Parkinson's Flashcards
(36 cards)
Parkinson’s
Progressive degeneration of the basal ganglion function
Basal ganglia fxn
slow coordinated mvts
Which cells are affected with parkinson’s
substantia nigra - cells in the basal ganglia that make dopamine
CM of Parkinson’s
- BIG 3–rest tremor, rigidity, bradykinesia with nonmotor CM
- upper tremor (pill roll), shuffling gait, flat affect, postural instability (fall risk)
Primary Parkinson’s
- idiopathic Parkinson’s disease
- genetic or sporadic
Secondary Parkinson’s
Parkinsonism but not the disease
- acquired–infx, drug tox, trauma
- most often drug-induced (antiemetic and antidepressive)
How to fix drug-induced parkinsonism
stop the drug and it usually resolves
Risk fx for Parkinson’s
- avg onset 60s, peak in 70s
- more men than women
- dom or recessive family (10%)
- enviro exposure to agricultures and pests
2nd fx that bring Parkinson’s out more
depression, head trauma, hysterectomy
Protective fx for Parkinson’s
coffee!
Dopamine in Parkinson’s
- inhibitory and excitatory NTs
- causes smooth motion w/o extra mvt normally
- lack inhibitory Dp receptors so unnecessary mvts aren’t inhibitory
ACh in Parkinson’s
- excitatory NT that causes uncoordinated mvts
- muscle fxn and balances with Dp so if Dp is wrong and ACh is right, still fxn well
Patho of Parkinson’s
- excess ACh with Dp –lose coordination
- don’t balance each other out
- primary–damage to sub nigra causes dec DP and dp/ACh imbalance, inc ACh and lose coordination
- secondary–altered Dp production
How do Parkinson’s sx progress
Gradual to prog–develop alone or in combo
- begin with 1 side and move to both
First sign of Parkinson’s often
resting tremor
- handwriting affected
- worse with stress and concentration
Parkinson’s vs essential tremor
Parkinson’s–DP deficit and ACh inc
- occur with rest and fixed with mvt
Essential–from faulty neuro impulses with motor fxn
- no other CM of parks
Rigidity
resistance to passive mvt
- “cogwheel rigidity”
- inc ACh causes continuous ctx with muscle soreness, aches, and pains
- often bilat but can be unilat
Bradykinesia
loss of automated mvt
- no blinking, no swing arms/balance, drool (no swallow), no self-expression with hands and feet
Major cause of disability with Parkinson’s
Bradykinesia
Comps of Parkinson’s
dementia (Lewy bodies form and cause memory, cog, hallucinations), sleep probs, fatigue, anx/dep, dec mobility (PNA, asp, malnut, UTIs (urine retention)), skin b/d)
Goals of Parkinson’s pharm
Maintain motor fxn best you can
- inc Dp or stim of Dp receptors
- block ACh with anticholinergic drugs
Levodopa/carbidopa (Sinemet) class and MOA
Dopaminergic
- Levodopa converts to Dp in brain and activates DP rec; carbidopa blocks destruction of levodopa–keep Dp in sys for longer
Levodopa/carbidopa (Sinemet) SE
- All r/t levodopa; N/V, dyskinesias (annoying to disabling uncontrolled mvts), CV postural hypotension and dysrhythmias, psychosis (hallucinate, nightmare, paranoia), dark sweat and urine, can activate malignant melanoma
Levodopa/carbidopa NC
- takes several months to work
- doesn’t work long-term–dose wears off
- may need shorter dose intervals
- abrupt loss of effect “on-off” phenomenon–can occur anytime w/ dosing and can’t predict (“off” pd inc with time)
- take with small food to dec GI (does dec drug abs tho)
- vit B6, antipsychotics, and pro can dec effect
- carbidopa, antiACh, MAOIs can inc fx (tox)–psychosis