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Blood Cell Abnormalities Flashcards

1
Q

What is leukemia

A

A bone marrow disease and overspill of abnormal cells into blood. Cancer that arises from a mutation in a precursor of myeloid or lymphoid cells.

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2
Q

How does leukemia differ from other cancers

A

The abnormal cells circulate in the blood stream and migrate to other tissues. It is difficult to apply the concepts of metastatic tumours etc.

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3
Q

Two types of leukemia

A

Acute and Chronic

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4
Q

Acute leukemia

A

If left untreated, it has profound pathological effects and leads to death in a matter of days, weeks or months

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5
Q

Chronic leukemia

A

Causes less impairment of function of normal tissues and although it will eventually lead to death, this does not occur for a number of years

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6
Q

4 types of leukemia

A

Acute lymphoblastic
Chronic lymphocytic
Acute myeloid
Chronic myeloid

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7
Q

why does leukemia occur

A

mutations occur in primitive cells that as a result have growth or survival advantage over normal cells that have not undergone mutations. This gives rise to a clone that steadily replaces normal cells. These mutations may be in the protooncogenes or the tumor suppressor genes.

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8
Q

where does the mutation take place in leukemia

A

Somatic cells and germ cells. The process of mutation in a somatic cell may be the result of undetected exposure to mutagens or it may be a random, spontaneous process. The older a person is, the more likely it is that enough spontaneous or induced mutations have accumulated in a single cell for the cell to expand into a clone that replaces normal cells.

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9
Q

common causes of acute lymphoblastic leukemia

A

usually unknown, sometimes mutagenic drugs or exposure to irradiation or chemicals in utero , possibly delayed exposure to a common pathogen or pathogens

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10
Q

common causes of acute myeloid leukemia

A

usually unknown, sometime irradiation or mutagenic drugs or chemicals (benzene, cigarette smoke)

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11
Q

common causes of chronic myeloid leukemia

A

usually unknown, rarely irradiation or mutagenic drugs

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12
Q

common causes of chronic lymphoid leukemia

A

unknown but some families are predisposed

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13
Q

how can acute myeloid leukemia that occurs in late and middle age

A

can often be as a result of multiple sequential mutations (therefore likelihood increases with age)

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14
Q

somatic mutations and acute lymphoblastic leukemia

A

somatic mutations occur well before birth and many cases of leukemia that occurs in infants ( acute lymphoblastic leukemia) due to events that occur in fetal development. antigenic stimulation may also be relevant to the development of some forms of ALL- leads to the rearrangement of DNA so that antibodies of greater affinity are produced. If the process goes wrong

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15
Q

what determines the whether a mutation is acute or chronic

A

acute = mutations in genes encoding transcription factors with a resultant profound abnormality in the cells ability to mature. But the cells continue to proliferate so there is an accumulation of primitive cells referred to as blast cells, either lymphoblasts or myloblasts

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16
Q

how does chronic myeloid leukemia progress

A

the mutation involves the activation of signalling pathways within the cell (in CML, this results from the fusion protein BCR-ABL 1 encoded by the Philadelphia chromosome).
However maturation still occurs and in the case of myeloid cells, mature end cells are still able to function. So impairment of normal physiological processes is much less than acute leukemias.

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17
Q

which type of leukemia predominantly affects the elderly

A

chronic lymphocytic leukemia

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18
Q

signs and symptoms of leukemia as a direct result of the proliferation of leukaemic cells

A

bone pain, enlarged liver (helatomegaly), enlarged spleen (splenomegaly) and swollen lymph nodes *lymphadenopathy- mainly in lymphoid leukemias”

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19
Q

signs and symptoms of leukemia as an indirect result of leukemic cell proliferation

A

replacement of normal bone marrow cells by leukemic cells (causing anaemia, thrombocytopenia and neutropenia)

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20
Q

clinical features of leukemia

A
  • fatigue, lethargy and pallor (anaemia)
  • fever and infections (neutropenia)
  • bruising and petechiae (thrombocytopenia)
  • bone pain(bone marrow expansion)
  • abdominal enlargement ( hepatomegaly, splenomegaly)
  • lumps and swellings (lymphademopathy)
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21
Q

what are the essential investigations needed to diagnose leukemia

A

full blood count and blood film. Also need to characterise the profile of the cell surface markers expressed to distinguish between B and T cells (flow cytometry). Basically look for markers such as Philadelphia chromosome.

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22
Q

Diagnosing acute myeloid lekemia from a blood film

A

Blast cells will be present (large size, high nuclei-cytoplasmic ratio, prominent nucleoli and open chromatin pattern)
Cytoplasm should also contain granules which will help to differentiate between lymphoid and myeloid (lymphoid will have no granules)
Platelets and neutrophils will be absent

23
Q

Possible symptoms/signs of AML

A

fatigue, lethargy, pallor (anaemia)
fever and infections (neutropenia)
bruising and petechiae (thrombocytopenia)
bone pain (bone marrow expansion)

24
Q

Diagnosing chronic myeloid leukemia from a blood film

A

Will see increase in all granulocytes (neutrophils, eaosinophils and basophils and an increase in their precursors so will see a left shift)
A basophil should have a lobed nuclei

25
Q

Possible symptoms/signs of chronic myeloid leukemia

A

patient may present with abdominal discomfort (hepatomegaly and splenomegaly)

26
Q

Possible symptoms/signs of chronic lymphocytic leukemia

A

lumps and swellings (lymphadenopathy)

fatigue, lethargy, pallor (anaemia)

27
Q

Diagnosing chronic lymphocytic leukemia from blood film

A

squashed CLL lymphocyte which is known as a ‘smear’ or ‘smudge’ cell which is characterised in the kind of leukemia

28
Q

diagnosing acute lymphoblastic leukemia from a blood film

A

blast cells
but the cytoplasm does not contain granules so not myeloid
neutrophils and platelets should be absent

29
Q

symptoms of acute lymphoblastic leukemia

A
  • fatigue, lethargy and pallor (anaemia)
  • fever and infections (neutropenia)
  • bruising and petechiae (thrombocytopenia)
  • bone pain(bone marrow expansion)
  • lumps and swellings (lymphadenopathy)
30
Q

What decreases in blood measures is associated with anaemia

A

reduction in RBC count and haemocrit (HCT ) level

31
Q

mechanisms that result in anaemia

A
  • reduced production of red cells by bone marrow
  • loss of blood from body
  • reduced survival of red cells in the circulation (haemolysis)
  • increased pooling pf red cells in an enlarged spleen
32
Q

appearance of microcytic anaemia in a blood film

A

hypochromic (appear pale when looked at with a microscope) and microcytic

33
Q

causes of microcytosis

A

microcytosis results from reduced synthesis of haemoglobin .

Reduced synthesis of haem (iron deficinecy anaemia)
Reduced globin synthesis - thalassemia

34
Q

iron deficiency microcytosis causes

A

Bleeding (imp to find the cause of the blood loos as often the gastrointestinal tract or heavy mentsrual bleeding.

35
Q

Causes of iron deficiency

A
  • Increased blood loss :
    Hookworm
    menstrual (menorrhagia)

Insufficientintake:
Dietary(vegetarians)
Malabsorption (coeliac disease or H pylori gastritis)

Increased requirements:
Physiological- pregnancy and infancy

36
Q

how to recognise iron deficiency anaemia from blood film

A

microcytosis(low MCV), hypochromia (low MCHC) and occasional target cells , pencil cells (elliptocytes)

37
Q

stages of iron depletion

A

1) iron depletion: storage iron reduced or absent
2) iron deficiency: low serum iron and transferrin saturation
3) Iron deficiency anaemia: low haemoglobin and haemocrit

38
Q

Anaemia of chronic disease causes

A

Usually and inflammatory aspect to the disease. Common causes include:
Rheumatoid arthiritis, autoimmune disease, malignancy, kidney disease and infections such as TB or HIV

39
Q

role of TNF alpha and interleukins in anaemia

A

They have a role to play in chronic disease and they decrease erythropoietin production and also prevent the normal flow of iron from the duodenum to the RBC.

40
Q

lab clues of anaemia of chronic disease

A
  • C-reactive protein is high (unlike iron deficiency)
  • Erythrocyte sedimentation rate (ESR ) is high (unlike iron deficiency)
  • Ferritin is high
  • Transferrin is low
  • Acute phase proteins increase
41
Q

how to treat people with anaemia of chronic disease

A

iron replacement therapy will not help and should be avoided as patients with anaemia of chronic disease have plenty of storage iron. Controlling the underlying disease to reduce inflammation (e.g. by treating the infection) will treat the anaemia

42
Q

How to differentiate between anaemia of iron deficiency and of chronic disease from fbc

A

in anemia of chronic disease, ferritin will be high and transferrin will be low (compared to iron deficiency)

43
Q

How yo detect polycythaemia in FBC

A

HB, RBC and Hct are all increased compared to normal subjects of the same age and gender

44
Q

pseudo causes of polycythaemia

A

reduced plasma volume so it seems like there are more rbcs

45
Q

true causes of polycythaemia

A

increase in total volume of red cells in the circulation.
blood doping or overtransfusion
appropriately increased erythropoietin
inappropriate erythropoietin synthesis or use
independent of erythropoietin

46
Q

polycythaemia independent of erythropoietin

A

myeloproliferative disorders in respect to CML (it refers to increased erythropoiesis)

It is an intrinsic bone marrow disorder called polycythaemia vera and leads to hyperviscoscity (thick blood) which can lead to vascular obstruction or arterial thrombosis. Blood can be removed by venesection to reduce viscocity and drugs can be given to reduce bone marrow production of red cells

47
Q

how to differentiate between thalassemia trait and iron defficiency anaemia

A

iron deficiency: reduced mch and mchc

thalassemia trait: reduced mch and normal mchc . rbc increased

48
Q

why is it imp to differentiate between the two causes of microcytic anaemia

A

to replace iron where this is deficient and not incorrectly prescribe iron supplements that have no effect on thalassemia trait
provide genetic counseling

49
Q

macrocytic anaemia

A

usually results from abnormal haemopoiesis so that the red cell precursors continue to synthesise hb and other cellular proteins but fail to divide normally so red cells are larger than normal.

50
Q

causes of macrocytic anaemia

A

megoblastic erythropoiesis (delay in maturation of the nucleus while the cytoplasm continues to mature and the cell continues to grow). Megoblasts are generally seen in bone marrow not in blood film

51
Q

common causes of macrocytic anaemia

A

lack of vitamin B12 or folic acid (megoblastic anarmia)
use of drugs interfering with dna sunthesis
liver disease and ethanol toxicity
recent major blood loos with adequate iron stores (reticulocytes increasrd)
haemolytic anaemia (reticulocytes increased)

52
Q

how to diagnose macrocytic anaemia by megoblastic erythropoiesis

A

Blood film; tear drop cells, hypersegmented neutrophil and oval macrocytes but need bone marrow examination to be sure

53
Q

causes of normocytic anaemia

A

recent blood loos (gastrointestinal haemorrage /trauma)
failure of production of red cells ( early stages of iron deficiency , bone marrow failure or supression like chemo, bone marrow infiltration (leukeamia)
Pooling of red cells in spleen - hypersplenism, e.g. liver cirrhosis and splenic sequestration in SCD.

54
Q

reticulocytes and anaemia

A

increased reticulocyte count is seen as a reponse to haemolytic anaemia and recent blood loss and also as a response to treatment with iron, votamin B12 or folic acid. Reduced reticulocyte count is seen when there is reduced output of red cells from bone marroe

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