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Fundamentals Of Pathology > RBCs: Production And Survival > Flashcards

RBCs: Production And Survival Flashcards

1
Q

How many RBCs are made per day?

A

10^12

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2
Q

What is the first recognisable RBC precursor in bone marrow?

A

Proerythroblast

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3
Q

What are the stages a RBC has to go through to mature (from proerythroblast to normoblast)?

A

Proerythroblast
Early erythroblast
Late erythroblast
Normoblast

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4
Q

What is the key regulator in the RBC - O2 pressure feedback loop?

A

EPO

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5
Q

How is the number of RBCs related to the ambient O2 pressure?

A

Inversely

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6
Q

How does the o2 pressure increase the o2 carrying ability of blood (5 steps)?

A 
Decreased o2 blood levels
Kidney releases EPO
EPO stimulates red marrow
Enhanced erythropoeisis increases RBC count
Increases o2 carrying ability  of blood
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7
Q

What does EPO stand for?

A

Erythropoietin

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8
Q

What does HiF do?

A

Enhances expression of iron absorbing gene

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9
Q

Give 4 sources of iron

A

Meat, eggs, vegetables, dairy foods

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10
Q

How much iron does a normal western diet provide daily?

A

15mg

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11
Q

Where is the iron form a western diet absorbed?

A

5-10% in duodenum and jejunum

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12
Q

What helps the absorption of iron?

A

HCL and ascorbic acid

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13
Q

What regulates iron absorption?

A

DMT-7 and ferroportin

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14
Q

What are the three causes of iron deficiency?

A

Decreased uptake
Increased demand
Increased loss

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15
Q

What causes decreased uptake of iron?

A

Inadequate intake or malabsorption

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16
Q

What causes increased demand of iron in the body?

A

Pregnancy or growth spurt

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17
Q

What causes increased loss of iron in the body?

A

GI bleed or excess loss in periods

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18
Q

What are the other (not iron) haematinics?

A

Vitamin B12 and folic acid

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19
Q

What processes are vitamin B12 and folic acid needed for (3)?

A

RBC maturation, DNA synthesis and formation of thymidine triphosphate

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20
Q

What does a deficiency in vitamin B12 and folic acid lead to?

A

A failure of nuclear maturation

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21
Q

What are the 3 causes of vitamin B12 deficiency?

A

Inadequate intake
Absorption defect
IF deficiency

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22
Q

What group of people are likely to inadequately intake vitamin B12?

A

Vegans

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23
Q

What are symptoms of tropical sprue?

A

Altered small bowel muscosa, chronic diarrhoea and all signs/symptoms of multiple vitamin and nutrient deficiencies

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24
Q

What is pernicious anaemia?

A

Most common cause of B12 deficiency

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25
Q

What causes pernicious anaemia?

A

Autoimmune gastric atrophy, which leads to the loss of an intrinsic factor production needed for absorption of B12

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26
Q

What are the four causes of folate deficiency?

A

Inadequate intake
Absorption defect
Increased demand/losses
Drugs

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27
Q

What causes inadequate intake of folate?

A

Poor nutrition

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28
Q

What are some folate absorption defects called?

A

Coeliac
Crohns
Tropical sprue

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29
Q

What causes increased demand/ losses of folate?

A

Pregnancy
Haemolytic
Cancer

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30
Q

What type of drugs cause a vitamin folate deficiency?

A

Anticonvulsant

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31
Q

What happens (on a cellular level) in folate and B12 deficiencies (5)?

A 
Oval macrocytes 
Reduced WBC and platelet count
Megoblast change in bone marrow
Hypersegmented neutrophils
B12 only- demyelination of CNS
32
Q

What causes renal dx?

A

Ineffective erythropoeisis

33
Q

What causes a reduction in bone marrow erythroid cells?

A

Aplastic anaemia or marrow infiltration by leukaemia or other malignancies

34
Q

How long do RBCs circulate for?

A

Approx 120 days

35
Q

What are the two processes by which RBCs are destroyed?

A

senescence and random haemolysis

36
Q

What is random haemolysis?

A

Process that destroys interact RBCs or portions of them independent of their age

37
Q

What does the ability of a RBC to survive depend on?

A

Cytoplasmic enzymes involved in metabolic pathways

38
Q

What sorts of enzyme defects cause the most significant metabolic reaction problems?

A

Concentration and activites of the enzymes catalysing the necessary reactions are essential for overall survival of the erythrocyte

39
Q

What parts of the RBC do the metabolism pathways protect (and what do they protect it from)?

A

Hb molecule, membrane lipids and structural proteins

From oxidative stress

40
Q

What is the red cells metabolism pathways main job (4)?

A

Maintaining osmotic balance, produce the necessary cofactors, electro neutrality and fighting oxidative stress

41
Q

What is another name for the embden-meyerhof pathway?

A

Glycolytic pathway

42
Q

What is the embdem-meyerhofs main job?

A

To generate ATP

43
Q

Why is it important that red blood cells generate ATP?

A
  • Maintain RBC shape and deformability

- Regulates intracellular cation conc via cation pumps

44
Q

What pathway is PK a disorder of?

A

Glycolytic

45
Q

What is PK?

A

Autosomal recessive disorder with >100 mutations documented

46
Q

What does PK cause?

A

Low intracellular ATP generation, which means cells lose large amounts of K and H2O, becoming dehydrated and rigid

Causes chronic non-spherocytic haemolytic anaemia

47
Q

What happens when there’s a block in glycolysis in a RBC?

A

build up of 2,3 biphosphate, which shifts the oxygen dissociation curve to the right

48
Q

What do defects in band 3, spectrin, ankyrin or protein 4.2 lead to?

A

Destabilisation of the overlying lipid bilayer and release of lipid into microvesicles

49
Q

What is HS?

A

Deficiency in ankyrin spectrin

50
Q

What is HE?

A

Mutant spectrin, leasing to spectrin-ankyrin association.

51
Q

What causes HE?

A

Protein 4.1 deficiency

52
Q

What happens in the luebering rapaport shunt?

A

2,3 DPG binds to deoxyhaemoglobin to stabilise at lower o2 affinity state

53
Q

How much of the RBC glucose is metabolised through the hexose monophosphate shunt?

54
Q

What does NADPH stand for?

A

Nicotinic adenine dinucleotide phosphate

55
Q

What is NADPH’s role?

A

Protecting the RBC from oxidative damage

56
Q

What is another name for the pentose phosphate pathway?

A

Hexose monophosphate shunt

57
Q

What does G6PD do in the pentose phosphate pathway?

A

Catalysed first step in the pathway which is needed for producing NADPH

58
Q

What causes G6PD deficiency?

59
Q

What do people with a G6PD deficiency need to avoid?

A

Specific oxidative drugs

60
Q

What does a G6PD deficiency cause?

A

Acute haemolysis on exposure to oxidant stress, oxidative drugs, fava beans or infections

61
Q

What does NADH do in the RBC?

A

Reduced cytochrome b5 which reduces oxidised ferric ion of haemoglobin

62
Q

What would happen if NADH wasn’t present in RBC?

A

Without the reaction haem iron would be oxidised to methemoglobin

63
Q

Can methemoglobin transport oxygen?

64
Q

What are the acquired immune haemolytic anaemia?

A
  • autoimmune
  • alloimmune
  • drug induced
65
Q

What are the acquired non-immune haemolytic anaemias?

A
  • red cell fragmentation
  • infection
  • secondary
66
Q

What are the hereditary red cell membrane haemolytic anaemias?

A
  • hereditary spherocytosis

- hereditary elliptocytosis

67
Q

What are the hereditary red cell enymopathic haemolytic anaemias?

A
  • G6PD deficiencies

- PK deficiency

68
Q

What are the hereditary haemoglobinopathic haemolytic anaemias?

A
  • sickle cell diseases

- thalassaemias

69
Q

What is autoimmune haemolytic anaemia caused by?

A

Antibiotic production by the body against its own red cells

70
Q

What two groups is autoimmune haemolytic anaemia divided into?

A

Warm or cold depending on whether the antibody reacts more strongly with red cells at 37C or 4c

71
Q

What happens in hereditary spherocytosis?

A

Loss of membrane integrity, RBCs become spherical

72
Q

What happens in hereditary spherocytosis ?

A

Deficiency in proteins with vertical interactions between the membrane skeleton and the lipid bilayer

73
Q

What happens in hereditary elliptocytosis?

A

Mutations in horizontal interactions

74
Q

Where do the genes for globin chains occur on chromosomes?

A

11 (epsilon, gamma, delta, beta)

16 (zeta and alpha)

75
Q

What may mutations or deletions in globin chain genes lead to?

A

Abnormal synthesis of globin chains (like sickle cell diseases)

Reduced rate of synthesis of normal globin chains as in thalassaemia

Fundamentals Of Pathology (20 decks)

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