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MEH A > Session 5 Lecture 1 > Flashcards

Session 5 Lecture 1 Flashcards

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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
How is haemoglobin broken down?
Broken down into haem and globin.
26
What happens to the globin once broken down from haemoglobin?
It is protein therefore broken down into its amino acids and then recycled.
27
What happens to the haem once it has been broken down from haemoglobin?
Excreted and converted to biliverdin, then to bilirubin.
28
What happens to the bilirubin?
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.
29
When is erythropoietin production increased?
Reduce pO2 detected in interstitial peritublar cells in kidney
30
What is the function of erythropoietin?
Stimulates maturation and release of red cels from marrow
31
What are the two main metabolic pathways of red cells?
- Glycolysis | - Pentose Phosphate Pathway
32
What are the different stored forms of iron?
Ferritin and Haemosiderin
33
What are the functional forms/available forms of iron?
Haemoglobin, myoglobin, tissue iron and transported serum iron.
34
What are the different types of iron?
Haem iron and non haem iron
35
What is haem iron?
Better source of iron. Come from meat. Iron is in the desired ferrous form
36
What is non-haem iron?
This is from pulses and beans. It is in the ferric form therefore needs to be converted to the ferrous form first.
37
What happens to ferrous iron when it is in the enterocyte?
Can either be stored as ferritin or transported into the blood stream
38
How is iron exported out of the cell?
Ferroportin
39
What is lactoferrin?
The primary source of iron in infants
40
How is iron taken into cells eg RBC?
By binding of iron-transferrin complex to transferrin receptor (TfR)
41
Which cells contain the highest amount of transferrin receptors?
Erythroid cells
42
What helps the absorption of non-haem iron?
Vitamin C
43
What inhibits the absorption of iron?
Tea, chapatis and antacids
44
Give an example of a negative regulator of iron absorption?
Hepcidin
45
How does hepcidin work?
Binds to ferroportin and stops it from working so iron can't leave cell
46
What is the central regulator of iron metabolism?
Hepcidin
47
When is the synthesis of hepcidin increased?
Iron overload
48
What are the possible reasons for iron deficiency?
Insufficient intake or increased use age
49
Give a physiological reason why you may have an increased use age of iron?
Pregnancy
50
Give a pathological reason why there might be an increased useage of iron?
Increased bleeding
51
What are the physiological effects of anaemia?
Tiredness, reduced oxygen carrying capacity (pallor, reduced exercise tolerance) and cardiac symptoms eg angina
52
What are the signs of anaemia?
Pallor, tachycardia, increase respiratory rate and epithelial changes (angular stomatitis and spooning of nails)
53
Define hypochromic?
Low haemoglobin content
54
Define microcytic
Small RBC-low mean cell volume (MCV)
55
Define anisopoikilocytosis
Medical condition illustrated by a variance in size (anisocytosis) and shape (poikilocytosis) of a red blood cell.
56
What is used to test for iron deficiency?
Ferritin | reduced levels definitely indicate iron deficiency
57
What is a reticulocyte?
An immature red blood cells without a nucleus
58
Which test is recommended by NICE for identifying functional iron deficiency?
CHR - reticulocyte haemoglobin content
59
Why is CHR better to use than ferritin?
CHR is not an acute phase protein therefore remains low during inflammatory response
60
What is the disadvantage of using CHR?
It is also low in patient with thalasaemia so can't be used in this setting
61
What is the treatment of iron deficiency?
Dietary advice, oral iron supplements, intramuscular iron injections, IV iron or transfusion
62
When would you give a patient IV iron?
If they can't tolerate oral iron
63
When is transfusion given to patient?
Not given unless there is severe anaemia with imminent cardiac compromise
64
Why is iron excess dangerous?
We have no mechanism of excreting it.
65
What is haemochromatosis?
Disorder or iron excess resulting in end organ damage due to iron deposition
66
Where is the excess iron usually deposited?
Liver, pancreas, sexual organs
67
What can haemochromatosis cause?
Liver cirrhosis, diabetes mellitus, hypogonadism, cardiomyopathy, arthropathy and skin pigmentation
68
What are the different types of haemochromatosis?
Hereditary haemochromatosis | Transfusion associated haemosiderosis
69
How is heriditary haemochromatosis inherited?
Autosomal recessive
70
What gene is responsible for hereditary haemochromatosis?
Mutation in a gene designated HFE on chromosome
71
What pathology is associated with hereditary haemochromatosis?
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
How do you treat a patient with heriditary haemochromatosis?
Venesection
73
What is the function of iron chelating agents?
Slow down the accumulation of iron rather than stopping it

MEH A (19 decks)

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