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MCD Y2 > Haem > Flashcards

Haem Flashcards

1
Q

What can a multipotent stem cell in the bone marrow become?

A

A myeloid or a lymphoid stem cell.
A myeloid stem cell can become a red cell, a granulocyte, a monocyte or platelets (/megakaryocytes).
A lymphoid stem cell can become any type of lymphocyte.

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2
Q

Explain the pattern of differentiation from a multipotent stem cell to an erythrocyte.

A

Multipotent stem cell becomes proeryhtocyte.
Proeryhtorcyte divides 3 times before this cell eventually squeezes out its cytoplasm into the sinusoid, leaving the nucleus behind. The nucleus then gets digested by a macrophage, and the cytoplasm becomes the erythrocyte.

This process is called erythropoiesis.

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3
Q

What are two physiological conditions that stimulate erythropoietin production?

A

Hypoxia and anaemia.

As these are two states where the body’s haemoglobin is insufficient.

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4
Q

Where is erythropoietin produced?

A

In the juxtatubular interstitial cells of the kidney (90%) or in the hepatocytes/interstitial cells in the liver (10%).

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5
Q

Recall the intravascular life span of red cells.

A

120 days

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6
Q

White cells: explain the origin and function of white cells and recall their intravascular life span, including neutrophils, monocytes, eosinophils and lymphocytes

A

Granulocyte maturation can become one of these:
Myeloblast divides and starts forming primary granules. It divides 4 times, and then undergoes conformational change and becomes a neutrophil. Neutrophils survive for only 7-10 hours in the circulation, before migrating to tissues. Main function is defense against infections.
Eosinophil spends even shorter time in circulation. Play important role in allergic responses.
Monocytes spend several days in the circulation. They become macrophages in tissues and act as scavengers. Macrophages also store and release iron.
Lymphocytes re-circulate the circulation, have variable life span.

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7
Q

Platelets: explain the origin and function of platelets and recall their intravascular life span

A

Haemapoietic stem cell gives rise to megakaryocytes which gives rise to platelets.
Platelets have role in primary haemostasis.
Survive about 10 days in circulation.

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8
Q

What are the terms for:

  • red cells showing abnormal variation in size (between smallest and largest cells)
  • red cells showing abnormal variation in shape
A

Size: Anisocytosis
Shape: Poikilocytosis

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9
Q

Explain the terms:
Hypochromia
Hyperchromia

A

Hypochromia: central pallor is larger than normal, lack of haemoglobin
Hyperchromia: central pallor is smaller than normal,

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10
Q

What are the two types of hyperchromia?

A

spherocytes and irregularly contracted cells

Spherocytes: lack of central pallor. result from loss in membrane without proportional loss in cytoplasm. Membrane becomes untethered from cytoskeleton.

Irregularly contracted cells: usually result from oxidant damage.

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11
Q

What does polychromasia indicate?

A

That the cell is young.
The younger a cell is the bluer it is.
A deep blue shade usually indicates a cell has been pushed out of the bone marrow prematurely.

Another way to identify young cells is through a reticulocyte stain.

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12
Q

Can you name some different types of poikilocytes?

A 
Spherocytes
Target cells
Sickle cells
Elliptical cells
Fragments of red cells
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13
Q

What causes erythrocytes to take on a target cell-like appearance?

A

Target cell = accumulation of haemoglobin in centre of central pallor
Obstructive jaundice, liver disease, haemoglobinopathies and hyposplenism

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14
Q

What is the difference between rouleaux and agglutinates? What’s the cause of both of them?

A 
Rouleaux = "stack" of cells. Result from plasma protein alterations.
Agglutinates = clump of cells. Results from antibodies on surface of erythrocytes.
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15
Q

What do we call a remnant of a nucleus in an erythrocyte? What does the presence of this say about a patient?

A

A Howell-Jolly body.
These are normally removed by the spleen, so if these are present something might be wrong with the patient’s spleen or the patient might have had a splenectomy.

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16
Q

What do we refer to be the term ‘left shift’?

A

That there’s been a left-shift in the chronological order of cell development for a lymphocyte. This means unsegmented lymphocytes are increasingly present in the blood or myelocytes /promyelocytes are present in peripheral blood.

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17
Q

What would be another term to describe hypersegmented neutrophil?

A

‘Right shift’.

Abnormally high number of segmentations of the nucleus. Usually results from lack of Vitamin B12 or folic acid.

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18
Q

Define the terms ‘reference range’ and ‘normal range’.

A

A reference range is a range derived from a healthy population. It needs to be defined however, e.g. “reference range for healthy males aged 50-65”
A normal range includes 96% of the population.

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19
Q

what are the blood parameters you should learn to check first?

A

WBC
MCV
Platelets
Haemoglobin

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20
Q

What happens to the MCHC of a spherocyte?

A

Tends to increase as the area of low haemoglobin, the central pallor, is reduced.

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21
Q

What is a reduced white cell count usually to do with?

A

A reduced neutrophil count, as they are the most numerous white cells in the blood.

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22
Q

What is polycythaemia? What is pseudopolycythaemia?

A

too many red blood cells in the circulation.

Pseudopolycythaemia, rather than true polycythaemia, refers to a reduction in blood plasma.

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23
Q

Define anaemia

A

A reduction in the amount of haemoglobin in a given volume of blood below what would be expected in comparison with a healthy subject of the same age and gender.
RBC and Hct are often reduced as well.

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24
Q

Outline the main mechanisms of anaemia.

A

Loss of blood.
Loss of production of RBC.
Reduced survival of RBC.
Pooling of RBC in the spleen.

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25
Q

What are the two major MECHANISMS of macrocytic anaemia?

A

Macrocytic erythropoiesis - delayed maturation of nucleus, so cytoplasm continues to expand whilst cell isn’t dividing appropriately.
Premature release of young blood cells - as young red blood cells are about 20% bigger

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26
Q

What are the main causes of macrocytic anaemia?

A
  1. Megaloblastic anaemia – as a result of lack of vitamin B12 or Folic acid.
  2. DNA synthesis interfering drugs.
  3. Liver disease and ethanol toxicity.
  4. Recent major blood loss with adequate iron stores (reticulocyte numbers increase) – body pumps more out.
  5. Haemolytic anaemia (reticulocyte number increases) - RBCs are lysed
27
Q

What are the three ways haemolytic anaemia can be classified?

A

Inherited or acquired.
Intrinsic (cell membrane, Hb etc) or extrinsic (drugs, microorganisms etc.)
Intravascular (acute damage to RBC) or extravascular (removed by spleen)

28
Q

List major mechanisms of haemolysis and state important causes of haemolytic anaemia.

A

Sickle cell anaemia - inherited defect of haemoglobin
Hereditary spherocytosis - inherited defect of membrane (leading to premature removal of RBC by spleen)
Glucose-6-phopshate dehydrogenase deficiency - inherited defect of enzyme
Autoimmune haemolytic anaemia - autoimmune acquired defect of membrane

29
Q

When should one suspect haemolytic anaemia?

A
  • When anaemia seems to have no other cause
  • Presence of irregularly shaped cells
  • MCHC is normal
  • Evidence of increased RBC breakdown or irregular bone marrow activity.
30
Q

What are Heinz bodies?

A

In a type of G6PD deficiency, irregularly contracted RBC form round balls that we call Heinz bodies. Heinz bodies are removed by the spleen and leaves behind a cleaved cell.

31
Q

What type of anaemia is likely due to iron deficiency?

A

Microcytic anaemia.

32
Q

List dietary sources of iron.

A

We need 20 mg of iron per day, of which we get 12-15 from our diet from things like meat, fish, vegetables, whole grain and chocolate
Some iron can be recycled in the body.

33
Q

Describe the absorption of iron.

A

Iron freely absorbs into the cell, but needs help to cross from the cell to the blood, uses ferroportin for this.
Hepcidin inhibits ferroportin and therefore acts as a regulator of iron absorption.
Once absorbed into the cell, iron can either have a protein shell form around it to form ferritin, or can be transferred in blood attached to transferrin. TF (transferrin) is usually 20-40% saturated with iron. Iron exits the blood bound to TF, they bind to receptor TF-R.

34
Q

List causes of iron deficiency.

A

Major: bleeding
Minor: Increased use (pregnancy), dietary deficiency (vegan) or malabsorption (coeliac’s disease)

35
Q

Describe useful investigations in a patient who might be iron deficient.

A

If patient is male, or is female above age 40 —> full investigation
Full investigation: upper GI endoscopy, duodenal biopsy, colonoscopy

Urinary blood loss
Antibodies for coeliac’s disease

To outrule/diagnose Anaemia of Chronic Disease:
Levels of C-reactive protein –> if increased, can be Anaemia of Chronic Disease (ACD)
Higher Erythrocyte Sedimentation Rate –> ACD

36
Q

What are the expected ferritin levels and ferritin saturation levels of someone with:

a. thalassemia
b. Classic ACD
c. Classic iron deficiency

A

a. ferritin: normal
ferritin saturation: normal

b. ferritin: normal/low
ferritin saturation: normal

c. ferritin: high
ferritin saturation: low

37
Q

Explain roles of B12 and folate in haemopoiesis

A

All rapidly diving cells will be affected by deficiency in Vitamin B12 and folate.
As opposed to iron deficiency anaemia, this will lead to macrocytic anaemia.

38
Q

Explain terms macrocytic and megaloblastic

A

Macrocytic – average red cell size is increased.

Megaloblastic – a morphological change in RBC precursors within the bone marrow.

39
Q

Describe Laboratory features of megaloblastic anaemia.

A

In peripheral blood: anisocytosis, large RBCs, hypersegmented neutrophils and giant metamyelocytes

Vitamin B12 and folate blood levels

40
Q

List dietary sources & absorption of B12 and folate.

A

B12: meat, fish, vegetables, whole grain
folate: leafy greens that haven’t been overcooked

41
Q

List biochemical pathways requiring B12 and /or folate

A

Both Vit. B12 and folate are required for DNA synthesis and an absence can lead to a severe anaemia.

§ Vitamin B12 is required for:

o DNA synthesis.

o Integrity of the immune system.

§ Folic acid is required for:

o DNA synthesis.

§ To get from dUMP à dTMP (in DNA synthesis), you need a methyl group which is provided indirectly by dietary folate.

o Homocystine metabolism – look to diagram on left.

42
Q

Explain the contribution of Vit. B12 and/or folate deficiency to clinical disease.

A

Folate deficiency can lead to:

  • Megaloblastic, macrocytic anaemia.
  • Neural tube defects in developing foetuses – spina bifida, anencephaly.
  • Increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism.

Vitamin B12 deficiency can lead to:

  • Neurological problems – bilateral peripheral neuropathy, subacute combined degeneration of cord (can cause paralysis), optic atrophy and dementia.
  • Subacute combined degeneration of the cord is the scariest one à paralysis!
  • Paraesthesia.
  • Muscle weakness.
  • Difficult walking.
  • Visual impairment.
  • Psychiatric disturbance
43
Q

What is pernicious anaemia?

A

An autoimmune condition associated with a lack of Intrinic Factor (needed for Vitamin B12 absorption)

44
Q

What are the components of haemoglobin and where are they synthesised?

A

Haem + globin chains.

Haem is synthesised in mitochondrion. Iron is needed fot this (transported into cell with ferritin)

45
Q

List dietary sources of iron.

A

Meat and fish (haem iron), vegetables, whole grain cereal, chocolate

46
Q

Describe the absorption of iron.

A

20 mg of iron needed per day to make up for lost RBCs, however iron can be recycled so this makes up for part of iron needs.
Only 1 mg (for men) or 2mg (for women) needs to be ABSORBED per day.
Iron can freely be absorbed into enterocyte, but needs ferroportin to cross basal membrane. After absorption into enterocyte it can also be stored in the cell bound to ferritin.
It can exit cell using ferroportin and bind to transferrin in blood, in which case it can be transported in body.

47
Q

Explain the clinical causes and hematological features of ACD

A

ACD = Anaemia of Chronic Disease (there will be no obvious cause of the anaemia, such as haemorrhage, B12/folate deficiency)
Laboratory signs: High CRP, high ESR (erythrocyte sedimentation rate)

48
Q

What is Pancytopenia?

A

Reduction of all lineages of blood cells

49
Q

How can you differentiate a malignant from a benign haematopoiesis?

A

Only expected to see mature cells in peripheral blood

50
Q

When can you find myeloblasts, promyelocytes, myelocytes or metamyelocytes in the peripheral blood?

A

Following GCSF - cancer treatment
In sepsis - bone marrow is trying to compensate for stress by releasing myeloid precursors into blood (nucleated RBC can also be seen)
Bone marrow

51
Q

What does it mean if you can see immature white cells and nucleated red cells in the peripheral blood?

A

Leukoerythroblastic feature - means there is cancer in bone marrow
Patient is very unwell

52
Q

What can cause leukopenia?

A

B12 or folate deficiency

Autoimmune conditions

53
Q

What can cause eosinophilia?

A

Reactive:
Parasitic infestation, allergic disease (asthma, rheumatoid etc.), neoplasms (Hodgkin’s lymphoma, T-cell NHL) or hypereosinophilic syndrome

Important to establish whether it is reactive or malignant (autonomous cell growth)
Malignant can be caused by leukaemia.

54
Q

What are features of CML (Chronic Myeloid Leukemia)

A

High white cell count

White cells at every stage of white cell maturation

55
Q

What are the investigations of a raised WCC (White Cell Count)?

A
  • history (recent travel history e.g.)
  • haemoglobin
  • automated differential (no differential available can only be consequential to GCSF injection or in presence of a malignant condition)
  • examine blood film

Raised WCC can be discovered accidentally, patient can be completely asymptomatic.
Reactive lymphocytosis common in smokers.

Three steps essentially:

  1. White cells only, or all 3 lineages? (white cells/red cells/platelets)
  2. One type of white cells only, or all lineages?
  3. Mature cells only or mature and immature cells?
56
Q

What is usually associated with an isolated neutrophilia?

A

Reactive leukopenia.

57
Q

If there is an increase in all lineages, what is this usually associated with? What’s the exception?

A

Reactive pancytopenia or AML.

CML is the exception, increased basophils and eosinophils.
These two types of cells are rarely increased in an acute response.

58
Q

How fast can neutrophilia develop?

A

In minutes due to demargination (marginating pool –> circulating pool)
In hours due to early release from bone marrow
In days due to infection (increased production)

59
Q

What is associated with white granules inside neutrophils?

A

Toxic granulation. Response to infection

60
Q

Do all infections cause neutrophilia?

A

No.
Few viral infections do.
Most bacterial and fungal ones do, exceptions are
E.g. Brucella, typhoid

61
Q

What is associated with monocytosis?

A

Can be seen as part of an inflammatory process.
TB, brucella, typhoid.
Chronic myelomonocytic leukemia (MDS)

62
Q

How can immature lymphocytes be recognised in blood?

A

Lots of very large polychromatic cells, high nucleo-cytoplasmic ratio

63
Q

What are common causes of reactive lymphocytosis?

A

Smoking
Infection
Autoimmune disorders (usually lymphopenia though)

64
Q

How can you differentiate EBV (glandular fever) from leukemia?

A

EBV - only lymphocytes affected

Leukemia - some degree of anaemia and other lineages being affected is expected

MCD Y2 (1 decks)

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