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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
What does hepcidin do?
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
What ids erythropoietin's effect on hepcidin?
Suppresses it, causing ferroportin in duodenum to increase, causing an increase in iron absorption
27
What are folate and vitamin B12 used for?
Synthesis of deoxythymidine phosphate
28
Which cells do folate and vitamin D deficiencies affect?
Rapidly dividing cells: - Bone marrow - Epithelial surfaces of mouth and gut
29
How is a reference range derived?
- 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
How can a 'normal' reference range be affected?
Age • Gender • Ethnic origin • Physiological status • Altitude • Nutritional status • Cigarette smoking • Alcohol intake
31
Define anaemia
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
Define the 4 mechanisms of anaemia
- 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
State three causes of microcytic anaemia
- Iron deficiency - anaemia of chronic inflammation - Defect in globin synthesis (thalassaemia)
34
Describe the causes of iron deficiency
-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
Which type of anaemia is usually hypochromic (low in colour) ?
microcytic
36
What is a common mechanism of macrocytic anaemia?
Abnormal haemopoiesis. Often RBC precursors continue to synthesize Hb and other cellular proteins but fail to divide normally
37
What is megaloblastic macrocytic anaemia?
Cytoplasm matures and cell grows before nucleus does - occurs in bone marrow
38
List 5 causes of megaloblastic anaemia
- 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
Where can you see megaloblastic anaemia?
Bone marrow, not blood film. Shows nucleoplasmic dissociation
40
Describe the mechanisms and causes of normocytic anaemia
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
What happens during acute myeloid leukemia?
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
What happens during chronic myeloid leukemia?
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
What happens during acute lymphoblastic leukemia?
Build up of immature lymphocytes (lymphoblasts) cannot perform their function
44
What happens during chronic lymphoid leukemia?
mature but functionally deficent cells are formed
45
Define polycythaemia
Too many RBCs in the circulation
46
What is the difference between pseudo and true polycythaemia?
Pseudo - reduced plasma volume (dehydration/shock) | True - increase in total volume of red cells in the circulation
47
What is the cause of pseudo polycythaemia?
Dehydration or shock
48
What are the mechanisms and causes of true polycythaemia?
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
What happens during polycythaemia vera?
Hyperviscosity - vascular obstruction - causes spleen to enlarge as it is working harder than normal
50
What are the treatments for polycythaemia vera?
Blood removed (venesection) and drugs given to decrease the production of RBCs
51
What is leukemia?
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
Give 5 examples of types of mutation which may lead to leukemia
- proto-oncogene mutation - creation of novel gene - loss of function of tumour-suppressor - dysregulation - translocation (under the influence of another gene)
53
Symptoms and classic features of leukemia
Leukocytosis; bone pain (acute) ; hepatomegaly ; splenomegaly ; lymphadenopathy; thymic enlargement; skin infiltration; lack of production of normal cells --> anaemia; leukopenia; thrombocytopenia
54
Haematological features of acute lymphoblastic leukemia
leucocytosis with lymphoblasts in the blood; anaemia; neutropenia; thrombocytopenia; replacement of normal bone marrow cells by lymphoblasts
55
Clinical features of acute lymphoblastic leukemia
enlarged liver, enlarged spleen, enlargement of lymph nodes, enlargement of the testes, peripheral lymphadenopathy

Principles Of Medicine (6 decks)

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