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Principles Of Medicine > Blood Cells > Flashcards

Blood Cells Flashcards

1
Q

Name the three types of granulocyte?

A

Basophils, neutrophils, eosinophils

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2
Q

what are the functions of a neutrophil?

A

chemotaxis, phagocytosis, killing phagocytosed bacteria

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3
Q

how are granulocytes and monocytes derived?

A

Mutipotential haematopoetic stem cell –> common myeloid progenitor –>myeloblast–> specific cell type

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4
Q

What are monocytes precursors of?

A

tissue macrophages

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5
Q

What is the function of an eosinophil?

A

Kills parasites and engulfs immunocomplexes

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6
Q

What is the function of a basophil?

A

Immune and inflammatory responses

Stores histamine, heparin, proteolytic enzymes

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7
Q

During maturation of granulocytes, what happens to the cells?

A

Smaller and develop granules

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8
Q

What do monocytes do?

A

Migrate into tissues –> macrophages
Present antigens to lymphoid cells
Phagocytic and scavenging function

neutrophil functions (chemotaxis. phagocytosis, killing some microorgansims) plus antigen presentation

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9
Q

Describe the origin of a lymphocyte

A

Haematopoetic stem cell -> lymphoid progenitor -> stem cell -> NK cell/small lymphocyte -> T cell/ B cell

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10
Q

Link types of infection with types of leukocytosis

A

Bacterial - neutrophilia/monocytosis
Viral- lymphocytosis
Parasitic - eosinophilia

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11
Q

List 5 common causes of lymphopenia

A 
HIV
Chemo
Radiotherapy
Corticosteroids
Severe infection
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12
Q

Describe 3 specific abnormalities of neutrophil morphology

A

Left shift - non segmented neutrophils/ precursors

Toxic granulation - heavy, coarse granules

Hypersegmentation - more than 5 lobes

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13
Q

List possible causes (non infectious) of lymphocytosis, and neutrophilia/basophilia/eosinophilia

A

Chronic lymphocytic leukaemia and chronic myeloid leukaemia

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14
Q

List 4 common causes of neutropenia

A

Autoimmune,
Bacterial
Viral
Medication

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15
Q

Describe the pathway for erythrocyte production

A

HSCs -> myeloid stem cell -> erythroblast ->erythrocyte

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16
Q

How does the biconcave shape benefit the erythrocyte?

A

Manouevrability through small blood vessels

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17
Q

How many haem groups and globin chains does haemoglobin have?

A

4 haem groups, 4 globin chains 2 beta and 2 alpha

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18
Q

Which type of chains does foetal haemoglobin contain?

A

2 alpha and 2 gamma

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19
Q

How many erythrocytes are produced per day?

A

500 billion

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20
Q

How many days do red blood cells remain in the circulation?

A

120 days

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21
Q

Where is erythropoietin produced?

A

Kidney

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22
Q

When is erythropoietin production increased?

A

Hypoxia

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23
Q

Which form of iron is easily absorbed?

A

Fe2+ (haem)

24
Q

Which form of iron requires vitamin C (ascorbic acid) for absorption?

A

Fe3+ (non haem)

25
Q

What does hepcidin do?

A

Inhibits iron transport by binding to and degrading ferroportin, preventing efflux of iron from enterocyte (bound to ferritin) which is lost when the cell is shed from the gut

26
Q

What ids erythropoietin’s effect on hepcidin?

A

Suppresses it, causing ferroportin in duodenum to increase, causing an increase in iron absorption

27
Q

What are folate and vitamin B12 used for?

A

Synthesis of deoxythymidine phosphate

28
Q

Which cells do folate and vitamin D deficiencies affect?

A

Rapidly dividing cells:

  • Bone marrow
  • Epithelial surfaces of mouth and gut
29
Q

How is a reference range derived?

A
  • Collect samples from a carefully defined reference population
  • Using the same instrument and techniques that will be used for patient samples
  • Using an appropriate statistical technique
30
Q

How can a ‘normal’ reference range be affected?

A

Age • Gender • Ethnic origin • Physiological status • Altitude • Nutritional status • Cigarette smoking • Alcohol intake

31
Q

Define anaemia

A

Reduction in the amount of haemoglobin in a given volume of blood below what would be expected in comparison with a subject of the same age and gender

32
Q

Define the 4 mechanisms of anaemia

A
  • Reduced proportion of RBCs/Hb in bone marrow
  • Loss of blood from the body
  • Reduced survival of RBCs in the spleen
  • Pooling of red cells in large spleen
33
Q

State three causes of microcytic anaemia

A
  • Iron deficiency
  • anaemia of chronic inflammation
  • Defect in globin synthesis (thalassaemia)
34
Q

Describe the causes of iron deficiency

A

-Increased blood loss eg. cancer in GI tract, hookworm, menorrhagia (menstrual) -Physiological (pregnancy and infancy) - Dietary eg. vegetarian - Malabsorption eg.coeliac disease, H.Pylori gastritis

35
Q

Which type of anaemia is usually hypochromic (low in colour) ?

A

microcytic

36
Q

What is a common mechanism of macrocytic anaemia?

A

Abnormal haemopoiesis. Often RBC precursors continue to synthesize Hb and other cellular proteins but fail to divide normally

37
Q

What is megaloblastic macrocytic anaemia?

A

Cytoplasm matures and cell grows before nucleus does - occurs in bone marrow

38
Q

List 5 causes of megaloblastic anaemia

A
  • Vit B12/ folate deficiency
  • drugs interfere with DNA synthesis
  • liver disease and ethanol toxicity
  • recent blood lost, ADEQUATE iron stores, reticulocytes increase
  • Haemolytic anaemia, reticulocytes increase
39
Q

Where can you see megaloblastic anaemia?

A

Bone marrow, not blood film. Shows nucleoplasmic dissociation

40
Q

Describe the mechanisms and causes of normocytic anaemia

A

mechanism - recent blood loss - cause - GI haemorrhage, trauma

mechanism - failure to produce RBCs - cause - early Fe deficiency, bone marrow failure or suppression, bone marrow infiltration eg. leukemia

mechanism - pooling of red cells in the spleen - cause - hypersplenism eg. liver cirrhosis, splenic sequestration

41
Q

What happens during acute myeloid leukemia?

A

Cells of myeloid heritage continue to proliferate but fail to mature; and build up. There is a failure to produce myeloid end cells eg. neutrophils.

42
Q

What happens during chronic myeloid leukemia?

A

Increase in production of end cells, but there is usually a mutation in the proteins signalling between the cell surface receptors and nucleus. These cells are usually functionally deficient.

43
Q

What happens during acute lymphoblastic leukemia?

A

Build up of immature lymphocytes (lymphoblasts) cannot perform their function

44
Q

What happens during chronic lymphoid leukemia?

A

mature but functionally deficent cells are formed

45
Q

Define polycythaemia

A

Too many RBCs in the circulation

46
Q

What is the difference between pseudo and true polycythaemia?

A

Pseudo - reduced plasma volume (dehydration/shock)

True - increase in total volume of red cells in the circulation

47
Q

What is the cause of pseudo polycythaemia?

A

Dehydration or shock

48
Q

What are the mechanisms and causes of true polycythaemia?

A

mechanism - overtransfusion of cells - caused by blood doping
mechanism - appropriately increased erythropoietin - caused by high altitude or hypoxia
mechanism - innappropriate erythropoietin synthesis - administered to athletes or tumour cells can sometimes secrete erythropoietin innappropriately
independent of erythropoeitin - mechanism - bone marrow produces too many red blood cells - caused by myeloproliferative neoplasm in the bone marrow (slow growing cancer)

49
Q

What happens during polycythaemia vera?

A

Hyperviscosity - vascular obstruction - causes spleen to enlarge as it is working harder than normal

50
Q

What are the treatments for polycythaemia vera?

A

Blood removed (venesection) and drugs given to decrease the production of RBCs

51
Q

What is leukemia?

A

Cancer of the blood that results from a series of mutations in a single lymphoid or myeloid stem cell in the bone marrow. It circulates the tissues and blood.

52
Q

Give 5 examples of types of mutation which may lead to leukemia

A
  • proto-oncogene mutation
  • creation of novel gene
  • loss of function of tumour-suppressor
  • dysregulation - translocation (under the influence of another gene)
53
Q

Symptoms and classic features of leukemia

A

Leukocytosis; bone pain (acute) ; hepatomegaly ; splenomegaly ; lymphadenopathy; thymic enlargement; skin infiltration; lack of production of normal cells –> anaemia; leukopenia; thrombocytopenia

54
Q

Haematological features of acute lymphoblastic leukemia

A

leucocytosis with lymphoblasts in the blood; anaemia; neutropenia; thrombocytopenia; replacement of normal bone marrow cells by lymphoblasts

55
Q

Clinical features of acute lymphoblastic leukemia

A

enlarged liver, enlarged spleen, enlargement of lymph nodes, enlargement of the testes, peripheral lymphadenopathy

Principles Of Medicine (6 decks)

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