My Patients Flashcards

1
Q

Multiple Myeloma – which interleukin may be increased?

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Txs that treat Hyperkalemia by increasing its excretion from the body?

A
  • Kayexylate (exchanges Na for K in gut)
  • Diuretics (furosemide)
  • Dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Txs that treat Hyperkalemia by driving K+ into cells?

A
  • Insulin
  • Bicarbonate (use esp. if acidemic drives K into cells in exchange for H)
  • β-2 agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common primary malignancy of bone?

A

Multiple Myeloma

note: only “primary” – otherwise most common would be bone mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does Multiple Myeloma cause bone lesions?

A

Neoplastic cells activate RANK (osteoclast activating factor), activating osteoclasts which cause lytic “punched out” lesions that can be seen on X-ray, esp. in vertebrae & skull (inc’d risk of fracture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does “SPEP” stand for?

A

Serum Protein ElectroPhoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

“M spike” in Multiple Myeloma is seen via what procedure? What is the “M spike”?

A

SPEP will show M spike of monoclonal antibodies, which are usually IgG or IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is the M spike problematic in Multiple Myeloma patients?

A

B/c monoclonal antibodies lack genetic diversity, so you are left susceptible to many other infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common cause of death in Multiple Myeloma?

A

Infection

due to monoclonal antibodies lacking genetic diversity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is seen on RBC smear in Multiple Myeloma & why?

A
  • Rouleax Formation: RBCs pile up on each other like “poker chips” due to the fact that the increased serum protein decreases charge between RBCs
  • Also a marked increase in ESR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Likely urine findings in Multiple Myeloma?

A

Bence Jones proteins: free immunoglobulin light chains (either kappa or λ) that are often found in significant quantities in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Serum chemistry changes in Multiple Myeloma?

A
  • Hypercalcemia (2ary to bone destruction)
  • Alkaline phosphatase is NOT increased (in contrast to most cases of hypercalcemia)
  • Anemia (due to neoplastic encroachment on myeloid precursors)

& possibly:

  • Leukopenia
  • Thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dx?

B-cell neoplasm of lymphoid cells that produce a monoclonal IgM protein.

A

Waldenstrom Macroglobulinemia (similar to MM, but no bone lesions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What other organ system might likely be affected by Multiple Myeloma & how so?

A

Renal insufficiency w/ azotemia due to myeloma kidney (myeloma nephrosis).
The renal lesion is characterized by prominent tubular casts of Bence Jones protein, numerous multinucleate macrophage-derived giant cells, & metastatic calcification, & sometimes by interstitial infiltration of malignant plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is amyloid?

A
  • Abnormally folded protein w/ a β-pleated sheet configuration
  • deposits extracellularly, usually near BM
  • Amorphous, eosinophilic appearance in routine hematoxylin & eosin sections
  • Stained w/ Congo Red dye, demonstrating apple-green birefringence (other stains work too)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Primary Amyloidosis & what is it ass’d w/?

A
  • Amyloid fibrils derived from Ig light chains (AL protein)
  • deposits in mesodermal tissue such as heart, muscle, tongue, kidney, etc.
  • Most frequently ass’d w/ Plasma Cell Disorders, like Multiple Myeloma
17
Q

Chronic Kidney Disease - Electrolyte abnormalities?

A
  • Hyperkalemia w/ metabolic acidosis
  • Hypocalcemia (due to dec’d l-alpha-hydroxylation of vit D by proximal
    renal tubule cells and hyperphosphatemia)
  • Hyperphosphatemia
  • Acidosis
18
Q

Rhabdomyolysis triad?

A

Muscle pain (usually proximal), weakness, & dark urine

19
Q

Muscle damage generally tends to cause what types of electrolyte abnormalities?

A
  • Hyperkalemia & Hyperphosphatemia (K+ & PO4- released from damaged cells)
  • Hypocalcemia (Ca2+ deposits in damaged muscle & bone)
  • Hyperuricemia (from nucleic acids released from damaged cells)
  • Acidosis
20
Q

Organ injury complications seen in Rhabdomyolysis?

A

AKI