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PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Seven: Neurodegenerative DX- Myasthenia Gravis MG > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Seven: Neurodegenerative DX- Myasthenia Gravis MG Flashcards

Exam 4 (Final)

1
Q

Myasthenia Gravis MG:

What is the normal function of cholinesterase?

A

Normal function of cholinesterase is to break down ACh –> choline & acetic acid

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2
Q

Myasthenia Gravis MG: What is it?

A

MG is a rare chronic, progressive autoimmune disease

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3
Q

Myasthenia Gravis MG:
What occurs?

A

Antibodies destroy acetylcholine receptors (AChR) at post-synaptic membrane of neuromuscular junction

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4
Q

Myasthenia Gravis MG:
What occurs:
Antibodies destroy acetylcholine receptors (AChR) at post-synaptic membrane of neuromuscular junction

What does this lead to?

A

Breakdown in the normal communication between nerves and muscles.

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5
Q

Myasthenia Gravis MG:

What causes MG?

A

Cause: acquired immunological or genetic abnormality, thymic tumors or changes

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6
Q

Myasthenia Gravis MG:

What are typical complaints?

A

Typical complaints:

muscle weakness,

ocular motor disturbances,

ptosis (droopy eyelid),

or diplopia are the initial symptoms.

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7
Q

Myasthenia Gravis MG:

How is severity of weakness throughout the day?

A

Severity of weakness fluctuates during the day, usually being least severe in the morning and worse as the day progresses, especially after prolonged use of affected muscles

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8
Q

Myasthenia Gravis MG:

What does weakness involve?

A

Weakness can involve oropharyngeal and limb muscles.

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9
Q

Myasthenia Gravis MG:

What is treatment for? Is there a cure?

A

There is no cure for MG, but treatment can help relieve signs and symptoms

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10
Q

Prevalence and Exacerbating Factors of Myasthenia Gravis:

How common is it? Who is it in more?

A

Rare

More common in women

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11
Q

Prevalence and Exacerbating Factors of Myasthenia Gravis:

Precipitating Factors for Exacerbations

A

Emotional stress

Pregnancy or menses

Trauma

Temperature extremes

Hypokalemia

Ingestion of drugs

Psychotropic drugs

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12
Q

Prevalence and Exacerbating Factors of Myasthenia Gravis:

Precipitating Factors for Exacerbations:

Ingestion of what drugs can aggravate MG?

A

Ingestion of drugs, including aminoglycoside, macrolide, tetracycline & fluoroquinolone antibiotics, β-adrenergic & Ca++ ch blockers, and phenytoin aggravate MG

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13
Q

Patho of MG:
What happens first?

A

Autoantibodies bind to the receptors at the NMJ, preventing acetylcholine from binding to them

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14
Q

Patho of MG:
What happens after Autoantibodies bind to the receptors at the NMJ, preventing acetylcholine from binding to them?

A

Eventually autoantibodies attack specific receptors found at the neuromuscular junction

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15
Q

Patho of MG:

Eventually autoantibodies attack specific receptors found at the neuromuscular junction

What does this cause?

A

Prevents muscle from responding to the nerve signal.

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16
Q

Patho of MG

In MG, - antibodies bind & attack the acetylcholine (nicotinicM) receptors at the neuromuscular junction.

What happens to the number of sites?

A

Decreased ACh receptor sites at the NMJ

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17
Q

Patho of MG

In MG, when there is a decreased number of acetylcholine receptor sites at the NMJ

What happens to the acetylcholine?

A

ACh can’t attach to receptors and induce muscle contraction

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18
Q

Patho of MG

When ACh can’t attach to receptors and induce muscle contraction –>? What happens?

A

skeletal muscle weakness, and fatigue of the affected muscles.

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19
Q

Patho of MG

When ACh can’t attach to receptors and induce muscle contraction –> skeletal muscle weakness, and fatigue of the affected muscles

What muscles are usually affected initially?

A

The facial and ocular muscles are usually affected initially, followed by the arm and trunk muscles.

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20
Q

Patho of MG:

What is acetylcholine responsible for normally?

A

Ach is responsible for movement.

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21
Q

Patho of MG:

Normally, how is normal voluntary movement possible?

A

ACh moves across the neuromuscular junction to the nicotinicM receptors & makes voluntary movement possible.

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22
Q

Patho cont’d:

90% of patients with generalized MG have what?

A

90% of patients with generalized MG have anti-acetylcholine receptor antibodies detectable in their blood.

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23
Q

Patho cont’d:

What other disorders are common in patients with MG? What does this suggest?

A

Disorders of the thymus such as hyperplasia and tumors are common in patients with MG, suggesting autoantibody production occurs in the thymus.

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24
Q

Clinical Presentation & DX of MG:

How do AchR receptor sites and autoantibody attacks occur?

A

AchR receptor sites and Ab attack varies

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25
Q

Clinical Presentation & DX of MG:

How is onset?

A

Insidious onset

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26
Q

Clinical Presentation & DX of MG:

What is first effected?

A

Face, throat & neck muscles 1st affected

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27
Q

Clinical Presentation & DX of MG:

Face, throat & neck muscles 1st affected

What are the effects?

A

Facial drooping

Throat muscles, esophagus: dysphagia

Vision issues:

Drooling, diff chewing & swallowing

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28
Q

Clinical Presentation & DX of MG:

Face, throat & neck muscles 1st affected

What are the visual issues effects?

A

diplopia, ptosis, blurred vision, difficulty moving eyes

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29
Q

Clinical Presentation & DX of MG:

What are other effects?

A

Muscle fatigue after exercise

Progressive weakness

Dyspnea, impaired ventilation (severe MG)

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30
Q

Clinical Presentation & DX of MG:

When may symptoms first appear?

A

Sx may 1st appear in pregnancy, PP, or with anesthesia

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31
Q

Clinical Presentation & DX of MG

Diagnostics

A

PE & neuro assessment

Serum antibody levels

Nerve conduction study

Electromyographic (EMG) studies

Thymus CT, MRI

Edrophonium

Autoimmune testing

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32
Q

Clinical Presentation & DX of MG

Diagnostics: What is included in autoimmune testing?

A

ESR
ACh receptor antibodies
Antinuclear antibody

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33
Q

Myasthenic Crisis: What is it?

A

Acute exacerbation

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34
Q

Myasthenic Crisis: What is it characterized by?

A

Characterized by an increase in weakness and fatigue, and respiratory impairment may develop requiring ventilator support to maintain oxygenation.

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35
Q

Myasthenic Crisis: How does it develop?

A

Develops as disease progresses

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36
Q

Myasthenic Crisis: What happens to muscles?

A

Muscles too weak to maintain ventilation

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37
Q

Myasthenic Crisis:

There is Muscles too weak to maintain ventilation

A

Paralysis –> death
Quadriparesis, quadriplegia –> resp arrest

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38
Q

Myasthenic Crisis:

Muscles too weak to maintain ventilation- why does this occur?

A

Caused by inadequate medication

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39
Q

Myasthenic Crisis

Exacerbating factors

A

Fatigue, illness, stress, pregnancy

Extreme heat, emotional distress, infections

EtOH consumption/med exposure/inadequate medication

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40
Q

Myasthenic Crisis

How is it treated?

A

TX with cholinesterase inhibitor

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41
Q

Myasthenic Crisis

TX with cholinesterase inhibitor includes what?

A

Neostigmine (Bloxiverz, Prostigmin),

Pyridostigmine (Mestinon)

42
Q

Management of MG:

Before patient takes PO meds, what must be assessed? How?

A

Assess swallow ability for PO

Sips of H2O

43
Q

Management of MG:

Medications

A

Cholinesterase inhibitors

Immunosuppressive drugs

44
Q

Management of MG:

Medications: Cholinesterase inhibitors

What do these drugs do?

A

↑ neuromuscular transmission & muscle strength

45
Q

Management of MG:

Medications: Immunosuppressive drugs

What is the drug? How is it used?

A

Azathioprine (off-label)

46
Q

Management of MG:

Medications: Immunosuppressive drugs

Azathioprine (off-label)- What does this drug do?

A

May improve muscle strength

Suppress production of abnormal antibodies

47
Q

Management of MG:

Non-drug measures include:

A

Thymectomy

Plasmapheresis

High doses of immunoglobulins

48
Q

Management of MG:

Non-drug measures include:

Plasmapheresis - what is this?

A

Plasmapheresis ~ removal of abnormal antibodies

49
Q

Management of MG

Self-care strategies

A

Proper nutrition

Adequate rest

Assistive devices

Coping strategies & support

50
Q

Cholinesterase Inhibitors: What do they prevent?

A

Prevent degradation of acetylcholine by acetylcholinesterase (AChE or cholinesterase)

51
Q

Cholinesterase Inhibitors:

Prevent degradation of acetylcholine by acetylcholinesterase (AChE or cholinesterase)

What does this lead to?

A

More ACh available; this can intensify transmission at virtually all Ach junctions

52
Q

Cholinesterase Inhibitors

Cause More ACh available; this can intensify transmission at virtually all Ach junctions

What is the result of this?

A

Result: more acetylcholine to activate receptors –> enhances cholinergic action

53
Q

Cholinesterase Inhibitors

Sufficient doses of Cholinesterase Inhibitors produce what?

A

Sufficient doses produce skeletal muscle stimulation

54
Q

Cholinesterase Inhibitors

What responses do these drugs cause?

A

Muscarinic responses:

Neuromuscular Effects:

CNS:

55
Q

Cholinesterase Inhibitors

Responses do these drugs cause:

Muscarinic responses:

A

bradycardia,

bronchial constriction,

urinary urgency,

increased glandular secretions,

increased GI tone & motility of smooth muscle,

miosis, & focusing lens for near visions

56
Q

Cholinesterase Inhibitors

Responses do these drugs cause:

Neuromuscular Effects:

A

increase force of contraction but toxic doses reduce force of contractions because excessive amt of Ach at NMJ keep motor-end plate in state of constant depolarization

57
Q

Cholinesterase Inhibitors

Responses do these drugs cause:

CNS: What do therapeutic effects produce? What do toxic levels cause?

A

CNS: therapeutic effects produce stimulation,

but toxic levels depress CNS if cross BBB

58
Q

Cholinesterase Inhibitors

What kind of inhibitors exist?

A

Reversible & irreversible inhibitors

59
Q

Cholinesterase Inhibitors

Reversible

A

Reversible (PO, IM, IV, Sq) – used for: MG, reversal of NM blocking agents in postops (pancuronium) & OD to reverse muscle relaxation & paralysis

60
Q

Cholinesterase Inhibitors

Reversible: What is it caused by?

A

by causing accumulation of Ach

61
Q

Cholinesterase Inhibitors

Irreversible

A

Irreversible (topical) – excessive muscarinic effects (cholinergic crisis)

62
Q

Cholinesterase Inhibitors

Irreversible: How safe is it? What is it used for?

A

Highly toxic, used as insecticides, WWII used as nerve agents, warfare, terrorism

Lipid soluble – poisons agricultural workers

63
Q

Cholinesterase Inhibitors

Irreversible:

What disease is it used for?

A

Used for glaucoma to stimulate muscarinic receptors on the ciliary and the sphincter muscle to contract to lower IOP

64
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

Mainstay of therapy

A

Neostigmine (bloxiverz, prostigmin) – PO, IM, IV, subQ

Pyridostigmine (mestinon) – PO

65
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What do these drugs prevent?

A

Prevents acetylcholine inactivation so these agents intensify the effects of Ach released from motor neurons

66
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What is the goal of treatment?

A

Goal: Muscle strength increases

Symptomatic relief

67
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

When is atropine given?

A

Atropine given if muscarinic responses excessive

68
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

How are initial doses?

A

Small initial doses

69
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What are symptoms of improvement?

A

Sx of improvement:

ease of swallowing, increased ability to raise eyelids

70
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What should patients be educated on?

A

Pt ed: monitor times of drug adm, when fatigue occurs, state of muscle strength before & after rx, sx of excessive muscarinic stimulation

71
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

When can patients modify their dose?

A

Pts can occasionally modify their dose (eg anticipation of exertion, supplemental doses 30-60 min before)

72
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What are symptoms of undermedicated?

A

Sx of undermed: ptosis, difficulty swallowing

73
Q

Cholinesterase Inhibitors used for Myasthenia Gravis

What are symptoms of overmedicated?

A

Sx of overmed:

excessive salivation & other muscarinic responses

74
Q

Cholinergic Crisis:

What occurs?

A

Adverse effects/acute toxicity

75
Q

Cholinergic Crisis:

Excessive muscarinic stimulation - What will accumulate?

A

SLUDGE & the Killer Bs

DUMBELS

Resp depression

76
Q

Cholinergic Crisis:

Excessive muscarinic stimulation - What will accumulate:

SLUDGE & the Killer Bs:

A

(Salivation, Lacrimation, Urination, Diaphoresis/Diarrhea, GI cramps, Emesis, Bradycardia, Bronchospasm)

77
Q

Cholinergic Crisis:

Excessive muscarinic stimulation - What will accumulate:

DUMBELS

A

DUMBELS (Diaphoresis/Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Salivation)

78
Q

Cholinergic Crisis:

Excessive muscarinic stimulation - What will accumulate:

A

Resp depression from combo of depolarizing neuromuscular blockade & CNS depression

79
Q

Cholinergic Crisis: What is treatment?

A

Treatment with antagonist [IV Atropine]

80
Q

Cholinergic Crisis:

What does treatment with antagonist [IV Atropine] do?

A

Alleviate muscarinic effects of cholinesterase inhibition

81
Q

Myasthenia Gravis (Cont.): What is treatment?

A

Treatment with cholinesterase inhibitors

82
Q

Myasthenia Gravis (Cont.):

What are beneficial effects of this particular treatment?

A

Increased muscle strength

83
Q

Myasthenia Gravis (Cont.):

Dosage adjustment?

A

Start small and adjust to patient response

84
Q

Myasthenia Gravis (Cont.):

Dosage adjustment: How is timing of medication?

A

Timing is individualized to pt & is required around the clock to maintain blood levels

85
Q

Myasthenia Gravis (Cont.):

Dosage adjustment: What should you teach patient?

A

Teach pt to modify dose depending on sx of over/under-medication

86
Q

Myasthenic crisis and Cholinergic crisis

Cholinergic crisis: What is it characterized by?

A

Characterized by extreme muscle weakness or frank paralysis and signs of excessive muscarinic stimulation

87
Q

Myasthenic crisis and Cholinergic crisis

Cholinergic crisis: What causes the extreme muscle weakness, paralysis and signs of excessive muscarinic stimulation?

A

Overstimulation at a neuromuscular junction, excess of acetylcholine (ACh), due to inactivity of acetylcholinesterase, which normally breaks down acetylcholine. The crisis is the result of patients with MG who take too much of their cholinesterase inhibitor

88
Q

Myasthenic crisis and Cholinergic crisis

Cholinergic crisis: What is involved in treatment?

A

Treatment with respiratory support and atropine

89
Q

Myasthenic crisis and Cholinergic crisis

Myasthenic crisis: What is it caused by?

A

Inadequate medication

90
Q

Myasthenic crisis and Cholinergic crisis

Myasthenic crisis: What is it characterized by?

A

Extreme muscle weakness

91
Q

Myasthenic crisis and Cholinergic crisis

Myasthenic crisis: What is it caused by?

A

Caused by insufficient ACh at the neuromuscular junction

92
Q

Myasthenic crisis and Cholinergic crisis

Myasthenic crisis: What happens if left untreated?

A

Left untreated, myasthenic crisis can result in death as a result of paralysis of the muscles of respiration

93
Q

Myasthenic crisis and Cholinergic crisis

Myasthenic crisis: What is used to relieve a crisis?

A

A cholinesterase inhibitor (such as neostigmine) is used to relieve the crisis

94
Q

Myasthenia Gravis (Cont.)

Distinguishing myasthenic crisis from cholinergic crisis

A

History of medication use, or signs of excessive muscarinic stimulation assist with differential diagnosis

Challenging dose of edrophonium (tensilon)

95
Q

Myasthenia Gravis (Cont.)
Distinguishing myasthenic crisis from cholinergic crisis

Challenging dose of edrophonium (tensilon): What is edrophonium?

A

Ultra-short acting cholinesterase inhibitor

96
Q

Myasthenia Gravis (Cont.)

If edrophonium-induced elevation of acetylcholine levels alleviates symptoms, then the crisis is ___.

A
97
Q

Myasthenia Gravis (Cont.)

If edrophonium-induced elevation of acetylcholine levels intensifies symptoms, the crisis is _____.

A
98
Q

Myasthenia vs Cholinergic Crisis

Myasthenic Crisis: Causes of it?

A

Exacerbation of myasthenia following precipitating factors or failure to take drug as prescribed or drug dose too low

99
Q

Myasthenia vs Cholinergic Crisis

Myasthenic Crisis: Differential diagnosis?

A

Improved strength after IV administration of anticholinesterase drugs

100
Q

Myasthenia vs Cholinergic Crisis

Cholinergic Crisis: What are causes?

A

Overdose of anticholinesterase drugs, resulting in increased ACh (acetylcholine) at the receptor sites,

101
Q

Myasthenia vs Cholinergic Crisis

Differential Diagnosis: What is differential diagnosis?

A

Weakness within 1 hr after ingestion of anticholinesterase drugs

Increased weakness of skeletal muscles manifesting as ptosis, dyspnea, effects on smooth muscle include pupillary miosis, salivation, diarrhea, nausea or vomiting, abdominal cramps, increased bronchial secretions, sweating, or lacrimation

PATHO/PHARM II (27 decks)

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