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review / wrong answers > DIT review - Heme 4 > Flashcards

DIT review - Heme 4 Flashcards

1
Q

What is the most common type of NHL

A

Diffuse large B-cell

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2
Q

What is the translocation in follicular lymphoma

A
  • t(14;18) = heavy chain Ig (14) and BCL-2 (18)
    • Overexpression of BCL-2 = decreased apoptosis
      • Recall that BCL2 stabilizes mitochondrial membranes, preventing leakage of cytochrome C, and thus preventing apoptosis
      • Follicle is where B-cells are produced, so lack of apoptosis = malignant B-cell proliferation
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3
Q

What is the translocation in Burkitt lymphoma

A
  • t(8;14) = c-myc (8) and heavy chain Ig (14)
    • Overexpression of c-myc oncogene
    • THINK: “B” in Burkitt = 8 and “tt” = 14
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4
Q

Histology of Burkitt lymphoma

A
  • “Starry sky” appearance – sheet of lymphocytes with interspersed “tingible body” macrophages
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5
Q

Presentations of Burkitt lymphoma

A
  • Different forms:
    • Endemic/African form = jaw
    • Sporadic form = abdomen
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6
Q

Translocation in mantle cell lymphoma

A
  • t(11;14) = cyclin D1 (11) and heavy chain Ig (14)
    • Overexpression of cyclin D1 = G1 to S transition
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7
Q

What is small lymphocytic lymphoma

A
  • Lymphoma equivalent of CLL
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8
Q

Translocation in marginal zone lymphoma

A
  • t(11;18)
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9
Q

What is a MALToma

A
  • Marginal zone lymphoma within lymphoma a of mucosal tissue
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10
Q

What diseases are associated with marginal zone lymphoma

A
  • Associated with chronic inflammatory states:
    • Sjogren syndrome
    • Hashimoto thyroiditis
    • H. pylori
  • The marginal zone is only produced when the cells in germinal center are activated (i.e. inflammation), so it makes sense that this lymphoma occurs in chronic inflammatory states
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11
Q

What are the T-cell NHL’s

A

Adult T-cell lymphoma

Mycosis fungoides

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12
Q

What disease is associated with adult T-cell lymphoma

A

HTLV

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13
Q

What is Sezary syndrome

A

If malignant T-cells of Mycosis fungoides leave the skin lesions and get into the blood it is called Sezary Syndrome

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14
Q

What cancer is associated with t(8;14), and what is the effect of the translocation

A
  • Burkitt lymphoma
  • C-myc activation
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15
Q

What cancer is associated with t(9;22), and what is the effect of the translocation

A
  • CML, rarely ALL
  • BCR-ABL oncogene (constitutively active tyrosine kinase)
  • Responds to Imatinib (tyrosine kinase inhibitor)
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16
Q

What cancer is associated with t(11;14), and what is the effect of the translocation

A
  • Mantle cell lymphoma
  • Cyclin D1 activation
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17
Q

What cancer is associated with t(14;18), and what is the effect of the translocation

A
  • Follicular lymphoma
  • BCL-2 activation
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18
Q

What cancer is associated with t(15;17), and what is the effect of the translocation

A
  • APL (subtype of AML)
  • Responds to all-trans retinoic acid
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19
Q

What is the most common leukemia in childre

A

ALL

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20
Q

What serum markers indicated ALL

A
  • TdT (+) and PAS (+)
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21
Q

What disorder is associated with ALL

A

Down syndrome

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22
Q

Presentation of T-ALL

A
  • May present as mediastinal/thymic mass
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23
Q

Marker indicative of B-ALL

A

CD10+

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24
Q

Translocation associated with B-ALL

A
  • t(12;21) = better prognosis
  • t(9;22) = poor prognosis
25
Q

Markers and histology associated with AML

A
  • MPO (+) and PAS (+)
  • Auer rods
    • Crystal aggregates of MPO
    • Especially seen in Acute promyelocytic leukemia, AML
26
Q

Risk factors for AML

A

Chemotherapy, radiation, myelodysplastic syndrome, Down syndrome

27
Q

Common presentation of AML

A
  • DIC is a common presentation
    • Auer rods activate coagulation cascade
28
Q

Treatment of AML

A
  • Treatment:
    • Retinoic acid
  • Think:
    • Auer sounds like Fuer (Hitler) – Sound of music
    • I am 16 going on 17 (15;17)
    • Poke Hitler in the eye with a carrot – treat with retinoic acid
29
Q

Common cell markers in CLL

A
  • 95% have B-cell markers (rather than T-cell) -> CD20+ and CD5+
30
Q

Histology of CLL

A

Smudge cells

  • THINK: CLL = Crushed Little Lymphocytes = smudge cells
31
Q

What is Richter transformation

A

Progression of CLL to aggressive lymphoma, usually diffuse large B-cell lymphoma

32
Q

What cancer is associated with autoimmun hemolytic anemia and why/

A
  • CLL (usually involves B-cells) may cause autoimmune hemolytic anemia (both warm of cold cell agglutinins)
    • If neoplastic B-cells do make Ig, it will be defective and can attack the bod
33
Q

Common complication of CLL

A
  • Hypogammaglobulinemia
    • Neoplastic B-cells don’t make Ig
34
Q

What is the leukemic version of small cell lymphocytic lymphoma

A

CLL

35
Q

What are the distinguishing features of hairy cell leukemia

A
  • Neoplastic proliferation of mature B-cells with hairy cytoplasmic processes
  • Causes bone marrow fibrosis – dry tap on aspiration
  • Stains TRAP (+)
36
Q

Treatment of hairy cell leukemai

A
  • Treat with Cladribine (adenosine deaminase inhibitor)
37
Q

What are the myeloproliferative disorders

A

Aka chronic leukemias of myeloid cells:

  • Chronic myeloid leukemia (CML)
  • Polycythemia vera
  • Essential thrombocytopenia
  • Myelofibrosis
38
Q

Translocation associated with CML

A
  • t(9;22) – Philedalphia chromosome
    • THINK: Carry Mai, Lord, because she is able
      • Mai’s birthday is 9/22
      • BCR-ABL (because she is able)
39
Q

What does CML progress to?

A
  • May progress to AML (80%) or ALL (20%)
40
Q

Treatment of CML

A
  • Responds to Imatinib (bcr-able tyrosine kinase inhibitor)
41
Q

Mutation in polycythemia vera

A
  • JAK2 kinase mutation
42
Q

Presentation of polycythemia vera

A
  • Plethora (flushed face)
  • Blurred vision and HA (due to hyperviscosity)
  • Thrombosis (e.g Budd Chiari)
  • Itching after bathing
  • Erythromelalgia (severe, burning pain and red-blue coloration in the extremities)
43
Q

Mutation in essential thrombocytopenia

A
  • JAK2 kinase mutation
44
Q

Presentation of essential thrombocytopenia

A
  • Increased bleeding – too many platelets
  • Thrombosis – dysfunctional platelets
45
Q

What is myelofibrosi

A
  • Obliteration of bone marrow with fibrosis
46
Q

Mutation in myelofibrosis

A
  • JAK2 kinase mutation
47
Q

Presentation of myelofibrosis

A
  • “Teardrop” RBCs – due to marrow fibrosis
  • Splenomegaly – extra-medullary hematopoiesis
48
Q

Describe the problem in myelodysplastic syndrome

A
  • Defect in cell maturation of all non-lymphoid lineages
    • Stem-cell disorder and dysplasia involving ineffective hematopoiesis
    • Cause by de novo mutations or environmental exposures
49
Q

Histology of myelodysplastic syndrome

A
  • Pseudo-Pelger-Huet anomaly
    • Neutrophils with bilobed nuclei, connected by a thin strand
    • Typically seen after chemotherapy
50
Q

Describe the classic presentation of multiple myeloma

A
  • Anemia – plasma cells packed in bone marrow inhibit production of other cells
  • Renal insufficiency – excessive antibodies plug up kidney and form casts
  • Back pain – plasma cells stimulate osteoclasts
  • Hypercalcemia – plasma cells stimulate osteoclasts
51
Q

What changes in immunoglobulin levels do you see in multiple myeloma

A
  • Increased production of IgG and IgA
    • M spike of serum electrophoresis (M spike = increased gamma)
    • Increased risk of infection (monoclonal antibodies lack antigenic diversity)
52
Q

What is the X-ray finding in multiple myeloma

A
  • Lytic bone lesions
    • Plasma cells activate RANK on osteoclasts
53
Q

Histology of multiple myeloma

A
  • Rouleaux formation of RBCs
    • Increased serum protein leads to decreased charge between RBCs
54
Q

What are some of the effects of increased immunoglobulin in multiple myeloma

A
  • Primary AL amyloidosis
  • Ig light chains in urine (Bence Jones protein)
    • Do not show up on routine urinalysis
    • Shows up on urinary protein electrophoresis
  • Renal damage
    • Excessive antibodies plug up kidney and form casts
55
Q

Findings in Waldenstrom macroglobulinemia

A
  • M spike due to increased IgM (vs. Multiple myeloma with IgM and IgA)
  • Hyperviscosity:
    • Blurred vision
    • Raynoud phenomenon
  • Amyloidosis
  • No lytic bone lesions (vs. multiple myeloma)
56
Q

Describe the presentation of monoclonal gammopathy of undetermined significance (MGUS)

A
  • Monocloncal proliferation of plasma cells
  • Production of monoclonal immunoglobulins = M spike
  • No symptoms
  • 1-2% progress to multiple myeloma
57
Q

Positive markers found in Langerhans cell histiocytosis

A
  • S-100 (+) and CD1a (+)
58
Q

Presentation of Langerhans cell histiocytosis

A
  • In children
  • Lytic bone lesions
  • Skin rash
  • Recurrent otitis media

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