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Step I > White Blood Cell Disorders > Flashcards

White Blood Cell Disorders Flashcards

1
Q

Normal WBC count

A

5-10 K/ul

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2
Q

Leukopenia

A

low WBC count; <5 K/ul

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3
Q

Leukocytosis

A

high WBC count; >10 K/ul

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4
Q

Causes of neutropenia

A
  1. Drug toxicity (e.g. chemo with alkylating agents)– damage to stem cells results in decreased production of WBCs, particularly neurtrophils 2. Severe infection (e.g. gram-negative sepsis)– Increased movement of neutrophils into tissues results in decreased circulating neutrophils
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5
Q

What can be used to boost granulocyte production after chemotherapy?

A

GM-CSF or G-CSF (colony stimulating factor)

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6
Q

What cell type is most sensitive to radiation?

A

Lymphocyte

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7
Q

Causes of lymphopenia

A
  1. Immunodeficiency (DiGeorge syndrome- failure to develop 3rd and 4th pharyngeal pouch, no thymus; HIV) 2. High cortisol state (e.g. exogenous corticosteroids or Cushing syndrome)– induces apoptosis of lymphocytes 3. Autoimmune destruction (SLE) 4. Whole body radiation
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8
Q

Neutrophilic leukocytosis

A

Increased circulating neutrophils

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9
Q

Causes of neutrophilic leukocytosis

A
  1. Bacterial infection or tissue necrosis- induces release of marginated pool and bone marrow neutrophils, ncluding immature forms (left shift); immature cells are characterized by decreased Fc receptors (CD16) 2. High cortisol state- impairs leukocyte adhesion, leading to release of marginated pool of neutrophil
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10
Q

What is a marker of immature neutrophil?

A

Immature cells are characterized by decreased Fc receptors (CD16)

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11
Q

Causes of monocytosis

A

Increased circulating monocytes 1. chronic inflammatory states (autoimmune, infectious) 2. Malignancy

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12
Q

Causes of eosinophilia

A

Increased circulating eosinophils. 1. Allergic reactions (type I hypersensitivity) 2. Parasitic infections 3. Hodgkin lymphoma

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13
Q

What is eosinophila driven by?

A

Eosinophila is driven by increased eosinophil chemtactic factor and IL-5 production.

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14
Q

Cause of basophilia

A

Increased circulating basophils; classically seen in chronic myeloid leukemia

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15
Q

Cause of lymphocytic leukocytosis

A

Increased circulating lymphocytes 1. Viral infection- T lymphocytes undergo hyperplasia in response to virally infected cells 2. Bordetella pertussis infection- bacteria produces lymphocytosis promoting factor, which blocks circulating lymphocytes from leaving the blood to enter the lymph node

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16
Q

How does Bordetella pertussis cause lymphocytic leukocytosis?

A

Increased circulating lymphocytes The bacteria produces lymphocytosis promoting factor, which blocks circulating lymphocytes from leaving the blood to enter the lymph node. This is an exception for bacteria, which normally increases neutrophils.

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17
Q

Name 2 viruses that cause lymphocytic leukocytosis with reactive CD8+ T cells.

A

EBV infection is most common. CMV is less common cause.

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18
Q

How is infectious mononucleosis screened?

A

Monospot test- detects IgM antibodies that cross-react with horse or sheep red blood cells (heterophile antibodes)

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19
Q

How is infectious mononucleosis diagnosed?

A

Definitive diagnosis is made by serologic testing for the EBV viral capsid antigen.

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20
Q

What are heterophile antibodies?

A

Monospot test- detects IgM antibodies that cross-react with horse or sheep red blood cells (heterophile antibodes)

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21
Q

In the case of lymphadenopathy (LAD) due to T-cell hyperplasia following EBV infection, what part of the lymph node is enlarged?

A

The lymph node is composed of 3 layers: Cortex, Paracortex, and medulla. T cells normally hang out in the paracortex. Therefore, the paracortex is enlarge following EBV infection.

22
Q

In the case of splenomegly due to T-cell hyperplasia following EBV infection, what part of the spleen is enlarged?

A

Spleen is divided into white pulp and red pulp. Red pulp is vascular; white pulp contains lymphoid tissue. T cells proliferate in the periarterial lymphatic sheath (PALS) in the white pulp. Histology: dense blue color around arteries.

23
Q

What does a negative monospot indicate in a patient suspected of infectious mononucleosis?

A

A negative monospot test suggests CMV as a possible cause of IM.

24
Q

Complications of infectious mononucleosis

A
  1. Increased risk of splenic rupture- pts are generally advised to avoid contact sports for one year 2. Rash if exposed to ampicillin 3. Dormancy of virus in B cells leads to increase risk for both recurrence and B-cell lymphoma, esp. if immunodeficiency develops.
25
Q

Causes of erythrocytosis

A
  • Polycythemia vera - Tumors - High altitude - Smoking - Hypoxia - Blood doping - High O2 affinity Hb
26
Q

Tumors that cause erythrocytosis

A

“PHUCK” Phenochromocytoma Hepatic Uterine leiomyoma Cerebellar Hemangioblastoma Kidney

27
Q

DDx for painless lymphadenopathy

A
  1. Chronic inflammation (chronic lymphadenitis) 2. Metastatic carcinoma 3. Lymphoma
28
Q

Which specific region of the lymph nodes is enlarged in the following cases: 1. Rheumatoid arthritis 2. HIV infection 3. Viral infection 4. Cancerous tissue drained by lymph nodes

A
  1. Follicle 2. Follicle 3. Paracortex 4. Hyperplasia of sinus histiocytes (in medulla)
29
Q

How is follicular lymphoma distinguished from reactive follicular hyperplasia?

A
  1. Disruption of normal lymph node architecture 2. Lack of tingible body macrophages in germinal centers 3. Bcl2 expression in follicles 4. Monoclonality
30
Q

Translocation in Follicular Lymphoma

A

t(14;18) chr 14 = IgH chr 18 = Bcl2 (antiapoptotic)

31
Q

Translocation in Mantle Cell Lymphoma

A

t(11;14) chr 11 = cyclin D1 chr 14 = IgH Overexpression of cyclin D1 promotes G1/S transition in the cell cycle, facilitating neoplastic proliferation.

32
Q

What is marginal zone lymphoma associated with?

A

Marginal zone lymphoma is associated with chronic inflammatory states, such as Hashimoto thyroiditis, Sjogren Syndrome, H pylori gastritis.

33
Q

What is MALToma?

A

MALToma is marginal zone lymphoma in mucosal sites.

34
Q

Translocation in Burkitt Lymphoma

A

t(8;14) chr 8 = c-myc chr 14 = IgH

35
Q

How does diffuse proliferation of large B cells arise?

A

Arise sporadically or from transformation of low-grade lymphoma (e.g. follicular lymphoma).

36
Q

Features of Hodgkin Lymphoma

A
  • Presence of Reed-Sternberg (RS) cells, large B cells with multilobed nuclei and prominent nucleoli (owl-eyed nuclei) - Classically positive for CD15 and CD30, but NEGATIVE for CD20 - RS cells secrete cytokines, resulting in ‘B symptoms” (fever, chills, might sweats) and attract reactive cells, which form tumor.
37
Q

Subtypes of Hodgkin Lymphoma. Which one is most common?

A
  1. Nodular sclerosis- most common 2. Lymphocyte-rich- best prognosis 3. Lymphocyte-depleted- most aggressive 4. Mixed cellularity- associated with abundant eosinophils
38
Q

How to differentiate between multiple myeloma and MGUS?

A

MGUS (monoclonal gammapathy of undetermined significance) - Increased serum protein with M spike on SPEP, with other features of multiple myeloma absent (no lytic bone lesions, hypercalcemia, AL amyloid, or Bence Jones proteinuria).

39
Q

What is the most common primary malignancy of bone?

A

Multiple myeloma

40
Q

What is the most common malignant lesion of bone?

A

Metastatic cancer

41
Q

Clinical features of multiple myeloma

A

MM is the malignant proliferation of plasma cells in the bone marrow. It is the most common PRIMARY malignancy of bone. 1. Bone pain with hypercalcemia and lytic bone lesions 2. Elevated serum protein (M spike present on serum protein electrophoresis, most commonly due to monoclonal IgG or IgA) 3. Increase risk of infection (monoclonal antibody lacks antigenic diversity 4. Rouleaux formation of RBCs on blood smear (increased serum protein decreases charge between RBCs) 5. Primary AL amyloidosis- free light chains circulate in serum and deposit in tissue 6. Free light chain is excreted in the urine as Bence Jones protein; deposition in kidney tubules leads to risk for renal failure (myeloma kidney)

42
Q

What is the most common cause of death in multiple myeloma?

A

Infection! Monoclonal antibody lacks antigenic diversity.

43
Q

What is a myeloma kidney?

A

In multiple myeloma, free light chain is excreted in the urine as Bence Jones protein; deposition in kidney tubules leads to risk for renal failure (myeloma kidney)

44
Q

Bence Jones protein

A

In multiple myeloma, free light chain is excreted in the urine as Bence Jones protein; deposition in kidney tubules leads to risk for renal failure (myeloma kidney).

45
Q

Clinical features of Waldenstrom Macroglobulinemia

A

B cell lymphoma with monoclonal IgM production: 1. Generalized lymphadenopathy 2. No lytic bone lesions 3. Increased serum protein with M spike (comprised of IgM) 4. Visual and neurologic deficits due to retinal hemorrhage or stroke (IgM, large pentamer, causes serum hyperviscosity) 5. Bleeding- viscous serum results in defective platelet aggregation

46
Q

Name 3 types of dyscrasias

A
  1. Multiple myeloma 2. MGUS 3. Waldenstrom Macroglobulinemia
47
Q

Acute treatment for Waldenstrom Macroglobulinemia

A

Plasmapheresis to remove IgM

48
Q

Langerhans Cell Histiolcytosis. Histological features and 3 subtypes.

A

Neoplastic proliferation of Langerhans cells. Characteristic histological features: 1. Birbec granules (tennis racket) are seen on EM 2. Cells are CD1a+ an S100+ by ICH. Subtypes: 1. Letterer-Siwe disease- malignant, skin rash, cystic skeletal defects in infants (< age 2), rapidly fatal 2. Eosinophilic granuloma- benign, pathologic fracture in adolescent, NO skin involvement. 3. Hand-Schuller-Christian Disease- Malignant, scalp rash, lytic skull defects, diabetes insipidus, exophthalmos in a child (> age 3)

49
Q

Langerhans Cells

A

Langerhans cells are specialized dendritic cells found predominant in the skin. rare disease involving clonal proliferation of Langerhans cells, abnormal cells deriving from bone marrow and capable of migrating from skin to lymph nodes. Clinically, its manifestations range from isolated bone lesions to multisystem disease.

50
Q

Letterer-Siwe disease

A
  • A subtype of Langerhans Cell Histiolcytosis. - Malignant, skin rash, cystic skeletal defects in infants (< age 2), rapidly fatal
51
Q

Eosinophilic granuloma

A
  • A subtype of Langerhans Cell Histiolcytosis. - Benign, pathologic fracture in adolescent, NO skin involvement.
52
Q

Hand-Schuller-Christian Disease

A
  • Malignant, scalp rash - Triad of lytic skull defects, diabetes insipidus (from pituitary stalk infiltration), exophthalmos in a child (> age 3).

Step I (3 decks)

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