MM / call Flashcards

1
Q

Cauda equina Sx

A
  • acute (<24h; rarely subacute or chronic)
  • LMN signs: weakness/paraparesis in multiple root distributions, reduced reflexes
  • urinary retention (or –> overflow incontinence), fecal incontinence (loss of anal sphincter tone)
  • sensory: low back pain radiating to legs, aggravated by Valsalva & sitting, relieved by lying down; bilat sensory loss or pain; saddle anesthesia; sexual dysfunction (late finding)
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2
Q

What is multiple myeloma?

A

cancer of plasma cells: produce monoclonal immunoglobulin, invade and destroy adjacent bone tissue

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3
Q

What are the most common presenting features of multiple myeloma?

A

bone pain and anaemia.

May also be IDed via Ix of fatigue, infections, hypercalcaemia, or renal impairment.

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4
Q

Clinical manifestations of multiple myeloma

A

CRAB:

  • Calcium (hypercalcemia)
  • Renal disease
  • Anemia
  • Bone pain
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5
Q

Why is calcium elevated in multiple myeloma?

A

Plasma cells secrete osteoclast activating factor, leading to increased resorption & hypercalcemia

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6
Q

Why does anemia occur in multiple myeloma?

A

Bone marrow is infiltrated by plasma cells, so it is less able to produce RBCs

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7
Q

Why does renal disease occur in multiple myeloma?

A
Light chains (of Ig) deposit in tubules (aka "light chain nephropathy" or "myeloma kidney"
(other kinds of kidney issues can happen: type 2 renal tubular acidosis, secondary amyloidosis, hypercalcemia)
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8
Q

Why does bone pain occur in multiple myeloma?

A
  • lytic bone lesions
  • spinal cord compression (if tumour infiltrates from vertebrae)
  • infections (plasma cells produce Ig that’s not useful for infections: impairs immunity)
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9
Q

What is the epidemiology of multiple myeloma?

A

average about 3 in 100 000. Increased frequency with age; median age of Dx is about 68.
M:F is 1.6:1
Black:white is 2:1
(BMJ: black men 2x white men, black women 3x white women)

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10
Q

What is lenalidomide?

A

Immunomodulator, used to treat multiple myeloma; inhibits hematopoetic cell proliferation. Also inhibits proinflammatory cytokines (altering immune response).

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11
Q

What are the diagnostic criteria for multiple myeloma?

A
  1. serum or urinary monoclonal protein
  2. presence of clonal plasma cells in bone marrow (>60% without “CRAB”) or a plasmacytoma
  3. presence of end-organ damage related to plasma cell dyscrasia, such as:
    ◆ increased serum Ca2+
    ◆ lytic bone lesions
    ◆ anemia
    ◆ renal failure
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12
Q

What bloodwork abnormalities are seen in multiple myeloma?

A

CBC: Normocytic normochromic anaemia
Lytes: elevated Ca2+
Creatinine, urea: elevated (renal)
Serum albumin

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13
Q

What is the prognosis of multiple myeloma?

A

Incurable; 3-7y. Newer therapies are improving prognosis but not by a whole lot.
ISS stage I: median 62mo
ISS stage II: median 44mo
ISS stage III: median 29mo
Staging is based on serum beta2-microglobulin and serum
albumin

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14
Q

What do people with MM die from?

A

Seems like (based on complication list in BMJ):

  • renal failure
  • infection
  • less commonly: cardiac failure (CHF or ischemic; amyloid deposits in heart)
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15
Q

What is a Bence-Jones protein?

A

only part of an immunoglobulin; in MM, sometimes only these parts are made instead of full Ig

Bence Jones proteinuria: “free monoclonal kappa (κ) or lambda (λ) light chains in the urine”

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16
Q

What makes multiple myeloma different from Waldenström macroglobulinemia?

A

Waldenström macroglobulinemia (IgM myeloma):

  • rare type of B cell lymphoma
  • often presents with hyperviscosity (IgM stick together –> ischemia)
  • can be asymptomatic; may alternately have fatigue, freq infections, pancytopenia–> easy bleeding, hepatosplenomegaly, lymphadenopathy
17
Q

What makes multiple myeloma different from MGUS?

A

Monoclonal Gammopathy of Undetermined Significance (MGUS):
- no end-organ damage
- less than 10% plasma cells on bone marrow biopsy
The risk of MGUS progressing to multiple myeloma is 1% a year. No treatment, but monitoring required (labs)