parkisons Flashcards

1
Q

what are the classifications of PD

A

primary/idiopathic

secondary

heredogenerative

multiple-system degeneration or parkinsonism-plus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

give examples of primary/idiopathic PD

A

parkinson’s disease

juvenile parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

give examples of secondary PD

A

infections, drugs, toxins, vascular or trauma

toxoplasmosis
- from feces of cats c parasites; common in HIV pts that causes lesion on BG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

give examples of heredogenerative PD

A

huntington’s or wilson disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

give examples of multiple-system degeneration or parkinsonism-plus

A

progressive supranuclear palsy

corticobasal degeneration

lew body dementia

multisystem atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

discuss progressive supranuclear palsy

A

PSP
- rigidity
- diff c vertical gaze
- has ssx of PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

discuss lewy body dementia

A

LBD
- combi of parkinsons and dementia
- no cure; often presesnt c depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

discuss multisystem atrophy

A

striatonigral degeneration - affects striatum and SN

olivopontocerebellar atrophy - OCPA
- bradykinesia
- balance probs
- sporadic or sponty in occurence

shy drager syndrome
- ssx of PD but has autonomic probs; BP or cant sweat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

discuss prevalence of PD

A

20-30 per 100k and more common in males (3:2)

rising prevalence with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

discuss the pathogenesis of PD

A

neurodegenerative disease c depigmentation of the substantia nigra = loss of dopaminergic input in BG = extrapyramidal sx

from imbalance bet dopamine (inhib) and ACH (excitatory); normal ACH but onti dopamine kaya hyperkinetic - resting tremors

PD is both hypokinetic and hyperkinetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

discuss the etiology of PD

A

unknown tlaga but

influence of aging - since neurons also degenerate

environmental toxins - aluminum cans

genetics pero saks lng

oxidative stress - seen in DM AND HTN

X-LINKED DYSTONIA - PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

exp oxidative stress theory

A

alterations of SN in PD is suggestive of oxidative damage

  • inc iron, aluminum
  • lack of isoferritins
  • reduced glutathione
  • selective defect in complex 1 of mitochondrial respiratory chain
  • damage to lipids, DNA and proteins
  • DM and HTN that leads to dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

in essence what are the possible causes of PD

A

oxidative stress

mitochondrial dysfunction

abnormal protein clearance

excitotoxicity

protein handling dysfucntion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

age for young onset PD

A

onset < 40 yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

age for juvenile onset PD

A

onset < 20 yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is parkin mutation

A

major cause of young onset autosomal recessive PD and isolated juvenile PD

17
Q

this is usually seen in autosomal dominant PD

A

mutations in the 𝝰 synuclein and ubiquitin carboxyl hydrolase:

18
Q

most PD symptoms do not appear til striata DA levels decline by ______

A

at least 70-80%

19
Q

symptoms of PD

A

TRAP

  • tremors: resting
  • rigidity: cogwheel
  • akinesia or brady: rebound or slow initiation and execution
  • postural instab: imbalance, stoop posture; pwede din gait; shuffling gait c lack of heel strike; righting reflex
20
Q

further discuss resting tremors

A

4-6 Hz

will begin in the hand unilaterally and usually at early stage

disappears c voluntary movement but in advanced di na nawawala

disappears with sleep; more present in > 80 yo and if stressed

pill rolling - unconscious movement of index and thumb

basta dapat ma differentiate with essential (8 Hz) and physiological (12Hz) which are more of cerebellar problem

21
Q

further discuss limb rigidity

A

inc tone and resistance to movement of both UE and LE

should be cogwheel and differentiated from spastic

ratchet like resistance dapat not matigas then mag give in which is spastic

22
Q

further discuss akinesia or bradykinesia

A

dec speed & amplitude of complex voluntary movement

slowness in initiating and sustaining movement

how to elicit:
- micrographia: lumiliit sulat
- tapping fingers
- twiddling of hands
- pinching and circling
- tapping c heel

usually one side is slower in early stages; misdiagnosed as stroke

akinesia is for late stage

23
Q

further discuss postural instab

A

how to elicit
- ask pt to stand parang romberg tas usually wide based
- pt will fall is positive test
- off balanced when turning
- parkinsonian gait
- stoop posture

24
Q

discuss diagnosis for PD from ward and gibb

A

presence of at least 2/4 cardinal signs; but 2/3 lng at their time since wala pa postural instab

presence of 2 of the ff
- marked response to levodopa
- assym of signs; unilateral
- assymetry at onset

evidence of disease progression

absence of clinical features of alternative dx

absence of etiology known to cause similar features; secondary PD

25
Q

stage 0 PD

A

no clinical signs or evidence

26
Q

stage 1 PD

A

Unilateral involvement

major features of tremor, rigidity or bradykinesia

minimal functional impairment

27
Q

stage 2 PD

A

bilateral involvement but no postural abnormalities

28
Q

stage 3 PD

A

mild to mod bilateral disease; mild postural imbalance

but can still function indep

29
Q

stage 4 PD

A

bilateral involvement c postural instab and requires assistance

30
Q

stage 5 PD

A

severe; pt is restricted to bed or w/c unless aided

31
Q
A