Oncology Flashcards

0
Q

History and PE of acute leukemias

A

Rapid onset w/ si/sx of anemia (pallor, fatigue), thrombocytopenia (petechiae, purpura, bleeding), and bone pain (medullary expansion and periosteal involvement)
Hsm and swollen/bleeding gums

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1
Q

Blasts

A

immature blood cells

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2
Q

BM findings in acute leukemia

A

BM with 20-30% blasts
AML = myeloblasts
ALL = lymphoblasts

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3
Q

AML vs ALL blasts appearance

A

AML: large, uniform myeloblasts with round or kidney-shaped nuclei and prominent nucleoli
ALL: large, uniform lymphoblasts- large cells w/ high N:C ratio

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4
Q

Leukostasis

A

Occurs when WBC is very high

Blasts occlude the microcirculation -> pulmonary edema, CNS symptoms, ischemic injury, and DIC

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5
Q

Leukemoid reaction vs. CML

A

Both have increased WBC count, but leukemoid reaction has increased LAP
Leukemoid reaction: leukocytosis 2/2 infection/sepsis

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6
Q

Auer rods

A

Rods present in APL

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7
Q

APL treatment

A

all-trans retinoic acid

-ATRA therapy

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8
Q

APL associations

A

Increased incidence of DIC

Chromosomal translocation: q15,17

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9
Q

Treatment of acute leukemia

A

Patients should be well hydrated prior to therapy
High WBC = start allopurinol to prevent TLS
Chemotherapeutic agents; antibiotics, transfusions, and colony-stimulating factors are also used
BM transplantation may be required for those who do not achieve remission

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10
Q

Treatment of leukostasis

A

Hydroxyurea +/- leukopharesis to rapidly decrease the WBC

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11
Q

Ages of leukemia

A

0-20: ALL
20-40: AML
40-60: CML
60-80: CLL

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12
Q

CLL

A

Clonal proliferation of functionally incompetent lymphocytes
-accumulates in BM, blood, LN, spleen, liver

Involves well-differentiated B cells

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13
Q

Diagnosis of CLL

-cell markers

A
Biopsy is rarely required for diagnosis
Clinical picture (fatigue, malaise, infection, LAD, splenomegaly)
Flow cytometry: CD5, CD20, CD2 positive together (normally CD5 is T cell specific while CD20 and CD2 are B cell specific)

Peripheral smear: abundance of small, normal appearing lymphocytes and ruptured smudge cells on smear
-smudge cells 2/2 cover slip crushing fragile leukemic cells

Labs: granulocytopenia, anemia, thrombocytopenia 2/2 marrow infiltration

Abnormal leukemic function = hypogammaglobulinemia

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14
Q

Tx of CLL

A

Palliative treatment, often withheld until pts are symptomatic
-ie recurrent infection, anemia, thrombocytopenia, splenomegaly, LAD

Tx: chemo
Not curable, but long dz-free intervals can be achieved

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15
Q

CML

A

Clonal proliferation of myeloid progenitor cells -> leukocytosis with excess granulocytes and basophils
-sometimes increased erythrocytes and platelets also

CML = BCR-ABL translocation must be present (Philadelphia chromosome of q(9,22)

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16
Q

Sx of CML

A

Anemia, splenomegaly (LUQ pain and early satiety), hepatomegaly, constitutional symptoms

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17
Q

Disease phases of CML

A

Chronic: without treatment, usually anemia, splenomegaly, constitutional symptoms

Accelerated: transition to blast crisis -> increased peripheral and BM blood counts
-suspected when diff shows abrupt increase in basophils and thrombocytopenia

Blast crisis: resembles acute leukemia

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18
Q

Blast crisis

A

Occurs in CML
Increased basophils and thrombocytopenia
Resembles acute leukemia

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19
Q

Granulocytes in all stages of maturation

A

CML

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20
Q

Lab values in CML

A

Low LAP

High LDH, uric acid, and B12levels

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21
Q

Diagnosis of different leukemias

A

Acute: Circulating blasts in the peripheral blood, leukocytosis
CLL: Flow cytometry, lymphocytosis, granulocytopenia, anemia, thrombocytopenia, smudge cells
CML: luekocytosis (very high), granulocytes in all stages of maturation

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22
Q

Treatment of CML

A

Chronic: Imatinib, a non-receptor tyrosine kinase inhibitor

Blast crisis: same as for acute leukemia; can also involve dasatinib + stem cell transplantation

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23
Q

Hairy Cell Leukemia

A

Malignancy of well-differentiates B lymphocytes, usually affects older males
Presents: pancytopenia, BM infiltration, splenomegaly
Hx: weakness, fatigue, bruising and petechiae, infection (esp w/ MAC), abdominal pain, early satiety, weight loss

24
Q

Dx of Hairy Cell Leukemia

A

Hairy cells in the blood, marrow, or spleen
TRAP staining: tartrate-resistant acid phosphatase staining of hairy cells, electron microscopy, and flow cytometry are helpful in distinguishing hairy cells
CBC: leukopenia

Peripheral smear: hairy cells OR monocytes with abundant pale cytoplasm and cytoplasmic projections

25
Q

Treatment of Hairy Cell Leukemia

A

10% don’t need therapy
Those who develop progressive pancytopenia and splenomegaly need therapy
-mainstay = nucleoside analogs ie cladribine
Can also use splenectomy and IFN-a

26
Q

Non-Hodgkins Lymphoma definition

A

Diverse group of diseases characterized by progressive clonal expansion of B cells, T cells, and/or NK cells
-2/2 chromosomal translocation especially t(14,18), the inactivations of tumor suppressor genes, or the introduction of exogenous genes by oncogenic viruses

27
Q

MALT gastric lymphoma

A

a/w H pylori infection

28
Q

Origin of most NHLs

A

B cell origin

29
Q

NHL disease staging

A

Ann Arbor classification

Based on number of nodes and whether the disease involves sites on both ides of the diaphragm

30
Q

Hodgkins Disease definition

A

Predominantly B cell malignancy with an unclear etiology
Types:
-nodular sclerosing: peak in the 3rd decade
-lymphocyte-depleting type: peak around age 60

31
Q

Pel-ebstein fevers

A

1-2 weeks of high fever alternating with 1-2 afebrile weeks

-rare sign specific for Hodgkin’s disease

32
Q

Alcohol induced pain

A

Rare sign specific for Hodgkin’s disease

33
Q

Anemia + bone pain + renal failure

A

Multiple myeloma

34
Q

Multiple myeloma: which cells

A

Clonal proliferation of malignant plasma cells, which then produce excessive Ig (IgA or IgG0 or Ig fragments

35
Q

Diagnosis of Multiple Myeloma

A

> 10% plasma cells in the bone marrow
lytic bone lesions
M protein

36
Q

M proteins

A

Present in MM, MGUS, CLL, lymphoma, Waldenstrom’s macroglobulinemia, and amyloidosis

37
Q

Diagnostic tests for multiple myeloma

A

Skeletal survey, bone marrow biopsy, UPEP, SPEP,CBC

38
Q

Treatment of Multiple Myeloma

A

Chemotherapy: melphalan + prednisone + other agents

Melphalan = oral alkylating agent

39
Q

Waldenstrom’s macroglobulinemia

A

Clonal B cell disorder -> malignant monoclonal gammopathy

Elevated IgM -> hyperviscosity syndrome, coagulation abnormalities, cryoglobulinemia, cold agglutinin disease (autoimmune hemolytic anemia), and amyloidosis

40
Q

Cryoglobulinemia

A

IgM disorder usually seen in HCV

Palpable purpura + proteinuria + hematuria + arthralgias + hsm + hypocomplementemia

41
Q

Cold agglutinins

A

IgM disorder which causes numbness upon cold exposure

-seen with EBV, mycoplasma infection, and Waldenstroms

42
Q

Waldenstrom’s symptoms

A

Lethargy, weight loss
Raynaud’s phenomenon
Neuro problems: AMS, sensorimotor peripheral neuropathy, blurry vision
Organ dysfxn affecting skin, GI, kidneys, lungs
MGUS is a precursor

43
Q

Waldenstrom’s diagnosis

A

Labs: elevated ESR, uric acid, LDH, and alk phos
BM biopsy: abnormal plasma cells with Dutcher bodies
-Dutcher bodies = PAS + IgM deposits around the nucleus
SPEP and UPEP and immunofixation are helpful

44
Q

Treatment of Waldenstrom’s

A

Plasmapharesis to remove excess IgG

Chemo to treat underlying pathology

45
Q

Amyloidosis

-definition and classification

A

Extracellular deposition of protein fibrils

Types:

  • AL: plasma cell dyscrasia. deposition of monoclonal light chains. a/w MM and Waldenstroms
  • AA: deposition of acute phase reactant serum amyloid A. a/w chronic inflammatory dz ie rheumatoid arthritis, infections, and neoplasms
  • Dialysis related: deposition of B2 microglobulin which accumulates in patients with long term dialysis requirements
  • Heritable: deposition of abnormal gene products ie transthyretin which is prealbumin; heterogenous group of disorders
  • Senile-systemic deposition of otherwise normal transthyretin
46
Q

Major sites of amyloid deposition

A

Kidneys, heart, liver

47
Q

Amyloidosis diagnosis

A

Tissue biopsy showing apple green birefringence on Congo red stain under polarized light

48
Q

Definition of neutropenia

A

ANC < 1500

49
Q

Acute neutropenia infections

A

S aureus, Pseudomonas, E. coli, Proteus, Klebsiella sepsis

50
Q

Chronic/autoimmune neutropenia infections

A

Recurrent sinusitis, stomatitis, gingivitis, perirectal infection

51
Q

Treatments for neutropenic fever

A

Broad spectrum antibiotics ie cefipime
Anti-fungals
G-CSF to shorten duration of neutropenia
IVIG and allogenic BM transplant can help

52
Q

Causes of secondary eosinophilia

A
NAACP
Neoplasm
Allergies
Asthma
Collagen vascular disease
Parasites
53
Q

CSF eosinophilia

A

Suggestive of drug reaction or infection with cocci or a helminth

54
Q

Hematuria + eosinophilia

A

Schistosomiasis

55
Q

Hyperacute transplant rejection

-timing, pathophys, tissue findings, prevention, tx

A
Timing: Within minutes
Pathophys: 2/2 preformed antibodies
Tissue findings: vascular thrombi; tissue ischemia
Prevention: check ABO before
Tx: cytotoxic agents
56
Q

Acute transplant rejection

-timing, pathophys, tissue findings, prevention, tx

A

Timing: 5 days - 3 months
Pathophys: T-cell mediated
Tissue findings: tissue destruction ie increased GGT, alk phos, LDH, BUN, or Cr
Prevention: n/a
Tx: confirm w/ sampling of tissue; tx with corticosteroids, antilymphocyte antibodies ie OKT3, tacrolimus, or MMF

57
Q

Chronic transplant rejection

-timing, pathophys, tissue findings, prevention, tx

A

Timing: months to years
Pathophys: Chronic immune reaction causing fibrosis
Tissue findings: gradual loss of organ function
Prevention: n/a
Treatment: No treatment

58
Q

Graft vs Host Disease

A

T cells from the donor organ starts to attach the person needing the transplant
-affected tissues include skin, liver, GI
Timing: acute = 100 days

Pathophys: 2/2 MHC incompatibilitiy

Sx: skin changes, cholestatic liver dysfunction, obstructive lung disease, GI problems

Tx: high-dose corticosteroids