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Apex > Musculoskeletal Disease > Flashcards

Musculoskeletal Disease Flashcards

1
Q

What causes Myasthenia Gravis?

A

Autoimmune destruction of POST junctional nicotinic acetylcholine receptors

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2
Q

Key features of MG are:

A

Muscle fatigue that gets works as the day progresses

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3
Q

Removal of ______ can improve symptoms of myasthenia gravis

A

The thymus

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4
Q

What situations exacerbate MG?

A
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5
Q

What are the early symptoms of MG?

A
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6
Q

What is the first line treatment for MG?

A
  1. ORAL PYRIDOSTIGMINE
  2. Immunosuppression
  3. Thymectomy
  4. Plasmapheresis
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7
Q

What test is used to determine whether muscle weakness is caused by MG?

A
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8
Q

In terms of NM blockade, MG creates sensitivity to ________ and resistance to _______

A

sensitivity to non-depolarizers

resistance to depolarizers

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9
Q

In a patient with MG, what is an appropriate dose of Rocuronium?

A

You should reduce your dose by 1/2 to 2/3 and give repeat doses based on ToF

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10
Q

If you have to give a patient with MG succinylcholine, what dose is appropriate?

A

1.5 - 2 mg/kg

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11
Q

Will a patient with MG who receives succinylcholine have a decreased or increased duration of action?

A

Increased. Pyridostigmine is an acetylcholinesterase inhibitor, so break down of Succ will be delayed

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12
Q

All patients with MG are at risk for requiring postoperative ventilation, but this risk is especially high in which circumstances?

A
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13
Q

What causes Eaton-Lambert Syndrome?

A

IgG mediated destruction of PREsynaptic voltage-gated CALCIUM channels

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14
Q

What are alternative names of Eaton Lambert Syndrome?

A

Myasthenic Syndrome
LEMS

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15
Q

How does ELS impact acetylcholine receptors?

A

It doesn’t! It inhibits PRE synaptic calcium channels, which means Ach is never released into the NMJ

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16
Q

Which muscles are effected by ELS?

A

The proximal muscles first (opposite of MG)

Eventually the diaphragm and respiratory muscles

Worst in the morning and improves throughout the day (opposite of MG)

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17
Q

What is the treatment for ELS?

A

DAP, which increases Ach release by presynaptic neurons

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18
Q

Which cholinesterase inhibitor is recommended for ELS?

A

NONE! Cholinesterase inhibitors are not helpful, and a Tensilon test is not diagnostic

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19
Q

Which NMBA should be used in patients with ELS?

A

They have increased sensitivity to BOTH

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20
Q

Which comorbidity is present in 60% of ELS patients?

A

Small cell carcinoma.

If a patient is coming in for surgery to remove an SCC, you should be suspicious they may have presynaptic dysfunction and be judicious with NMBAs

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21
Q

What causes Guillain-Barre syndrome?

A

Autoimmune destruction of the myelin sheath in peripheral nerves

Action potentials can’t be conducted

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22
Q

When does GBS occur?

A

1-3 weeks after a flu-like illness

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23
Q

How long does GBS last?

A

2-4 weeks

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24
Q

What are the most common causes of GBS?

A

Campylobacter
Mono
CMV
Vaccines
Surgery
Lymph Disease

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25
Q

What are the s/s of GBS?

A
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26
Q

What is the treatment for GBS?

A

Plasmapheresis
IVIG
Steroids are NOT helpful

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27
Q

How do patients with GBS respond to ephedrine?

A

They have an exaggerated response, because sympathetic receptors upregulate in an attempt to improve conduction

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28
Q

What is another name for GBS?

A

Acute idiopathic polyneuritis

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29
Q

Which NMBAs should be used for patients with GBS?

A

Succ should be avoided because they have upregulated receptors

They will be MORE sensitive to non-depolarizers

30
Q

What is familial periodic paralysis?

A

The blanket disorder for HYPO-PP and HYPER-PP

31
Q

HypoPP is exacerbated by:

A

Glucose-insulin infusions that reduce serum potassium levels

32
Q

HyperPP is exacerbated by:

A

Potassium infusion

33
Q

Both types of familial periodic paralysis are treated with:

A

Acetazolamide
Strict avoidance of HYPOthermia

34
Q

Which NMBAs should be used in patients with FPP?

A

Never Succ

With HyperPP (because it increases K)

but also with HypoPP, because it’s often associated with MH

35
Q

Which medications should be avoided in the patient with HypoPP

A

All MH triggering agents

36
Q

There are three coexisting diseases that are DEFINITIVELY related to MH:

A

King-Denborough
Central Core Disease
Multiminicore Disease

37
Q

Which four states have the highest incidence of MH?

A

Wisconsin
Nebraska
West Virginia
Michigan

38
Q

How long after exposure can an MH crisis occur?

A

Up to 6 hours later!

39
Q

Which diseases should be considered in an MH differential?

A

Thyroid Storm
Pheochromocytoma
Serotonin Syndrome
Cocaine Intoxication

40
Q

What is trismus?

A

A tight jaw that can still be opened. It’s a common effect of Succ and is NOT the same as a masseter spasm

41
Q

What is masseter rigidity?

A

A tight jaw that CANNOT be opened

42
Q

Can masseter rigidity be resolved with Roc?

A

No. The problem is with the calcium outflow, downstream of anything the NMBA can effect

43
Q

Which drug class should absolutely never be used during an MH crisis?

A

Calcium Channel Blockers

Coadministration with dantrolene can cause life-threatening hyperkalemia

44
Q

What is the immediate treatment for MH?

A
45
Q

What is the MOA of dantrolene?

A
46
Q

When should you stop dantrolene?

A

When symptoms of hypermetabolism subside

47
Q

When a patient in MH crisis moves into the ICU, how should dantrolene be given?

A
48
Q

What dose of calcium and insulin should be given to control hyperkalemia during an MH crisis?

A
49
Q

If dysrhythmias occur during an MH crisis, which drugs can be used?

A

Procainamide or Lidocaine

NOTHING WITH CCB ACTION!

50
Q

How long should a patient be monitored in the ICU after an MH incident?

A

At least 48 hours. MH can reoccur up to 36 hours later

51
Q

What causes DMD?

A

An absence of dystrophin leaves the sarcolemma unmoored and subject to destruction during normal muscle contraction

52
Q

Why does DMD cause hyperkalemia with Succ?

A

Absence of dystrophin allows extrajunctional receptors to populate the sarcolemma

53
Q

What are the respiratory effects of DMD?

A

They develop kyphoscoliosis, leading to restrictive lung disease

AND have respiratory muscle weakness

54
Q

What are the cardiac effects of DMD?

A
55
Q

What EKG changes may be seen in patients with DMD?

A
56
Q

What are the GI effects of DMD?

A

They have delayed gastric emptying

57
Q

What is the Cobb Angle?

A

Measures severity of kyphoscoliosis

58
Q

What Cobb angle necessitates surgery?

A
59
Q

How does severe kyphoscoliosis impact cardiac function?

A

These patients have pHTN due to restrictive disease, so they have right sided heart failure

They very commonly also have mitral valve prolapse

60
Q

How does RA impact the airway?

A
61
Q

What is the most common airway complication with RA?

A

atlantoaxial subluxation

62
Q

What is rheumatoid arthritis?

A

An autoimmune disease that targets SYNOVIAL joints

63
Q

What are the most common SLE exacerbating triggers?

A
64
Q

Treatment of SLE includes:

A
65
Q

Are patients with SLE hyper or hypocoaguable?

A

They may have a prolonged aPTT, but they’re prone to hypercoagulability and thrombosis

66
Q

What are the most common complications from Ehlers Danlos?

A

AAA and bleeding into joints (because the vessels are damaged)

67
Q

Which disease can cause a blue sclera?

A

Osteogenesis imperfecta

68
Q

Myotonic dystrophy is characterized by:

A

a prolonged contracture after a voluntary contraction

69
Q

What three things should you avoid in the patient with myotonic dystrophy?

A

Succ
Ach reversal after NMB
Hypothermia

70
Q
A

Apex (46 decks)

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