Parkinsons Flashcards

1
Q

some symptoms of Basal Ganglia Disorders

A
  • Abnormal motor control
  • Altered posture
  • Affects muscle tone
  • Dyskinesia
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2
Q

pattern of disorders with basal ganglia

A

right basal ganglia probelm

contralateral symptoms

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3
Q

define Basal ganglia disease

A

is a group of physical dysfunctions that occur when the group of nuclei in the brain known as the

basal ganglia fail to properly suppress unwanted movements or to properly prime upper motor neuron circuits to initiate motor function

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4
Q

what happens to the direct and indirects pathways on the cortex in parkinsons?

A

overall inhibitory effect!

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5
Q

normal effect of dopamine in the direct and indirect pathway?

A

D1 receptors>> stimulates direct>> increase cortex stimulation

D2 recepters>> inhbits indirect> increase cortex stimulation

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6
Q

what is parkinsons disease?

A

Chronic, progressive movement disorder characterised by a triad of bradykinesia, tremor and rigidity

Degeneration of substantia nigra causes deficiency of dopamine

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7
Q

which part of SN in parkinsons is defected?

A

SN>> pars compacta

degeneration

(ily yam 3yoona)

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8
Q

pathophysiology of parkinsons

A
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9
Q

Causes of parkinsons?

A
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10
Q

What is seen under the microscope?

A
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11
Q

clinical features of Parkinson’s

A
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12
Q

what type of tremor do ppl w/ parkinsons present?

A

A ‘pill-rolling’ movement of the index and middle fingers against the thumb pad is characteristic.

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13
Q

how is the rigidity described? why do they get it?

A

lead pipe rigidity>> resistance through the full range of movement.

if tremor is also seen w/ the rigidity >> cogwheel sensation (tremor superimposed on rigidity).

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14
Q

why do patients display ‘resting tremor’, with supposedly inactive muscles?

A

It just so happens that when the forearms are resting on the lap or on the arms of a chair, the forearm/hand muscles are not fully at rest. If the limb is fully supported at the elbow and wrist, the tremor disappears. The tremor also disappears during sleep.

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15
Q

describe how the handwriting of PD patients

A

Micrographia

Difficulty in writing is a common early feature of PD, written letters become small and irregular. Loss of writing skill is attributable to concontraction of wrist flexors and extensors, owing to a marked reduction of supraspinal activation of 1a interneurons synapsing on antagonist motor neurons.

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16
Q

why do they get Bradykinesia?

A

Bradykinesia means slowness of movement. Patients report that routine activities, such as opening a door, require deliberate planning and consciously guided execution. theres a reduction of the ‘initial agonist burst’ of electrical charge accompanying the first contraction of relevant prime movers.

Normally, the basal ganglia contribution to movement is initiated some milliseconds after the premotor cortex and cerebellum have raised the firing rate of motor-cortex neurons to threshold at a spinal lower motor neuron level.

In PD the boost to lower motor neuron activation is weak because of the weakened contribution from the supplementary motor area SMA.

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17
Q

which symptoms does not progress at the same rate as bradykinesia, rigidity, or gait problems?

describe why it occurs?

A

Tremor

(The aetiology of tremor in PD may reflect the combination of dysfunction of the basal ganglia and the cerebello–thalamo–cortical pathway, which then results in the appearance of a tremor

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18
Q

in tremor, what is the commonest sequence of limb involvement?

A

1 upper limb to the ipsilateral lower limb within 1 year,>>> followed by contralateral limb involvement within 3 years

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19
Q

what is Parkinsonism plus syndrome

A

Parkinsonism plus syndrome is a group of heterogeneous degenerative neurological disorders, which differ from the classical idiopathic Parkinson’s disease in certain associated clinical features, poor response to levodopa, distinctive pathological characteristics and poor prognosis

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20
Q

what is Multiple system atrophy

A

is a Parkinson plus degenerative disorder of the brainstem, basal ganglia, and central autonomic neurons.

Patients present with one or more of the following:

  • Akinesia/rigidity with little or no tremor.
  • One or more signs of autonomic failure: postural hypotension, bladder/bowel dysfunction, impotence, dry eyes and mouth, pupillary abnormalities, impaired sweating.
  • Bilateral pyramidal tract degeneration leading to pseudobulbar palsy and ‘upper motor neuron signs’ in the limbs.
  • Poor ocular convergence.
  • L-dopa is of little value.
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21
Q

when examining patient, explain his gait and features that come along with it?

A
  • Bradykinesia
  • Patient will be slow to initiate movement
  • May see a ‘festinating gait’
  • Hypertonia (rigidity)
  • Will take more steps to turn around
  • Reduced arm swing
  • Slightly ‘stooped’ (flexed) posture
22
Q

what posture will they present with?

A

•Slightly ‘stooped’ (flexed) posture

23
Q

term for Reduced facial expressions?

A

•Hypomimia

masked face (reduced facial expression)

24
Q

when examining tone, how can the situation be accentuated?

A

•by asking the patient to perform a distracting activity

e.g. counting backwards, moving arm up and down

25
What r the general side effects of parkison drugs?
N&V, confusion, sedation, hypotension, physociss, hallucinations, delusions, dyskineaseia
26
Which drug is ineffective in those whose parkinsons disease has progressed and lost all their dopaminergic cells in the SN? Why?
Levadopa, in order to work the dopaminergic cells in the SN have to take up the levadopa in order to comvert it to dopamine
27
What do u give with levadopa? Why
Peripheral dopa decarboxylase inhbitor 1. to get more levadopa into the CNS rather than the peripheries and skin. 2. to reduce dose required 3. reduce side effects
28
Which vitamen antagonizes levadopa? And breaks it down
VB6 pyridoxine
29
Which drug has more psyciatric Side effects?
Dopamine receptor agonists bromocryptine, rotiginr, cabergoline
30
Parkinsoniam is a side effects of whatcdrugs?
Sodium valproate Antipsycotics
31
Which drugs r less likely to produce dyskineasea? Why?
Dopamine receptor agonists they have a DIRECT EFFECT
32
Which class may have neuroprotective actions?
Dop, recep, agomists
33
How do u reverse the on and off symotoms of parkinson s drugs? And motor symtoms that come in and off
APOMORPHINE SC
34
What is used in those who have a very BAD TREMOR.
Anticholinergics
35
Non motor manifestations of parkinsons
Mood changes- anxiety depression pain-on affected side cognitive changes-dementia urinary symptoms- frequency sleep disorder-REM SLEEP behaviour sweating excessive drooling
36
Prognosis in PD, 15 yr follow up early parkinsons does NOT SHOW......
FALLS!
37
Differentials!
Exclude other causes of parkinsonsim
38
Their must be \_\_\_\_\_% loss of neurons in parkisons to present with motor symptoms
50
39
Why can anticholinergics durgs be used to treat parkinsons?
40
How is dopamine made and broken down?
41
What should u warn ur patient when taking levadopa? What should they mot take it with?
A high protein meal u wont absorb much of it, lana it competes with amino acids for absorption
42
Long term side effects oflevadopa
Involutary movements motor complicaitons on and off wearing off! Dyskinesia dystonia freezing
43
which antiemetic should u not give with parkinsosn?
Antiemetic\>\> metaclopremide , bc it blocks dopamine give donperidome
44
What can be used as a patch ? how is it good?
Dopamine recepter agonist Rotigotine good for those who have dysphagia
45
What is imoulse contril disorder?
Also called dopamine dysregulation syndrome Always ask ppl about this when taking drug. u have the desire to increase the dose! - pathalogical gambling - hypersexualtily - compulsive shopping - desire to increase dose - punding
46
Which drug maku salfa u give it alone? what do u give it with then?
COMT inhbitior lana it has no benifit on its own, must be given with levadopa
47
What is used for those witha very bad tremor?
Anticholinergics dry mouth, dry eyes, urinary retention
48
What is deep brain stimulation targeting?
Subthalamic nuclei
49
What it co-carledopa?
Its a combination
50
What is Stalevo? Moa
Stalevo is an oral drug formulation developed by Novartis that contains a combination of **three** different drugs — carbidopa, levodopa and entacapone — to treat Parkinson’s disease Levodopa will converted into dopamine in the brain. When levodopa is administered orally, it is rapidly broken down by a biological process called decarboxylation that limits the amount reaching the brain. This is prevented by carbidopa, a dopa decarboxylase inhibitor Levodopa is also broken down by another process called methylation. This is prevented by entacapone, a selective inhibitor of the methylating enzyme called catechol-O-methyltransferase (COMT), which methylates and causes levodopa to break down. When entacapone is given in conjunction with levodopa and carbidopa, levels of levodopa in the blood are greater and more sustained than after the administration of levodopa and carbidopa alone.