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PATTY PHARM FINAL (NEW STUFF) > Drugs for Neurodegenerative Diseases > Flashcards

Drugs for Neurodegenerative Diseases Flashcards

1
Q

Parkinson’s Disease

Drugs that Increase Dopamine Levels

A
  • Levodopa/Carbidopa (Sinemet)
  • Entacapone (Comtan)
  • with Ldopa/Cdopa (Stalveo)
  • Carbidopa (Lodosyn)
  • Tolcapone (Tasmar)
  • Rasagiline (Azilect)
  • Selegeline (Eldepryl)
  • Amantadine (Symmetrel)
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2
Q

Parkinson’s Disease

Dopamine Receptor Agonists

A
  • Apomorphine (Apokyn)
  • Bromocriptine (Parlodel)
  • Pramiprexole (Mirapex)
  • Ropinirole (Requip)
  • Rotigotine (Neupro)
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3
Q

Parkinson’s Disease

Cholinergic Receptor Antagonists

A
  • Benztropine (Cogentin)
  • Trihexyphenidyl
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4
Q

Alzhimer’s Disease

Central Acetylcholinesterase Inhibitors

A
  • Donepezil (Aricept)
  • Galantamine (Razadyne)
  • Rivastigmine (Exelon)

offset EP side effects

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5
Q

Alzhimer’s Disease

Other Agents

A
  • Caprylidene (Axona)
  • Dextromethorphan and Quinidine (Nuedexta)
  • Memantine (Namenda)
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6
Q

Drugs for Huntington’s Disease

Drugs for Huntington’s Disease

A

Diazepam (Valium)
Haloperidol (Haldol)
Tetrabenazine (Xenazine)
Sertraline (Zoloft)

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7
Q

Drugs for Multiple Sclerosis

A
  • Dalfampridine (Ampyra)
  • Fingolimod (Gilenya)
    * Interferon beta B-1b (Betaseron)
  • Prednisone (Deltasone)
  • Teriflunomide (Aubagio)
  • Dimethyl fumarate (Tecfidera)
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8
Q

Drugs for Amyotrophic Lateral Sclerosis (ALS) (Lou Gehrig’s Disease)

A
  • Gabapentin (Neurontin)
  • Riluzole (Rilutek)
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9
Q

Anti-Spastic Drugs

A

* Baclofen (Lioresal)
* Cyclobenzaprine (Flexeril)
* Carisoprodol (Soma)
* Orphenadrine (Norflex)
* Tizanidine (Zanaflex)
* Methocarbamol (Robaxin)
* Dantrolene (Dantrium)
* Botulinum toxin A (Botox)

ine = muscle relaxants = drowiness (anticholinergic aka no pee, no spit)

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10
Q

PARKINSON’S DISEASEDrugs that increase dopamine levels

Levodopa

A
  • Biosynthetic precursor to dopamine
  • Used to alleviate motor dysfunction
  • Ingestion of high protein levels can impede response to levodopa
  • Most common side effect is nausea and vomiting followed by orthostatic hypotension, and cardiac dysrhythmias caused by B-adrenoceptor activation (B-agonist effect)
  • Dyskinesia (involuntary movements) occurs as a result of excessive dopamine concentrations
  • Psychotic effects including hallucinations, or distorted thinking may also occur
  • Other side effects include sedation, agitation, delirium, vivid dreams, euphoria
  • Drug interaction with MAO Inhibitors (anti-psychotics) may lead to over accumulation of dopamine and cause HTN
  • Metabolized by L-amino acid decarboxylase (LAAD) (requires B6)
  • and Catechol-O-methyltransferase (COMT)
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11
Q

PARKINSON’S DISEASE Drugs that increase dopamine levels

Carbidopa

A
  • Structural analog of levodopa and inhibits LAAD thereby reducing the conversion of levodopa to dopamine in peripheral tissues thereby increasing the amount of levodopa that enters the brain
  • Highly ionized and does not cross the blood brain barrier
  • Substantially reduces the GI and CV side effects of levodopa and allows for a 75% reduction in the dose of levodopa
  • Used in combination with levodopa in different concentrations both in immediate release and sustained release formulations to reduce wear off of the drug
  • Does not inhibit the formation of dopamine in the CNS

INCREASES Levadopa

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12
Q

PARKINSON’S DISEASE Drugs that increase dopamine levels

Entacapone/Tolcapone

A
  • Drugs used to enhance the effectiveness of levodopa in the treatment of PD
  • Inhibits the COMT enzyme that metabolizes levodopa to 3OMD in the gut and liver
  • 3OMD competes for transport with levodopa into brain tissue
  • Produces a twofold increase in the oral bioavailability and half life of levodopa
  • Contributes to more sustained improvement in motor function
  • Found to increase efficacy of levodopa while reducing the dosing requirement
  • Side effects include nausea, diarrhea, and in rare cases hepatitis
  • Entacapone has no reports of hepatic toxicity and is available in a Ldopa/Cdopa combination
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13
Q

PARKINSON’S DISEASE Drugs that increase dopamine levels

Selegiline (Eldepryl) and Rasagiline (Azilect)

A

* MOA Inhibits MOA-B and prevents oxidation of dopamine to dihydroxyphenylacetic acid and hydrogen peroxide
* Increases dopamine levels in the basal ganglia and decreases the formation of hydrogen peroxide
* Inhibits the progression of PD by inhibiting the formation of free radicals or by inhibiting the formation of an active metabolite of an environmental toxin
* Does not inhibit MAO-A an enzyme that catalyzes degradation of catecholamines
* Can cause adverse effects if administered with meperidine or with other selective serotonin reuptake inhibitors (Fluoxetine)
* Used in early PD as a single drug and in combination with ldopa/cdopa in moderate or progressive advanced disease

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14
Q

PARKINSON’S DISEASE Dopamine Receptor agonists

Pramipexol/Ropinirole

A

*** Act as selective D2 receptor agonists
* May delay the need for levodopa when used in early stages of **PD
* Also indicated for the treatment of Restless Leg Syndrome
* Rotigotine a newer agent is also selective for D2 receptors as well as D3 receptors and is used as an adjunct to ldopa/cdopa
* Available as a patch formulation
* Apomorphine is available as an injection for intermittent hypomobility or freezing episodes
* Acts as a dopamine receptor agonist even though it is structurally related to morphine

Restless leg syndrome

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15
Q

PARKINSON’S DISEASE Dopamine Receptor agonists

Bromocriptine

A
  • Ergo alkaloid in same class as LSD used to treat migraine headaches
  • D2 receptor agonist and D1 receptor angagonist
  • Used as an adjunct to ldopa/cdopa in patients with wearing off effects and on off motor fluctuations
  • New diagnosis in formulation (Cycloset) to treat type 2 diabetes
  • Adverse effects include nausea, diarrhea, confusion, dyskinesias, sedation, vivid dreams and hallucinations
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16
Q

Management of Parkinson’s disease
(Early disease of mild intensity)

A
  • Exercise, Nutrition, Education
  • Speech, Occupational, Physical Therapy
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17
Q

Management of Parkinson’s disease
(Mild tremor and slowness)

A
  • Anticholinergic drugs like amantadine may be helpful
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18
Q

Management of Parkinson’s disease
(More severe functional disabilities)

A
  • Dopaminergic drugs are the most effective treatment
  • Combination therapy with levodopa/carbidopa is usually prescribed
  • Drugs have a delayed onset of action and improvement may not be noted for 2-3 weeks
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19
Q

ALZHEIMER’S DISEASE (Central Acetylcholinesterase Inhibitors)

Rivastagimine (Exelon)

A
  • Significantly delays the global cognitive impairment associated with AD
  • Available in a patch formulation
    *
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20
Q

ALZHEIMER’S DISEASE (Central Acetylcholinesterase Inhibitors)

Donepezil (Aricept)

A
  • Slow the deterioration of cognitive function
  • They do not affect the underlying neuro-degenerative process
  • Donepezil demonstrates a better cognitive function in comparative studies at 24 weeks
  • Reversible cholinesterase inhibitor that selectively inhibits cholinesterase in the CNS and increases Acetylcholine levels in the cerebral cortex
  • Side effects include diarrhea, nausea, and vomiting
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21
Q

Alzheimer’s Disease Treatment

Quinidine with Dextromethorphan

A

Used to treat pseudobulbar affect of emotional lability seen in patients with neurodegenerative diseases

22
Q

Alzheimer’s Disease Treatment

Caprylidene

A

Is a medical food that replaced depleted glucose levels to treat patients with neurodegenerative diseases

23
Q

Alzheimer’s Disease Treatment

Memantine (Namenda)

A
  • Low potency non-competitive antagonist at the NMDA receptor
  • Attenuates the ex ectocytotoxic effects of glutamate
  • Combination of memantine extended release with donepezil is also available and has shown increased efficacy as a combination in more of a synergist effect that either agent alone
24
Q

HUNTINGTON’S DISEASE Treatment

Diazepam

A

potentiates GABA and can also reduce excess movements in patients with HD

25
Q

HUNTINGTON’S DISEASE Treatment

Haloperidol (Haldol)

A

blocks dopamine receptors as does other anti-psychotic drugs

26
Q

HUNTINGTON’S DISEASE Treatment

Tetrabenazine

A

is the only drug for the treatment of chorea in HD and acts as a monoamine depletory by reversibly inhibiting the human vesicular monoamine transporter type 2 (VMAT2)

27
Q

HUNTINGTON’S DISEASE Treatment

SSRIs

A

have been incorporated as primary treatment for patients with Huntington’s disease particularly Sertraline (Zoloft)

28
Q

MULTIPLE SCLEROSIS Treatment

Interferon B-1b

A
  • the first drug to demonstrate an ability to halt and even reverse the progression of the disease
  • Effects are postulated to be from its immunomodulating properties.
  • Shown to reduce the frequency of relapses and the number of new lesions detected by MRI
  • Interferon B-1a is also approved to treat the relapsing forms of MS
29
Q

MULTIPLE SCLEROSIS Treatment

Peginterferon B-1a

A

provides a longer duration of action

30
Q

MULTIPLE SCLEROSIS (Other Treatments)

Mitoxantrone

A

an antineoplastic agent approved for MS suppresses the activity of T cells, B cells, and macrophages thought to lead the attack on the myelin sheath

31
Q

MULTIPLE SCLEROSIS (Other Treatments)

Glatiramer acetate

A

acetate is a synthetic protein that mimics the structure of myelin basic protein

32
Q

MULTIPLE SCLEROSIS (Other Treatments)

Dalfampridine

A

has been shown to improve walking in patients with MS

33
Q

MULTIPLE SCLEROSIS (Other Treatments)

Teriflunomide

A

a new agent used to treat relapsing forms and is believed to reduce the proliferation of overactive immune cells and has major risk of hepatic toxicity

34
Q

MULTIPLE SCLEROSIS (Treatment acute exacerbations)

Prednisone

A
  • Acute exacerbations are treated with adrenal corticosteroid drugs mostly prednisone
  • Prednisone shortens the duration of exacerbations and ameliorates the symptoms
35
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Baclofen

A
  • GABA B receptor agonist
  • controls spastity
36
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Gabapentin

A

may slow decline in muscle strength

37
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Riluzole

A

has been shown to prolong the time before patients require a tracheotomy and have prolonged life by approximately 3 months and has been more effective in patients with bulbar onset disease

38
Q

Antispastic Agents

Baclofen (Lioresal)

A

Most effective in treating spasticity from MS as a GABA b receptor agonist

39
Q

Antispastic Agents

Cyclobenzaprine (Flexeril)

A

MOA unknown but has significant Anticholinergic properties and sedation

40
Q

Antispastic Agents

Orphenadrine (Norflex)

A

MOA unknown but has significant Anticholinergic properties and sedation

41
Q

Antispastic Agents

Methocarbamol (Robaxin)

A

CNS depressant with a sedative and musculoskeletal relaxant property

42
Q

Antispastic Agents

Carisoprodol (Soma)

A

Meprobamate Barbiturate derivative with active metabolites

43
Q

Antispastic Agents

Tizanidine (Zanaflex)

A

MOA unknown but has significant Anticholinergic properties and sedation

44
Q

MYASTHENIA GRAVIS

Thymectomy

A

This operation to remove the thymus gland (which often is abnormal in individuals with myasthenia gravis) can reduce symptoms and may cure some people, possibly by rebalancing the immune system. A NINDS-funded study found that thymectomy is helpful both for people with thymoma and those with no evidence of the tumors. The clinical trial followed 126 people with myastenia gravis and no visible thymoma and found that the surgery reduced muscle weakness and the need for immunosuppressive drugs.

45
Q

MYASTHENIA GRAVIS

Monoclonal antibody

A

This treatment targets the process by which acetylcholine antibodies injure the neuromuscular junction. In 2017, the U.S. Food and Drug Administration approved the use of eculizumab for the treatment of generalized myasthenia gravis in adults who test positive for the antiacetylcholine receptor (AchR) antibody.

46
Q

MYASTHENIA GRAVIS

Anticholinesterase medications

A

Medications to treat the disorder include anticholinesterase agents such as mestinon or pyridostigmine, which slow the breakdown of acetylcholine at the neuromuscular junction and thereby improve neuromuscular transmission and increase muscle strength.

47
Q

MYASTHENIA GRAVIS

Immunosuppressive drugs

A

These drugs improve muscle strength by suppressing the production of abnormal antibodies. They include prednisone, azathioprine, mycophenolate mofetil, and tacrolimus. The drugs can cause significant side effects and must be carefully monitored by a physician.

48
Q

MYASTHENIA GRAVIS

Plasmapheresis and intravenous immunoglobulin

A

These therapies may be options in severe cases of myasthenia gravis. Individuals can have antibodies in their plasma (a liquid component in blood) that attack the neuromuscular junction. These treatments remove the destructive antibodies, although their effectiveness usually only lasts for a few weeks to months.

49
Q

MYASTHENIA GRAVIS

Plasmapheresis

A

is a procedure using a machine to remove harmful antibodies in plasma and replace them with good plasma or a plasma substitute.

50
Q

MYASTHENIA GRAVIS

Intravenous immunoglobulin

A

is a highly concentrated injection of antibodies pooled from many healthy donors that temporarily changes the way the immune system operates. It works by binding to the antibodies that cause myasthenia gravis and removing them from circulation.

PATTY PHARM FINAL (NEW STUFF) (6 decks)

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