Basics Flashcards

1
Q

What are some of the possible causes of low cell count?

A

Blood loss

Haemolytic anaemia

Bone marrow abnormalities

Chronic disease

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2
Q

What are some of the causes of high cell count?

A

Infection

Malignancy

Steroids

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3
Q

What terms are used to describe excess in haematology?

A

Cytosis or philia

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4
Q

What term is used to describe shortage in haematology?

A

Penia

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5
Q

Where does haematopoiesis occur in the embryo?

A

Yolk sac, then liver, then marrow

Spleen in the 3rd - 7th months

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6
Q

In an adult, where is the common site for bone marrow aspiration and biopsy?

A

Posterior iliac crests

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7
Q

What happens to the nucleus as red blood cells mature?

A

As the cell matures it loses its nucleus, once it leaves the bone marrow into the circulation it leaves the nucleus behind

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8
Q

Which granulocyte is a polymorph with a segmented nucleus and has neutral staining granules?

A

Neutrophils

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9
Q

Which granulocytes is usually bi-lobed and has bright orange/ red granules?

A

Eosinophils

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10
Q

Which granulocytes has large deep purple granules which obscure the nucleus?

A

Basophils

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11
Q

Which type of granulocyte is a circulating version of a tissue mast cell and mediates hypersensitivity reactions? This cell type has Fc receptors which bind IgE and granules which contain histamine.

A

Basophils

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12
Q

Which cell type circulates for a week before entering tissues to become macrophages?

A

Monocytes

These phagocytose invaders and attract other cells

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13
Q

Which cell type cognates responses to infection and ccan thus be considered the ‘brains’ of the immune system?

A

Lymphocytes

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14
Q

What is Hb called when it is oxidised with Fe3+?

A

Methaemoglobin

Can’t carry oxygen in this state

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15
Q

What does the RBC do for energy production?

A

Relies on glycolysis for energy production as it has no mitochondria

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16
Q

Why do red blood cells have a limited lifespan?

A

They have no nucleus so can’t divide or replace damage

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17
Q

What happens to the levels of erythropoietin in hypoxia?

A

Erythropoietin levels rise in hypoxia

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18
Q

How is hypoxia sensed and what happens as a consequence?

A

Interstitial fibroblasts in the kidneys detect hypoxia in the blood flowing through the kidneys

This results in increased production of erythropoietin

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19
Q

How does an increase in levels of erythropoietin levels in conditions of hypoxia act to increase red blood cell production?

A

Erythropoietin stimulates cell division red cell precursors and recruits more cells to the marrow

The result is erythroid hyperplasia (more machinery to produce RBCs)

20
Q

What are red blood cells called for the first few days after production?

A

Reticulocytes

21
Q

Worn out red blood cells are recycled into raw materials. What are these raw materials?

A

Iron, amino acids, bilirubin

22
Q

Where does red cell destruction usually occur?

A

Spleen

23
Q

How are aged red blood cells taken out of the circulation?

A

They are taken up by macrophages

24
Q

Describe how red blood cell contents are removed/ recycled

A

Globing chains are made into amino acid

Heme is broken down into iron and bilirubin

Bilirubin is taken to the liver, conjugated and then excreted in bile

25
Q

At the same p02, do HbF and myoglobin bind more or less oxygen than normal Hb?

A

At the same p02, both HbF and myoglobin can bind more 02

26
Q

What happens to the levels of 2,3 DPG in chronic anaemia?

A

2,3 DPG is increased in chronic anaemia

27
Q

How is most carbon dioxide transported?

A

Most carbon dioxide is transported as bicarbonate (60%)

10% is dissolved in solution
30% is bound directly to Hb as carbamino Hb

28
Q

Reactive oxygen species such as hydrogen peroxide are free radicals which have unpaired free electrons and can damage haemoglobin. How does glutathione counteract this?

A

Glutathione reacts with hydrogen peroxide to form water and oxidised glutathione product GSSG

29
Q

What does the Rapapoport Lubering shunt do?

A

Generates 2,3 DPG that shifts the oxygen dissociation curve to the right and allows more oxygen to be released

30
Q

What does the Embden-Myerhof pathway do?

A

Anaerobic glycolysis pathway

Reverses Fe3+ to Fe2+

31
Q

How much iron is absorbed and lost per day?

A

1mg absorbed and 1mg lost

32
Q

Where does iron absorption mainly occur?

A

In the duodenum

33
Q

What things enhance or inhibit iron absorption?

A

Enhance iron absorption;

  • Ascorbic acid
  • Alcohol

Inhibit iron absorption;

  • Tannins (e.g tea)
  • PPIs
34
Q

What is the role of ferroportin?

A

Facilitates iron export from cells

Iron is then passed on to transferrin to be transported elsewhere

35
Q

What is the role of DMT (divalent metal transporter)?

A

Transports ferrous iron into the duodenal enterocyte

36
Q

What is the role of duodenal cytochrome B?

A

Reduces ferric iron (Fe3+) to ferrous form (Fe2+)

37
Q

What is the role of hepcidin?

A

It is the major negative regulator of iron uptake

It binds to ferroportin and causes its degradation

Produced in the liver in response to iron load and inflammation

38
Q

Different tests can be done to assess iron status. What is used to measure functional iron?

A

Haemoglobin concentration

39
Q

Different tests can be done to assess iron status. What is used to measure transport iron (iron supply to tissues)?

A

Transferrin saturation (saturation is normally 20-50%)

40
Q

Different tests can be done to assess iron status. What is used to measure storage iron?

A

Serum ferritin

41
Q

What is hereditary haemochromatosis?

A

An inherited condition involving decreased synthesis of hepcidin and thus iron loading

42
Q

Hereditary haemochromatosis can be caused by several different mutations but what is the most common?

A

Mutations in the HFE gene

43
Q

What would be the expected results of transferrin saturation and serum ferritin measurement in hereditary haemochromatosis?

A

Transferrin saturation >50%

Serum ferritin >300ug in men/ 200ug in women

44
Q

How is hereditary haemochromatosis managed?

A

Weekly venesection

Family screening

45
Q

Venesection is not a suitable treatment option for patients with secondary iron overload if they are already anaemic. What other management options can be considered?

A

Iron chelating agents - deferrioxamine- subcutaneous or IV

Deferiprone/ deferasirox - oral gents