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NEC 3 > PARKINSON'S DISEASE & MYASTHENIA GRAVIS > Flashcards

PARKINSON'S DISEASE & MYASTHENIA GRAVIS Flashcards

1
Q

What is parkinson’s disease?

A

A chronic, progressive neurodegenerative disorder

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2
Q

Parkinson’s disease are characterized by:

A

-bradykinesia
-rigidity
- tremor at rest
- gait changes

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3
Q

what is bradykinesia?

A

slowness in the initiation & execution of movement

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4
Q

what is rigidity?

A

increased muscle tone

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5
Q

Etiology of Parkinson’s disease

A

-idiopathic
- traumatic brain injury
- Exposure to manganese, pesticides, herbicides, and chemicals
-gene mutations

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6
Q

What is parkinsonism?

A

A syndrome made up of disorders that mimic parkinson’s disease

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7
Q

Parkinsonism symptoms occur at

A

Symptoms occur after exposure to chemicals and metals

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8
Q

Degeneration of nerve cells in the brain

A

Parkinson Disease

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9
Q

Drug-induced, head trauma, neurological disease

A

Parkinsonism

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10
Q

Progresses slowly

A

Parkinson disease

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11
Q

Progresses more rapidly

A

Parkinsonism

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12
Q

Lesion in the basal ganglia

A

Parkinson disease

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13
Q

Bradykinesia, stiffness and tremor

A

Parkinsonism

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14
Q

Ongoing loss of motor control and non-motor control symptoms

A

Parkinson Disease

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15
Q

Similar to PD; symptoms disappear after removing the cause

A

Parkinsonism

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16
Q

Continuation etiology of parkinson disease

A

-degeneration of the DA- producing (dopamine producing) neurons in the substantia nigra of the midbrain

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17
Q

What is DA producing neurons?

A

needed for normal function of the extrapyramidal motor system

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18
Q

What are the extrapyramidal motor system?

A

-posture
- support
- voluntary motion

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19
Q

What is lewy bodies?

A

-unusual clumps of protein inside neurons
-indicates abnormal brain function

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20
Q

What is the common manifestation of Parkinson disease?

A

-Tremor
-Rigidity
- Bradykinesia
- Postural instability

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21
Q

What is tremor?

A

-often the first sign
- worsened by increased concentration
- can involve the diaphragm, tongue, lips and jaw

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22
Q

What is pill rolling?

A

Hand tremor; rolling a pill or coin

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23
Q

What is rigidity?

A

-increased resistance to passive motion when the limbs are moved through their range of motion (ROM)
-muscles do not relax; muscles soreness, feeling tired and achy

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24
Q

Bradykinesia

A

-slow movement
- due to decreased impulses from the basal ganglia
- task become frustratingly slow
- Lack natural activities like blinking, swinging of arms while walking, and swallowing saliva

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25
Q

Characteristics Appearance of PD

A

-Blank facial expression
- Slow, monotonous, slurred speech
- Tremor
- Short, shuffling gait ( festination)
- Forward tilt to posture

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26
Q

What is posture instability?

A

-Being unable to stop themselves from going forward (propulsion) or backward (retropulsion)
-they are at risk for falls/injury

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27
Q

Complications of PD

A

-dysphagia
- malnutrition
- aspiration
- neuropsychiatric problems (depression, hallucinations)
- dementia

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28
Q

Diagnosis of PD

A

-Pull test
- DaT Scan (gold standard)

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29
Q

Examiner stands behind the patients and by pulling on their shoulder tries to make them fall backwards

A

Pull Test

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30
Q

What is pull test?

A

Examiner stands behind the patients and by pulling on their shoulder tries to make them fall backwards

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31
Q

A special CT scan; detects DA function in the brain and distinguish PD from similar diseases

A

Dat Scan

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32
Q

The purpose of the drug for PD

A

to correct the imbalance of neurotransmistters

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33
Q

Examples of antiparkinsonian drugs

A

-Levodopa with carbidopa (Sinemet)

34
Q

Purpose of antiparkinsonian drugs

A

-Enhance the release of supply of DA (dopaminergic)
- blocks the effects of the overactive cholinergic neurons in the striatum

35
Q

Excess amount of dopamine drugs which worsens condition

A

Paradoxical intoxication

36
Q

Primary treatment for symptomatic patients

A

Levodopa with carbidopa

37
Q

More ____ reaches brain

A

levodopa

38
Q

What is levodopa with carbidopa?

A

primary treatment for symptomatic patients

39
Q

What is levodopa?

A

Precursor of DA; converted go DA in the basal ganglia

40
Q

Precursor of DA; converted go DA in the basal ganglia

A

Levodopa

41
Q

What is carbidopa?

A

inhibits the enzyme dopa-decarboxylase ( breaks down levodopa)

42
Q

Example of anticholinergic drugs

A

Trihexyphenidyl & Benztropine (Cogentin)

43
Q

Trihexyphenidyl & Benztropine (Cogentin)

A

-decreases the activity of acetylcholine
-helps with tremors & rigidity

44
Q

Examples of monoamine oxidase type B (Mao-B inhibitors)

A

Rasagiline (Azilect)

45
Q

Rasagiline (Azilect)

A

-combined with carbidopa/levodopa
- Inhibits mao-b; increases DA levels
- Less effective in treating motor symptoms

46
Q

What is the surgical management of PD?

A

-Deep Brain Stimulation
- Ablation Surgery

47
Q

Deep brain stimulation

A

-PD for more than 5 years
-Involves placing an electrode and deliver a specific current to the targeted brain location
-Reduces the increased neuronal activity produced by DA depletion

48
Q

Involves placing an electrode and deliver a specific current to the targeted brain location

A

Deep Brain Stimulation

49
Q

Reduces the increased neuronal activity produced by DA depletion

A

Deep Brain Stimulation

50
Q

Ablation Surgery

A
  • Involves finding, targeting, and destroying an area of the brain affected by PD
  • Destroys tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms
51
Q

Involves finding, targeting, and destroying an area of the brain affected by PD

A

Ablation Surgery

52
Q

Destroys tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms

A

Ablation Surgery

53
Q

Nursing Management of PD

A

-Promotion of Exercise
- referral to physical therapy programs and speech therapists
- Promotion of safety
- Aspiration precaution
- Give diet that can be chewed easily (6 meals a day is less tiring than 3 big meals daily)
- Emotional support

54
Q

An autoimmune disease of the neuromuscular junction

A

Myasthenia Gravis

55
Q

Presence of fluctuating weakness of certain skeletal muscle groups

A

Myasthenia Gravis

56
Q

Weakness increases with muscle use

A

Myasthenia Gravis

57
Q

What is Myasthenia Gravis?

A
  • An autoimmune disease of the neuromuscular junction
  • Presence of fluctuating weakness of certain skeletal muscle groups

-Weakness increases with muscle use

58
Q

What is the etiology & pathophysiology of Myasthenia Gravis

A

-Autoimmune process
- Medications (can worsen MG)

59
Q

Autoimmune process

A

-Antibodies attack ACh receptors, resulting in a decreased number of ACh receptor (ACHR) sites at the neuromuscular junction.

-Prevents ACh molecules from attaching and stimulating muscle contraction

60
Q

Medication is one of the cause of myasthenia gravis, what medications that can worsen the MG?

A

-B-adrenergic blockers
- quinidine
- phenytoin (dilantin)
- Certain anesthetics
- aminoglycoside antibiotics

61
Q

What is myasthenic crisis?

A

an acute exacerbation of muscle weakness triggered by:

      -infection
      -surgery
      -emotional distress
     -pregnancy
      -corticosteroids
62
Q

Myasthenic crisis are triggered by:

A

-infection
- surgery
- emotional distress
- pregnancy
- corticosteroids

63
Q

Myasthenic crisis occurs at

A

Occurs in the first 2 years after diagnosis

64
Q

Complications of Myasthenia Gravis

A

Muscle weakness in areas that affect swallowing and breathing

    -aspiration
    - respiratory insufficiency
   - respiratory infection
65
Q

Clinical Manifestations of Myasthenic crisis

A

-Fluctuating weakness of skeletal muscle
- Strength restored after resting
- muscles are the strongest in the morning; become exhausted with continued activity

66
Q

Clinical Manifestations of Myasthenia Gravis

A

-Change in facial expression
- Chronic muscle fatigue
- Difficulty breathing
- Difficulty chewing or swallowing
- Drooping eyelids (Ptosis)

67
Q

Diagnostics of Myasthenia Gravis

A
  • Physical examination
  • AChr antibody test
  • Single-fiber electromyography (EMG)
  • Nerve stimulation testing
  • CT scan
68
Q

Drugs for Myasthenia Gravis

A

Anticholinesterase medications

69
Q

What is anticholinesterase medications?

A
  • enhances function of the neuromuscular junction
  • prolongs the action of ACH and facilitate transmission of impulses by inhibiting acetylcholinesterase
70
Q

Examples of Anticholinesterase Medications

A

-Pyridostigmine (Mestinon)

71
Q

Surgical Management of Myasthenia Gravis

A

Thymectomy

72
Q

For patients with thymoma

A

Thymectomy

73
Q

Removal of thymus gland

A

Thymectomy

74
Q

What enhances the thymus?

A

Thymus enhances the production of ACHR antibodies

75
Q

What is thymectomy?

A

-for patients with Thymoma
- Removal of thymus gland
- Thymus enhances the production of ACHR antibodies

76
Q

Other therapies of myasthenia gravis

A

Plasmapheresis

77
Q

Directly removes circulating ACHR antibodies in the blood

A

Plasmapheresis

78
Q

Initial choice in myasthenic crisis

A

Plasmapheresis

79
Q

decreases symptoms

A

Plasmapheresis

80
Q

What is plasmapheresis?

A

-directly removes circulating ACHR antibodies in the blood
-initial choice in myasthenic crisis
- decreases symptoms

NEC 3 (16 decks)

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