2NEURO- Myasthenia Gravis

Question 1

What is destroyed in the neuromuscular junction in Myasthenia Gravis?

Answer 1

AUTOantibodies destroy AcH receptor is degraded w/in muscle

Question 2

What is function of NT ACH?

Answer 2

Motor nerve receptor on muscle. Motor pathway

Question 3

This theory involves rapid endocytosis L/2 turnover of receptors?

Answer 3

Cross linking Mech

Question 4

This theory involves blocking of Ach receptor via what protein?

Answer 4

Autoantibodies

Question 5

This theory involves damage of post-synaptic membrane?

Answer 5

Loss of folding d/2 complement mediate process

Question 6

What is relationship btwn MG and normal msk function?

Answer 6

MSK- needs more stimulate. MG- 1. reduced transmiter d/t down reg or damaged membrane. 2. =30% less stimulation to target. 3. Atrophy, dec endurance 4. progressively decreasing response to repeate nerve stim.

Question 7

Which tissue is affected in MG?

Answer 7

Skeletal msk. NO smooth, cardiac or sensory

Question 8

What msk is must concerning if affected in MG?

Answer 8

Diaphragm

Question 9

This structure is linked to play a role in MG?

Answer 9

Thymus retrosternal space. Adults should dissappear. Theory is thymus tissue migrate and destroy receptors. 75% have thymus or thymoma 10%

Question 10

MG pts with Weakness in eye, limp, gait, and ptosis, diplopia are worsen by?

Answer 10

Stress, infx, menses, surgery, exertion

Question 11

What is preserved on PE w/ MG?

Answer 11

DTRs. Proximal and Asymmetric limb weakness. Focus on

Question 12

When the muscles that control breathing weaken to the point that ventilation is inadequate, creating a medical emergency and requiring a respirator for assisted ventilation?

Answer 12

Myasthenia Crisis- infx MCC

Question 13

What is special to symptoms of MG?

Answer 13

1. Upper limb common 2. Asymmetric 3. disappear w/ rest 4. Cooling nerve improves conduction

Question 14

This lab test is will show +in 85% of the time?

Answer 14

Antibodies

Question 15

If antibodies is negative, this test acetylcholinesterase inhibition increases pool of
available ACh. Improvement of symptoms immediate .

Answer 15

Edorphonium

Question 16

What treatments are ideal for MG pts?

Answer 16

Neostigmine- ACHe inhibition allow ACh to accumulate. 2. PT very important 3. Steroids maybe . Thymectomy

Question 17

What is no evidence based that supplement may work?

Answer 17

Vit K to suppress IL-6 related to thymus

Question 18

Tx of MG can include cholinesterase inhibitors like neostigmine but these can be used for flare ups.

Answer 18

Steroid- help w/ suppression

Question 19

This end result is the cause of fatigue associated with MG.

Answer 19

Depletion of NT stores - from more NT release required to facilitate contraction.

Question 20

A female college student comes into your clinic complaining of weakness. She says when she goes to the gym her muscles fatigue really quickly like after a couple reps. She’s also wondering if she needs an eye exam because she starts to have trouble reading the words after ten minutes. The words become blurred. DeRosa suggested doing this task during your PE to help with you DD.

Answer 20

Pt hold sustained position. Ex. Hold gaze toward the celling.
If ptosis is a Sx an ice pack can be used to temporarily reverse the Sx

Question 21

A Pt presents to your ER gasping for air and looking cyanotic. Her boyfriend says that she’s had a bad cold all week and is always coughing. When asked about medications he pulls a bottle from her purse with neostigmine printed on it. This is the probable cause for her respiratory distress.

Answer 21

Myasthenia Crisis –

Tx: inhabation, plasmapherisis, and intravenous immune globulin (IVIG)

Question 22

In MG this mechanism, along with damage of post synaptic muscle membranes by antibodies and accelerated turnover of receptors by cross linking and endocytosis are the main cause of MG Sx.

Answer 22

Blockade of active sites on Ach receptor