Bone Marrow, Blood And Cells Prac

Front 1

What are the various mature cells generated as a result of haemopoeisis?

Back 1

Diagram

Front 2

What factors are involved in controlling proliferation, differentiation and maturation of haematopoietic precursor cells?

Back 2

Transcription factors (master controllers) and cytokines

Front 3

What is ratio of fat to tissue in adult bone marrow?

Back 3

50% tissue, 50% fat

Front 4

What happens to the ratio of haemopoietic cells and adipose cells as we age?

Back 4

Red marrow (tissue) gets replaced with adiposed fat.

Front 5

Why is there a zone of central pallor in erythrocytes?

Back 5

Due to their biconcave disk shape

Front 6

What is anisocytosis?

Back 6

Abnormal variation of erythrocyte size

Front 7

What is poikilocytosis?

Back 7

Abnormal shape of erythrocytes

Front 8

What is the size differentiation between RBC and WBC?

Back 8

RBC is approx 2/3 the size of WBC

Front 9

What is pictured? Where is this cell derived from? and what is the function of this particular cell?

Back 9

-Platelet
-Cell fragments produced from megakaryocytes
-Functions in clotting and coagulation

Front 10

How do you differentiate between reticulocytes and erythrocytes on a blood film?

Back 10

-Reticulocytes will stain a different colour due to presence of residual DNA
-They are bigger than a mature erythrocyte

Front 11

In what circumstances would you expect to see an increased number of reticulocytes in peripheral blood smears?

Back 11

-When there is an increased need to replace mature RBc
-Anaemia, haemolysis, acute blood loss

Front 12

What are the two types of neutrophils?Which is more mature?

Back 12

-Banded and segmented
-Segmented is mature form

Front 13

At what stage are neutrophils released into the bloodstream?

Back 13

When matured into segmented neutrophils

Front 14

What does banded neutrophils in circulation indicate?

Back 14

Inflammatory cytokines are present causing early release of immature form

Front 15

What is the function of a neutrophil?

Back 15

-Phagocytosis of invaders by squeezing through capillary walls into infective tissue by chemotactic process

Front 16

What are the functions of macrophages?

Back 16

Phagocytic cells that engulf antigens as well as dead an dying cells of the body

Front 17

What is the function of eosinophils?

Back 17

Engulf parasitic worms and release cytotoxic basic granules as part of immune response

Front 18

What is the function of basophils?

Back 18

Accumulate at site of infection and discharge acidic granules

Front 19

What are the 2 classes of lymphocytes?

Back 19

B cells and T cells

Front 20

What is the function of B cells?

Back 20

Responsible for making antibodies

Front 21

What is the 3 subclasses of T cells and their functions?

Back 21

-Helper t cells; enhance Bcell produced antibodies, produced lymphocytes that attract macrophages and neutrophils to infection
-Cytotoxic T cells; Kill virus infected and tumour cells
-Regulatory T cells; down regulate immune response, maintains tolerance to self antigens

Front 22

What measurements are made in full blood examination?

Back 22

-Total RBC (per litre)
-Hb (amount in blood grams/decilitre)
-Haematocrit (fraction of whole blood volume that consists of RBC)
-Red blood cell indicies (MCV, MCH, MCHC, RDW)
-Total white blood cells (neutrophils, lymphocytes, monocytes, eosinophils, basophils)

Front 23

What conditions cause low MCV (micrcytosis)?

Back 23

Iron deficiency, anaemia of chronic disease, thalassemia/haemoglobinopathies, hypothyroidism, siderblastic anaemia

Front 24

What conditions cause high MCV (macrocytosis)?

Back 24

B12/folate deficiency, myelodysplasia, reticulocytosis, alcohol abuse, liver disease, medications

Front 25

What conditions would you expect the MCV to remain unaltered (normocytic)?

Back 25

Acute blood loss, anaemia of chronic disease, chronic renal failure, endocrine (hypothyroidism/hypopituitarism)

Front 26

In what conditions would you expect the various WBC counts to increase?

Back 26

Infections, tissue necrosis, allergic disorders, some forms of malignancy, autoimmune diseases, chronic infections

Front 27

What happens to size, shape and pallor of RBC in iron deficiency anaemia?

Back 27

-Shape becomes altered (get pencil, target cells)
-Size decreases (microcytic) due to lack of Hb
-Pallor increased (hypochromic) due to lack of Hb also

Front 28

What happens to MCV and MCH in iron deficiency anaemia?

Back 28

-MCV decreases due to less Hb and decreased size
-MCH will also decrease as iron needed to create Hb

Front 29

What are the defining characteristics of Macrocytic anaemia?

Back 29

-RBC with increase MCV
-Due to primary DNA failure resulting in restriction of cell division of progenitor

Front 30

What conditions may give rise to macrocytic anaemia?

Back 30

-Megaloblastic anaemias; B12 and folate deficiencies
-Bone marrow disorders
-Reticulocytosis
-Alcohol abuse
-Liver disease
-Medications
-All of which result in defective DNA synthesis

Front 31

What are the intrinsic causes of heamolysis?

Back 31

-Usually hereditary
-Membrane defects
-RBC ezyme defect
-Haemoglobinopathies

Front 32

What are the acquired causes of haemolysis?

Back 32

-Environmental causes
-Immune mediated
-Microangiopathic (anaemia caused by factors in small blood vessels)

Front 33

What would you expect to see in bone marrow in patients with Haemolytic anaemia?

Back 33

Increased proginetors of RBC

Front 34

What would you expect to see in peripheral blood in patients with Haemolytic anaemia?

Back 34

-Increased reticulocyte count
-Increased uncongugated billirubin
-Increased lactate dehydrogenase
-Decreased haptoglobin
-Increased urobilinogen

Front 35

What are spherocytes?

Back 35

-RBCs that have assumed a spheroidal shape due to loss of membrane proteins
-This produced membrane instability and disconnection with cytoskeletal elements that lead te cell to take the shape with the smallest surfface area, a sphere

Front 36

How do you differentiate between an RBC and spherocyte under the microscope?

Back 36

Spherocytes appear smaller in diameter and have lost their central pallow and therefore have a dense uniform colour

Front 37

What causes spherocytosis?

Back 37

-Hereditary spherocytosis and autoimmune haemolytic anaemia

Front 38

What features in a slide would indicate a patient has suffered from acute blood loss?

Back 38

-Normal RBC size
-Decreased RCC
-Increased plasma volume
-Increased neutrophils
-Increased platelets
-2-3days increase in reticulocytes
-Hb may take a week to rise

Front 39

What is a way to classify haemotological disorders? (4 different ways)

Back 39

-Cellular deficiencies; either of a single lineage or multiple lineages, depending on where on the differentiation pathway the disorder has occurred (eg anaemia, thrombocytopaenia)
-Proliferative disorders; the cells have differentiated and have relatively normal function but are proliferating out of control (eg chronic myeloproliferative leukemia, polycythaemia vera)
-Cellular (non malignant) disorders; that lead to an affect on cell function (eg thalassemia)
-Malignant disorders; defect in proliferation and differentiation and there is a loss of normal function, the extent on the latter will be dependant on where the differentiation pathway the defect has occurred (eg AML, ALL, lyeloma, lymphoma)

Front 40

What is aplastic anaemia?

Back 40

Pancytopaenia resulting from aplasia of bone marrow (aplasia being failure of normal cell generation and development in bone marrow)

Front 41

What changes in WCC, Hb and platelet count would you expect in aplastic anaemia?

Back 41

-Leukopenia (selective fall of granulocytes, neutrophils appear normal)
- Thrombocytopaenia
-Normocytic/normochromic cells (occasionally macrocytic)

Front 42

What conditions would a patient with aplastic anaemia be predisposed to?

Back 42

-Infections, bruising, bleeding etc
-Any condition as a result of low cells of all types

Front 43

Are cells in aplastic anaemia morphologically normal?

Back 43

Yes, normal production but due to fatty build up in bone marrow there is a shortage of production

Front 44

What is myelodysplasia?

Back 44

-Condition where bone marrow is unable to produce adequate RBC, WBC or platelets

Front 45

What is the difference between aplastic anaemia and myelodysplasia?

Back 45

In myelodysplasia there is not a shortage of HSC like in aplastic anaemia but the stem cells are defective and do not mature normally leading to defective end stage cells

Front 46

Define leukaemia?

Back 46

An accumulation of malignant white cells in the bone marrow or blood displacing normal haematopoiesis

Front 47

Which lineages do leukaemias affect?

Back 47

Myeloid or lymphoid lineages

Front 48

What conditions would leukemic patients be pront to and what would be the common complications that arise?

Back 48

-Lack of functional WBC leaves patient prone to infections
-Mass of leaukemic cells in the marrow can also crowd out other cell lineages causing dysfunction of other cells

Front 49

What is acute leukaemia?

Back 49

Agressive cancers in which the malignant transformation has occurred in the haemopoietic stem cell or early progenitors

Front 50

How do leukaemia cells differ to normal healthy cells?

Back 50

-Increased rate of proliferations
-Decreased rate of differentiation
-Decreased apoptosis

Front 51

How does chronic myeloid leukemia differ from other leukemia?

Back 51

-myeloproliferative disorder at all stages of differentiation particularly in the latter maturational stages

Front 52

How are lymphomas diagnosed as either B or T cell lymphomas?

Back 52

Lymph node biopsy

Front 53

When cell is affected in chronic lymphocytic leukaemia (CLL)?

Back 53

Mature B cells with weak surface expression of IgM or IgD accumulate in the peripheral blood, bone marrow and lymphoid organs as a result of prolonged life span with limited apoptosis

Front 54

What are the blood groups?

Back 54

A, B, O

Front 55

How does the body develop antigen to certain blood types?

Back 55

After birth an infant gut becomes colonised with normal flora which express these A-like and b-like antigens causing the immune system to make antibodies to those antigens that the red cells do not possess (eg people who are blood type A will have anti-b antibodies, blood type O will have both anti A and anti B and blood type AB will have neither)

Front 56

What is the rhesus system in blood grouping?

Back 56

-The term negative or positive refer to either the presence or absence of the RhD antigen

Front 57

What is important when working out who you can receive blood from?

Back 57

Antibodies that are important as these will recognise foreign antigen on donated red blood cells and destroy them

Front 58

What is important when working out who you can donate blood to?

Back 58

Antigens present on your red blood cells and the antibodies that are present in the recipients blood

Front 59

What blood types can donate to other blood types?

Back 59

-O+ can donate to O+,A+,B+,AB+
-O- can donate to All
-A+ can donate to A+, AB+
-A- can donate to A+, A-,AB+,AB-
-B+ can donate to B+ and AB+
-B- can donate to B-,B+, AB-, AB+
-AB+ can donate to AB+
-AB- can donate to AB- and AB+

Front 60

What blood types can receive blood from other blood types?

Back 60

-O+ can receive from O+ O-
-O- can receive from O-
-A+ can receive from O-,O+,A-,A+
-A- can receive from O-,A-
-B+ can receive from O-, O+, B-, B+
-B- can receive from O-, B-
-AB+ can receive from All
-AB- can receive from O-, A-, B-, AB-