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**PATHOLOGY AND MEDICINE > pt10 > Flashcards

pt10 Flashcards

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1
Q

What two stem lineages give rise to all leukocytes?

A

Myeloid stem cells generate granulocytes and monocytes; lymphoid stem cells generate B and T lymphocytes

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2
Q

What are colony-forming units (CFUs) in leukopoiesis?

A

Intermediate progenitors (CFU-Granulocyte/Monocyte, CFU-Eosinophil, CFU-Basophil) that commit myeloid precursors before forming blasts

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3
Q

Define leukocytosis and leukopenia.

A

Leukocytosis: ↑ total WBC count; Leukopenia: ↓ total WBC count

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4
Q

What distinguishes leukemia from a leukemoid reaction?

A

Leukemia is clonal neoplastic proliferation with massive ↑ WBCs; leukemoid reaction is benign, reactive ↑ WBCs with immature cells

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5
Q

What are the five diagnostic value patterns of WBC changes?

A
  • Neutrophilia: bacterial infection, tissue damage
  • Lymphocytosis: viral infection
  • Eosinophilia: parasites, allergy
  • Monocytosis: chronic bacterial infection, malignancy
  • Basophilia: myeloproliferative disorders
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6
Q

What defines neutrophilia?

A

Neutrophils >7.5 × 10⁹ /L

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7
Q

List six causes of neutrophilia.

A

Bacterial infections; inflammation/tissue necrosis; metabolic disorders; malignancy; myeloproliferative disease; drugs (e.g., steroids); physiological (pregnancy, exercise)

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8
Q

What is neutropenia, and what is its threshold?

A

Neutrophils <1.5 × 10⁹ /L

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9
Q

Name five causes of selective neutropenia.

A

Viral infection; severe bacterial (e.g., typhoid); drug-induced (anti-inflammatories); autoimmune (e.g., rheumatoid arthritis); hypersplenism

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10
Q

How can neutropenia occur as part of pancytopenia?

A

Bone marrow failure/infiltration (cytotoxic therapy, irradiation, malignancy) or severe megaloblastic anaemia impairing DNA synthesis

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11
Q

What are key clinical features of severe neutropenia?

A

Frequent, serious infections (pneumonia, septicaemia); mucositis and ulceration in the mouth

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12
Q

When does lymphocytosis occur?

A

Acute viral infections (e.g., infectious mononucleosis), chronic infections (e.g., TB), lymphocytic leukemia (CLL, ALL), non-Hodgkin’s lymphoma

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13
Q

What is the hallmark clinical feature of lymphocytosis?

A

Lymphadenopathy (enlarged lymph nodes)

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14
Q

Define leukemia and lymphoma.

A
  • Leukemia: malignant, monoclonal proliferation of WBC precursors in bone marrow/blood without solid mass
  • Lymphoma: malignant tumour of lymphoid cells presenting as a tissue mass in lymphoid tissue
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15
Q

What is the incidence of leukemia?

A

~10 per 100,000 per year

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16
Q

Describe the common pathologic consequence of leukemia.

A

Replacement of normal bone marrow by leukemic cells → bone marrow failure (anemia, neutropenia, thrombocytopenia)

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17
Q

How are leukemias classified?

A

By acuity (acute vs chronic) and lineage (myeloid vs lymphoid)

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18
Q

What are the two acute leukemia types and their features?

A
  • AML (myeloblastic): all ages, incidence ↑ with age, FAB M0–M7
  • ALL (lymphoblastic): mainly children, FAB L1–L3
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19
Q

What defines acute leukemia on bone marrow biopsy?

A

> 20% blasts in marrow

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20
Q

What are key clinical consequences of acute leukemia?

A

Bone marrow failure (infections, anemia, bleeding), bone pain, organ infiltration (e.g., CNS)

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21
Q

What distinguishes chronic leukemias?

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A

Occur mainly in adults; leukemic cells retain some differentiation; more indolent course

22
Q

What are the two chronic leukemia types and their hallmarks?

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A
  • CLL: B-cell proliferation in >50 yrs, lymphocyte count often >100 × 10⁹/L
  • CML: neutrophil-predominant, WBC >15 × 10⁹/L, Philadelphia chromosome (t(9;22))
23
Q

What is the Philadelphia chromosome?

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A

t(9;22) fusion creating BCR-ABL tyrosine kinase oncoprotein in CML

24
Q

Name four clinical features of chronic leukemia.

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A

Very high WBC counts, anemia, thrombocytopenia, splenomegaly, hepatomegaly, lymphadenopathy

25
What proportion of cancers in the UK are lymphomas, and what are the two main types?
7th most common; Hodgkin’s lymphoma and non-Hodgkin’s lymphoma
26
What is the diagnostic cell in Hodgkin’s lymphoma?
Reed–Sternberg cell (multinucleate B lymphocyte)
27
What are the typical “B symptoms” of lymphoma?
Fever, night sweats, weight loss
28
How does non-Hodgkin’s lymphoma differ from Hodgkin’s?
85–90% are B-cell origin; often extranodal involvement (GI, lung); lacks Reed–Sternberg cells; broader spectrum of aggressiveness
29
What is the primary clinical presentation common to both Hodgkin’s and non-Hodgkin’s lymphoma?
Lymphadenopathy; may have extranodal masses in non-Hodgkin’s
30
Which leukocyte change indicates acute viral infection?
Lymphocytosis
31
Which leukocyte change indicates parasitic infestation or allergy?
Eosinophilia
32
Which leukocyte change is a hallmark of bacterial infection?
Neutrophilia
33
Who is the patient in this case study?
Mary Wilson, a 27-year-old web designer with new bruising on arms and legs for 3 days
34
What are the first three steps a GP should take when presented with unexplained bruising?
1) Detailed patient history (including recent medications and alcohol) 2) Physical examination (inspection for purpura, lymph nodes, spleen) 3) Obtain blood samples for lab tests
35
Which specific physical findings did Mary have?
Numerous tiny purpura on arms/legs, no lymphadenopathy, no splenomegaly, no IV injection marks
36
What initial lab tests did the GP order?
Full blood count (including platelet count), coagulation screen, blood film, and routine biochemistry
37
What did Mary’s initial lab results show?
Normal Hb, WBC and differential, normal coagulation tests; markedly reduced platelet count
38
Why did normal Hb and WBC counts help narrow the diagnosis?
Excluded bone-marrow failure or malignant infiltration, which would also lower RBCs and WBCs
39
What three broad mechanisms cause thrombocytopenia?
1) ↓ Production (bone-marrow failure/infiltration) 2) ↑ Sequestration (splenomegaly) 3) ↑ Destruction (immune or non-immune)
40
How were ↓ production and ↑ sequestration excluded in Mary’s case?
Normal biochemistry, normal spleen size on ultrasound, no other cytopenias
41
What was the most likely mechanism for Mary’s thrombocytopenia?
Immune-mediated destruction of platelets (suspected ITP)
42
Which specialist did the GP refer Mary to?
Haematologist for further evaluation
43
What further investigations did the haematologist perform?
Repeat blood counts and film, abdominal ultrasound, biochemical screen, then bone-marrow aspirate & biopsy
44
What did Mary’s bone-marrow aspirate reveal?
Normal cellularity with increased megakaryocytes, no abnormal cells
45
How does increased megakaryocyte count support ITP?
Shows compensatory platelet production in marrow with peripheral destruction
46
What key features confirm a diagnosis of ITP?
Isolated thrombocytopenia, normal marrow and spleen size, absence of other causes
47
How is childhood ITP usually managed?
Often self-limiting; observe if bleeding mild, treat only if severe
48
What are first-line treatments for adult ITP?
Corticosteroids to suppress autoimmunity; IV immunoglobulins to neutralize autoantibodies
49
What are second-line options if medical therapy fails?
Platelet transfusions for acute bleeding; splenectomy to remove major site of platelet destruction
50
Why is vaccination needed before splenectomy?
To prevent overwhelming post-splenectomy infections (e.g., pneumococcus)

**PATHOLOGY AND MEDICINE (24 decks)

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