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Fundamentals Of Pathology > RBCs: Production And Survival > Flashcards

RBCs: Production And Survival Flashcards

(75 cards)

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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
What causes pernicious anaemia?
Autoimmune gastric atrophy, which leads to the loss of an intrinsic factor production needed for absorption of B12
26
What are the four causes of folate deficiency?
Inadequate intake Absorption defect Increased demand/losses Drugs
27
What causes inadequate intake of folate?
Poor nutrition
28
What are some folate absorption defects called?
Coeliac Crohns Tropical sprue
29
What causes increased demand/ losses of folate?
Pregnancy Haemolytic Cancer
30
What type of drugs cause a vitamin folate deficiency?
Anticonvulsant
31
What happens (on a cellular level) in folate and B12 deficiencies (5)?
``` Oval macrocytes Reduced WBC and platelet count Megoblast change in bone marrow Hypersegmented neutrophils B12 only- demyelination of CNS ```
32
What causes renal dx?
Ineffective erythropoeisis
33
What causes a reduction in bone marrow erythroid cells?
Aplastic anaemia or marrow infiltration by leukaemia or other malignancies
34
How long do RBCs circulate for?
Approx 120 days
35
What are the two processes by which RBCs are destroyed?
senescence and random haemolysis
36
What is random haemolysis?
Process that destroys interact RBCs or portions of them independent of their age
37
What does the ability of a RBC to survive depend on?
Cytoplasmic enzymes involved in metabolic pathways
38
What sorts of enzyme defects cause the most significant metabolic reaction problems?
Concentration and activites of the enzymes catalysing the necessary reactions are essential for overall survival of the erythrocyte
39
What parts of the RBC do the metabolism pathways protect (and what do they protect it from)?
Hb molecule, membrane lipids and structural proteins From oxidative stress
40
What is the red cells metabolism pathways main job (4)?
Maintaining osmotic balance, produce the necessary cofactors, electro neutrality and fighting oxidative stress
41
What is another name for the embden-meyerhof pathway?
Glycolytic pathway
42
What is the embdem-meyerhofs main job?
To generate ATP
43
Why is it important that red blood cells generate ATP?
- Maintain RBC shape and deformability | - Regulates intracellular cation conc via cation pumps
44
What pathway is PK a disorder of?
Glycolytic
45
What is PK?
Autosomal recessive disorder with >100 mutations documented
46
What does PK cause?
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
What happens when there’s a block in glycolysis in a RBC?
build up of 2,3 biphosphate, which shifts the oxygen dissociation curve to the right
48
What do defects in band 3, spectrin, ankyrin or protein 4.2 lead to?
Destabilisation of the overlying lipid bilayer and release of lipid into microvesicles
49
What is HS?
Deficiency in ankyrin spectrin
50
What is HE?
Mutant spectrin, leasing to spectrin-ankyrin association.
51
What causes HE?
Protein 4.1 deficiency
52
What happens in the luebering rapaport shunt?
2,3 DPG binds to deoxyhaemoglobin to stabilise at lower o2 affinity state
53
How much of the RBC glucose is metabolised through the hexose monophosphate shunt?
10%
54
What does NADPH stand for?
Nicotinic adenine dinucleotide phosphate
55
What is NADPH’s role?
Protecting the RBC from oxidative damage
56
What is another name for the pentose phosphate pathway?
Hexose monophosphate shunt
57
What does G6PD do in the pentose phosphate pathway?
Catalysed first step in the pathway which is needed for producing NADPH
58
What causes G6PD deficiency?
X-linked
59
What do people with a G6PD deficiency need to avoid?
Specific oxidative drugs
60
What does a G6PD deficiency cause?
Acute haemolysis on exposure to oxidant stress, oxidative drugs, fava beans or infections
61
What does NADH do in the RBC?
Reduced cytochrome b5 which reduces oxidised ferric ion of haemoglobin
62
What would happen if NADH wasn’t present in RBC?
Without the reaction haem iron would be oxidised to methemoglobin
63
Can methemoglobin transport oxygen?
No
64
What are the acquired immune haemolytic anaemia?
- autoimmune - alloimmune - drug induced
65
What are the acquired non-immune haemolytic anaemias?
- red cell fragmentation - infection - secondary
66
What are the hereditary red cell membrane haemolytic anaemias?
- hereditary spherocytosis | - hereditary elliptocytosis
67
What are the hereditary red cell enymopathic haemolytic anaemias?
- G6PD deficiencies | - PK deficiency
68
What are the hereditary haemoglobinopathic haemolytic anaemias?
- sickle cell diseases | - thalassaemias
69
What is autoimmune haemolytic anaemia caused by?
Antibiotic production by the body against its own red cells
70
What two groups is autoimmune haemolytic anaemia divided into?
Warm or cold depending on whether the antibody reacts more strongly with red cells at 37C or 4c
71
What happens in hereditary spherocytosis?
Loss of membrane integrity, RBCs become spherical
72
What happens in hereditary spherocytosis ?
Deficiency in proteins with vertical interactions between the membrane skeleton and the lipid bilayer
73
What happens in hereditary elliptocytosis?
Mutations in horizontal interactions
74
Where do the genes for globin chains occur on chromosomes?
11 (epsilon, gamma, delta, beta) | 16 (zeta and alpha)
75
What may mutations or deletions in globin chain genes lead to?
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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