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2) Patho 2 > 14) Degenerative Medicine > Flashcards

14) Degenerative Medicine Flashcards

1
Q

Parkinson’s Disease

A

Neuromuscular disorder where the substantia nigra loses its ability to produce dopamine, so it leads to a disinhibition of the cholinergic system which causes tremors & rigidity (too much cholinergic activity) or akinesia & bradykinesia (too little dopamine)

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2
Q

What causes PD?

A
  • Idiopathic
  • Genetics
  • Encephalitis
  • Toxic encephalopathy
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3
Q

What does TRAPPED stand for?

A
  • Tremors (Resting)
  • Rigidity
  • Akinesia/Bradykinesia
  • Postural Instability
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4
Q

What is the 1st early clinical sign of PD?

A

Loss of trunk rotation w/gait

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5
Q

Most is the most common sx of PD?

A

Tremor

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6
Q

When PD tremors start, are they seen unilaterally or bilaterally?

A

Unilaterally

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7
Q

When PD rigidity starts, is it seen unilaterally or bilaterally?

A

Unilaterally

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8
Q

What is akinesia associated w/?

A

Fixed postures

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9
Q

Bradykinesia

A

Paucity of movement characterized by an inability to perform purposeful movements

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10
Q

What types of movements does akinesa/bradykinesia usually effect?

A

Sequential/simultanous movements

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11
Q

What does the postural instability & gait impairments associated w/PD cause?

A

Incr fall risk

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12
Q

What kind of gait deviations do pt’s w/PD have?

A
  • Decr heel strike
  • Loss of heel-toe progression
  • Decr step length
  • Loss of trunk rotation
  • Retropulsion
  • Festinating gait
  • Shuffling gait
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13
Q

What are the gait deviations associated w/PD caused by?

A

Rigidity & Bradykinesia

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14
Q

What percent of PD pt’s have intellectual changes?

A

>50%

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15
Q

Why do PD pt’s get depression?

A

Loss of dopamine neurons & sensory deprivation

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16
Q

Sx’s of PD

A
  • Resting tremors
  • Rigidity
  • Akinesia/Bradykinesia
  • Postural instability
  • Micrographia
  • Whispering, montone voice
  • Masked face
  • Incr salvation & sebaceous secretions
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17
Q

What are the gold standard drugs to tx PD?

A

Dopaminergics

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18
Q

What are the side effects of dopaminergics?

A
  • Orthostatic hypotension
  • On/Off Times
  • Dyskinesia
  • Hallucinations
  • Decr drug effectiveness over time
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19
Q

What do dopamine agonists do?

A

Make the brain think there’s more dopamine, so it delays the need for dopaminergics, but incr need for YOPD

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20
Q

Side Effects of Dopamine Agonists

A
  • Drowsiness
  • Edema
  • Obsessive problems
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21
Q

What do anticholinergics do?

A

Restores the ACh/Dopamine balance to control early tremors

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22
Q

Side Effects of Anticholinergics

A
  • Dry mouth
  • Confusion
  • Urinary retention
  • Sedation
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23
Q

What do MAO-B inhibitors do?

A

Slows the breakdown of dopamine by decr free radical production

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24
Q

What are the side effects of MAO-B inhibitors?

A

Orthostatic hypotension & Insomnia

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25
Q
A
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26
Q

What do COMT inhibitors do?

A

Blocks the enzyme that deactivates dopamine

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27
Q

What do antivirals do for PD?

A

Helps w/rigidity & bradykinesia

  • Low doses smooth fluctuations
  • High doses suppress dyskinesia
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28
Q

Why is botox given to PD pt’s?

A

For hypertonia

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29
Q

What surgical procedure can be done to help alleviate the sx’s of PD & what is the problem w/it?

A

Deep Brain Stimulation–>Not always effective

  • Can only return pt to their best “on time”
30
Q

True or False: Deep brain stimulation can decr the amount of meds a PD pt needs to take by up to 30%.

A

True

31
Q

What is the On/Off Phenomenon & what causes it?

A

Short duration therapeutic response followed by rapid decr in that response–>Occurs bc PD meds are toxic to receptor sites

32
Q

Huntington’s Disease

A

Progressive autosomal dominant disorder characterized by movement abn’s (chorea), personality disturbances, & dementia bc of atrophy of the BG & striatum

33
Q

When do sx’s of HD usually start?

A

40’s or 50’s

34
Q

True or False: Anyone who inherits the HD gene will eventually have sx’s.

A

True

35
Q

Explain the pathophys of HD

A

Neurons that project from the striatum to the substantia nigra are depleted so there’s decr GABA, ACh, & metenkephalins, which causes incr potency of dopamine & NE, which goes on to cause imbalance of excitatory & inhibitory responses between the BG & thalamus

36
Q

What body parts does Huntington’s chorea effect more?

A

UE & face more than LE’s

37
Q

When does Huntington’s chorea incr/decr?

A
  • Incr during complex/stressful tasks
  • Disappears during sleep
38
Q

What other issues can arise w/HD?

A
  • Vision changes
  • Oromotor Impairments
  • Sleep disturbances
  • B&B dysfxn
  • Neuro & psych disorders
39
Q

For a pt w/HD, what will movement testing reveal?

A

Dysmetria & dysdiadochokinesia

40
Q

Clinical Manifestations of HD

A
  • Early chorea can look like restlessness or be integrated into normal movement strategies
  • MMT can be normal in the early stages, but may be difficult bc of motor disturbances
  • Hypotonia can be present initally, progressing to rigidity & bradykinesia
  • Choreiform gait
41
Q

Why are eye movement abn’s are common w/HD commo & why?

A
  • Disturbed saccades
  • Decr smooth pursuit

*Bc of disturbances w/ocular & extraocular muscles

42
Q

What oromotor impairments are commonly seen w/HD?

A
  • Dysarthria
  • Dysphagia
  • Cachexia
43
Q
A
44
Q

What is a common early sign of HD?

A

Neuro & psych disorders

45
Q

Is there a cure for HD?

A

No

46
Q

What meds are given for HD & why?

A

Anticonvulsants &/or antipsychotics–>Block dopamine transmission if chorea is interfering w/fxn

47
Q

What are the side effects of HD meds?

A
  • Acute dystonia
  • Psudo-parkinsonism
  • Akasthesia
  • Tardive dyskinesia
48
Q

Prognosis for HD

A
  • Earlier the onset, the more severe the disease
  • Death usually occurs 15-20yrs after onset
49
Q

ALS

A

Degenerative scarring/sclerosis in the lateral regions of the spinal cord, brainstem, & cortex causing UMN & LMN sx’s

50
Q

Who does ALS most commonly effect?

A

Males

51
Q

What is the mean age of onset for ALS?

A

57y/o

52
Q

What causes ALS?

A

Possibly genetics

53
Q

What can be used to r/o a dx of ALS?

A

Presence of:

  • Cognitive sx’s
  • Oculomotor sx’s
  • B&B sx’s
  • Sensory sx’s
54
Q

Explain the patho of ALS

A
  • Demyelination & glisosis of the corticospinal & corticobulbar tracts
  • Death of motor neurons in the brainstem & spinal cord cause denervation & subsequent atrophy
55
Q

True or False: Before HD sx’s start, 80% of motor neurons in the affected area may already be dead.

A

True

56
Q

What is the pattern of onset for ALS sx’s?

A

UE, LE, Bulbar

57
Q

What are the significant features of ALS?

A
  • Asymmetrical weakness w/muscle fiber sparing
  • CN3 & B&B sparing
58
Q

Outcomes of ALS

A
  • Paralysis of all spinal musculature
  • Paralysis of all muscles innervated by CN’s
  • Sensory issues
  • Pt’s w/bulbar onset tend to have a more rapid progression
  • Occasional improvement bc of collateral sprouting
  • Death occurs 4-5yrs after onset
59
Q

What does the medical management of ALS consist of?

A
  • Riluzole–>Glutamate anatagonist that slows excitotoxic cell death to extend life by 1-2yrs
  • Antioxidants–>Limits further injury to motor neurons & protects against cell death
  • Neurotrophic factors–>Aid in the recovery of injured but still viable motor neurons
  • PROM or antispasmodics–>Muscle spams
  • Adequate nutrition
  • Mechanical ventilation
  • End of life care
60
Q

Alzheimer’s Disease

A

Condition of progressive dementia characterized by slow decline in memory, language, visuospatial skills, & cognition

61
Q

In pt’s w/AD, what is the 1st structure to show pathological changes?

A

Cerebral cortex

62
Q

What is the most significant finding in pt’s w/AD?

A

Amyloid plaque & Neurofibrillary tangles

63
Q

What is the clinical presentation of AD?

A
  • Personality changes (Indifference, Impulsivity, & Irritability)
  • Loss of ability to do basic math
  • Eating, sleeping, & sexual behavior disorders
  • Bouts of inappropriate behavior
  • Lack of spontaneity
  • B&B dysfxn
  • Akinesia & dystonia
  • Rigidity
64
Q

What are the most common sx’s of of AD?

A

Loss of ability to learn new info & spatial disorientation

65
Q

True or False: In pt’s w/AD, there can by UMN signs, but the’yre typically related to another pathology.

A

True

66
Q

Medical management of AD

A
  • Anticholinesterase Therapy–>Blocks the enzyme that degrades ACh to help w/memory, language, thinking, & judgement
  • NMDA Receptor Agonists–>Improves memory, attention, reasoning, & language skills
  • Manipulation of the environment
67
Q

PT Management of AD

A
  • Use structured environment
  • Maximize repetition & use of fxnl movement patterns
  • Use procedural memory tasks
68
Q

Why do AD pt’s not have declarative memory?

A

Bc of hippocampal damage

69
Q

If a pt w/AD can’t follow directions, what should you do ID fxn limitations?

A

Rely on observational analysis

70
Q

Dx Criteria for AD

A
  • By exclusion
  • MMSE score
  • Presence of personality changes
  • Normal MRI

2) Patho 2 (20 decks)

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