parkinson's Flashcards

1
Q

what keeps dopamine in balance in Parkinson’s

A

acetocholine

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2
Q

Parkinson’s

A

Progressive disorder with degeneration of nerve cells in the basal ganglia with generalized decline in muscular function.
There is depigmentation of the substania nigra of the basal ganglia.
Is a disorder of the extrapyramidal system. This includes all descending fibers in the cortical and subcortical motor centers that reach the medulla and spinal cord by pathways other than corticospinal tracts. Important in maintenance of equilibrium & muscle tone.

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3
Q

effects of Parkinson’s

A

Selective depletion of dopamine producing neurons in the substania nigra in midbrain.
Dopamine influences purposeful movement. Without it there is a loss of the inhibitory influence of the excitatory mechanisms of acetycholine which goes unopposed.
Depletion of dopamine results in degeneration of the basal ganglia

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4
Q

Statistics of Parkinson’s

A

Affects men more than women.
Cause is unknown. Predominately idiopathic but research suggests several causative factors: genetics, atherosclerosis, excessive accumulation of oxygen free radicals, viral infections, head trauma, chronic antipsychotic medication and some environmental exposures.
100 to150 persons/ 100,000 or about 50,000 new cases per year.
Symptoms usually appear in fifth decade but some have been diagnosed by age 30.

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5
Q

Four classic symptoms of of Parkinson’s

A

Tremors
Rigidity
Akinesia
Postural Instability

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6
Q

Tremors in parkinson

A

a slow, unilateral, resting tremor present in about 70% at the time of diagnosis. Disappears with purposeful movement. Starts on one side and progresses to the other.

usually have resting tremors that will go away with purposeful movement

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7
Q

rigidity in parkinsons

A

have stiffness of neck, trunk and shoulders commonly. Cogwheel rigidity common.

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8
Q

Akinesia

A

(bradykinesia)
slowness of movement. May exhibit “freezing phenomenon”. As dexterity declines, micrographia develops.
tiny tiny writing is common in parkinsons

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9
Q

Postural Instability

A

loss of postural reflexes. Stands with head bent forward. Shuffling, propulsive gait.

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10
Q

autonomic symptoms of parkinsons

A

sweating, paroxyzsmal flushing, lacrimation, orthostatic hypotension, gastric and urinary retention, constipation, drooling, sensitivity to heat and sexual disturbances.

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11
Q

psychiatric changes in parkinsons

A

depression, dementia, sleep disturbances, and hallucinations. May have cognitive, perceptual, & memory deficits though intellect is usually not affected. May see personality changes, psychosis, dementia and acute confusion in the elderly.

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12
Q

what is a parkinsons patient at risk for as the disease progresses

A

respiratory & urinary infection, skin breakdown, and injury from falls.

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13
Q

stage 1 of parkinson’s

A

mild tremors. unilateral . patient doesn’t even realize there is something going. inconsistent. Little problem with locomotion

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14
Q

stage 2 of parkinson’s

A

symptoms are bilateral. slightly more tremors. Friends and family start to see something is wrong.

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15
Q

stage 3 of parkinson’s

A

starting to slow with body motion . moderately severe disability. More issues with gait and stability.

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16
Q

stage 4 parkinson’s

A

at this point they can’t live alone. very rigid. full blown tremors.

17
Q

stage 5 parkinson’s

A

they can’t stand or walk. Require nursing care

18
Q

what is usually the final demise of Parkinson’s patients

A

urinary tract or respiratory infection. They go septic

19
Q

diagnostic findings in parkinsons

A

Laboratory and imaging studies are not helpful in diagnosing condition. PET scanning is used to evaluate levodopa ( precursor to dopamine ) uptake.
Disease is diagnosed by history and presence of 2 or more of the cardinal manisfestations.

20
Q

medical management of parkinson’s

A

control the symptoms

Directed at controlling symptoms and maintaining functional independence because there is no medical or surgical treatment to prevent or cure the disease.
We now have better symptom control measures.

21
Q

pharmacological therapy in parkinsons acts by

A

Increasing striatal dopaminergic activity

b. Reducing excessive influence of excitatory       cholinergic neurons.
c. Acting on neurotransmitter pathways other than dopaminergic pathways.
22
Q

surgical management of parkinson’s

A

Thalamotomy and pallidotomy are effective in relieving many symptoms. Interrupts nerve pathways and alleviates tremor and rigidity.
b. During thalamotomy stereotactic electrical stimulator destroys a portion of the thalmus to decrease tremors. Complications can be ataxia and hemiparesis.
c. Pallidotomy destroys part of globus pallidum. Helps to decrease rigidity, bradykinesia & dyskinesia. Improves motor function and ADLs. Complications:
stroke, visual changes, hemiparesis
Use MRIs, CT scans and angiography to localize appropriate site. Have a stereotactic frame and make a burr hole to pass the electrode through it to target the area.
Stereotactic procedures are completed on one side of the brain at a time. If there are bilateral symptoms, 6 months interval is suggested.

23
Q

neural transplantation in parkinson’s

A

Implantation of adrenal medulla tissue into corpus striatum to reestablish normal dopamine release.
Research to transplant human fetal brain cells or genetically engineered cells .
Recently (2000) fetal pig neuronal cells survived transplantation so may be alternate to human cell transplants.

24
Q

deep brain stimulation in parkinson’s

A

Recently approved by the FDA, pacemaker like brain implants show promising results in relieving tremors.
Stimulation can be bilateral or unilateral. Electrode is placed in thalmus and connected to a pulse generator implanted in a subcutaneous subclavicular or abdominal pouch.
Generator sends high frequency impulses through a wire placed under the skin to a lead anchored in the skull. The electrode blocks nerve pathways in the brain that cause tremor. Complication: lead leakage.

25
Q

nursing interventions in parkinson’s

A
Provide a safe environment.
 Measures to increase mobility.
 Activities to limit postural deformities.
 Improve communication.
 Maintain adequate nutrition.
 Enhance swallowing
Improve urinary and bowel elimination.
 Support coping abilities.
 Promote home and community based care.
26
Q

drugs used for parkinson’s

A
Dopaminergic Agents
	a.  Replacement ( Levodopa, Sinemet )
	b.  Dopaminergic Agonists:
         Bromocriptine
         Cabergoline ( Cabaser )
         Pramipexole ( Mirapex )
         Ropinirole ( Requip )
 COMT Inhibitors ---Entacapone ( Comtress )
 Monomine Oxidase B Inhibitor---Selegiline
 Anticholinergics
27
Q

dopaminergic agents for parkinsons

A

A. Dopaminergic agents help replace lost dopamine or enhance function of the few neurons that are left to produce their own.
B. Categories:
1. Replacement—replace dopamine to increase levels in the brain. Examples: Levodopa and Sinemet ( levodopa and carbidopa).
2. Dopaminergic Agonists—direct acting. Bind to receptor and stimulate receptor function. Mimic body’s own regulatory function. Examples:
a. Bromocriptine
b. Cabergoline ( Cabaser)
c. Pramipexole (Mirapex)
d. Ropinirole (Requip)
3. Indirect acting—Those that release dopamine. Example: Amantadine.
C. Goal: Increase levels of dopamine in the brain to create a balance with acetycholine.

28
Q

COMT inhibitors

A

Entacapone (Comtress) for parkinsons
Action: Increases availability of levodopa by inhibiting COMT activity. COMT
( Catechol-O-Methyltransferase ) is an enzyme which is important in the central
and peripheral metabolism of catecholamines ( dopamine, adrenalin,
noradrenalin ) and levodopa. COMT activity in periphery reduces the amount of
levodopa available for central conversion to dopamine. COMT inhibitors increase
availability of levodopa in the brain and prolong its availability in plasma. Results
in reduced requirement for levodopa.
B. Example: Entacapone ( Comtress, Comtan)
(4)

 C.  Side effects / Adverse reactions:
      1.  Orthostatic hypotension, Hepatic Failure, nausea, vomiting, diarrhea, 
           electrolyte imbalances.
      2.  Tolcapone was suspended because of concerns over severe hepatic reactions.
29
Q

Monomine Oxidase B inhibitor for parkinsons

A

SELEGILINE (ELDEPRY)

 A.  Most non selective MAO Inhibitors have tyramine effect if taken with foods like
       cheese, red wins, beer, and yogurt that results in a severe hypertension.  Selegiline
       does not elicit classic cheese effect at doses of 10mg or less per day.  Is able to 
       slow the progression of P.D. because it is neuro-protective and blocks the
       metabolism of dopamine.
 B.  Theory is that substantia nigra’s destruction of cells is caused by MPP, the 
      enzymatically active toxin of MPTP.  Conversion is accomplished by MAO-B.
      By blocking enzyme, substantia nigra is spared.
 C.  Selegiline has less side effects than most MAO Inhibitors so it is approved for
       use with levodopa and sinemet.  It allows those doses to be decreased.  Helps
       to delay levodopa’s loss of control of P.D. in 5 to 10 years.  May delay it for
       9 to 18 years.  Dose is usually 5m BID.
 D.  Side effects / Adverse reactions—usually mild
       1.  Nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion,
            dry mouth, hypotension.
       2.  If dose is increased more than 10mg per day, hypertensive crisis is possible.
30
Q

anticholinergics for parkinsons

A

used more for drug induced parkinson’s

 A.  Action is to inhibit action of acetycholine resulting in a decrease in sweating,
       salivation, muscle tremors, and rigidity.  Does little for bradykinesia.  It
       reduces excessive cholinergic activity in the brain.
 B.  Example:
      1.  Cogentin
      2.  Artane
 C.  Side effects / Adverse reactions:
      1.  CNS—drowsiness, memory confusion, disorientation,hallucinations.
      2.  Constipation, nausea, vomiting, dry mouth
      3.  Urinary retention, pain on urination.
      4.  Blurred vision, dilated pupils, sensitivity to sun, tachycardia.
31
Q

replacement Dopaminergic agents for parkinsons

A
  1. Replacement—replace dopamine to increase levels in the brain. Examples: Levodopa and Sinemet ( levodopa and carbidopa).
    Levodopa
    a. Initially 250mg every 6 to 12 hours PO. Increase daily dose by 100 to
    750mg every 3 to 7 days until desired response. Max dose-8 grams/day.
    Usual dose-3 to 6 grams /day. Requires 3 to 6 months to achieve optimal
    therapy.
    b. Increases levels of dopamine in the brain and relieves tremors,
    bradykinesia, and rigidity. Crosses blood-brain barrier. Metabolized in
    the liver and GI tract. Excreted by the kidneys.
    c. Interactions:
    1. Haldol and phenothiazines block dopamine receptors in the brain so
    decrease levodopa effect.
    2. B6 reverses effect of levodopa by promoting levodopa breakdown.
    3. MAO I increase the risk of hypertensive crisis when used with
    levodopa. Must discontinue 2-4 weeks prior to starting levodopa.
    d. Contraindications:
    1. Acute glaucoma, Melanoma, history of MI with residual arrhythmias,
    psychotic state.
    e. Side effects/ adverse reactions:
    1. Orthostatic hypotension, cardiac arrhythmias, hemolytic anemias
    2. May aggravate peptic ulcer and bronchial asthma.
    3. Diplopia ,blurred vision, anorexia, nausea, vomiting, false positive
    urine glucose. Drowsiness.
    4. Confusion, agitation, hallucinations, psychotic episodes, seizures,
    5. Hepatoxicity. May cause urinary retention with renal disease.
    6. May cause urine and sweat to turn dark. Incontinence.
    7. Skin rash, increased sweating.
    (2)
    f. Benefits of levodopa do not persist indefinitely. Within 5 to 10 years many
    patients develop drug related symptoms like drug induced involuntary
    movements, end-of-dose deterioration, on-off motor fluctuations, psychiatric
    effects.
    g. Nursing Implications:
    1. Proper history ie. hypotension, seizures, melanoma, glaucoma, meds
    patient is on.
    2. Assess LFTs, RFTs, CBC
    3. Assess for toxicity ( involuntary muscle twitching, facial grimacing,
    spasmotic winking, exaggerated protrusion of the tongue or behavioral
    changes.
    4. Do not take with meals, however MD may order them taken 15 minutes
    after a meal to decrease gastric irritation. Taking with a meal may retard
    drug effect.
    5. Move slowly for position changes. No driving if drowsy or visual
    problems. Routine follow-up. Therapeutic effect takes 2 to 3 weeks to
    achieve. Wait 8 hours before switching to sinemet—can cause toxicity.
    2. Sinemet ( Carbidopa / Levodopa)
    a. Action—Carbidopa given with levodopa inhibits enzymatic conversion of
    levodopa to dopamine in the peripheral nervous system. Carbidopa does not
    cross the blood-brain barrier so levodopa is converted to active dopamine
    primarily in the brain. This decreases many unwanted effects caused by
    peripherally broken down levodopa. Carbidopa reduces the dose of
    levodopa needed.. Carbidopa is not effective alone.
    b. Dosages:
    1. 10/100 mg 3 to8 times a day
    2. 25/100 mg 3 to 6 times a day
    3. 25/250 mg 3 to 4 times a day
    4. Sinemet CR—1 tab BID
    * Maximum dose 200mg Carbidopa and 2 grams levodopa /day
    c. Side effects /adverse reactions
    1. Same as with levodopa but less since lower doses of levodopa are used.
    2. Mental depression, mood and mental changes.
    3. Hypotension, hypertension, arrhythmias, dizziness.
    4. Blurred vision, diplopia, dark urine and sweat, blood dyscrasias
    5. Nausea, vomiting, diarrhea, constipation, anorexia.
    d. May need drug holiday after several years. With long term use, patients
    experience periods when they have good control (on-time) and periods when
    they have bad control (off-time). Sinemet CR increases on-time and
    decreases off-time.
32
Q

dopaminergic agonists for parkinsons

A

Dopaminergic Agonists
1. Action: Stimulate dopamine 2 receptors and antagonizes or blocks dopamine 1
receptors so they stimulate the release of dopamine in the substantia nigra. Can
be given with sinemet so lower doses of levodopa needed to prolong “0n” time.

                                                     (3)
  2.  Examples:  Cabaser, Mirapex, Requip, Bromocriptine
  3.  Side effects / adverse reactions
            a.  Hypotension, leg cramps, shock
            b.  Drowsiness, confusion, dizziness, nightmares ,hallucinations,  visual
                 disturbances, uncontrolled movement of body, face, tongue, arms,
                 hands, and feet.
            c.  Nausea, vomiting, constipation, diarrhea, metallic taste.
  4.  Contraindications:  Hypersensitivity to ergot alkaloids.  Patients with severe
        ischemic PVD.  Don’t give to kids under 15 years. F.  Indirect Acting
  1.  Amantadine ( Symmetral)      
            a. Is an antiviral that blocks the reuptake and storage of catecholamines, 
                allowing for the accumulation of dopamine.  Elicits release of dopamine
                from the nerve endings causing higher concentrations of dopamine in the 
                CNS.
            b. Is more effective in early stages of P.D. when there is still a significant
                number of nerves to act on dopamine to be released.  Usually only
                effective for 6 to 12 months.
            c.  Dose:  100 to 400 mg / day
            d.  Caution with patients with seizures, liver disease, psych problems,
                 cardiac and renal disease.
            e.  Side effects / adverse reactions:
                  1.  Impaired concentration, mood changes, confusion, hallucinations,
                       visual impairment, headache, irritability, nervousness.
                  2.  Hypotension, nausea, vomiting, constipation ,anorexia
                  3.  Purple re skin spots, dry mouth, nose, and throat. increased weakness
             f.  Nursing Implications:
                  1.  Monitor blood pressure.  position changes slowly.
                   2.  Don’t give last dose HS because it will cause insomnia.
                   3.  Better to give in divided doses since it decreases the CNS side effects.
                   4.  Can mix content of capsules with food and fluids.
                   5.  Assess for purple mottling—usually disappears with continued
                        treatment.
                   6.  Therapeutic effects usually seen by end of first week.
33
Q

what vitamin should parkinson’s be careful with

A

B6. it diminishes levodopa in the body. So stay away from foods that have B6

34
Q

alcohol in parkinson’s

A

at later stages its good for them to have small amounts of alcohol to help with relaxation

35
Q

bowel habits for parkinson’s

A

try to keep them on their schedule. If they used to go to the bathroom after breakfast every morning, then place them on the commode every morning after breakfast.

36
Q

biggest side effects of parkinson’s drugs (across the board)

A

orthostatic hypertension

37
Q

parkinson’s drugs build up

A

you build up a tolerance. So you’ll have intermittent symptoms. They will usually take them off the drug for awhile and then re add it.

38
Q

what do you not want with parkinson’s drugs

A

we do not want peripheral metabolism in the brain

39
Q

major side effects of parkinson’s drugs (across the board)

A

Hypotension