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Drug Action III > Disorders Affecting Motor Function (Physiology) - Block 1 > Flashcards

Disorders Affecting Motor Function (Physiology) - Block 1 Flashcards

1
Q

What is Parkinsons?

A

Progressive degenerative CNS disorder and disorder of basal ganglia function

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2
Q

What is the mechanism of basal ganglia function disorder?

A

Progressive destruction of the nigrostriatal pathway leads to the reduction of strial dopamine concnetration

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3
Q

What is the clinical syndrome of parkinsonism?

A

Tremors, akinesia/bradykinesia, rigidity, postural instability

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4
Q

What is primary parkinsonism?

A
  1. Idiopathic
  2. Dopamine depletion -> degeneration of the dopamine nigrostriatal system
  3. Sx due to dx
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5
Q

What is secondary parkinsonism?

A

Sx occur due to cause other than dx:
1. Head trauma
2. Toxins
3. Metabolic disorders
4. Encephalopathy
5. Brain tumors’
6. Drugs

Some cases can be reversed

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6
Q

What are the RF of developing PD?

A
  1. Increased age
  2. Male
  3. Environmental exposure to toxins
  4. Family hx
  5. Genetics
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7
Q

What is the difference between autosomal recessive and dominant forms of PD?

A

Recessive: milder sx
* mutations is due to genetic code of protein, parkin (early onset of PD)

Dominant: rare and associated with increased a-synuclein and Lewy bodies

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8
Q

What is the function of parkin?

A

Acts as an enzyme in the Ub-conjugating system that targets defective and abnormally folded proteins for destruction.
* Loss of normal parkin cause abnormal proteins to aggregate -> neurodegenerative changes

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9
Q

The risk of PD is inversely related to?

A
  1. Cigarette smoking
  2. Caffeine
  3. High serum urate
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10
Q

How does PD cause brain abnormalities?

A
  1. Degeneration of nigrostrial dopamine neurons
  2. Loss of pigmented substantia nigra neurons (neuromelanin)
  3. Some residual nerve cells become atrophic and contain Lewy bodies
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11
Q

What is the most prominent sign of PD?

A

Progressive depletion of presynaptic dopamine in the basal ganglia, substantia nigra (SN), and pathwaysto the corpus striatum (caudate nucleus and putamen)

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12
Q

What is the consequence of progressive dopamine depletion?

A

Abnormal firing patterns that increase inhibition of the thalamus and reduce excitatory input to the motor cortex

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13
Q

What is proteolytic stress?

A

Unwanted proteins accumulate in cells interfering with UPS and inducing cytotoxitity

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14
Q

What are Lewy bodies?

A

Inclusions or abnormal protein filled neurons associated with proteolytic stress

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15
Q

What is in lewy bodies that misfold and aggregrate proteins?

A

alpha (a)-synuclein

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16
Q

What is oxidative stress?

A

ROS accumulation in cells -> toxicity and cellular damage

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17
Q

What causes oxidative stress in PD?

A

ROS are generated by oxidation of dopamine within cells of the SN

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18
Q

Describe how a heathy body copes with oxidative stress?

A
  1. α-synuclein facilitates endocytosis of transferrin receptor and iron-bound holo-transferrin.
  2. A cytoplasmic labile iron pool is tightly maintained by ferritin to enable ferroprotein function, including dopamine production by tyrosine hydroxylase (TH).
  3. α-synuclein facilitates multiple steps in synaptic dopamine release and repackaging
19
Q

Describe how a PD body copes with oxidative stress?

A
  1. Oxidation and phosphorylation of α-synuclein impair transferrin receptor-mediated iron import
  2. Combined with an age-dependent diminution in the iron storage capacity of ferritin, this elevates the labile iron pool, which reacts with free dopamine to produce ROS.
  3. Free dopamine is also elevated due to impaired dopamine packaging
  4. Oxidation and phosphorylation of α-synuclein is associated with Lewy pathology deposition, exacerbating nigral oxidative stress.
20
Q

What is the mitochondrial dysfunction theory?

A

Decrease in mitochondrial complex activity contributes to the development of PD

21
Q

How does PD cause inflammation?

A

Overactivation of microglia:
* leads to excess production of neuortoxic facotors -> neurodegeneration
* This accumulation triggers the activation of glial cells and the freeing of proinflammatory cytokines

22
Q

What is the most visible sign of PD?

A

Tremor

23
Q

What are motor sx of PD?

A
  1. Tremors (pill-rolling)
  2. Rigidity: increased muscle stiffness and tone (cogwheel-type or ratchet-like movements)
  3. Bradykinesia
  4. Postural instability (feeling of imbalance, classic sx)
24
Q

What is cogwheeling?

A

Slight hesitations during movement that produce a stop-and-go effect

25
Q

What is bradykinesia?

A

Slowing of voluntary muscle activity
* Festination: Acceleration while walking in an effort to “catch up”; result of flexed posture and postural instability.
* Freezing of gait: sudden and transient inability to move

26
Q

What are physical sx of PD?

A
  1. Fatigue
  2. Sleep disturbances
  3. Olfactory dysfunction
  4. Pain
  5. Autonomic dysfunction
27
Q

What are potential neuropsychiatric sx of PD?

A
  1. Cognitive dysfunction
  2. Deficit in frontal labe executive function
  3. Dementia
  4. Deficit in visuospatial discrimination
  5. Deficit in memory retrieval
  6. Psychosis
  7. Mood disorder
  8. Depression/Axiety
  9. Hallucinations
28
Q

How do we stage sx of parkinsons?

A

Hoehn and Yahr Staging of Parkinson Disease scale

Unified Parkinson Disease Rating Scale

29
Q

What is MS?

A

A chronic, inflammatory, demyelinating (white matter), and axonal degenerative disorder of the CNS inflammatory autoimmune disease

30
Q

What are the risk factors of MS?

A
  1. 20-50 YO
  2. Women
  3. Caucasians of northern descent
  4. Live farther from the equator
  5. People with the human leukocyte antigen HLA-DR2 haplotype are particularly susceptible
31
Q

What are the triggers of MS?

A
  1. Viral infection
  2. Environmental factors
  3. Genetic predisposition
32
Q

Describe plaque formation of MS?

A
  1. A trigger sets off an inflammatory process, and the protective blood-brain barrier (BBB) is disrupted
  2. Inflammatory T cells, B cells, and macrophages enter the brain and attack myelin.
  3. Demylination of neurons cause conduction abnormalities
  4. Axonal degen and atrophy of both gray and white matter
33
Q

What is a myelin?

A

Protein substance that coats the axon of a neuron and increases conduction velocity; produced by oligodendrocytes in the CNS.

34
Q

What are some of the causes of MS?

A
  1. Lesions
  2. Plaques
35
Q

What are the stages of lesions?

A

First: involves the sequential development of small inflammatory lesions
Second: lesions extend and consolidate; demyelination and gliosis (scar formation) occur

36
Q

Describe the types of progression of MS?

A

Relapsing-remitting multiple sclerosis (RRMS): patient remains stable or near but then transitions to secondary progression MS
Secondary progressive multiple sclerosis (SPMS): Gradually worsening sx w/ or w/o occassional relapses, minor remissions, and plateaus
Primary progressive multiple sclerosis (PPMS): Progressive deficit from the time of onset with occassional plateaus, temporary improvements, or acute relapses
Progressive-relapsing multiple sclerosis (PRMS): Gradual neurologic deterioration from the onset of sx but with subsequent superimposed relapses

37
Q

Identify some of the areas MS affects?

A

Optic nerve: visual field.
Corticobulbar tracts: speech and swallowing.
Corticospinal tracts: muscle strength.
Cerebellar tracts: gait and coordination.
Spinocerebellar tracts: balance.
Medial longitudinal fasciculus: conjugate gaze function of the extraocular eye muscles.
Posterior cell columns of the spinal cord: position and vibratory sensation.

38
Q

What is restless legs syndrome?

A

Strange sensation in the legs and an accompanying need to move the legs when resting or lying still

39
Q

What are the RF of RSL?

A
  1. Diabetes
  2. Pregnancy
  3. Uremia
  4. Iron def
  5. Anemia
  6. Obese
  7. Caffeine
  8. Smoking
  9. Sedetary
  10. Meds
40
Q

What is the difference between primary and secondary RLS?

A

Primary: hereditary component
Secondary: people with condditions that predispose them to iron-def anemia

41
Q

What are the causes of RLS?

A

Involves homeostatic mechanisms that regulate the influx and efflux of iron from cells of the CNS:
* Cerebrospinal fluid ferritin are lower with RLS
* Iron is involved in dopaminergic transmission in the CNS and cofactor of tyrosine hydroxylase (rate-limiting steps of dopamine synthesis)

42
Q

How does RLS cause both sleep and motor sx?

A

Low levels of iron in the brain:
1. Reduced tyrosine hydroxylase and dopamine production
2. decrease in the dopamine transporter (DAT).
3. number of transferrin receptors is decreased
4. Insufficient amount of iron regulatory protein 1 (IRP1), which represses degradation

43
Q

What are sx associated with RLS?

A
  1. Urge to move legs coupled with unpleasant sensations
  2. Rest provokes sx
  3. Getting active relieves sx
  4. Evening and night worsen sx

Drug Action III (23 decks)

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