Real Final Flashcards
(236 cards)
degenerative disease of the CNS*
aka neurodegenerative diseases
they are progressive, irreversible loss of neuron function in the brain and/or spinal cord
can affect any age group
pharmacotherapy treats symptoms -> no cure
depression is a common problem with these chronic/irreversible disorders
parkinson disease
progressive neurodegenerative disorder characterized by abnormal motor movement
onset 40-70yrs
men are more affected
fatigue, slow movement, slight tremor
cardinal sign of Parkinson disease
tremor
- hands and head develop palsy-like continuous motion, shaking when at rest
- pill rolling -> rub thumb and forefinger together in circular motion
muscle rigidity
- resistance to passive movement of arms/legs
- may resemble arthritis
- uncontrollable drooling -> rigidity of facial muscles
bradykinesia
- involuntary slowness of movement and speech
- difficulty chewing, swallowing, speaking
- shuffling gait
postural instability
- stooped over
-stumbling
- difficulty balancing
cause of Parkinson disease
caused by a lack of sufficient amounts of dopamine produced by the substantial nigra (part of the brain that plays a key role in controlling movement)
if dopamine levels decline, acetylcholine has a more dramatic stimulatory effect -> PIG
dopamine
is a chemical messenger and hormone that plays a role in many body functions
in the case of Parkinson disease it impacts movement
degeneration of 60% to 80% of dopamine producing neurons leads to Parkinson disease
pharmacotherapy of Parkinson disease*
the goal is to balance dopamine and Ach
may take 2-3 weeks of tx to see the benefits of the drug
dopamine agonists and anticholinergic drugs
dopamine agonists*
increase the available dopamine by:
- directly replacing dopamine,
- decreasing breakdown,
- increasing release,
- activating dopamine receptors
anticholinergic drugs in the tx of Parkinson*
block the excitatory actions of Ach in the striatum, reducing stimulation of abnormal muscle movements
striatum
cluster of interconnected nuclei that form a part of the basal ganglia
involved in decision making such as motor control, emotion
levodopa
most effective therapy for treating Parkinson disease
dopamine replacement therapy
usually is combined with carbidopa
dramatic improvement in symptoms early in treatment -> effects may diminish over time
-> on-off syndrome may worsen
extrapyramidal symptoms
major adverse effects that develop from deficiency of dopamine in striatum
can be treated with antiparkinson drugs
carbidopa
inhibits the peripheral metabolism of levodopa
greater proportion of peripheral levodopa will cross the blood-brain barrier for CNS effect
adverse effects of levodopa
- N/V
- anorexia
- headache
- choreiform (rapid, jerky movement)
- dry mouth
- urinary retention
- confusion/agitation
serious ADR
- agranulocytosis - low level of granulocytes
- leukopenia
- hemolytic anemia - blood cells break down faster than the body can replace them
considerations with taking Levodopa*
- take on an empty stomach
- avoid multivitamins/B6
- avoid high protein diets
- watch ANS VS -> BP, pulse, RR
- monitor safety with ambulation due to dizziness, assist with ADLs
- monitor liver and kidney function
- avoid alcohol;
- watch for mood or behavioural changes -> aggression/confusion
dopamine agonists
may be used as monotherapy for early symptoms of Parkinson disease or adjuncts to levodopa in pts with advances disease
less effective than levodopa
no dietary restrictions, no toxic metabolites produced, less likely to cause dyskinesias (abnormality or impaired voluntary movement)
pramipexole
pramipexole
antiparkinson agent
dopamine receptor agonist, nonergot
used to treat Parkinson’s disease:
- monotheraply early on
- with levodopa in advanced stages
non ergot
a class of dopamine agonists used to treat Parkinson’s disease
are not associated with the risk of heart damage
ex. pramipexole
dyskinesias
abnormal or impaired voluntary movement
levodopa worsens it
considerations when using pramipexole*
- assess baseline vital signs and symptoms of parkinsons disease
- monitor for orthostatic hypotension
- monitor for tar dive dyskinesia
- assess mental status
- alert pt and family about sleep attacks
- ensure family knows that PD tx is not a cure but might help with symptoms for a period of time
tardive dyskinesia*
stiff, jerky movements of your face and body that you can’t control
involuntary repetitive body movements
anticholinergics for tx of PD
are effective at reducing the tremor
less effective at reducing bradykinesia
restores the balance between Ach and dopamine, blocks reports that inhibit the effects of Ach which results in more available dopamine
most common is benzotropine and trihexyphenidyl
adverse effects for benztropine *
- sedation
-constipation - blurred vision
- dry mouth
- decreased sweating
- urinary retention
- confusion
serious:
- paralytic ileus
contraindication/precautions for benztropine*
- ALCOHOL!!!!!
- close angle glaucoma
- myasthenia gravis -> weakness in the voluntary muslces
- tardive syskinesia
-GI/urinary obstruction - prostatic hypertrophy
- peptic ulcers
- tachycardia
benztropine drug interactions*
Additive toxicity:
- antihistamines
- tricyclic antidepressants
- phenothiazines
- MAOIs
-Quinidine
Additive sedative effect:
- alcohol
- CNS depressants
Slow GI motility/decreased absorption
- antidiarrheals
Pregnancy category C -> benefits may outweigh the risks, but may be harmful to fetus
tx of overdose:
- physostigmine, 1-2mg subcutaneous or IV
- repeat in 2 hours if necessary
- will reverse symptoms of anticholinergic intoxication