressive or worsening MS. Very expensive mabs.

70
Q

Interferons B-1b and B-1a

A

First Generation DMT

  • Naturally occurring cytokines in the body
  • MOA unkown, affects suppressor cell function. Inhibiting that can taper down immune system.
  • Interferon B1a - Avonex
  • Interferon B1a - Rebif
  • Interferon B1b - Betaseron, Extavia
  • Interferon B1a - Plegridy
71
Q

Ptegylated Interferon B-1a

A
  • Largely supplanted other interferon
  • Added polyethylene glycol group
  • Decreases side effects.
72
Q

Adverse effects of Interferon B-1b and B-1a (First generation DMT)

A
  • Hepatotoxicity, must monitor
  • CBC may be depressed
  • Flu-like symptoms, bc they’re injected proteins (myalgia, fever, etc).
  • Menstrual irregularities
  • Injection site reactions
  • Depression, esp in 1b.
73
Q

Glatiramer Acetate (Copaxone)

A

First generation DMT

  • Mimics antigenic property of myelin basic protein.
  • Mimicking protein, it binds to the T cells and prevents them from being activated in the first place.

SIDE EFFECTS

  • Injection, can’t be taken orally. May have injection site RXN.
  • 10% pts have chest tightening, flushing, dyspnea. Lasts 20 mins.
74
Q

What should you warn your patient about when prescribing Glatiramer Acetate (Copaxone)?

A
  • 10% pts have chest tightening, flushing, dyspnea. Lasts 20 mins.
  • NOT a heart attack, will go away.
75
Q

Natalizumab (Tysabri)

A
  • Monoclonal antibody against very late antigen (VLA-1)
  • Binds to VLA-1, adhesion molecule prevents the lymphocytes from crossing BBB to get to SC to interact with neurons.
  • Prevents neutrophils from getting to their site of action.

ADR:
-Depression, fatigue, respiratory infection, hepatotoxicity

76
Q

What drug is in REMS Program? Why?

A

Natalizumab (Tysabril)

  • Risk Evaluation Mitigation Strategy
  • Due to concerns for multifocal leukoencephalopathy seen in clinical trials.
77
Q

Fingolimod (Gilenya)

A

-First oral DMT for MS (big deal); other drugs required infusion

  • MOA: agonizes sphingosine 1-phosphate receptor, which sequesters lymphocytes in lymph organs to prevent them from getting into CNS
  • ADR: first dose bradycardia (need to be monitored 6hrs), lymphoma can develop (but is reversible), risk of infection, and hepatotoxicity.

Do NOT give live vaccines during treatment; give before or after discontinuation of therapy - worried about live vaccines activating.

78
Q

Teriflunomide (Aubagio)

A

-MOA: Works on dihydroorotate dehydrogenase to prevent proliferation of B and T cells. –To stop inflammatory cells from getting into CNS.

  • Metabolite of Leflunomide (seen in RA)
  • Will increase INR when prescribed with Warfarin!!!
  • ADR: Transaminitis - increased LFTs, alopecia, paresthesia
  • BLACK BOX FOR TERATOGENICITY AND HEPATOTIXICITY
  • Stays in the blood for two years after D/C.
  • Cholestyramine wash out will help to bind the drug to draw levels down more quickly.

-Test for TB beforehand so you don’t activate a latent infection!!!

79
Q

Dimethyl Fumarate (Tecfidera)

A
  • No known mehanism
  • Oral agent
  • ADR: increased flushing, increased LFTs
80
Q

Alemtuzumab (Lemtrada)

A
  • Injected
  • MOA: causes cytolysis of inflammatory cells (T cells, macrophages, etc).
  • Infusion reactions are common
  • Third line medication
  • Increased risk for RTI, UTI, HSV, and TB.
  • Some patients can develop an AI disease with thyroid, diabetes, GN, hemolytic anemia.

Lots of reasons why not to use this drug!!!!!!

81
Q

When are DMTs used?

A
  • Pt w/ poor prognosis
  • Poor clinical presentation of MS
  • Can use natalizumab, fingolimod, teriflunomide, or dimethyl fumarate to control symptoms.
  • Efficacy and safety vary
82
Q

How do you manage symptoms of spasticity associated with MS?

A
  • Muscle relaxants - baclofen, cyclobenzaprine (Increase GABA receptor activity; will see drowsiness, sedation, nystagmus).
  • Gabapentin or pregabalin
  • Onabotulinum toxin A
83
Q

How do you manage bladder incontinence, etc. associated with MS?

A
  • Oxybutinin
  • Solifenacin, darifenacin - to hold onto urine and relax detrusor muscles
  • Self-catheterization
84
Q

How do you manage sensory symptoms in MS?

A
  • Carbamazepine
  • Phenytoin
  • TCAs
85
Q

How do you manage fatigue in MS?

A
  • Amantidine
  • Antidepressants
  • Modafinil/Armodafinil - resets sleep cycle
  • Amphetamines
86
Q

HEADACHES

A

HEADACHES

87
Q

Migraines

A
  • Vasodilation leads to edema and pressure

- Tx with vasoconstrictors to relieve the pressure/pain

88
Q

Common food triggers

A

Alcohol, caffeine, pickled foods, MSG, tyramine foods

89
Q

Mild to moderate migraine, tx:

A

NSAIDs, analgesics

  • Aspirin, ibuprofen, naproxen, Excedrin
  • Acetaminophen is ineffective as a single agent
  • Ketorolac (Toradol) for acute care setting
90
Q

Nausea/Vomitting symptoms, tx:

A

Phenothiazines

  • Promethazine
  • Metoclopramide (Reglan)

5HT3 receptor antagonists
-Odansetron (Zofran)

91
Q

Moderate to severe migraine, tx:

A

Ergots

  • Ergotamine tartrate (Ergomar)
  • DHE (Migranal) - nasal spray or parenteral

Triptans

  • Sumatriptan
  • Zolmitriptan
  • Rizatriptan
  • Naratriptan
  • Almotriptan
  • Frovatriptan
  • Eletriptan
92
Q

Ergots - vasoconstrictors

  • Ergotamine tartrate (Ergomar)
  • DHE (Migranal) - nasal spray or parenteral
A
  • Second line therapy
  • MOA: Bind to 5HT1D/1B to constrict vessels in the brain to relieve pressure on trigeminal nerve.
  • Decreases release of peptides that cause pain.
  • Decreased risk of occurence
  • Intranasal form good for patients with N/V
  • ADR: N/V, pain, HTN
  • CI: Don’t give to patients with vascular or coronary disease, don’t give to HTN patients bc it will raise BP, its CATEGORY X so don’t give to pregnant girls
93
Q

Triptans

  • Sumatriptan
  • Zolmitriptan
  • Rizatriptan
  • Naratriptan
  • Almotriptan
  • Frovatriptan
  • Eletriptan
A
  • 5HT1D/1B receptor agonists
  • Sumatriptan - nasal spray

-MOA: Activate 5HT1D/1B receptors to vasoconstrict, same as ergots
-Effective in 85% of patients;
40% have recurrence bc of short half life.
-Frovatriptan and Rizatriptan have longer half-life.
-ADR: Chest tightness, pressure, pain, paresthesia.
-CI: Don’t give to those with CAD, MI, angina, PVD, MAO inhibitors
-OK for pregnant; not teratogenic

94
Q

Why don’t you give Triptans within 24hrs of giving Ergots?

A

Too much vasoconstriction could lead to ischemia in the brain.

95
Q

Sumatriptan

A
  • GOLD STANDARD
  • Most respond well
  • SubQ injections
  • Covered by insurance
96
Q

Second generation agents

A
  • Designed to decrease headache recurrence, side effects, and increase bioavailability.
  • Have better lipophillicity to get to CNS quicker and have longer half-life.
97
Q

Zolmitriptan (Zomig)

A

Second generation

  • ODT (oral disintegrating tab) or nasal spray
  • Similar to sumatriptan
98
Q

Naratriptan (Amerge)

A
  • High bioavailability, longer-half life to limit HA recurrence.
  • CI: hepatic adn renal disease
  • Slow onset, low recurrece rate
  • More favorable profile to ADR than sumatriptan.
99
Q

Rizatriptan (Maxalt)

A
  • ODT
  • Drug interaction if given with propranolol. Can see 70% increase in AUC of drug you’re exposed to.
  • FAST onset for quick relief
100
Q

Almotriptan (Axert)

A

-Metabolized by CYP3A4 and MAO (inhibitors will increase dose effects).

101
Q

Eletripan (Relpax)

A

Metabolized by CYP3A4

102
Q

Frovatriptan (Frova)

A

Low bioavailability, long half-life

Similar to naratriptan

103
Q

Rules for acute treatment of migraines:

A

Use migraine-specific agents in patients with severe migraine or who respond poorly to NSAIDs
-Use non-oral route for early or significant N/V since they can’t keep it down

  • Allow 1hr for SubQ to work
  • Allow 2hrs for IN and PO forms to work
  • Do NOT use triptans within 24hrs of ergot, because it could have XS prolonged vasospasms = ischemia in brain.
  • Try to avoid exceeding 2 days a week of abortive therapy
104
Q

Medication overuse headaches

A
  • Occur with overuse of ergotamines, triptans, and opioids
  • HA ~15 days per month
  • Using drugs ~10 days per month
  • Switch to new med or put them on a better preventative med
  • Patient should be resolved over time
105
Q

Treatment for medication overuse headache:

A

<7-12 analgesic tabs or caps per day
Discontinue analgesic or taper over 4-6 weeks, then begin prophylaxis medications.
Withdrawal symptoms occur days to weeks.

> 12 analgesic tabs or caps per day or pregnant
Do not abruptly discontinue because you’ll see worsening side effects and headaches.

106
Q

Who is a candidate for preventative therapy for med overuse headaches?

A
  • Recurrent frequent migraine that interferes with daily routines, despite acute treatment.
  • CI to any acute treatment.
  • Significant ADRs, can’t tolerate abortive therapy or cost.
  • Patient preference.
107
Q

First line therapy for medication overuse headaches:

A

Beta blockers - dilate blood vessels; start low dose and titrate up slowly to avoid inducing a migraine.

  • First line therapy
  • Propranolol
  • Alternatives: atenolol, metoprolol, nadolol, timolol
  • May block vasodilation!!, inhibit serotonin release from PLTs (which cause migraines).
108
Q

Who don’t you use propranolol in?

A
  • Old people with CNS changes

- Non-selective beta blocker

109
Q

Anticonvulsants

-Preventative therapy

A

Divalproex and Valproic acid
-Inhibit early wave of spreading depression

Topamax

  • Migraine prevention
  • Blocks carbonic acid, Na, Ca, and glutamate receptors.
  • ADR: paresthesia, fatigue, CNS depression, decreased appetite
110
Q

Antidepressants

-Preventative therapy

A

Tricyclics

  • Amitriptyline, Nortriptyline, Protriptyline
  • Amitryptiline is most effective

SSRI’s

  • Not frequently used, can worsen migraine
  • Fluxotine, paroxetine
  • Effect NE and 5HT reuptake sites
111
Q

Calcium Channel Blockers

-Preventative therapy

A

Verapimil

  • Start low, go slow
  • Modest effect with nifedipine
112
Q

Botulinum toxin

A

Good for tension headaches to relieve spasms in neck

113
Q

If a patient has a migraine, what’s an abortive therapy we can use?

A

Imitrex

  • IN, SC, PO
  • MOA: Works on 5HT-1B and 5HT-1D receptors; cause vasoconstriction in cerebral vessels to take pressure off nerves.
  • Triptans and ergotamines work specifically by doing that
114
Q

What is CI in pregnancy?

A

Ergots

-Category X

115
Q

What are treatment options for patients experiencing a menstrual migraine?

A

NSAIDs, estrogen, triptans 2-3 days prior to onset of menses; continue for 5-7 days

116
Q

What can you do if oral contraceptives cause or increase migraine?

A
  • Different formulation OC
  • Progestin-only pill if migraine is related to estrogen component
  • Discontinue OC or decrease number of estrogen withdrawals
  • Vitamin B6 (supplement)
117
Q

If you have migraines during pregnancy, how do you treat?

A
  • Drug of choice: Acetaminophen
  • Short course opioids for a few days
  • Triptans are CAT C, could be an option if nothing else is working for them. No evidence for fetal harm, but unsure.
  • NSAIDs can be used early on in pregnancy, but are CAT D in 3rd trimester

-Avoid ergotamines - CAT X

118
Q

Why are NSAIDs CAT D in third trimester?

A

-It’ll close the patent ductus arteriosus and affect the fetal blood flow in the womb.

119
Q

How do you treat acute tension headaches?

A
  • NSAIDs, acetaminophen, Excedrin
  • Acetaminophen/aspirin combined with caffeine/butalbital (Fiorcet/Fiorinal)

Butalbital - barbiturate; if you have someone with urine drug screen, they’ll show positive for barbituates.

  • Can lead to rebound headaches from overuse
  • Use 2x/week and educate!
120
Q

What prophylaxis can be used to prevent tension headaches?

A
  • Amitriptyline
  • TCAs
  • SSRI - fewer ADR than TCAs, but less effective
  • Smoking cessation
121
Q

Cluster Headaches tx:

A

Tx with abortive therapy

  • Ergotamines
  • Triptans
  • Need subq or IV admin
  • Oxygen can be useful as well
122
Q

What prophylaxis can be used to prevent cluster headaches?

A

-Verapimil - most effective, better to use than Lithium.

  • Lithium - bipolar disorder; toxicity.
  • Ergotamine
  • Corticosteroids, but not for long term therapy due to SE.

Pharmacology II (10 decks)

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