Chapter 13: White Blood Cells Flashcards Preview

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Flashcards in Chapter 13: White Blood Cells Deck (116)
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What CDs are makers of HSC and ALL white blood cells?

HSC - CD34

WBC - CD45 (leukocyte common antigen)


What is HSC location throughout development?

3rd week --> yolk sac
3rd month --> liver
4th month --> bone marrow (puberty --> ONLY AXIAL)


Where is EPO generated from and what are its two production modes?

- generated by KIDNEY (peritubular capillary lining)

- released relative to Po2
(contantly Hb >10 or logarithmically Hb <10)


What is the normal % of T Cells in the peripheral blood?



What is the most common cause of agranulocytopenia?


- inc. susceptibility to bacterial or fungal infection, since it is a reduction in the number of neutrophils


What do infections occurring due to agranulocytosis look like (2)? When does serious infection normally occur?

- infections with ulcerating necrotizing lesions of mouth (agraun. angina)

- deep lesions w/dark necrotic membranes (Candida/Aspergillus)

serious infection occurs w/neutrophil count <500


How is Agranulocytosis treated?

broad spectrum antibiotics and GCSF to stimulate granulocyte production


When will LAP be elevated vs normal?

Elevated --> leukemoid reactions

Normal --> leukemia


What is the effect of Sepsis on neutrophils morphology (2) specifically?

appearance of toxic granulations (abnormal, dark azurophilic granules) and Dohle bodies (dilated endoplasmic reticulum)


Acute Nonspecific Lymphadenitis:

What is the difference between Localized, Systemic, and Mesenteric forms?

L: from direct microbiological draining

S: from bacteriemia and viral infections (usually kids)

M: mesenteric LN enlargement (looks like appendicitis)


Where is Chronic Nonspecific Lymphadenitis commonly seen in? What does the lymph node look like?

- commonly occurs in inguinal and axillary LNs

- LNs are nontender without acute inflammation or tissue drainage


What development in nonlymphoid tissue can chronic immune reactions lead to, and what is the common cytokine required?

- leads to Tertiary Lymphoid Organs

- chronic gastritis (H. pylori) and Rhematoid arthritis lead to MALToma's

- lymphotoxin required for Peyer Patch formation


What are 3 common causes of follicular hyperplasia and what are Tingible-body macrophages?

CC: rheumatoid arthritis, toxoplasmosis, early HIV

TBM = macrophages that have eaten apoptotic B Cells


What is a common cause of Paracortical Hyperplasia, and what happens when these reactions become exuberant?

- T cell mediated response like that to infectious mononucleosis (EBV)

- exuberant rxns cause immunoblasts to encroach on B-cell follicles, leading to sinusoidal/endothelial hypertrophy

- if immunoblasts (large, activated T-cells) are numerous, need special studies to exclude neoplasm from the differential


Sinus Histocytes (Reticular Hyperplasia)

- inc. in number and size of cells lining lymphatic sinusoids (expansion/distension)

- nonspecific, though seen in LNs draining carcinoma of the breast


Hemophagocytic Lymphohistiocytosis:

What is it and what is its pathogenesis? What is it most commonly caused by?

- aka "Macrophage Activating Syndrome" --> cytopenias and symptoms of systemic inflamm dur to macrophage activation

- macrophages and CD8+ cells destroy peripheral and marrow cell lineages, while releasing mediators that suppress hematopoiesis

- infection is most common trigger (EBV especially)


Hemophagocytic Lymphohistiocytosis:

What does it look like clinically and how can it be treated?

- acute febrile illness and hepatosplenomegaly with anemia/thrombocytopenia

- inc. LFTs/TG (hepatitis) and DIC may be present

Treatment: immunosuppressive drugs and mild chemo
- only about 50% survive (may have sequelae)


Myeloid Neoplasms

What is the difference between Acute Myeloid Leukemia, Myelodysplastic Syndrome, and Chronic Myeloproliferative Disease?

AML: blasts accumulate in bone marrow suppressing normal hematopoiesis (MOST SEVERE)

MDS: ineffective hematopoiesis, causing peripheral blood cytopenias (more severe than MPD)

CMD: inc. production of one or more adult myeloid elements leads to inc. peripheral blood counts

**less severe types can evolve over time into more aggressive forms of disease**


What kinds of cancer do these viruses lead to:

1. HTLV1
2. EBV
4. HIV

1. adult T-cell leukemia/lymphoma (ATLL)

2. Burkitt lymphoma, Hodgkins, other B-cell lymphoma
- paracortical response to B cell infection in Burkitt

3. B-cell lymphoma (malignant pleural effusions)

4. B-cell lymphoma


What is the difference in spread of Hodgkins vs Non-Hodgkins lymphoma?

Hodg: spreads in an orderly fashion, staging useful
- distinctive pathological features, unique treatment

NonHodg: spreads widely and is less predictable


Acute Lymphoblastic Leukemia (ALL):

What is it, who does it commonly affect, and what is its pathogenesis between T and B cells?

- immature lymphoblast neoplasm (mostly B-ALL)

- affects hispanics > white > blacks and is the MOST COMMON cancer/leukemia of childhood (< 15)

- B cells: 90% t(12;21) translocation (ETV6/RUNX1)
- also LOF in PAX5, E2A, RBF

- T cells: GOF in NOTCH1


Acute Lymphoblastic Leukemia (ALL):

What is the morphology and how can you tell this neoplasm apart from Acute Myeloid Leukemia?

- hypercellular bone marrow with "starry sky" appearance due to macrophages eating tumor cells

- scant basophilic cytoplasm with large nuclei

- ALL stains MPO (-) and TdT (+), while AML is MPO (+) and TdT (-), also more likely to cause NERVE PALSIES than AML


Acute Lymphoblastic Leukemia (ALL):

What does it look like clinically (4) and how is it treated?

- mass effect, "storm-onset" (onset in days to weeks), fatigue, fever, bleeding (due to cytopenia), and NEUROLOGICAL problems (nerve palsies, headaches, vomiting)

Treat: aggressive chemo (95% remission, 75-85% cured)


Acute Lymphoblastic Leukemia (ALL):

What is the difference between a good prognosis and bad prognosis?

Good: age 2-10, low WBC count, HYPER-DIPLOIDY, and t(12;21) translocation

Bad: age < 2, t(9;22) translocation (seen in adolescence w/WBC count >100,000)


What are common B and T cell markers that can be checked for when determining the kind of lymphoid neoplasm?

B cell: CD 10, 19, 20
- very immature will be CD 10 (-)

T cell: CD 1, 8
- very immature will be CD 3, 4, 8 (-)


What are the three "T's" of T-cell ALL?

presents Teenaged males as a Thymic mass (mediastinal) and has Thymocytes

- also see splenomegaly


Chronic Lymphocytic Leukemia (CLL):

What is it, who does it affect, and what chromosomal anomalies does it show?

- most common leukemia of adults in Western World

- affects males (2:1) that are 60 yo in Western countries

- translocations are RARE, has deletion 13q14.3 (microRNA 15/16) and 11q, 17q

PNEUMONIC: 11, tr12, 13q14, 15, 16, 17


Chronic Lymphocytic Leukemia (CLL):

What is the morphology and immunophenotype? What are 3 indicators of BAD prognosis?

M: develop proliferation centers (large lymphocytes gather in aggregates - mitotically active); promylocytes if LN is involved (Small Lymphocytic Lymphoma)

I: CD 5, 19, 20, 23 (B cell prolif. w/CD5 = CLL)

B: 11q, 17p deletions, ZAP70(+), NOTCH1 mutations


Chronic Lymphocytic Leukemia (CLL):

What are the clinical aspects and treatments for patients?

C: asymptomatic --> nonspecific signs (hepatosplenomegaly and lymphadenopathy), monoclonal Ig spike may be preset

- can cause hypogammaglobulinemia (low IgG)

T: gentle chemo, immunotherapy (CD20), BTK inhibitors, HSC transplant (median survival 4-6 yrs)


Richter Syndrome and CLL

- tendency of CLL/SLL to transform to diffuse B-cell lymphoma

- rapidly enlarging mass within LN or spleen

- BAD (survival < 1 yr)