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Atrial Fibrillation > Red Cell Disorders > Flashcards

Red Cell Disorders Flashcards

1
Q

Types of red cell disorders

A

Anaemia

Polycythaemia

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2
Q

Types of anaemia

A 
Iron deficiency
Megaloblastic
Haemolytic
Aplastic
Sickle
Thalassaemias
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3
Q

Clinical signs of anaemia

A

Reduced levels of Hb
Symptoms depend on severity - SoB, weakness/lethargy, tachycardia
Severe - potential for angina
Glossitis and angular cheilitis
DPG may be elevated in RBCs so O2 more readily given up in tissues

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4
Q

Characteristics of iron deficiency anaemia

A

microcytic, small, decreased MCV RBCs

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5
Q

Cause of iron deficiency anaemia

A

iron input reduced - poor diet, surgical removal of stomach
output increased - chronic/heavy menstruation, gastrointestinal bleeding (colon cancer?), ulcers (NSAIDs?)
demand increased - pregnancy
iron deficiency where bone marrow and macrophage Fe stores depleted, causing anaemia

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6
Q

Acute bleed

A

rapid blood loss as in haemorrhage
sever loss of blood
BP falls
over time there is haemodilution (more fluid in the blood)

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7
Q

Chronic bleed

A

long term bleeding

eg. gastric bleeding, excessive menstruation

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8
Q

How would Hb, haematocrit, MCV, retics, WBC, platelets, EPO and iron stores be affected 24 hours after an acute bleed?

A 
Hb - decreased
haematocrit - decreased
MCV - normal
retics - normal
WBC - decreased
platelets - decreased
EPO - increasing
iron stores - normal
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9
Q

How would Hb, haematocrit, MCV, retics, WBC, platelets, EPO and iron stores be affected after a chronic bleed?

A 
Hb - decreased
haematocrit - decreased
MCV - decreased
retics - increasing 
WBC - normal
platelets - normal
EPO - increased
iron stores - zero
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10
Q

Treatment for iron deficiency anaemia

A

find and treat underlying cause
give oral iron (FeSO4)
prophylaxis in pregnancy - oral iron folic acid
severe - transfusion

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11
Q

What can renal anaemia lead to?

A 
normocytic anaemia (normal size, not enough)
complicates chronic renal failure
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12
Q

How to treat renal anaemia?

A

Fe and EPO

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13
Q

How does pregnancy affect RBCs?

A

dilution/iron effiency

therefore normocytic RBCs as pregnancy increases MCV but iron deficiency decreases MCV

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14
Q

What is megaloblastic anaemia?

A

abnormal RBC maturation due to defective DNA synthesis
out of step with cytoplasmic development, bone marrow contains megaloblasts
macrocytic

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15
Q

What is a megaloblast?

A

larger than normal RBC

cytoplasmic development quicker than DNA synthesis

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16
Q

What is the cause of megaloblast anaemia?

A

vitamin B12 or folate deficiency

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17
Q

Symptoms of megaloblast anaemia

A

jaundice - XS breakdown of Hb due to increased ineffective erythropoiesis
many symptomless and diagnosed with blood test

18
Q

What is B12 essential for?

A

cofactor for purine and pyrimidine synthesis (therefore cell division), requires intrinsic factor for absorption

19
Q

Use of folic acid (folate)

A

essential for thymidylate synthesis

rate limiting step in DNA snythesis as thymidine is a pyrimidine base

20
Q

Action of folic acid and B12

A

methyl tetrahydrofolate and B12 as co-factor
THF -> THF polygultamate -> DHF reductase
causes deoxy-uracilmonophosphate (dUMP) to become deoxy thymine MP (dTMP)
DNA

21
Q

Issues associated with B12 and folic acid

A

methotrexate
pernicious anaemia
Crohn’s disease

22
Q

Methotrexate

problem

A

used in chemo, immunosupressant, rh. arthritis

inhibits dihydrofolate reductase

23
Q

Pernicious anaemia

problem

A

lack of intrinsic factor for absorption of B12 due to automimmune disease

24
Q

Crohn’s disease

A

malabsorption of B12, folate or iron

25
Q

What happens in haemolytic anaemias?

A

increased rate of RBC destruction

eg. megloblastic

26
Q

Types of haemolytic anaemias

A

spherocytosis

acquired

27
Q

Spherocytosis anaemia

A

type of haemolytic anaemis
genetic
abnormal reduction in RBC membrane protein, fragile cells

28
Q

Acquired anaemia

A

type of haemolytic anaemia

haemolytic transfusion reaction, malaria, drug-induced

29
Q

Give consequences of haemolytic anaemias

A

jaundice and enlarged spleen

30
Q

Cause of sickle cell anaemia

A

genetic - single nucleotide polymorphism
smino acid substitution, valine for glutamic acid
abnormal Hb - insoluble forms crystals at low O2, RBC form sickle shapes and may block microcirculation

31
Q

What can sickle cell anaemia cause?

A

haemolytic anaemia

32
Q

Cause of thalassaemias?

A

genetic
reduced rate of alpha/beta globin units production, variation
deletion of both alpha genes leads to death in uterus as Hb (gamma4) produced
one alpha gene deletion reduced RBC volume and haematocrit

33
Q

What is aplastic anaemia?

A

insufficient production of RBCs, WBCs and platelets, although can be just RBCs

34
Q

Consequences of aplastic anaemia

A

decreased resistance to infections, increased bleeding, increased tiredness

35
Q

Cause of aplastic anaemia

A 
viral, radiation, drugs
cytotoxic agents
chloramphenicol
sulphonamides
insecticides
bone marrow failure
36
Q

How to treat aplastic anaemia

A

bone marrow transplant with tissue match
immunosuppressants to prevent immune destruction of stem cells
colony-stimulating factors to increase WBC count

37
Q

What is polycythaemia?

A

increased Hb content and haematocrit, resulting in increased blood viscosity and poor tissue perfusion

38
Q

Symptoms of polycythaemia

A 
ruddy appearance
cyanosis
headaches
blurred vision
hypertension
39
Q

Causes of aplastic anaemia

A

primary - changes in bone marrow, stem cell defect

secondary - increased erythropoietin: altitude, smoking, renal, carcinoma

40
Q

How to treat primary cause of aplastic anaemia?

A

venesection (bleeding)
radioactive phosphorus - myelosuppression (bone mineralisation, kills off fast growing cells)
cytotoxic agents - myelosuppression

Atrial Fibrillation (9 decks)

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