multiple myeloma with pathophysiology
DESCRIPTION
This is a presentation made for our HEMATOLOGY report on Advanced Medical Surgical Nursing 1 (Pathophysiology) at University of Santo Tomas - Graduate School, Manila, PhilippinesTRANSCRIPT
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Prepared by: Maribec V. Pagaduan
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A 69 year old male complained of pain in his lower back upon bending over in his garage.
He worked in a petroleum plant for 15 years.
He also complained of easy fatigability.
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A radiograph of the spine shows a compression fracture of the lumbar vertebrae at L2 – L3.
Further evaluation reveals normocytic anemia, hypercalcemia, and a high globulin fraction. Bone marrow biopsy was also done.
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Other name: Plasma cell myelomaSecond most common hematologic
malignancy.It affects osseous and non-osseous
tissues.
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The cause of myeloma is unknownHigh occurrence among the following:
- Those exposed to radiation warheads
- Myeloma has been seen more commonly than expected among farmers, wood workers, leather workers, and those exposed to petroleum products.
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Occurrence: 2-4/100,000Age: Increases with age
Median Age of Px: 65 y/oGender: More men than womenRace: More common in Blacks than in
Caucasians, Asians – low incidence.
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RED BONE
MARROW
Composition
1.The PARENCHYME2.The STROMA
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- Continuous replacement of old bone tissue by new bone tissue
2 types of cells1.Osteoblasts2.Osteoclasts
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Used to determine size and shape of RBCs, WBCs and platelet precursors and to examine various maturational abnormalities.
Gold standard for diagnosing MM
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L2-L3 Compression
Non destructive method of inspection
Each specimen under evaluation will have differences in density, thickness, shapes, sizes, or absorption characteristics
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Randomly distributed, rounded, punched out lytic lesions throughout the skull.
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Patient Normal
WBC 3.4 X 103/uL (3.3-11.0)
Neut 9 % (44-88)
Lymph 27% (12-43)
Mono 4% (2-11)
Eos 0% (0-5)
Baso 0% (0-2)
RBC 3.2 X 106/uL (3.9-5.0)
Reticulocytes 1.% (0.5-1.5)
Hgb 8.6 g/dL (11.6-15.6)
HCT 26.1 % (37.2-50.4)
MCV 81.5 fL (79-99.0)
MCH 26.8 pg (26.0-32.6)
MCHC 32.9 g/dL (31.0-36.0)
Plts 110 thousands/uL (130-400)
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Test Patient Normal
Glucose 90 mg/dL (65-110)
Creatinine 1.9 mg/dL (0.7-1.4)
BUN 29 mg/dL (7-24)
Uric Acid 9 mg/dL (3.0-8.5)
Cholesterol 199 mg/dL (150-240)
Calcium 12 mg/dL (8.5-10.5)
Protein 10.9 g/dL (6-8)
Albumin 3.7 g/dL (3.7-5.0)
LDH 270 U/L (100-225)
Alk. Phos. 210 U/L (30-120)
AST 50 U/L (0-55)
GGTP 35 U/L (0-50)
Bilirubin/Bil. Direct 0.7 mg/dL/(.11 mg/dL) (0.0-1.5)/(.02-18)
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Test
Patient Normal
pH 6 (5.0-7.5)
Protein 3+ (Neg)
Glucose Neg (Neg)
Ketone Neg (Neg)
Occult blood Neg (Neg)
Color Yellow (Yellow)
Clarity Clear (Clear)
Sp. Grav. 1.050 (1.010-1.055)
WBC 3/HPF (0-5)
RBC 1/HPF (0-2)
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A process of separating electrically
charged particles in solution by passing an electric current through the solution
Particularly used to determinewhether the humoral immunity function normally or not.
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Albumin 1 2
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MAJOR CRITERIAI.Plasmacytoma by biopsyII.>30% marrow plasmacytosisIII.Monoclonal gammopathy Serum: IgG > 3.5 g/dL, IgA >2 g/dL Urine: >1 g/d of Bence Jones Proteins
MINOR CRITERIAA.10-30% marrow plasmacytosisB.Monoclonal gammopathies with lower values than aboveC.Lytic bone lesionsD.Suppressed normal immunoglobulins
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Durie-Salmon Staging SystemStage Criteria Estimated Tumor
Burden, x 1012 cells/m2
I All of the following: 1. Hemoglobin >100 g/L (>10 g/dL)
2. Serum calcium <3 mmol/L (<12 mg/dL) 3. Normal bone x-ray or solitary lesion 4. Low M-component production a. IgG level <50 g/L (<5 g/dL) b. IgA level <30 g/L (<3 g/dL) c. Urine light chain <4 g/24 h
<0.6 (low)
II Fitting neither I nor III 0.6–1.20(intermediate)
III One or more of the following: 1. Hemoglobin <85 g/L (<8.5 g/dL)
2. Serum calcium >3 mmol/L (>12 mg/dL) 3. Advanced lytic bone lesions 4. High M-component production a. IgG level >70 g/L (>7 g/dL) b. IgA level >50 g/L (>5 g/dL) c. Urine light chains >12 g/24 h
>1.20 (high)
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Age: 69 y/o, Male, Hx of working in a petroleum plant
DNA is damaged during the development of stem cell into a B – cell
Development of malignant plasmablasts
Produce adhesive molecules and bind to Bone Marrow Stromal Cells
Malignant plasmablast grows into malignant plasma cells
Uncontrolled proliferation of malignant plasma cell clones
Formation of Plasmacytomas
Production of Paraproteins (M-protein)
Production of Bence Jones
Protein
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Formation of Plasmacytomas
Compression of surrounding bone
tissue, bone marrow and nerve
endings
PAIN
↓ Hematopoesis
Release of IL-6 and TNF
Recruitment and activation of osteoclasts
Osteoclasts attach to bone tissue
Protein digesting enzyme
Acids
Digestion of collagen and fibers
Dissolves bone minerals
PUNCHED-OUT OSTEOLYTIC LESIONS
Continuous bone destruction
PATHOLOGIC FRACTURE
Calcium is released and
enters the bloodstream
HYPERCALCEMIA
Destruction of Bone marrow
stem cells
↓osteoblasts
↓bone deposition
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↓Hematopoiesis
↓RBC
ANEMIA
↓Megakaryocytes
↓Platelets
↑Susceptibility to bleeding
↓WBC
↑ Susceptibility to infection
Easy fatigability
THROMBOCYTOPENIA
Leukopenia
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Age: 69 y/o, Male, Hx of working in a petroleum plant
DNA is damaged during the development of stem cell into a B – cell
Development of malignant plasmablasts
Produce adhesive molecules and bind to Bone Marrow Stromal Cells
Malignant plasmablast grows into malignant plasma cells
Uncontrolled proliferation of malignant plasma cell clones
Formation of Plasmacytomas
Production of Paraproteins (M-protein)
Production of Bence Jones
Protein
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Production of Paraproteins (M-protein)
↑ Serum Monoclonal Antibodies
Normal Plasma cell breakdown
↓ Normal Antibody production
HYPERVISCOSITY SYNDROME
Binds with other serum protein
Disrupted antibody mediated immunity
↑ Susceptibility to infection
↑ Susceptibility to bleeding
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Age: 69 y/o, Male, Hx of working in a petroleum plant
DNA is damaged during the development of stem cell into a B – cell
Development of malignant plasmablasts
Produce adhesive molecules and bind to Bone Marrow Stromal Cells
Malignant plasmablast grows into malignant plasma cells
Uncontrolled proliferation of malignant plasma cell clones
Formation of Plasmacytomas
Production of Paraproteins (M-protein)
Production of Bence Jones
Protein
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Production of Bence Jones Protein
Blockage of tiny kidney tubules
Excreted in urine
↓erythropoietin
PROTEINURIA
↓ elimination of nitrogenous
waste
UREMIA
ANEMIA
↓RBC Production
Glomeruli filters large amounts of
Bence-Jones Protein
Proteinaceous inclusion bodies
accumulates in the tubules
Cellular degeneration and impairment of kidney/tubular
function
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Chronic PainActivity intoleranceRisk for InfectionFear/Anxiety
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Trials of Arsenic Trioxide in Multiple MyelomaMohamad A. Hussein, MD
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Anatomy and Physiology by Tortora, 11th ed. Clinical Physiology by Moran Campbell Pathophysiology By Porth, 4th ed. Harrison’s Principles of Internal Medicine, 17th ed. Wintrobe’s Clinical Hematology, Blood and Bone Marrow Pathology by
Wickramasinghe and McCullough