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Flashcards in Neuromuscular Junction Disorders Deck (13)
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1

Epidemiology of Myasthenia Gravis

F > M
Females 20-30 yo
Males 50-60 yo

2

Etiology of Myasthenia Gravis

antibodies against ACh receptors on postsynaptic membrane of NMJ

3

Signs/Sx of Myasthenia Gravis

- weakness and fatiguability of skeletal muscles
- sxs worse as day goes on
- facial weakness, ptosis, double vision

4

Associated disorders of Myasthenia Gravis

thymoma, thymus hyperplasia, hyperthyroid, pernicious anemia

5

What imaging/dx testing must be done on all Myasthenia Gravis patients?

CT/MRI to eval thymus
Thyroid function tests
Rheumatic factor

6

Myasthenia Gravis treatment

Long acting anti-cholinesterase (pyridostigmine)
Immunosuppressants (steroids, cyclosporines, etc.)

Thymectomy if thymoma

7

How is LEMS different than Myasthenia Gravis?

- antibodies against Ca2+ channels (MG against ACh)
- depressed/absent DTRs (MG DTRs are preserved)

8

What organism causes botulism? What are its characteristics?

Clostridium botulinum; a G+ spore forming, produces potent toxins that block ACh release

9

Sub-classifications of botulism and how are we infected

- Food born: home canned meats & veggies
- Wound botulism: soil contaminated wounds or IV heroin users (rare)
- Intestinal botulism: ingest spore; infants < 12 months who eat honey

10

Signs of botulism

- descending paralysis; cranial nerves affected first
- N/V if food born
- Mentation and sensation NOT affected

11

Botulism treatment

Hospitalization
Cathartic/enemas to purge gut
Antitoxins from CDC (prevent progression, but don't reverse)
Inform public health agency

If infant, use botulism immune serum globin

12

How is wound botulism different than other types?

No GI symptoms
Longer incubation of 10 days (normally 18-36 hrs)

13

Describe life cycle of Clostridium botulinum

spore -> organisms -> toxin release