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CPS > Case #3 Wrap Up > Flashcards

Case #3 Wrap Up Flashcards

1
Q

In comparison to neck or lower back pain, what is thoracic back pain usually due to?

A

serious spinal pathology

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2
Q

What are red flag signs/symptoms for thoracic back pain?

A
  1. Recent violent trauma (MVA, fall)2. Minor trauma, or even just strenuous lifting, in people with osteoporosis3. Age at onset of new back pain of < 20 or > 50 years4. History of cancer, drug abuse, HIV, immunosuppression or prolonged use of corticosteroids5. Constitutional symptoms - e.g. fever, chills, unexplained weight loss6. Recent bacterial infection7. Pain that is:—Constant, severe and progressive—Non-mechanical without relief from bed rest or postural modification—Unchanged despite treatment for 2-4 weeks—Accompanied by severe morning stiffness (rheumatoid arthritis and ankylosing spondylitis)8. Structural deformity9. Severe or progressive neurological deficit in the lower extremities
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3
Q

What were the important differential diagnosis considered in our back pain case?

A
  1. Symptomatic herniated nucleus pulposus i.e. “slipped disk” - rarely thoracic though2. Muscle spasm or strain3. Traumatic fracture of vertebra4. Pathologic fracture of vertebra —metastatic cancer —multiple myeloma —osteomyelitis —osteoporosis5. Aortic dissection6. Pulmonary Embolism7. Pneumothorax8. Inferior wall MI9. GI sources
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4
Q

Multiple Myeloma-type of cancer-type of cell

A

B-cell malignancy characterized by neoplastic proliferation of a single clone of plasma cells producing a monoclonal immunoglobulin

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5
Q

Epidemiology of Multiple Myeloma

A

5 cases/100,000 population/yearthemostcommonmalignant tumor arising within the bone of adults > 40 yrs10% of all hematologic malignanciesMost common in -elderly-black-menA family history gives a 4 fold increased risk

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6
Q

Red flags for multiple myeloma

A
  1. age over 502. pain that is worse supine3. pain worse at night or that awakens patient 4. pain with band like distribution5. pain that is not relieved with conventional methods6. associated constitutional symptoms7. progressive neurologic deficit in lower extremities
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7
Q

With multiple myeloma, 34 % of patients are asymptomatic at presentation with incidental findings of…

A

—Increased Total Protein(TP > 8)—Renal Insufficiency (Cr > 2)—Hypercalcemia (Ca > 11) —Anemia (Hemoglobin < 10)More asymptomatic patients being identified with increase in “routine blood work.”

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8
Q

What are common initial presentation symptoms of multiple myeloma?

A
  1. anemia - 73%2. Unexplained backache or other bone pain - 58%3. Elevated BUN/creatinine4. pathologic fracture5. fatigue/generalized weakness6. hypercalcemia7. weight lossRARELY - cord compression secondary to plasmacytoma or fracture
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9
Q

What is the underlying cause and pathogenic mechanism behind finding … hypercalcemia, osteoporosis, pathologic fractures, lytic bone lesions, and bone pain w/ multiple myeloma?

A

Tumor expansion, production of osteoclast activating factor by tumor cells, osteoblast inhibitory factors

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10
Q

What is the underlying cause and pathogenic mechanism behind finding … renal failure?

A

hypercalcemia, light chain deposition, amyloidosis, irate nephrophaty, drug toxicity, contrast dye

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11
Q

What is the underlying cause and pathogenic mechanism behind finding … easy fatigue/anemia?

A

bone marrow infiltration, production of inhibitory factors, hemolysis, decreased red cell production, decreased erythropoietin levels

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12
Q

What is the underlying cause and pathogenic mechanism behind finding … recurrent infections?

A

hypogammaglobulinemia, low CD4 count, decreased neutrophil migration

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13
Q

What is the underlying cause and pathogenic mechanism behind finding … nausea and vomiting?

A

renal failure, hypercalcemia

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14
Q

What is the underlying cause and pathogenic mechanism behind finding … bleeding/clotting disorder?

A

interferences with clotting factors, antibody to clotting factors, amyloid damage of endothelium, platelet dysfunction, AB coating of platelets, therapy-related hyper coagulable defects

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15
Q

What does POEMS stand for?

A

polyneuropathyorganomegalyendocrinopathymultiple myelomaskin changes

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16
Q

Myeloma bone disease is due to …–what does this do?

A

overexpression of Receptor Activator for Nuclear Factor κ B Ligand (RANKL) by bone marrow stroma. —RANKL activatesosteoclasts, which resorb bone —The resultant bone lesions are lytic (cause breakdown) in nature and are best seen in plain radiographs, which may show “punched-out” resorptive lesions (including the “pepper pot” appearance of theskullon radiography) —The breakdown of bone also leads to release ofcalciuminto the blood, leading to hypercalcemiaand its associated symptoms

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17
Q

What kind of imaging work up is don’t to detect bone lesions in multiple myeloma?

A

Skeletal surveyMRI–more sensitive–generally reserved for suspected spinal lesions

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18
Q

How do bone lesions with multiple myeloma progress?

A

Lesions begin in medullary cavity,erode cancellous bone thendestroy the bony cortex.

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19
Q

Describe the radiographic grading of multiple myelomaHow does MM compare to met static bone cancer?

A

0 - normal1 - extensive osteoporosis or osteopenia2 - osteolysis3 - pathologic fractureIn contrast to metastatic bone cancer MM is osteoclastic activity. Alkaline Phosphatase and bone scans reflect osteoblastic activity and will likely be near normal. They may be abnormal in met. CA prior to cortical bone destruction is noted on plain radiographs.

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20
Q

What can occur after a fracture?

A

osteomyelitis

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21
Q

Total protein consists mainly of …

A

Albumin-chronic dehydration-high protein dietsGlobulin-neoplastic plasma cell or lymphocyte production of Ig-chronic inflammatory diseases producing autoantibodies-liver cirrhosis with decreased albumin production with compensatory increase in globulins

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22
Q

WRT multiple myeloma, cast nephropathy is seen from …

A

light chainsthis is also called myeloma kidney

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23
Q

How does hypercalcemia manifest?

A

confusionweaknessletharyconstipationpolyuria

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24
Q

What kind of anemia is seen with MM?This can be related to…

A

normocytic, normochronic anemia-bone marrow replacement-kidney damage-dilution in the case of large M-protein-B12 deficiency

25
Q

What do we see in a peripheral blood smear of MM?Why?Where else do we similar findings?

A

RouleauxDue to high M protein causing red cells to stick to one anotheralso found in -Wadenstrom-SLE-early HIV-thickly prepared blood slide

26
Q

What are three rarer presentations of MM?

A
  1. plasmacytosis - soft tissue or solitary bone mass2. hyperviscosity-indcued arterial infarctions or venous thrombosis3. concomitant amyloidosis with GI symptoms, peripheral neuropathy, or cardiomegaly—due to light chain deposit
27
Q

Plasma cells

A

White blood cells which produce large volumes of antibodiesTransported by the blood plasma and the lymphatic systemOriginate in the bone marrowLeave bone marrow as B cellsTerminal differentiation in lymph nodes/spleen into plasma cells

28
Q

What happens after a B cell leaves the bone marrow normally?What happens in MM?

A

B cell acts as an antigen presenting cell (APC) and internalizes offending antigens by receptor-mediated endocytosis.Pieces of the pathogen (antigenic peptides) are loaded onto MHC II molecules, and presented on its extracellular surface.CD4+ T cells (T helper cells) bind to the MHC II/antigen molecule and cause activation of the B cell in germinal centers of secondary lymphoid organs like the spleen and lymph nodes.The activated B cell begins to differentiate by affinity maturation into more specialized cells, memory B cells or plasma cells. Most of these B cells will become plasmablasts, and eventually plasma cells, and begin producing large volumes of antibodies.In multiple myeloma the control over this process is lost.

29
Q

Pathogenesis of MM is complex and poorly understood, however it has been proposed that …

A

the abnormal precursor B-cells originate in the lymph nodes and migrate to the bone marrow, which provides a microenvironment conducive to terminal plasma cell differentiation

30
Q

Normally, plasma cells produce Ig to …In MM and MGUS a single cloned plasma cell…

A

to fight infectionsingle cloned plasma cell proliferates and overproduces the same Ig, “M-protein”M-protein is usually IgG (>50%)

31
Q

What are the consequences of producing lots of monoclonal immunoglobulins?

A

HyperviscosityKidney damage (from light chains only)Bone pain, hypercalcemia and pathologic fractures from bone lesionsAnemia/Pancytopenia from bone marrow invasion

32
Q

Pathophys-80% of MM cases arise how?-the other 20%?-Risk factors

A

80% de novo20% from MGUSRisk factors for progression from MGUS to MM include:–an elevated M protein level–non-IgG MGUS–abnormal free light chain ration

33
Q

What diagnostic tests can be done for MM?

A

SPEP & UPEP w/immunofixation –80% patients w/ + SPEP–The remainder have + UPEP only–About 3%have “non secretory” MM ( Neg SPEP & UPEP)Urine dipstick tests–Classic Test for Bence Jones Proteins, but insensitiveBone marrow –Anyone with abnormal SPEP/UPEP–May required multiple aspirates for focal dyscrasiasCBC, peripheral smear, BUN/CR, Calcium, ESR

34
Q

What are the indications for Serum Protein Electrophoresis?

A

Suspected multiple myeloma, Waldenström’s macroglobulinemia, primary amyloidosis, or related disorderUnexplained peripheral neuropathy New-onset anemia associated with renal failure or insufficiency & bone painBack pain in which multiple myeloma is suspectedHypercalcemia attributed to possible malignancy —associated weight loss, fatigue, bone pain, abnormal bleedingRouleaux formations noted on peripheral blood smearRenal insufficiency with associated serum protein elevation

35
Q

What does uPEP provide?What is seen in monoclonal gammopathies?

A

Urine protein electrophoresis (UPEP) can provide quantification of M-proteinIn monoclonal gammopathies, a proteinuria pattern may show a discrete band produced by monoclonal free light chains, or Bence-jones proteinuria (BJP)`

36
Q

What are Bence Jones proteins?How are they detected?

A

Normally, there is no protein (complete M components) in the urine because the glomerular filter does not allow the filtration of large molecules, such as globulins.The light chains in immunoglobulins (called Bence Jones proteins) are much smaller, may therefore not be filtered and appear in the urine. They are difficult to detect in the blood, because they are rapidly cleared by the kidneys. Usual dipstick reagents detect albumin & often do not detect Bence Jones proteins. Sulfosalicylic acid can be used to precipitate proteins in the urine, which can then be semi-quantitated.

37
Q

What is the important mnemonic for MM?

A

MMm + CRABM proteinCalcium excessRenal failureAnemiaBone pain with lytic lesions

38
Q

MGUS

A

Monoclonal Gammopathy Undetermined SignificanceAsymptomatic pre-malignant stage of clonal plasma cell proliferationDiagnostic criteria–serum M < 3– < 10% clonal plasma cells–no end organ damage

39
Q

SMM - smoldering asymptomatic MM

A

risk of progression to MM is 10% each yearDiagnostic criteria–serum M > 3– > 10% clonal plasma cells on bone marrow–no end organ damage - CRAB negativeObservation w/ labs every 3-4 monthsEarly treatment may worsen prognosis by increasing risk of acute leukemia

40
Q

Waldenstrom Macroglobulinemia

A

IgM MMLymphoplasmacytic lymphoma–IgM–Bone marrow > 10% lymphoplasmacytic infiltration–anemia–weakness, fatigue, fever, etcHyperviscosity (see notes)DOES NOT LEAD TO BONE LESIONS OR HYPERCALCEMIA

41
Q

Solitary plasmcytoma

A

Diagnostic–low or no serum and urine M protein–bone marrow not consistent with MM-no CRAB other than single bone lesions due to clonal plasma cells2X more common in med~50% may progress to MM over 3-4 yrs

42
Q

MM indications for treatment

A

End Organ Damage–HyperCalcemia (serum calcium >11.5 mg/dL)–Renal insufficiency (serum creatinine>2 mg/dL)–Anemia (hemoglobin <10 g/dL or 2 g/dL below normal)–Lytic Bone lesions or severe osteopeniaNo End Organ Damage but–Bone marrow aspirate clonal plasma cells ≥60%Extramedullary plasmacytoma

43
Q

International staging system for MM - stage I

A

Stage I (28%) median survival 62 monthsβ₂ Microglobulin < 3.5 mg/L Serum albumin ≥ 3.5 g/dL

44
Q

International staging system for MM - stage II

A

Stage II (39%) median survival 44 monthsβ₂ M < 3.5 mg/LSerum albumin < 3.5 g/dL ORβ₂ M 3.5 to 5.5 mg/L

45
Q

International staging system for MM - stage III

A

Stage III (33%) median survival 29 monthsβ₂ M ≥5.5 mg/L

46
Q

At initial diagnosis all myeloma patients are stratified into either standard, intermediate or high risk based on the results of …

A

FISH(fluorescence in situ hybridization) for specific translocations and/or deletions, conventional cytogenetics, and the plasma cell labeling index.

47
Q

What are the adverse effects of thalidomide?

A

somnolenceDVTneuropathy

48
Q

What is the treatment of choice for symptomatic MM?

A

Autologous stem cell transplantation (ASCT)

49
Q

Some patients are not eligible for autologous HCT. Which ones?

A

Age > 77 yearsDirect bilirubin > 2.0 mg/dL (34.2 µmol/liter)Serum creatinine > 2.5 mg/dL (221 µmol/liter) unless on chronic stable dialysisEastern Cooperative Oncology Group (ECOG) performance status 3 or 4 unless due to bone painNew York Heart Association functional status Class III or IV

50
Q

Proposed mechanism of action for MM therapies / why are they so successful?

A

The importance of all these new agents and why they are so successful in treating myeloma is that in addition to targeting the myeloma cells, they also target the microenvironment in the bone marrow, making it less hospitable to myeloma cells. These novel agents have effects on both the tumor and the tumor microenvironment.

51
Q

10% of pts die within ____ of diagnosis–what is the leading cause of death?–second leading cause?

A

within 60 daysinfection is the leading causesecond leading cause is renal failure

52
Q

How do we manage hypercalcemia as a complication of MM?

A

Aggressive hydration, corticosteroids, Lasix®PRN Bisphosphonates – inhibits osteoclastic bone resorption

53
Q

How do we manage osteoporosis/bone pain/fractures as a complication of MM?

A

All patients should be on bisphosphonate–IVpamidronate 60 mg over 120 min infusion every 4 weeks dosing OR –IV zoledronic acid 4 mg over 15 minute infusion very 4 weeks dosing(dose adjustment required for renal failure) –Beware of side effects

54
Q

What is the role of bisphosphonates?

A

After the initiation of bone resorption, the osteoclasts take up the bisphosphonates within the cell. This uptake inhibits osteoclast activity and, as a result, leads to a decrease in the number of osteoclasts by inhibiting their recruitment and activating apoptosis. Bisphosphonates may also modulate some of the signaling from osteoblasts to osteoclasts

55
Q

How do we manage manage renal insufficiency as a complication of MM?

A

Identifying reversible causes. Dialysis PRN.Plasmaphereis for hyperviscosity induced thrombosis

56
Q

How do we manage anemia as a complication of MM?

A

erythropoetintransfusion

57
Q

How do we manage infection as a complication of MM?

A

Consider prophylactic antibiotics during chemotherapy inductionTreat aggressively with broad spectrum antibioticsVaccinations: Influenza, Pneumococcal, HIB

58
Q

Mnemonic for breaking bad news to people

A

A - advanced preparationB - build a therapeutic environment/relationshipC - communicate wellD - deal with patient and family reactionE - encourage and validate emotions

CPS (6 decks)

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