CNS -Antiparkinsonian Drugs Discuss the signs and symptoms exhibited by a patient with Parkinson’s Disease Describe the actions and intended effects of.

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Presentation transcript:

CNS -Antiparkinsonian Drugs Discuss the signs and symptoms exhibited by a patient with Parkinson’s Disease Describe the actions and intended effects of medications used to treat the signs and symptoms of Parkinson’s Disease

CNS Antiparkinsonian Drugs Parkinson’s Disease:  Disease of the basal ganglia & related neuronal groups + neurotransmitter deficiencies  “shaking palsy”  Bradykinesia – slowing down in the initiation & execution of movement  Rigidity – increased muscle tone  Tremor at rest  Impaired postural reflexes

CNS Antiparkinsonian Drugs Degeneration of dopamine-producing neurons in the substantia nigra of the midbrain  Disrupts the balance of:  dopamine (DA) – neurotransmitter for normal functioning of the extrapyramidal motor system (control of posture, support, and voluntary motion)  Acetylcholine (Ach)  and the basal ganglia Symptoms do not occur until 80% of the neurons in the substantia nigra are lost

CNS Antiparkinsonian Drugs

Five Stages  Flexion of affected arm - tremor / leaning toward unaffected side  Slow shuffling gate  Increased difficulty walking – looks for support to prevent falls  Further progression of weakness – assistance with ambulation  Profound disability – may be confined to wheelchair

CNS Antiparkinsonian Drugs Tremor  First sign  Affects handwriting – trailing off at ends of words  More prominent at rest  Aggravated by emotional stress or increased concentration  “Pill rolling” – rotary motion of thumb and forefinger  NOT essential tremor – intentional

CNS Antiparkinsonian Drugs Rigidity  Increased resistance to passive motion when limbs are moved through their range of motion  “Cogwheel rigidity” -- Jerky quality – intermittent catches of movement  Caused by sustained muscle contraction Muscle soreness; feeling tired & achy Slowness of movement due to inhibition of alternating muscle group contraction & relaxation in opposing muscle groups

CNS Antiparkinsonian Drugs Bradykinesia  Loss of automatic movements:  Blinking of eyes, swinging of arms while walking, swallowing of saliva, self-expression with facial and hand movements, lack of spontaneous activity, lack of postural adjustment  Results in: stooped posture, masked face, drooling of saliva, shuffling gait (festination); difficulty initiating movement

CNS Antiparkinsonian Drugs Drug Therapy  Correcting the imbalance of neurotransmitters within the CNS  Dopaminergic – enhance release or supply of dopamine (DA)  Anticholinergic – antagonize or block the effects of overactive cholinergic neurons in the striatum  Monoamine Oxidase Inhibitor Decreases MAO (the degradative enzyme for DA) Results: DA levels are increased  Catechol-O-Methyl Transferase (COMT) Inhibitor  Betablocker  Antihistamine

CNS Antiparkinsonian Drugs

Anticholinergic Drugs: decrease the activity of Ach  Benztropine (Cogentin) Antihistamines – decreases rigidity  Benadryl Betablockers – decreases rigidity  Inderal Monoamine oxidase inhibitor (MAOI):  Selegiline (Eldepryl ) Catechol-O-Methyl Transferase (COMT) Inhibitor  Entacapone (Comtan)

CNS Antiparkinsonian Drugs Drug Therapy  Sinemet early in disease becomes ineffective  Early: DA receptor agonist -- directly stimulate DA receptors  Parlodel, Requip, Mirapex  Moderate to severe symptoms:  Sinemet is added to therapy

CNS Antiparkinsonian Drugs

CNS -- Antiparkinsonian Drugs Nursing Process Assessment  Head-to-toe  Neuro  GI/GU Ability to swallow  Psychological and emotional coping  Parkinson progression Medication History  Length of time on medications  Changes in medications and effects Safety  Ability to perform ADLs independently

CNS -- Antiparkinsonian Drugs Nursing Process Nursing Actions  Exact timing of medication – cannot be administered late  Oral doses given with food  Avoid foods in Vit B6 – reverse effects of levodopa  Wheat germ, whole grain cereals, muscle & glandular meats (particularly liver), legumes, green leafy vegetables, bananas  Force fluids >2,000 mL/day  High roughage, high fiber diet

CNS -- Antiparkinsonian Drugs Patient Education “Wearing off” – “On-Off” phenomenon – gradual worsening of symptoms as medication begins to lose effectiveness, despite maximal doses “Drug Holiday” when levodopa no longer working effectively (usually 10-day period of hospitalization) Community resources to assist patient and family Safety Effect on blood pressure –  Hypotension  Hypertensive crisis of MAOI accidentally taken “Sleep attacks” – newer dopamine agonists (pramipexole & ropinirole) GI: Constipation – high fiber, high roughage, increased fluids GU: urine color changes – brownish-orange (entacapone)

CNS – Antiparkinsonian Drugs Monitoring Therapeutic Effects Therapeutic Response:  Improved sense of well being  Ability to perform ADLs  Ability to concentrate and think clearly  Less intense parkinsonian manifestations Observe for Adverse Effects:  Confusion, anxiety, irritability, depression, paranoia, headache, weakness, lethargy, nausea, vomiting, anorexia, palpitations, postural hypotension, tachycardia, dry mouth, constipation, urinary retention, blurred vision, dark urine, difficulty swallowing, and nightmares

CNS – Antiparkinsonian Drugs Carbidopa in Parkinson’s disease is to be used:  a. As successful monotherapy.  b. In conjunction with levodopa to block peripheral conversion to dopamine.  c. To decrease the incidence of gastrointestinal side effects associated with levodopa.  d. 2 and 3

CNS – Antiparksonian Drugs Discuss the normal course of progression of Parkinson’s disease. Include the rationale for drug therapy to alleviate the symptoms.