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A. Pharm II > EXAM 3 > Flashcards

EXAM 3 Flashcards

1
Q

What do you add to levodopa to increase the levels of dopamine in the brain?

A

Carbidopa.

This is a metabolism inhibitor which decreases the amount of levodopa metabolized in the periphery. This leads to an increase of available levodopa to enter the CNS… 10% can enter.

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2
Q

Besides the increase of available levodopa in the CNS, what other benefit is there to taking carbidopa with levodopa?

A

Since it inhibits its metabolism in the periphery, allowing more to reach the CNS, this also allows for a lower dose of levodopa.

Less in the GI and less in the periphery means less adverse side effects!

  • Less N/V
  • Not as much orthorstatic hypotension
  • Less cardiac effects
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3
Q

What sorts of things should we TEACH about the medications given for Parkinson’s Disease?

A
  1. Therapeutic levels are not reached right away.
  2. The side effects may be pretty bad at first but they will decrease as the therapeutic levels are reached.
  3. The patient needs to tolerate these adverse side effects until the drug becomes effective… DON’T stop abruptly!
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4
Q

Some patients may develop a tolerance to, or a physical dependence on Parkinson’s drugs.

A

Do NOT stop abruptly.

Risk of Neuroleptic Malignant Syndrome.

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5
Q

What is the difference between idiopathic Parkinson’s and secondary Parkinson’s disease?

A

Idiopathic - Michael J. Fox, no known cause.

Secondary - From another cause: Exposure to toxins, side effects of anti-psychotics (pseudo Parkinson)
Ex: Muhammad Ali, got it from repeated blows to the head.

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6
Q

What IS Parkinson’s disease?

A

A disorder of the extrapyramidal system. (Akathisia.)

Often accompanied by psychological problems such as dementia, depression.

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7
Q

When is the ONSET and what is the TREATMENT?

A

Onset: middle age. 40-70, peak around 60

Treatment: drugs that balance the neurotransmitters

No cure. Progressive disease.

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8
Q

What is the focus of antiparkinson drugs?

A
  • Restoring dopamine function (by increasing dopamine as well as activation of dopamine receptors).
  • Blocking cholinergic activity in the nigrostriatal pathway (by blocking Ach).

What IS the nigrostriatal pathway?!
Nigrostriatal pathway is the efferent connection between the susbtantia nigra and corpus striatum. It is one of the major dopamine pathways in the brain and is particularly involved in the production of movement, as part of a system called the basal ganglia motor loop.

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9
Q

What is Sinemet?

A

Trade name of combination drug of carbidopa and levodopa.

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10
Q

First line dopamine receptor AGONIST used for treating Parkinson’s Disease symptoms:

A

pramipexole (Mirapex).

Advantages:

  • No toxic metabolites
  • No competition for absorption
  • Fewer long term failures

Disadvantages:

  • More frequent hallucinations (risk increases as pt gets older, so it’s better for younger patients)
  • Daytime sleepiness (sleep attacks)
  • Orthostatic hypotension (again, less risk with younger)

May be good to add with another parkinson’s medication to help with the fine tremors… or if the pt is experiencing on-off loss of effect.

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11
Q

What are the following symptoms a sign of?
Open-mouthed, drooling
Bradykinesia, loss of balance
Rigid body structure

A

Parkinson’s Disease

Big concern for falls.
Other signs: tremors, shuffling gait/shortened steps

Tx: Block Ach and/or increase dopamine. There is a fine line of balance between adverse effects and a therapeutic balance.

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12
Q

What is the primary drug to increase dopamine levels?

A

Levodopa (aka L-dopa)

  • 75% of patients experience 50% reduction in symptoms.
  • May take several months for the full effect to take place.

This is only a temporary treatment because after about 5 years, the disease will have progressed enough to where this drug will no longer be helpful.

***TEACH not to take with protein = competes with amino acids for intestinal absorption.

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13
Q

Why would selegiline be used for Parkinson’s Disease?

A
  1. Has a sublingual form of administration.

2. Helps reduce side effects because does not have to be broken down since it dissolves under the tongue.

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14
Q

How does an increase in dopamine help Parkinson’s Disease?

A

By increasing the smooth movements. Dopamine is the primary NT for movement.

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15
Q

How does selegiline work?

A

It’s selective for the B receptors (regarding monoamine oxydase)… inhibits the breakdown of dopamine.

It’s a MAOBi

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16
Q

What is COMT?

A

Catechol-O-Methyltransferase (COMT) is one of several enzymes that degrade dopamine, epinephrine, and norepinephrine. COMT breaks down dopamine mostly in the part of the brain responsible for higher cognitive or executive function (prefrontal cortex).

This metabolizes the drug to inactive metabolites.
Has to do with levodopa.

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17
Q

What is decarboxylase?

A

An enzyme that catalyzes the decarboxylation of a particular organic molecule… this metabolizes the drug to dopamine.

Has to do with levodopa.

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18
Q

Psychosis can occur in 20% of patients.
Dyskinesias are more likely to affect the younger patients.
Which drug are these related to?

A

levodopa.

Also:

  • N/V is more common early on but will decrease over time.
  • Orthostatic Hypotension is from the peripheral dopamine… so will not be as much of a risk if taken with carbadopa.
  • Discoloration of urine, perspiration, saliva. Not harmful, but may stain.
  • The increased amt of dopamine in the periphery can lead to cardiac effects… force of contraction, hyper/hypotension.
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19
Q

What drug interactions do we need to be concerned about with levodopa?

A
  • Conventional antipsychotics (bc they BLOCK dopamine)
    Ex: Haloperidol
  • MAOis because they INCREASE dopamine (and norepinephrine). This can lead to hypertensive crisis secondary to dangerous levels of dopamine and norepinephrine causing vasoconstriction.
20
Q

What is acute loss of effect and what do we do to treat it?

A

Acute loss of effect can happen in one of two ways.
1. Wearing off: There is a gradual loss of effect at the end of the dosing interval. Ex: Supposed to take ev 6 hrs but it wears off at hour 4 or 5. We treat this by reducing the dosing interval (taking it more often).

  1. On-Off: The “off” may last minutes to hours, for no known reason, during the time it is supposed to be therapeutic. There is no easy fix… **make sure they aren’t taking with a protein! **Maybe add a direct-acting dopamine receptor agonist (like pramipexole)?
21
Q

What is a really good reason to take pramipexole during the initial treatment of parkinson’s with levodopa?

A

It can delay the onset of dyskinesia’s which are a side effect of levodopa.

It also has beneficial effects on non-motor symptoms like depression, anhedonia, and weight loss.

22
Q

Which dopamine receptor agonist drug is good for treating fine tremors, depression, anhedonia and may lead to weight loss?

A

pramipexole

can also delay onset of dyskinesias related to levodopa.

risks for hallucinations and psychotic behavior increase with age.

23
Q

What life threatening condition may occur if levodopa is abruptly discontinued?

A

Neuroleptic Malignant Syndrome

S/S:

  • High fever (maybe from shivering)
  • Muscle rigidity
  • Autonomic dysfunction (BP changes, tachycardia)
  • Altered mental status (delirium, coma)
24
Q

How do we treat neuroleptic malignant syndrome?

A
  • Dopamine agonist, this will directly activate the receptors.
  • Acetaminophen for the fever
  • Dantrolene for the muscle rigidity
  • Fluids for dehydration and increase BP
25
Q

Which Parkinson’s medication is not recommended for the elderly?

A

benztropine (Cogentin). Anticholinergic.

This medication is effective for treating the tremors and is often taken in addition to Sinemet.

It isn’t recommended for the elderly because it increases the risk for dementia, confusion, dry mouth, urinary retention and tachycardia.

26
Q

Which medication is used to treat Parkinson’s disease as well as dystonia seen with antipsychotics? What are some common drug interactions with this medication?

A

benztropine.

Dystonia: Involuntary muscle contractions that cause repetitive or twisting movements.

Interactions: Not good with other anticholinergic drugs bc it intensifies the effect (duh). Some of these are:

TCAs
Antipsychotics
First generation anticholinergics like diphenhydramine.

27
Q

What is diphenhydramine?

A

An antihistamine and anticholinergic.

28
Q

This drug is an antiviral that increases the release and inhibits the re-uptake of dopamine:

A

amantadine (Symmetrel)

The amantadine tells the neurons to let more dopamine out AND to not take it back up out of the synapse.

This only works for about 3-6 months, so very short term.

It can help with dyskinesia’s but can exacerbate psychosis and suicidal ideation (due to the increase of dopamine).

29
Q

What is entacapone used for?

A

It is used to inhibit the COMT. Purely metabolism related. By inhibiting the COMT, this increases the dopamine levels.

Similar to carbadopa in that it doesn’t have a direct fix on Parkinson’s.

COMT is one of several enzymes that degrade dopamine, epinephrine, and norepinephrine.

30
Q

This condition includes memory loss, confusion, disorientation, and the onset to death is 4-8 years.

A

Alzheimer’s Disease.
A progressive degenerative disease of memory loss. It progresses until no longer capable of performing ADLs.

70-90% develop behavioral problems and personality changes.

Sun-downing may occur: wandering, getting lost, agitation, screaming out.

31
Q

What happens to the Alzheimer’s patient if you have to add an antipsychotic to their regimen?

A

It hastens their death!

Depression is a common co-morbidity and should be treated ASAP.

Psychosis, delusions, and hallucinations are very concerning bc of the above safety issue.

32
Q

This disease pathophysiology begins with neuronal degeneration, starting in the hippocampus and ending in the cerebral cortex:

A

Alzheimer’s disease.

Neuritic plaques develop which have a beta-amyloid core (which is neuro-toxic).

Neurofibrillary tangles are structural problems which damage the health of cognitive ability.

Ach levels are found to be 90% below normal levels in late disease. Not sure if it’s the chicken or the egg…

33
Q

How do we treat Alzheimer’s disease?

A

We want to increase acetylcholine levels to slow the progression of the disease.

34
Q

What does an excess in glutamate do to neurons?

A

Damage and death.

35
Q

What is donepezil used for?

A

Alzheimer’s disease.

Inhibits AchE (acetylcholine esterase) which breaks down Ach.

  • 60 hour half-life.
  • 25-30% have some cognitive improvement.
  • Metabolized in the liver - P450 system
  • Excreted in the urine and bile
  • Standard AND ORAL disintegrating tablets; 5-10mg/day
36
Q

What are some adverse effects of a cholinesterase inhibitor?

A

Elevated Ach could lead to cholinergic effects:

  • HA
  • D/N/V
  • Low HR
  • Fatigue
37
Q

What drug interactions should we be concerned with in regards to donepezil?

A
  • Other cholinergic blockers reduce effectiveness.

- First generation antihistamines, TCAs, and conventional antipsychotics all block Ach.

38
Q

Which drug should we start low and increase to effect dose based on side effects?

A

donepezil

Abrupt cessation will result in rapid progression of effects.

Also, once therapeutic level is reached, taking more will have no benefit.

39
Q

This drug helps prevent brain cell death by lessening the excessive transmission of glutamate:

A

memantine (Nemanda)

Works by blocking the NMDA receptor. The NMDA receptor is a glutamate receptor and ion channel protein found in nerve cells. … It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane.

Calcium needs to be in a big group in order to “get the message.” Memantine allows for larger influx of Ca to get the neuron activated by keeping the channel blocked until there’s enough Ca built up. Restores the normal function of the neuron. Even if glutamate is high.

40
Q

What combination drug therapy do we normally see for Alzheimer’s disease partnered with memantine?

A

donepezil.

41
Q

Taking 800 mg of which drug is recommended 2 years before the onset of Alzheimer’s disease to help prevent it?

A

NSAIDS may prevent AD.

42
Q

No real significant evidence to support estrogen therapy and AD.

A

Have not seen any real improvement.

43
Q

Which drug is indicated for moderate to severe Alzheimer’s disease?

A

memantine (Nemanda)

Can be used as monotherapy or with donepezil.

Side effects: 7% may experience dizziness, 6% HA

44
Q

Which drug interactions with memantine have black box warning?

A

SSRI and Atypical antipsychotics.

Can lead to an increased risk of death.

45
Q

What are statins good for with AD?

A

lowers cholesterol and lowers neurotoxic chemicals.

A. Pharm II (7 decks)

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