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PoM Block 2 > Blood Cell Abnormalities (14) > Flashcards

Blood Cell Abnormalities (14) Flashcards

1
Q

What is anaemia?

A
  • a reduction in the amount of Hb in a given volume of blood below what would be expected w/ a healthy subject of same age and gender
  • Hb conc. reduced
  • RBC and Hct/PCV usually also reduced
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2
Q

What are the 4 mechanisms of anaemia?

A
  • reduced production of RBCs/Hb in bone marrow
  • blood loss
  • reduced survival of RBCs in circulation
  • pooling of RBCs in v. large spleen
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3
Q

How do we distinguish between the mechanism and cause of anaemia?

A
  • mechanism might be reduced synthesis of Hb in bone marrow

- cause could be a condition causing reduced synthesis of haem or globin

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4
Q

What is the relationship between RBC size and haemoglobinisation?

A

microcytic- usually also hypochromic
normocytic- usually also normochromic
macrocytic- usually also normochromic

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5
Q

What are common causes of microcytic anaemia?

A
  • defect in haem synthesis: iron deficiency or anaemia of chronic disease
  • defect in globin synthesis: alpha thalassaemia (defect in alpha chain synthesis) or beta thalassaemia (defect in beta chain synthesis)
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6
Q

What are causes of iron deficiency?

A
  • insufficient intake: dietary or malabsorption (coeliac disease, H.pylori gastritis)
  • increased blood loss: due to hookworm or menorrhagia
  • increased requirements: pregnancy or infancy
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7
Q

What do macrocytic anaemias usually result from?

A

abnormal haemopoiesis–> so that RBC precursors continue to synthesise Hb and other cellular proteins, but fail to divide normally, so cells end up larger than normal

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8
Q

What is megaloblastic erythropoiesis?

A
  • a delay in maturation of the nucleus in RBC (bc impaired DNA synthesis) while cytoplasm continues to mature and cell continues to grow
  • megaloblasts generally seen in bone marrow, not blood film
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9
Q

What are common causes of macrocytic anaemia?

A
  • lack of vitamin B12 or folic acid (megaloblastic anaemia)
  • drugs that interfere w/ DNA synthesis
  • liver disease and excess alcohol intake
  • recent major blood loss w/ adequate iron stores (inc. reticulocytes, inc. MCV bc young RBC 20% larger than mature)
  • haemolytic anaemia (inc. reticulocytes)
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10
Q

What is the difference between polychromasia and reticulocytosis?

A
  • polychromasia= presence of RBCs w/ a blue tinge to cytoplasm on a routinely stained blood film; indicates young cells, newly released from bone marrow
  • reticulocytosis= cells exposed to specific stain; indicates inc. numbers of young RBCs bc lots of ribosomes
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11
Q

What are the mechanisms and causes of normocytic anaemia?

A
  • recent blood loss due to GI haemorrhage, or trauma
  • failure of RBC production due to early stages of iron deficiency, or bone marrow failure/suppression (e.g. chemo), or bone marrow infiltration (e.g. leukaemia) where normal HSCs are crowded out
  • pooling of RBCs in spleen due to hypersplenism (e.g. liver cirrhosis), or splenic sequestration in sickle cell
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12
Q

What is polycythaemia?

A
  • too many RBCs in circulation

- Hb, RBC and Hct all increased compared to normal subjects of same age and gender

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13
Q

What can cause pseudo polycythaemia?

A
  • result of reduced plasma volume
  • acute or chronic
  • severe dehydration or shock
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14
Q

What are the mechanisms of true polycythaemia?

A
  • blood doping or overtransfusion
  • appropriately increased erythropoietin (as a result of hypoxia)
  • inappropriate erythropoietin synthesis or use (e.g. kidney tumour)
  • independent of erythropoietin (myeloproliferative neoplasm- polycythaemia vera)
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15
Q

What is hyperviscosity and how can we treat it?

A

polycythaemia can lead to thick blood–> high haematocrit can lead to vascular obstruction, thrombosis and heart attacks etc..–> blood can be removed by venesection to reduce viscosity and can give drugs to reduce bone marrow production of RBCs

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16
Q

What is leukaemia?

A
  • ‘white blood’–> cancer of the blood
  • 5% of all cancers are blood cancers
  • bone marrow disease (not all patients have abnormal cells in the blood)
17
Q

What is the mechanism of leukaemia?

A
  • results from a series of mutations in a single lymphoid/myeloid stem cell, HSC, or a B/T lymphocyte
  • these mutations lead the progeny of that cell to show abnormalities in proliferation, differentiation, or cell survival leading to steady expansion of leukaemic clone
18
Q

Why is leukaemia different from other cancers?

A
  • haemopoietic and lymphoid cells behave differently from other body cells
  • HSCs and cells derived circulate in the blood and can enter tissues, and normal lymphoid stem cells recirculate between tissues and blood
  • so we cannot use the concepts of invasion and metastasis
  • chronic = benign… disease goes on for a long time
  • acute = malignant… if not treated, disease is very aggressive and patient dies rapidly
19
Q

How is leukaemia classified?

A
  • acute or chronic
  • lymphoid (B, T or NK lineage) or myeloid (granulocytic, monocytic, erythroid, or megakaryocytic)

acute lymphoblastic leukaemia (resemble precursors)
chronic lymphocytic leukaemia (resemble mature lymphocytes)
acute myeloid leukaemia
chronic myeloid leukaemia

20
Q

Why do people get leukaemia?

A
  • some mutations result from identifiable or unidentifiable oncogenic influences (e.g. radiation)
  • others occur due to random errors that accumulate in individual cells
  • important leukaemogenic mutations: mutation in oncogene, creation of novel gene, or dysregulation of a gene due to translocation making it susceptible to a promoter/enhancer
  • loss of function of tumour suppressor gene (deletion or mutation)
  • inherited tendency to inc. chromosomal breaks
  • DNA repair inhibited, so error persists
21
Q

What are some identifiable causes of leukaemogenic mutations?

A
  • irradiation (therapeutic)
  • anti-cancer drugs
  • cigarette smoking
  • chemicals e.g. benzene
22
Q

What is the difference between acute and chronic myeloid leukaemia?

A
  • in AML: buildup of immature cells (myeloblasts) in bone marrow w/ spread to blood, as they continue to proliferate but not mature and cell behaviour= profoundly disturbed, as product of oncogene prevents normal function of protein
  • in CML: inc. production of end cells instead of failure, reduced apoptosis so that cells survive longer and leukaemic clone expands…cell function not as seriously affected as in AML
23
Q

What is the difference between acute and chronic lymphoid leukaemia?

A
  • in ALL: inc. in immature cells (lymphoblasts)- frozen at this stage of development, so don’t mature
  • in CLL: leukaemic cells are mature, but abnormal and clonal (T, B or NK cells)
24
Q

How does leukaemia cause the disease characteristics?

A
  • accumulation of abnormal cells in bone marrow leads to bone pain (acute), leucocytosis, hepatomegaly, splenomegaly, lymphadenopathy (if lymphoid), thymic enlargement (if T lymphoid), skin infiltration
  • lack of production of normal cells leads to anaemia, leucopenia, thrombocytopenia
25
Q

How does chronic myeloid leukaemia arise genetically?

A

results from translocation between chromosomes 9 and 22 in an HSC, leading to a chimeric gene, BCR-ABL1–> protein encoded by this new gene gives cell a growth and survival advantage over normal cells, so expands into leukaemic clone

26
Q

How does chronic myeloid leukaemia present?

A
  • inc. in all granulocytes: neutrophils, basophils and eosinophils (and their precursors)
  • anaemia (due to replacement of normal bone marrow cells by lymphoblasts)
  • splenomegaly
27
Q

How do we potentially cure chronic myeloid leukaemia?

A

BCR-ABL1 protein signals between cell surface and nucleus–> can be inhibited by specific tyrosine kinase inhibitor, leading to remission

28
Q

What are the haematological features of acute lymphoblastic leukaemia?

A
  • leucocytosis w/ lymphoblasts in blood
  • anaemia (normocytic+ normochromic)
  • neutropenia
  • thrombocytopenia
    ^due to replacement of normal bone marrow cells by lymphoblasts
29
Q

Why do we do cytogenetic and molecular genetic analysis for leukaemia patients?

A
  • useful for managing the individual patient bc it gives us info about prognosis: hyperdiploidy- good prognosis, whereas reciprocal translocation- poor prognosis
  • advances knowledge of leukaemia bc discovers mechanisms and targeted treatments
30
Q

What are the leukaemogenic mechanisms of acute lymphoblastic leukaemia?

A
  • formation of a fusion gene
  • dysregulation of a proto-oncogene by juxtaposition of it to promoter of another gene e.g. T cell receptor gene
  • point mutation of a proto-oncogene
31
Q

What treatments are there for acute lymphoblastic leukaemia?

A
  • supportive: red cells for anaemia, platelets to prevent haemorrhage, ABs for infection due to neutropenia
  • systemic chemotherapy: IV and oral
  • intrathecal chemotherapy: bc leukaemic cells can get into CSF

PoM Block 2 (9 decks)

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