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MEH A > Session 5 Lecture 1 > Flashcards

Session 5 Lecture 1 Flashcards

1
Q

Where are RBC, platelets and most WBC produced?

A

Bone marrow

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2
Q

Compare the amount of active bone marrow in an adult compared to an infant?

A

Infant has more active bone marrow

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3
Q

Where are the main locations of active bone marrow in an adult?

A

Pelvis, sternum, skull, ribs and vertebrae

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4
Q

What is a trephine biopsy?

A

Bone marrow taken from the left posterior iliac crest

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5
Q

What drives more RBCs to be made?

A

Erythropoietin

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6
Q

What drives more platelets to be made?

A

Thrombopoietin

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7
Q

What does RES stand for?

A

Reticuloendothelial system

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8
Q

What is the function of the RES?

A

To break down old and senescent blood cells

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9
Q

What makes up the RES?

A

Network in blood and tissues which is part of the immune system containing phagocytic cells: monocytes, macrophages etc

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10
Q

What are the main organs involved in the RES?

A

Spleen and liver

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11
Q

What does MCV stand for?

A

Mean cell volume

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12
Q

What does MCV show?

A

The size of the red blood cells

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13
Q

What does a low MCV indicate?

A

Small RBC

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14
Q

What is the main function of red blood cells?

A

Deliver oxygen to tissues

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15
Q

List other functions of red blood cells

A

Carry haemoglobin, maintain haemoglobin in its reduced (ferrous state), generate energy (ATP) and maintain osmotic equilibrium

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16
Q

Describe the shape of RBC?

A

Flexible biconcave disc

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17
Q

What is special about the membrane of a RBC?

A

It is well developed and is a lipid bilayer. Allows flexibility

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18
Q

What is the advantage of a RBC being flexible?

A

Facilitates passage through the microcirculation

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19
Q

What is spherocytosis?

A

Autohaemolytic anaemia that is characterised by the production of spherocytes. Red blood cells are sphere shaped rather than biconcave

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20
Q

What is the structure of haemoglobin?

A

Tetramer of 2 pairs of globin chains each with its own haem group

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21
Q

What is the structure of adult haemoglobin?

A

alpha and beta chains

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22
Q

On which chromosome do the globin genes cluster on?

A

Chromosome 11 and 16

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23
Q

When do you switch from foetal haemoglobin to adult haemoglobin?

A

3-6 months of age

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24
Q

Why is an oxygen dissociation curve sigmoid shape?

A

It is hardest for the first molecule of oxygen to bind but gets easier for consequent oxygens to bind

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25
Q

How is haemoglobin broken down?

A

Broken down into haem and globin.

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26
Q

What happens to the globin once broken down from haemoglobin?

A

It is protein therefore broken down into its amino acids and then recycled.

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27
Q

What happens to the haem once it has been broken down from haemoglobin?

A

Excreted and converted to biliverdin, then to bilirubin.

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28
Q

What happens to the bilirubin?

A

Intestinal bacteria convert bilirubin to urobilogens. Some of which is absorbed by intestinal cells and transported to the kidney and excreted itch urine. Other travels down the digestive tract and is converted to sterobilin.

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29
Q

When is erythropoietin production increased?

A

Reduce pO2 detected in interstitial peritublar cells in kidney

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30
Q

What is the function of erythropoietin?

A

Stimulates maturation and release of red cels from marrow

31
Q

What are the two main metabolic pathways of red cells?

A
  • Glycolysis

- Pentose Phosphate Pathway

32
Q

What are the different stored forms of iron?

A

Ferritin and Haemosiderin

33
Q

What are the functional forms/available forms of iron?

A

Haemoglobin, myoglobin, tissue iron and transported serum iron.

34
Q

What are the different types of iron?

A

Haem iron and non haem iron

35
Q

What is haem iron?

A

Better source of iron. Come from meat. Iron is in the desired ferrous form

36
Q

What is non-haem iron?

A

This is from pulses and beans. It is in the ferric form therefore needs to be converted to the ferrous form first.

37
Q

What happens to ferrous iron when it is in the enterocyte?

A

Can either be stored as ferritin or transported into the blood stream

38
Q

How is iron exported out of the cell?

A

Ferroportin

39
Q

What is lactoferrin?

A

The primary source of iron in infants

40
Q

How is iron taken into cells eg RBC?

A

By binding of iron-transferrin complex to transferrin receptor (TfR)

41
Q

Which cells contain the highest amount of transferrin receptors?

A

Erythroid cells

42
Q

What helps the absorption of non-haem iron?

A

Vitamin C

43
Q

What inhibits the absorption of iron?

A

Tea, chapatis and antacids

44
Q

Give an example of a negative regulator of iron absorption?

A

Hepcidin

45
Q

How does hepcidin work?

A

Binds to ferroportin and stops it from working so iron can’t leave cell

46
Q

What is the central regulator of iron metabolism?

A

Hepcidin

47
Q

When is the synthesis of hepcidin increased?

A

Iron overload

48
Q

What are the possible reasons for iron deficiency?

A

Insufficient intake or increased use age

49
Q

Give a physiological reason why you may have an increased use age of iron?

A

Pregnancy

50
Q

Give a pathological reason why there might be an increased useage of iron?

A

Increased bleeding

51
Q

What are the physiological effects of anaemia?

A

Tiredness, reduced oxygen carrying capacity (pallor, reduced exercise tolerance) and cardiac symptoms eg angina

52
Q

What are the signs of anaemia?

A

Pallor, tachycardia, increase respiratory rate and epithelial changes (angular stomatitis and spooning of nails)

53
Q

Define hypochromic?

A

Low haemoglobin content

54
Q

Define microcytic

A

Small RBC-low mean cell volume (MCV)

55
Q

Define anisopoikilocytosis

A

Medical condition illustrated by a variance in size (anisocytosis) and shape (poikilocytosis) of a red blood cell.

56
Q

What is used to test for iron deficiency?

A

Ferritin

reduced levels definitely indicate iron deficiency

57
Q

What is a reticulocyte?

A

An immature red blood cells without a nucleus

58
Q

Which test is recommended by NICE for identifying functional iron deficiency?

A

CHR - reticulocyte haemoglobin content

59
Q

Why is CHR better to use than ferritin?

A

CHR is not an acute phase protein therefore remains low during inflammatory response

60
Q

What is the disadvantage of using CHR?

A

It is also low in patient with thalasaemia so can’t be used in this setting

61
Q

What is the treatment of iron deficiency?

A

Dietary advice, oral iron supplements, intramuscular iron injections, IV iron or transfusion

62
Q

When would you give a patient IV iron?

A

If they can’t tolerate oral iron

63
Q

When is transfusion given to patient?

A

Not given unless there is severe anaemia with imminent cardiac compromise

64
Q

Why is iron excess dangerous?

A

We have no mechanism of excreting it.

65
Q

What is haemochromatosis?

A

Disorder or iron excess resulting in end organ damage due to iron deposition

66
Q

Where is the excess iron usually deposited?

A

Liver, pancreas, sexual organs

67
Q

What can haemochromatosis cause?

A

Liver cirrhosis, diabetes mellitus, hypogonadism, cardiomyopathy, arthropathy and skin pigmentation

68
Q

What are the different types of haemochromatosis?

A

Hereditary haemochromatosis

Transfusion associated haemosiderosis

69
Q

How is heriditary haemochromatosis inherited?

A

Autosomal recessive

70
Q

What gene is responsible for hereditary haemochromatosis?

A

Mutation in a gene designated HFE on chromosome

71
Q

What pathology is associated with hereditary haemochromatosis?

A

Normal HFE protein competes with transferrin for binding to the transferrin receptor. Mutated HFE cant bind hence transferrin has no competition. Too much iron enters cells.

72
Q

How do you treat a patient with heriditary haemochromatosis?

A

Venesection

73
Q

What is the function of iron chelating agents?

A

Slow down the accumulation of iron rather than stopping it

MEH A (19 decks)

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