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Phase 1 - S2 Metabolism, Endocrinology, Haematology > Haemopoiesis > Flashcards

Haemopoiesis Flashcards

1
Q

what are produced in the bone marrow

A

RBC, platelets and WBC

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2
Q

where is bone marrow found

A

throughout the skeleton in infancy but limited to the pelvis, skull, ribs, sternum and vertebrae in adults

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3
Q

what are the 2 types of bone marrow test

A

bone marrow trephine biopsy (taking a 1-2cm core of bone marrow to look at structure) or bone marrow aspiration (taking bone marrow cells to look at finer details)

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4
Q

what type of cells do blood cells come from

A

multipotent hematopoietic cells

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5
Q

what are hematopoietic cells differeniate into

A

myeloid progenitor cells or common lymphoid progenitor cells

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6
Q

what controls haematopoiesis

A

the reduced oxygen is detected by the peritubular kidney cells which then increase their production of erythropoietin which stimulates release and maturation of RBC

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7
Q

what cells are involved in the reticuloendotheial system

A

monocytes, macrophages, kupffer cells, microglial cells

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8
Q

what do cells in the RES system do

A

identify old, abnormal blood cells and phagocytose them mainly in the spleen or liver.

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9
Q

how long do erythrocytes live for

A

120 days

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10
Q

what are the functions of erythrocytes

A
  • carry haemoglobin
  • maintain the ferrous/reduced state of haemoglobin
  • generate ATP
  • maintain osmotic pressure
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11
Q

describe the structure of RBCs

A
  • have proteins in their membranes making them flexible so can bend through capillaries
  • large SA to vol ratio
  • biconcave shape
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12
Q

which gene codes for the production of haemoglobin and where is it found

A

globin gene found on chromosomes 11 and 16

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13
Q

at what age do you switch from foetal to adult haemoglobin

A

3-6 months

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14
Q

what do the globin chains do

A
  • prevent the haem molecule from oxidation, preventing the ferric form being produced from the ferrous
  • allows variation in oxygen affinity by changing shape
  • allow solubility
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15
Q

describe the break down of haemoglobin

A

macrophage or kupffer cells break it down into globin (a protein which is then broken down into amino acids) and heme. The irons is taken from the heme to be used. the rest of the molecule is converted to bilirubin in the liver and conjugated to be excreted

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16
Q

what does an excess in bilirubin result in

A

jaundice

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17
Q

why do you get anaemia with damaged kidneys

A

cant produce erythropoietin hormone so there is a decrease in haemoglobin production

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18
Q

what are the 2 main metabolic pathways in RBC

A
  • glycolysis

- pentose phosphate pathway

19
Q

what happens if metabolism is altered in RBC

A

their membrane changes and so they break down quicker so you become anaemic

20
Q

what are the types of available iron

A
  • in haemoglobin
  • in myoglobin
  • tissue iron e.g. iron used in enzymes
  • serum/transported iron
21
Q

what are the types of stored iron

A
  • ferritin

- haemosiderin

22
Q

what happens to iron requirement in pregnancy

A

increases

23
Q

where does most of the active iron in our body come from

A

breakdown of RBC (not absorption in the gut from food)

24
Q

what is 95% of iron in the liver stored as and in what cells?
what about the remaining 5%

A
  • ferritin in hepatocytes

- the other 5% is as haemosiderin in kupffer cells

25
Q

how is iron excreted from the body

A

its not excreted - only small amounts are lost each day by the loss of skin, hair and gut cells

26
Q

how much iron enters and leaves the body in a day

A

1-2mg

27
Q

what are the differences between haem and non-haem iron

A
  • haem is a better source of iron found in meat which enters enterocytes (cells lining intestines) as Fe 2+ (ferrous)
  • non-haem is found in pulses and grains and exists as Fe3+ (ferric)
28
Q

what happens to non-haem iron in order to be taken up by enterocytes

A

stomach acid converts it into ferrous which then binds to transferrin which allows it to be taken up by the enterocytes in the duodenum and upper jejunum. can then be stored in the liver as ferritin or transported in the blood for use

29
Q

what exports iron out of the cells

A

ferroportin

30
Q

what is lactoferrin

A

primary iron source in infants

31
Q

how is iron taken into cells such as RBCs

A

binding of iron transferrin complex to a transferrin receptor

32
Q

what cells contain the highest number of transferrin receptors

A

RBCs

33
Q

what controls iron absorption

A
  • levels are sensed by villi of enterocytes
  • can regulate transporters
  • control transferrin and HFE receptor expression
  • cytokines
34
Q

outline the role of hepcidin

A

it is a negative regulator of iron absorption which works by binding to ferroportin and so stops iron leaving enterocytes or macrophages giving a build up of non-functional iron

35
Q

what does an iron deficiency result from

A
  • insufficient intake

- increased use

36
Q

what are the signs and symptoms of an iron deficiency

A
  • tiredness
  • reduced oxygen carrying capacity
  • cardiac symptoms
  • tachycardia
  • increased respiratory rate
  • epithelia changes (shiny tongue and spooning of nails)
37
Q

what is hypochromic iron deficiency

A

low haemoglobin content

38
Q

what is a microcytic iron deficiency

A

small RBCs as the cells will carry on dividing

39
Q

what is anisopoikilocytosis

A

change in size and shape of RBC

40
Q

how can you test for an iron deficiency

A
  • ferritin test (but this is an acute phase protein so will increase in infection)
  • Recticulocyte haemoglobin content - CHR (this is low in thalasaemias)
41
Q

what are the treatments to an iron deficiency

A
  • dietary advice
  • oral supplements
  • intramuscular injections
  • intravenous
  • transfusion (but only in severe anaemia)
42
Q

why is excess iron dangerous

A

it can produce highly reactive hydroxyl and lipid radicals which damage lipid membranes, nucleic acids and proteins. the excess iron is deposited in tissues

43
Q

what is haemochromatosis

A
  • iron excess resulting in organ damage due to deposition
  • can causes liver cirrhosis, diabetes, cardiomyopathy
  • can be hereditary or transfusion associated
44
Q

what is hereditary haemochromatosis

A

an autosomal recessive disease due to mutation on the HFE gene
HFE normally competes with transferrin for binding to the transferrin receptor so without there is no competition so too much iron enters cells. treated with venesection

Phase 1 - S2 Metabolism, Endocrinology, Haematology (22 decks)

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