Hey this is Dr K from imedicalschool and today we are going to talk about multiple myeloma.
Let's first start off by talking about the different forms of immunity.
Your body can fight off infections via two main types of immunity.
The types of immunity are cellular immunity and humoral immunity.
Cellular immunity, as it sounds, utilizes cells to fight off infections such as cytotoxic
or killer T cells.
The second form of immunity is humoral immunity.
Humoral immunity works through the utilization of antibodies.
Now cells are needed to produce the antibodies.
These cells that produce antibodies are called plasma cells.
Plasma cells are important in the pathophysiology of multiple myeloma.
Multiple myeloma is the expansion of a single clone or type of plasma cell.
Due to the proliferation of a single clone of plasma cells there is a sharp rise in the
production of a single type of antibody resulting in what is called a monoclonal gammopathy.
The rapid expansion of a clone of plasma cells and antibody production can lead to bone pain,
lytic lesions, anemia, hypercalcemia, and acute kidney injury.
Generally multiple myeloma is quite rare and only makes up about 1% of all cancers.
There has been a noted increased incidence of multiple myeloma among African Americans
while there is a decreased incidence of myeloma among Asians and Mexicans.
The median age of onset for multiple myeloma is 66 and the cases of familial inheritance
are extremely rare.
Now the symptoms and signs of myeloma are quite generalized and numerous.
Symptoms and signs include anemia, fatigue, weight loss, acute kidney injury, hypercalcemia,
and bone pain.
In terms of the anemia it is usually a normochromic normocytic anemia.
The anemia results due expansion of plasma cells in the bone marrow impairing RBC production,
as well as, progressive kidney injury leading to poor erythropoietin production.
Erythropoietin or EPO is a hormone made famous by Lance Armstrong and is a hormone that stimulates
the bone marrow to increase RBC production.
One of the hallmarks of multiple myeloma is extreme bone pain.
A common finding is a reduction height that results due to vertebral fractures.
Generally bone pain worsens with movement and tends to be seen in up to sixty percent
of multiple myeloma patients.
Proteinuria is another common finding in multiple myeloma . It is important to point out that
urinalyses only detect albumin in the urine.
In multiple myeloma patients are spilling immunoglobulins into the urine and thus their
urine dipsticks will show no protein though in reality they are spilling a significant
amount into their urine.
If sulfosalicyclic acid is added to the urine sample the immunoglobulins present can be
visualized.
In addition to using sulfosalicyclic acid you can obtain a 24 hour urine and send it
for protein electrophoresis and immunofixation to determine the amount and type of protein
present in the urine.
The electrophoresis should show a single large peak indicating one type of immuglobulin replicating
out of proportion to other immunoglobulins.
The significant proteinuria that develops in myeloma leads to acute kidney injury.
There are two types of acute kidney injury encountered in multiple myeloma.
Myeloma can cause light chain cast nephropathy, otherwise known as myeloma kidney, and light
chain amyloidosis.
In myeloma kidney the immunoglobulins result in large waxy casts in the urine with a negative
dipstick urine.
In light chain amyloidosis the immunoglobulins deposit into the kidney causing significant
glomerular damage and loss of albumin into the urine resulting in a positive dipstick.
In rare circumstances patient can develop cord compression.
Spinal cord compression is an oncological emergency.
In myeloma it can be due to an extramedullary plasmacytoma.
A plasmacytoma is a mass of proliferating plasma cells that can occur within or outside
the bone marrow.
If it occurs in the spine it can compress the spinal cord causing severe damage.
The first step is to obtain STAT imaging of the spinal cord to determine if compression
is present.
Patients with cord compression diagnosed clinically or via imaging should be started on dexamethasone.
Neurosurgery should be consulted for further evaluation and decompression.
Other features you may see in multiple myeloma include the rouleax formation.
In a peripheral blood smear you may see red blood cells stacked on top of one another
like a stack of coins.
This occurs due to the hyperviscocity linking of RBCs by immunoglobulins.
You can see the coin stacks that are created as pictured here.
In a bone marrow biopsy you will notice a large proliferation of plasma cells.
Finally patients will usually undergo a skeletal survey if they are diagnosed with myeloma.
These films may show osteolytic lesions of the skull and vertebra.
In addition they may show diffuse osteopenia and even vertebral fractures.
Now that we discussed signs and symptoms let's talk about the initial workup.
If you suspect someone has multiple myeloma it is important to order the proper initial
workup.
First start off with a CBC with a differential to identify if an anemia is present.
In addition look at a peripheral blood smear to identify if rouleax formations are present.
Next obtain an SPEP and UPEP to identify production of a monoclonal production of antibodies.
Other labs include LDH and CRP to identify inflammation and cell turnover.
In addition obtain a chemistry to identify any electrolyte abnormalities or kidney dysfunction.
Lastly obtain a beta 2 microglobulin as an elevation is this test is a poor prognostic
sign.
If the workup is consistent with myeloma obtain a bone marrow sample and a bone survey.
The diagnostic criteria for myeloma stress whether organ damage is taking place.
A patient needs three criteria met before diagnosing multiple myeloma.
These include M protein in serum and/or urine.
In addition the bone marrow must consist of at least 10% of plasma cells, and finally
there must be some evidence of organ impairment.
The organ damage that is described can be represented by the acronym CRAB and includes
calcium levels, renal insufficiency, anemia, and bone lytic lesions.
Differential diagnoses include MGUS or monoclonal gammopathy of undetermined significance and
smoldering multiple myeloma.
MGUS a serum monoclonal gammopathy but has plasma cells at less than 10 % of the bone
marrow with no end organ impairment as represent by CRAB or lytic lesions.
In smoldering multiple myeloma serum monoclonal gammopathy is elevated with > 10% of plasma
cells in the bone marrow but there is no organ impairment.
Treatment of multiple myeloma includes stem cell transplant and chemotherapy.
Chemotherapeutic agents include bortezomib and thalidomide.
Well that is a brief review of multiple myeloma.
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This is Dr K and I will see you next time.