Lymphomas Flashcards
Where do T cells mature?
thymus
What are the 3 types of lymphocytes and which are most prevalent?
- T-cell (80%)
- B-cell (15%)
3 NK cell (<5%)
Where do B cells mature??
Mature in bone marrow, then go into circulation
Primary lymph organs
Bone marrow and thymus
-Where B cells and T cells mature and differentiate
Secondary Lymph organs
Where mature antigen specific B and T cells interact with APC and each other
Ex. Spleen, Lymph nodes, tonsils, MALT
NK cells
- kill cancer cells
- Live 40-60 years
Non- Hodgkin’s Lymphoma: Staging
Stage I: lymph node
Stage II: lymph node in two places
Stage III: multiple lymph nodes and crosses the diaphragm
Stage IV: multiple lymph nodes, Invasion of major organs and bones
Non-Hodgkin’s Lymphoma: Labs
LDH - often elevated
Beta 2 microglobulin- often elevated
Uric Acid - elevated
Non-Hodgkin’s Lymphoma: Dx
CT scan - check nodes
PET scan - check for biological activity
Biopsy lymph nodes**
Cutaneous T-cell lymphoma
-scaly rash (looks like psoriasis), but doesn’t respond to steroids or vitamin D
Non-Hodgkin’s Lymphoma: Tx
Elderly patient:
- low grade: watchful waiting
- CVP (cyclophosphamide, vincristine, prednisone)
Younger patient/curative intent:
-CHOP +/-Rituxan
cyclophosphamide, doxyrubicin, oncovin, and prednisone
[CHOP is harsher and less well tolerated]
Very high risk:
Autologous stem cell transplant
Hodgkin’s Disease
- Reed-sternberg cells***
- Bimodal (20s-50s)
Labs: EBV titer since this can be cause
Hodgkin’s Staging: A versus B
A - no constitutional symptoms
B - constitutional symptoms (fever, night sweats, weight loss)
Hodgkin’s: Treatment
Early or in bulky disease: Radiation
Standard Chemo:
AVBD (Adriamycin, bleomycin, vinblastine, and dacarbaine)
Prognosis: generally good! :)
Hodgkin’s Disease: increased risk for other malignancies
- leukemia
- gastric CA
- Lung CA
- breast CA
Multiple Myeloma: etiology
Plasma cell (B cells)
Multiple Myeloma: clinical manifestation
Anemia**** Bony pain (back pain)** Kidney disease (AKI)
- Fatigue
- Infections
- hyperviscous blood due to immunoglobulins (retinal vein engorgement)
What causes the kidney disease in multiple myeloma?
-hypercalcemia
or
-accumulation of gammaglobulins in tubules
What causes the cytopenias/anemia and bony pain?
osteoclast activating factors that eat bone marrow
Multiple Myeloma: Labs
CBC: anemia*
CMP: Total protein elevated, decreased albumin, Na+ (low)
Peripheral smear: Rouleaux formation**
SPEP: M-spike****
Immunofixation: monoclonal protein (IgG, IgA, or IgM)
24 hour urine (UPEP): Bence Jones proteins
Multiple myeloma staging depends on what two things?
- Beta 2 Micro
2. Albumin
Multiple Myeloma: indications to treat
CRAB I
Calcium (increasing) Renal insufficiency Anemia Bone-lytic lesions Infections
Multiple Myeloma: treatment
Ex.
Velcade + Decadron
Revlamid + Decadron
Thalidomide + Decadron
Younger patient:
consider autologous stem cell transplant
Monthly IV bisphosphonate - zoledronic acid
AKI in Multiple Myeloma
-Vigorous hydration
-Zoledronic Acid
+/- calcitonin
+/- loop diuretic
Hypercalemia
Stones, bones, groans, moans, and psychiatric overtones
groans = constipation
psychiatric overtones = confusion
Monoclonal gammopathy of undetermined significance (MGUS)
-elevated IgG, IgA, or IgM on SPEP
but, no other symptoms
Waldenstrom Macroglobinemia
- Diseased B cells that contain lymphocytic and plasma cell parts
- Proliferation of IgM macromolecule, very large and hyperviscosity
- No lytic lesions
Waldenstrom: Dx
SPEP: IgM spike**
Physical Exam: retinal vein engorgement (sausage link)
Waldenstrom: Tx
- emergent plasmapheresis
- chemotherapy
