Page 1 of 1: med: multiple myeloma

quincy · Credits: 3617 My Scrapbook

true about mm is :[ pgi q]
1.inc uric acid
2.inc urea
3.inc ca
inc ALP

drlouis · Credits: 5374 My Scrapbook

increase calcium and increased uric acid

alkaline phosphatase does not increase as the lesions are predominatly osteolytic and there is no osteoblastic activity

and we can expect a increase in sr creatinine rather than urea if myeloma kidney sets in

changu · Credits: 583 My Scrapbook

options 1,2&3 are true for multiple myeloma.serum alkaline phosphatase levels are normal because of absence of osteoblastic activity.

changu · Credits: 583 My Scrapbook

which 1 of the following is not associated with multiple myeloma?
1.punched out lesions in skull.
2.amyloid deposits in joints.
3.aseptic necrosis of femoral head.
4.metastatic calcification.

Akil · Credits: 28114 My Scrapbook

mdi · Credits: 250 My Scrapbook

1 2 3

mdi · Credits: 250 My Scrapbook

1 2 3

josephdhar · Credits: 1143 My Scrapbook

Patients with myeloma commonly develop hypercalcemia. The mechanisms include bony involvement and, possibly, humoral mechanisms. Treatment for myeloma-induced hypercalcemia is the same as that for other malignancy-associated hypercalcemia. uric acid, which is high if the patient has high cell turnover or is dehydrated
Beta-2 microglobulin
o Beta-2 microglobulin is a very strong predictor of outcome; some studies suggest it is more powerful than stage.
o Beta-2 microglobulin is a surrogate marker for the overall body tumor burden.
o The level of beta-2 microglobulin is increased in patients with renal insufficiency without myeloma, which is one reason that it is a useful prognosticator in myeloma. The prognosis of patients with myeloma and impaired renal function is reduced.
answer-
increase calcium and increased uric acid

ppraveen · Credits: 152 My Scrapbook

its inc in uric acid alk phosp n ca

paco · Credits: 545 My Scrapbook

[b] Hypercalcemia,
pathologic
fractures, cord
compression,
lytic bone
lesions,
osteoporosis,
bone pain Skeletal destruction Tumor expansion;
production of osteoclast
activating factors
(OAF) by tumor cells

Renal failure Light chain proteinuria,
hypercalcemia, urate
nephropathy, amyloid
glomerulopathy (rare)
Pyelonephritis
Toxic effects of tumor
products, light chains,
OAF, DNA breakdown
products
Hypogammaglobulinemia

Anemia Myelophthisis, decreased
production, increased
destruction
Tumor expansion;
production of inhibitory
factors and
autoantibodies by
tumor cells

Infection Hypogammaglobulinemia,
decreased neutrophil
migration
Decreased production
due to tumor-induced
suppression; increased
IgG catabolism

Neurologic
symptoms
Hyperviscosity,
cryoglobulins, amyloid
deposits
Hypercalcemia, cord
compression
Products of tumor;
properties of M
component; light chains
OAF

Bleeding Interference with clotting
factors, amyloid damage
of endothelium, platelet
dysfunction
Products of tumor;
antibodies to clotting
factors; light chains;
antibody coating of
platelets

Mass lesions Tumor expansion

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