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Health Studies > Parkinson's Disease Roop/Reza > Flashcards

Parkinson's Disease Roop/Reza Flashcards

1
Q

A 68 year old man presents to the doctor’s office complaining of trembling hands and difficulty walking. No significant health problems besides kidney stones 12 years ago. Vitals WNL. It is noted that the patient’s facial expressions are reduced. Upon examination of his walking, it is noted that he has difficulty taking the first step, but then walks smoothly with a shuffling gait. What is the diagnosis?

A

Parkinson’s Disease

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2
Q

The patient diagnosed with Parkinson’s disease was found to have resting tremor L hand that diminishes when performing a task. During passive movement of the left arm, muscles are rigid, resulting in a ‘cogwheel’ motion during stretching. What does cogwheeling mean/what is it?

A

-early sign of Parkinson’s disease
-muscular stiffness throughout the range of passive movement in both extension and flexion
-muscle feels stiff/rigid/inflexible
-jerking feeling in arm or leg when rotating affected limb/joint

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3
Q

What are some Parkinson’s disease symptoms?
Hint: there’s 10

A

-stooped posture
-back rigidity
-flexed elbows and wrists
-tremors in the legs
-shuffling, short stepped gait
-slightly flexed hip and knees
-hand tremor
-reduced arm swing
-forward tilt of trunk
-masked face

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4
Q

What are the four primary motor symptoms of Parkinson’s?

A

1) bradykinesia
2) rigor
3) postural instability
4) resting tremors

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5
Q

What is the (unified Parkinson’s disease rating scale) UPDRS?

A

Clinical rating system with a total UPDRS score that includes 31 items contributing to three subscales

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6
Q

What is the (Movement Disorder Society-Sponsored Revision of the Unified Parkinson’s Disease Rating Scale) MDS-UPDRS?

A

-a comprehensive 50 question assessment of both motor and non-motor symptoms associated with Parkinson’s
-features sections that require independent completion by people with Parkinson’s and sections to be completed by the clinician

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7
Q

What does the (Movement Disorder Society-Sponsored Revision of the Unified Parkinson’s Disease Rating Scale) MDS-UPDRS Parts I – IV refer to?

A

Part 1: non-motor experiences of daily living (THIS was a major update to the UPDRS)

Part 2: motor experiences of daily living

Part 3: motor examination

Part 4: motor complications

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8
Q

Which disorders are the leading cause of disability in the world?

A

neurological disorders

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9
Q

What is the fastest growing neurological disorder?

A

Parkinson’s disease

2015- approx. 7 mil cases worldwide

2040- estimated to be 13 mil cases worldwide

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10
Q

In 2040, it is projected that there will be about 13 million cases of parkinson’s disease worldwide. Why?

A

-better diagnoses, growing older population (aging), medications
-papers now talk about a genetic component
-environmental component: pesticide pollution

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11
Q

The basal ganglia is a _______ nuclei of the cerebral hemispheres

A

deep

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12
Q

What are the components of the basal nuclei?
hint: 6 things

A

1) Caudate
2) putamen
3) substantia nigra (pars compacta and pars reticularis)
4) red nucleus
5) globus pallidus
6) subthalamic nucleus

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13
Q

Which neurotransmitter is released from the neurons of the striatum that innervate the globus pallidus and the pars reticularis of the substantia nigra?

A

GABA (inhibitory neurotransmitter)

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14
Q

Damage to the striatum causes what?

A

Huntington’s disease

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15
Q

Which neurotransmitter is released from the neurons of the globus pallidus that project to the thalamus and subthalamic nuclei?

A

GABA (inhibitory neurotransmitter)

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16
Q

Damage to the globus pallidus causes what?

A

Progressive supranuclear palsy or Tourettes (more common)

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17
Q

Which neurotransmitter is released from the neurons of the subthalamic nucleus that project to the internal globus pallidus?

A

glutamate (excitatory neurotransmitter)

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18
Q

Damage to the subthalamic nuclei causes what?

A

hemiballismus

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19
Q

What is the commonality between damage to the striatum, globus pallidus, and subthalamic nuclei?

A

all 3 of them lead to uncontrolled movement

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20
Q

The major output of the substantia nigra is through dopaminergic neurons to the striatum. Damage to these neurons causes what?

A

Parkinson’s disease

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21
Q

Dopamine receptors are what type of receptors?

A

GPCRs

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22
Q

What is the role of dopamine?

A

to regulate movement

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23
Q

What are the 2 pathways that operate in the basal ganglia? What is the difference?

A

direct and indirect pathway

direct pathway boosts movement

indirect pathway inhibits movement

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24
Q

Parkinson’s disease is a defect in which pathway? What does this result in?

A

defect in direct pathway

result in increased signal from the indirect pathway

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25
Q

Does parkinson’s disease have a gradual onset?

A

yes

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26
Q

How does parkinson’s disease usually begin?

A

w/ mild tremor of the hands or feet while at rest

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27
Q

How does a resting tremor differ from an intentional tremor?

A

Resting tremor is a tremor at rest. Intention tremor is produced with purposeful movement toward a target, such as lifting a finger to touch the nose.

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28
Q

Intention tremors are characteristic of ________________ diseases.

A

cerebellar

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29
Q

T/F:

intention tremors can be benign

A

true!

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30
Q

What is often mistaken for Parkinson’s disease and sometimes misdiagnosed?

A

essential tremor (ET)

31
Q

Compre essential tremor symptoms to parkinson’s disease symptoms

A

essential tremor=
-tremors mostly seen during action
-family history reported in more than 50% of pts
-tremor usually affects both sides of the body initially (symmetrical)
-alcohol improves tremor

parkinson’s disease symptoms=
-tremors mostly seen at rest
-family hx not as prominent (less than 10%)
-tremor usually starts on one side of the body and progresses to the other side; usually remains symmetrical
-tremor is not impacted by the consumption of alcohol

32
Q

What happens as parkinson’s disease progresses?

A

-tremor becomes more pronounced
-bradykinesia
-postural instability

33
Q

What are the non-motor symptoms that develop in the advanced stages of Parkinson’s disease?

A

-Mild cognitive decline
-Vertigo
-GI issues → constipation
-Urinary issues
-Sweating

34
Q

What are the motor skill symptoms of parkinson’s disease?

A

-bradykinesia (mask-like face, decreased blinking, degrading fine motor skills)
-vocal symptoms
-rigidity and postural instability
-tremors
-walking or gait difficulties
-dystonia (repetitive muscle movements that makes body parts twist)

35
Q

What are the non-motor skill symptoms of parkinson’s disease?

A

-mental/behavioral issues
-loss of smell
-sweating and melanoma
-GI issues (urinary issues, weight loss, sexual concerns)
-pain
-depression, anxiety, fatigue, sleep problems, and cognitive ability, and personality changes

36
Q

Parkinson’s disease course has a prodromal phase. Prodromal symptoms may occur ________ years before motor symptoms

A

15-20

37
Q

What are some examples of prodromal symptoms for parkinson’s disease?

A

-RBD (REM sleep behavior disorder)
-EDS (excessive daytime sleepiness)
-hyposmia (reduced ability to smell and to detect odors)
-constipation
-hypotension
-urinary and erectile dysfunction
-anxiety and depression
-subtle motor impairment

38
Q

What are the clinical symptoms of parkinson’s disease?

A

-tremor
-bradykinesia (slowness of movement/speed)
-rigidity
-postural instability
-fluctuations
-dyskinesias (involuntary, erratic, writhing movements of the face, arms, legs or trunk)
-PIGD (Postural instability and gait disorders)
-dysphagia (difficulty swallowing)
-fatigue
-apathy (lack of interest, enthusiasm, or concern)
-MCI (mild cognitive impairment)
-pain
-dysautonomia (disorder of autonomic nervous system (ANS) function)
-dementia
-psychosis (lose touch w/ reality)

39
Q

What is REM sleep behavior disorder (RBD)?

A

-loss of REM sleep
-Start to fling arms
-Laughing or talking in sleep

40
Q

What is EDS?

A

excessive daytime sleepiness

41
Q

What is hyposmia?

A

reduced ability to smell and to detect odors

42
Q

What is bradykinesia?

A

slowness of movement/speed

43
Q

What is dyskinesias?

A

involuntary, erratic, writhing movements of the face, arms, legs or trunk

44
Q

What is PIGD?

A

Postural instability and gait disorders

45
Q

What is MCI?

A

mild cognitive impairment

46
Q

What is dysautonomia?

A

-disorder of autonomic nervous system (ANS) function
-usually involves failure of the sympathetic and parasympathetic parts of the ANS

47
Q

Where does substantia nigra get its name?

A

Nigra = because of the “black” color

Melanin is causing the dark black color

48
Q

What is the pathology/pathophysiology of parkinson’s?

A

loss of neurons of substantia nigra

Damage to the neurons is associated with disruption of post-translational trafficking of proteins. The protein α-synuclein binds to ubiquitin which now cannot be transported for secretion.

-Endoplasmic Reticulum → releases calcium under stress
-Mitochondrial dysfunction
-ETC disrupted
-Accumulation of ROS! → progresses parkinson’s

Ubiquitin + α-synuclein accumulates within the cells as Lewy bodies.

49
Q

What does normal histology of substantia nigra look like?

A

pigmented neurons

50
Q

What does parkinson’s disease histology look like?

A

diminished numbers of pigmented neurons

51
Q

Are lewy bodies only seen in parkinson’s?

A

no, also seen in lewy body dementia

52
Q

What is the pathogenesis of parkinson’s disease?

A

Impaired protein clearance
■ UPS system (ubiquitin proteasome system) malfunction
■ Autophagy-lysosome system malfunction
○ Mitochondrial dysfunction
■ Complex 1 deficiency → increased cytochrome C → triggers apoptosis → causes neuronal cell death
○ A-synuclein misfolding and aggregation → forms Lewy Bodies
○ Neuroinflammation
■ Impaired cellular and humoral immunity → increased pro-inflammatory cytokines and microglia activation

Manganese dust → in pesticides
-Biggest pesticide that we’re trying to get rid of right now = roundup
>Linked to a lot of neurological diseases

53
Q

How does levodopa work?

A

Crosses BBB, then is metabolized to dopamine

54
Q

Why is L-dopa usually combined with carbidopa?

A

Maintains structure so dopamine can get to neuron before getting degraded

55
Q

Are other drugs besides L-dopa w/ carbidopa effective for parkinson’s disease?

A

no, there is currently no other drugs as effective

56
Q

What is deep brain stimulation?

A

-Implant electrodes
-Looks like pacemaker
-Brain is linked to electrodes to stimulate neurons

57
Q

What is focused ultrasound of the thalamus or subthalamic nuclei?

A

-Removes BBB so that the drugs can travel to the brain
-Seems to benefit motor symptoms

58
Q

Give examples of diseases caused by protein aggregation.

A

1) Alzheimer’s disease
2) ALS
3) Progressive supranuclear palsy
4) Parkinson’s disease
5) Lewy body dementia
6) Huntington’s

59
Q

What is the cause of sickle cell disease?

A

-HbS- gene expression
-Hbs → heme can be released → causes hydrogen peroxide (damages cell membrane)
-Can be detected with isoelectric focusing
-Treated with hydroxyurea that aids in the expression of HbF (pathway unknown)
-IF HbF can be expressed → can help pt (HYDROXYUREA CAN DO THIS)

60
Q

What is the cause of Alzheimer’s disease?

A

-A combination of age-related changes in the brain, along with genetic, environmental, and lifestyle factors
-Caused by the abnormal build-up of proteins in and around brain cells (amyloids)
-Aggregation of hydrophobic patches in the peptide
-Amyloid peptides are generated
>Hydrophobic → aggregates together
>Can affect cellular metabolism (enters through mitochondrial pores, inhibits pyruvate dehydrogenase complex, can also be deactivated by pyruvate DH kinase)
>Activates pyruvate dehydrogenase kinase
>Shortage of ACh
>Oxidative phosphorylation and tryptophan metabolism are disrupted
>Produces radicals → interacts with chlorine and tryptophan enzyme 5-HT which causes less release of acetylcholine and melatonin (also antioxidant so there is more ROS)
>Monoamine oxidases → responsible for decreasing hydroxy form of tryptophan (melatonin (antioxidant) not produced)

61
Q

What are the potential treatments for alzheimer’s disease?

A

-MOA-B (specifically cholinesterase)
-Making sure that peptides are not being produced (inhibit these proteins and immunize the individual)
-Scavengers (use it for imaging through a probe)

62
Q

How does protein aggregation affect the eye lens transparency?

A

-Protein aggregation can make the lens cloudy
-Glutathione is found at high concentrations in the lens and maintains protein thiols in the reduced state, which helps to maintain lens transparency by preventing the formation of high molecular weight crystallin aggregates
-Crystallin aggregation (denatures and makes lens cloudy)
-Photochemical damage occurs when light is absorbed by a photosensitizer that, upon photoexcitation, forms a transient excited triplet state that is long lived, allowing for interaction with other molecules producing free radicals or singlet oxygen. The continuous entry of optical radiation into the lens, in particular the absorption of shorter wavelengths (295–400 nm),
makes lens tissue particularly susceptible to photochemical reactions. The major ultraviolet (UV) absorbers in the lens are free or bound aromatic amino acids (tryptophan), numerous pigments (3-hydroxykynurenine), and fluorophores
-ROS have the capacity to damage the lens in many ways:
>Peroxidizing membrane lipids results in the formation of aldehydes, which in turn can form cross-links between membrane lipids and proteins.
>Introducing damage into the bases of the DNA (base modifications) and reducing DNA repair efficiency.
>Polymerizing and crosslinking proteins result in crystallin aggregation and inactivation of many essential enzymes, including those with an antioxidant role (catalase and glutathione reductase)
-The protein conc. within the lens is highest in the body
-As the lens ages, it changes from colorless or pale yellow to darker yellow in adulthood, and brown or black in old age
-The increased capacity of the lens to absorb visible light, in combination with the increased scattering properties of the lens (because of the aggregation of lens proteins and possibly the release of bound water), results in a decrease in transparency

63
Q

What is the cause of Parkinson’s disease?

A

-Caused by a loss of nerve cells in the part of the brain called the substantia nigra
-A combination of genetic and environmental factors
-Dopamine breaking down MAO (monoamine oxidase) and COMT (catechol-O-methyltransferase)
- MAO-B oxidizes glutathione (GSH) to glutathione disulfide (GSSG)→ generates excess H2O2 → suppression of PDHc and complex II (pyruvate and succinate) → quinones become oxidized → damage to mtDNA and mitochondrial swelling → oxidative stress-> Cytochrome C efflux from mitochondria-> intrinsic apoptosis occurs via stimulation of pro-apoptotic executioner proteins
>Chaperone mediated autophagy is disrupted
-The pathology of PD is characterized by specific death of dopaminergic neurons. Neural loss is most likely due to the induced damage of the Lewy bodies, which are formed from the insoluble nucleation of misfolded alpha-synuclein (a-syn) protein in addition to the mitochondrial alteration. The mitochondrial alteration is characterized by ATP depletion. This disrupts the storage of dopamine in vesicles, contributing to cytoplasmic formation of oxidized dopamine metabolites.
-In Parkinson disease, the major mitochondrial defect is associated with complex I (NADH dehydrogenase activity).

64
Q

What are the potential treatments for parkinson’s disease?

A

-The symptomatic treatment of Parkinson disease (PD) using pharmacotherapy can include L-Dopa, dopamine agonists, inhibitors of monoamine oxidase (MAO)-B and catechol-o-methyltransferase (COMT).
-Dopamine agonists- can bind to receptors and have the same outcomes
-Inhibitors of MAO-B and COMT (enzymes responsible for breaking down dopamine)
-Prevention of alpha-syn aggregation
-epinephrine

65
Q

List the disorders that have parkinson-like symptoms
Hint: there’s 8

A

*Progressive supranuclear palsy
*Multiple system atrophy
*Viral parkinsonism
*Drug and toxin-induced parkinsonism
*Post-traumatic parkinsonism
*Cortical basal ganglionic degeneration
*Lewy body disease
*Normal pressure hydrocephalus (NPH)

66
Q

What symptoms are similar to Parkinson’s disease as to progressive supranuclear palsy? Which symptoms are different?

A

Same=
-Sleep disturbances
-Bradykinesia
-Muscle rigidity
-Postural instability

Progressive supranuclear palsy only=
-Pseudobulbar palsy
-Photophobia, blurred vision
-You can treat this with L-dopa, but not as effective

67
Q

What symptoms are similar to Parkinson’s disease as to multiple system atrophy? Which symptoms are different?

A

Same=
-Muscle rigidity
-Unsteady gait
-Bradykinesia

MSA only=
-difficulty bending arms and legs
-slurred speech, slow or low volume
-visual disturbances

Multiple system atrophy responds to L-dopa better than Parkinson’s disease

68
Q

What symptoms are similar to Parkinson’s disease as to viral parkinsonism? Which symptoms are different?

A

Same=
-Bradykinesia
-Masked face

Viral parkinsonism only=
-Acute onset of fever
-Myalgia (muscle weakness)
-Respiratory symptoms
-Hypotonia (decreased muscle tone)
-Influenza type A–> responds more to L-dopa than the other drug-induced Parkinsonism

69
Q

What symptoms are similar to Parkinson’s disease as to drug and toxin-induced parkinsonism ? Which symptoms are different?

A

Same=
-Bradykinesia
-Gait disturbance
-Resting tremor
-Postural instability

Drug and toxin-induced parkinsonism only=
-Impaired speech
-SOB, cough, fever, nausea, vomiting, diarrhea, headache, metallic taste, salivation
-Decreased color vision

***Antipsychotics are the most likely to cause this

These medications block the dopamine receptors in nerve cells. The resulting reduction in dopamine levels causes parkinsonism. Typically, when someone stops taking these medications, the symptoms of parkinsonism decrease over time.

70
Q

How is post-traumatic parkinsonism different from parkinson’s disease?

A

It is hypothesized that a traumatic brain injury can damage neural tissue and induce the release of cellular breakdown products from damaged cells in the surrounding area. The cellular breakdown products can then act on neighboring healthy cells and promote intracellular alpha-synuclein aggregation.

Does post-traumatic parkinsonism respond better to L-dopa than parkinson’s disease? NO

TBI is similar to clinical PD
Spiders = astrocytes

know this diagram!!!

71
Q

How is cortical basal ganglionic degeneration different from parkinson’s disease?

A

-Cerebral cortex and basal ganglia waste away
-Rigidity and impaired balance usually begins on one side and spread to the other over time
-Responds to L-dopa? → no
-Any treatment? → no

72
Q

How is Lewy body disease similar/different to parkinson’s disease?

A

-dementia w/ lewy bodies (DLB) is generally diagnosed when at least 2 of the following features also occur with dementia:
1) Changes in attention and alertness. These changes may last for hours or days. Signs of these changes include staring into space, being lethargic or drowsy, and having speech problems.
2) Visual hallucinations. These hallucinations recur and are very detailed. They generally don’t bother the person having them.
3) Movement symptoms consistent with PD. These include slow movement, shuffling gait, rigidity, and falls. The person may also have tremors. But they are not as pronounced as in a person with PD with dementia.

-POST-mortem diagnosis
-Respond to L-dopa? Yes w/ small doses, cannot tolerate higher doses for unknown reason

73
Q

How is normal pressure hydrocephalus similar/different to parkinson’s disease?

A

-The cause of excess fluid in the ventricles of the brain may be due to injury, bleeding, infection, brain tumor, or surgery on the brain. However, the cause is often not known.
-NPH though rare, most often affects older adults, and its symptoms can be similar to those of Alzheimer and Parkinson diseases.
-Surgery → tube/shunt will get rid of fluid (excess in the brain)
-Doesn’t need L-dopa as treatment if surgery works
-Surgery should decrease pressure in the brain

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