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Pharm Block 5 > CNS degenerative diseases > Flashcards

CNS degenerative diseases Flashcards

1
Q

What does excitotoxicity result from?

A

Sustained intracellular calcium causes protease activation, free radical formation, and lipid peroxidation. Due to NMDA glutamate receptor activation.

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2
Q

What happens to the CNS when there are misfolded proteins?

A

Forms extracellular or intracellular aggregates leading to Neurotoxicity.

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3
Q

What is the deficiency in Parkinson’s disease?

A

dopamine deficiency

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4
Q

How is the substantia nigra involved in Parkinson’s?

A

Substantia nigra is the source of dopaminergic neurons that terminate in the neostriatum. In parkinson’s there is degeneration of the pars compacta of the SN.

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5
Q

What happens in the neostriatum in Parkinon’s

A

When cells are destroyed in SN, there is reduced secretion of Dopamine in Neostriatum, leading to overproduction of ACh.

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6
Q

What drugs shouldn’t you use in Secondary Parkinsonism

A

Dopamine receptor blockers.

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7
Q

What is Levodopa?

A

immediate precursor of dopamine that is actively transported across the BBB. Has short half life so is dosed 3x/day.

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8
Q

What are adverse effects of L-Dopa?

A

Brown saliva and urine (important to tell families!), tachycardia, involuntary movement, mood changes, anxiety and psychosis

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9
Q

What’s the deal with antipsychotics and dopamine receptor antagonists?

A

Antipsychotics are dopamine receptor antagonists, so antipsychotics diminish the effect of dopamine receptor agonists.

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10
Q

What are drug interactions with LevaDopa?

A

MAOIs can product hypertensive crisis, watch out for arrhythmias in cardiac patients, and intraocular pressure in glaucoma patients.

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11
Q

What is the function of Carbidopa

A

reduces levodopa metabolism in the GI tract and peripheral tissues so more enters the CNS. Percent increases from 1-3% to 10%.

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12
Q

What is the negative consequence of combining Carbidopa and Levadopa?

A

The breakdown product, 3-O-Methydopa, of carbidopa competes for entrance into the CNS with Levadopa.

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13
Q

What is the mechanism for Selegiline and Rasagiline?

A

Both are MAOIs, that inhibit the metabolism of dopamine and reduce the dose of levodopa required.

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14
Q

What is the side effect of Selegiline?

A

it is broken down into methamphetamine and amphetamine, thus can produce insomnia if administered later in the day.

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15
Q

What is the benefit of Ragailine?

A

It an irreversible inhibitor and is 5x as potent as Selegiline and not metabolized into a stimulant.

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16
Q

What are the adverse effects of Ragailine and Selegiline

A

dyskinesia, mood changes, GI

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17
Q

What are the COMTIs?

A

The “capones”, entacapone and tolcapone.

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18
Q

What is the function of the COMTIs

A

reversibly inhibits Catechol-O-methyltransferase. Can be used to decrease 3-O-methydopa, as with what occurs when levadopa and carbidopa are taken together.

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19
Q

What is the adverse effect of Tolcapone?

A

It can cause hepatic necrosis. Entacapone doesn’t not.

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20
Q

What are AE related to the COMTIs?

A

sleep issues, hallucinations, postural hypertension

21
Q

What are the dopamine receptor agonists?

A

Bromocriptine, Apomorphine, Pramipexole, Ropinirole

22
Q

What is the action of Bromocriptine?

A

actions similar to levodopa, but causes many CNS issues, orthostatic hypotension that can lead to falls, and Pulmonary and retroperitoneal fibrosis.

23
Q

What type of patient do you avoid treating with Bromocriptine?

A

Patients with COPD.

24
Q

What does it mean to be nonergot vs ergot for the dopamine agonists?

A

Ergot is hallucinogenic, like Bromocriptine, and nonergot is non-hallucinogenic like apomorphine, pramipexole, and ropinirole.

25
Q

for what type of management is apomorphine used?

A

acute, since it’s given IV

26
Q

Which dopamine agonist do you avoid giving to a patient with kidney failure?

A

Pramipexole, since its dependent of the kidney for its elimination.

27
Q

What is amantadine?

A

limited use, maybe 6 months, but increases release of dopamine is release not already maxed out. AE: livedo reticularis, psychosis, restlessness

28
Q

Which antimuscarinic agents are used to treat Parkinson;s?

A

Benztropine, Trihexyphenidyl, and Biperiden

29
Q

What are the uses of animuscarinics in treatment for Parkinson’s?

A

Used as an adjuvant only.

30
Q

For What conditions are the antimuscarinics, Benztropine, Trihexyphenidyl, and Biperiden contraindicated?

A

glaucoma, prostatic hyperplasia, pyloric stenosis. AE are similar to atropin usage (DUMBELLS)

31
Q

In Huntington’s Disease, what is the loss of function?

A

GABA neurons from the corpus striatum degenerate.

32
Q

What groups of drugs are used to treat Huntington’s Disease?

A

Dopamine antagonists, Amine-depleting drugs, GABA agonists

33
Q

What are the dopamine antagonists used to treat Hungington’s

A

Haloperidol and Chlorpromazine. Both block at D2 receptors and for each there is s risk for Neuroleptic malignant syndrome.

34
Q

What are the mechanisms of Reserpine and Tetrabenazine, the amine depleting treatments for huntington’s?

A

inhibits Vesicular monamine transporter that transports stores of catecholamines.

35
Q

What are the adverse effects of Reserpine and Tetrabenazine, the VMAT inhibitors.

A

Severe depression. Avoid MAOIs.

36
Q

What is Baclofen?

A

A GABA B receptor agonist causing spinal inhibition of motor neurons. Leads to sedation and muscle weakness.

37
Q

What AChE Inhibitors are used in the treatment of Alzheimers?

A

Donepezil, Galantamine, Rivastigmine, Tacrine.

38
Q

What is the competitive inhibitor of the AChE inhibitors?

A

Galantamine.

39
Q

What is the function of the AChE inhibitors in the treatment of Alzheimers?

A

modest reduction in rate of loss of cognitive function.

40
Q

What are the adverse effects of the AChE inhibitors

A

tremors, bradycardia, myalgia, anorexia and hepatoxicity with Tacrine.

41
Q

What are the NMDA receptor antagonists in the tx of Alzheimers?

A

Memantine partially blocks ion channel to limit calcium influx?

42
Q

What are SE of NMDA receptor antagonists?

A

confusion and agitation exacerbated by drug

43
Q

What drugs are used to treat MS?

A

interferon B1a, interferon B1b, Mitoxantrone, Fingolimod, Dalfampridine, Glatiramer, Natalizumab

44
Q

What is the mechanism for Mitoxantrone?

A

kills T cells and inhibit WBC-mediated attacks. Injection only.

45
Q

What is the action of the interferons in tx of MS?

A

disrupt T-helper cell signal pathways and taper immune system

46
Q

What is the action of Fingolimod?

A

coats lymphocyte so when it goes into lymph node, it can’t get out. First oral drug to slow disease progression.

47
Q

What is the action of Dalfampridine and the major SE?

A

it is an oral potasstium chanel blocker that can improve walking speeds. Can cause arrhythmias.

48
Q

What is the action of Glatiramer?

A

Mimics 4 a.a. chain in myelin, so WBCs attack Glatiramer instead of myelin. Leaves huge welts, think sticking your arm in a hive, same idea.

49
Q

What is the action of natalizumab and the major SE?

A

coats integrin on WBCs so they can’t cross BBB, decreasing sx of MS. SE: death in 1/1000 from PML, Progressive multifocal leukoencephalopathy caused by JC virus.

Pharm Block 5 (9 decks)

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