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2a Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

What is anaemia?

A

A decrease in haemoglobin due to a reduction in cell mass or increased plasma volume. Accompanied by a fall in red cell count and packed cell volume.

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2
Q

How is anaemia classified?

A

Mean Corpuscular Volume (MCV):
<80 = microcytic
80-100 = normoctyic
>100 = macrocytic.

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3
Q

What are the symptoms of anaemia

A 
Fatigue
Lethargy
Dyspnoea
Palpitations 
headache.
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4
Q

What are the compensatory mechanisms in anaemia?

A
  1. Increased tissue perfusion
  2. increased O2 transfer to tissues
  3. Increased RBC production.
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5
Q

How do microcytic RBC appear in microcytic anaemia?

A

Hypochromic (less colour).

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6
Q

What are the main causes of microcytic anaemia?

A
  1. Iron deficiency
  2. Thalassemia
  3. Anaemia of chronic disease.
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7
Q

Where is iron absorbed?

A

Duodenum.

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8
Q

What are the main causes of iron deficient anaemia?

A

Blood loss (GI bleed, menorrhagia, hookworm), low iron diet, malabsorption.

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9
Q

What are the signs of iron deficient anaemia?

A

Brittle hair and nails, atrophic glossitis, koilonychia (spoon shaped nails) and angular stomatitis (inflammation of corners of the mouth).

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10
Q

What would appear on a blood film for iron deficient anaemia?

A

Hypochromic, microcytic anaemia.
Anisocytosis (variation in size), poikilocytosis (variation in shape).
Pencil cells.

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11
Q

Is ferritin raised or low in iron deficient anaemia?

A

Low. May be normal.

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12
Q

Is reticulocyte count raised or reduced?

A

Reduced.

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13
Q

What is the treatment for iron deficient anaemia?

A

Ferrous sulphate (oral iron). SE: nausea and abdominal discomfort. Give for at least 3 months to allow Hb to normalise.

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14
Q

What shows a response to iron treatment?

A

An increase in reticulocyte count followed by a gradual increase in haemoglobin until it is normal.

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15
Q

What kind of inheritance is thalassaemia?

A

Autosomal recessive.

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16
Q

When does alpha-thalassaemia tend to present?

A

In utero.

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17
Q

When does beta-thalassaemia tend to present?

A

In infancy.

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18
Q

What makes up a haemoglobin molecule?

A

2 alpha and 2 beta chains.

4 genes produce the production of alpha and 2 genes produce the production of beta.

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19
Q

What does the imbalance of chains in thalassaemia cause?

A

In red cell precursors it causes ineffective erythropoiesis e.g. reduced production of RBCs.
In mature red cells causes haemolysis e.g. premature rupture/destruction of red blood cells.

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20
Q

What causes alpha-thalassaemia?

A

Gene deletions.

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21
Q

What causes beta-thalassaemia?

A

Gene defects.

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22
Q

What is the prognosis for alpha-thalassaemia?

A

1 deletion= blood picture normal.
2 deletions = asymptomatic with possible mild microcytic anaemia.
3 deletions = patients have low levels of HbA and Hb Barts. Severe haemolytic anaemia and splenomegaly. Sometimes transfusion dependant.
4 deletions = no alpha chain-synthesis, only Hb Barts present. Hb Barts cannot carry oxygen and is incompatible with life. Infants are still born, they are pale, oedematous with huge livers and spleens.

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23
Q

What is an evolutionary advantage of thalassaemia?

A

Carriers are protected against falciparum malaria.

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24
Q

What is the pathophysiology of beta thalassaemia?

A

In homozygous beta-thalassaemia, there is little/no normal beta chain production and so therefore excess alpha chain production. This means alpha chains combine with whatever beta, delta or gamma chains are available and therefore increased production of HbA2 and Hbf which results in ineffective erythropoiesis and haemolysis.
HbA = 2 alpha and 2 beta chains
HbA2 = 2 alpha and 2 delta chains
HbF = 2 alpha and 2 gamma chains.

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25
Q

Are reticulocytes and nucleated RBCS raised or lowered in peripheral circulation in thalassaemia?

A

Raised.

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26
Q

How is thalassaemia diagnosed?

A

Hb electrophoresis. It shows increased HbF and low/absent HbA.

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27
Q

What is the management for thalassaemia>

A

Blood transfusions regularly. Give SC desderrioxamine and ascorbic acid to reduce the risk or iron overload.
Bone marrow transplant if more severe.

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28
Q

What are the main causes of normocytic anaemia?

A
  1. Acute blood loss/haemorrhage
  2. B12 and iron deficiency
  3. Anaemia of chronic disease.
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29
Q

In which patients does anaemia of chronic disease occur in?

A

Patients with chronic inflammatory disease e.g. Crohn’s, and rheumatoid arthritis, chronic infection e.g. TB and malignancy.

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30
Q

What do the conditions in anaemia of chronic disease cause?

A

A shortening of RBC life or reducing RBC production.

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31
Q

Is serum iron and total iron binding capacity low or high in anaemia of chronic disease?

A

Low.

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32
Q

Is serum ferritin low or high in anaemia of chronic disease?

A

Increased or normal.

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33
Q

What is the management for anaemia of chronic disease?

A

Treat underlying cause and recombinant erythropoietin.

34
Q

Where are old RBCs removed?

A

In the spleen.

35
Q

What are the causes of haemolytic anaemia?

A

Inherited: sickle cell, thalassaemia, inherited spherocytosis and elliptocytosis and glucose-6-phosphate deficiency.
Acquired: autoimmune, malaria, secondary to systemic disease.

36
Q

What are signs of haemolytic anaemia?

A

Gallstones and jaundice from excess bilirubin.

37
Q

Is haemoglobin raised or low in haemolytic anaemia?

A

Low.

38
Q

Is reticulocyte count raised or low in haemolytic anaemia?

A

Raised because bone marrow provides compensatory reticulocytes.

39
Q

What is present on blood films in haemolytic anaemia??

A

Schistocytes.

40
Q

What is the treatment for haemolytic anaemia?

A

Folate and iron supplementation.
Immunosuppressives if autoimmune.
Splenectomy if hereditary or other approaches fail.

41
Q

What are the main causes of macrocytic anaemia?

A

Megaloblastic: B12 deficiency (pernicious anaemia) and folate deficiency.
Non-Megaloblastic: alcohol excess.

42
Q

What does megaloblastic mean?

A

Megaloblastic means that there has been an inhibition of DNA synthesis, occurs with B12 and folate deficiency. The RBCs cannot progress onto mitosis causing continuing growth without division and hence the macrocytosis.

43
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum.

44
Q

What are the causes of pernicious anaemia?

A

Dietary, malabsorption, congenital metabolic errors.

45
Q

What is the pathophysiology of pernicious anaemia?

A

An autoimmune condition in which atrophic gastritis leads to a lack of IF secretion from parietal cells in the stomach. Dietary B12 therefore remains unbound and consequently cannot be absorbed by the terminal ileum.

46
Q

What are the signs of pernicious anaemia?

A

Glossitis, angular stomatitis, jaundice (due to excess breakdown of haemoglobin), polyneuropathy.

47
Q

What would FBC show in pernicious anaemia?

A

Decreased Hb, increased MCV. WCC and platelets low if severe.

48
Q

What investigation would you perform for pernicious anaemia?

A

Autoantibody screen to check for IF and parietal cell antibodies.

49
Q

What is the treatment for pernicious anaemia?

A

Vitamin B12 (hydroxocobalamin).

50
Q

Where is folate absorbed?

A

In the jejunum.

51
Q

What foods is folate found in?

A

Green vegetables, nuts, yeast and liver.

52
Q

What are the causes of folate deficiency?

A

Poor folate diet, malabsorption, pregnancy (increased demand) and anti-folate drugs e.g. methotrexate and trimethoprim.

53
Q

What is the difference between folate deficiency and pernicious anaemia?

A

Folate deficiency does not cause neuropathy.

54
Q

What does prophylactic doses of folic acid help prevent?

A

Spina bifida.

55
Q

What type of inheritance if sickle cell?

A

Autosomal recessive.

56
Q

What is an evolutionary advantage of sickle cell?

A

Protects against malaria.

57
Q

What is the pathophysiology of sickle cell anaemia?

A

Point mutation of the B globin gene (glutamic acid to valine) resulting in HbS variant. Under stress (cold/infection/dehydration/hypoxia/acidosis), the RBCs become deoxygenated and the HbS polymerises causing the cells to become rigid and sickle. This process worsens with repeated oxygenation/deoxygenation.

58
Q

What can sickling of cells produce?

A

Premature destruction of RBCs (intravascular haemolysis).

Obstruction of microcirculation (vaso-occlusion) which leads to tissue infarction.

59
Q

What are the symptoms of sickle cell anaemia?

A

Acute pain in hands and feet due to vast-occlusion.
Jaundice due to haemoglobin breakdown)
Anaemia symptoms.
Acute chest syndrome sue to vaso-occlusion.

60
Q

What would FBC show in sickle cell anaemia?

A

Low haemoglobin and high reticulocyte count.

61
Q

How do you diagnose sickle cell anaemia?

A

Hb electrophoresis. HbSS present and HbA absent.

62
Q

What is the management of sickle cell anaemia?

A

Supportive: folic acid, opiates, antibiotics for underlying cause, fluids.
Disease modifying: hydroxycarbamide.

63
Q

What are the most common causes of death in adults?

A

Pulmonary hypertension and chronic lung disease.

64
Q

What is bone marrow failure, ‘aplastic anaemia’?

A

A reduction in the number of pluripotent stem cells causes a lack of haemopoiesis (production of blood cells and platelets).

65
Q

What are the causes of aplastic anaemia?

A

Congenital, acquired, chemotherapy drugs, infections (EBV, HIV, TB, hepatitis), pregnancy.

66
Q

What is the pathophysiology of aplastic anaemia?

A

Reduction in the number of pluripotential stem cells together with a fault in those remaining or a immune reaction against them, such that they are unable to repopulate. This can occur in only one cell line, leading to isolated deficiencies.

67
Q

What symptoms are specific to aplastic anaemia?

A

Increased susceptibility to infection.
Increased bruising.
Increased bleeding, especially from nose and gums.

68
Q

What would the FBC in aplastic anaemia show?

A

Pancytopenia (low levels of all blood cells).

69
Q

What is the reticulocyte count in aplastic anaemia?

A

Low or absent.

70
Q

What would a bone marrow biopsy show in aplastic anaemia?

A

Hypocellular marrow with increased fat spaces.

71
Q

What is the management for aplastic anaemia?

A

Remove causative agent.
Blood/platelet transfusion.
Bone marrow transplant.
Immunosuppressive therapy: anti-thymocyte globulin (ATG) and ciclosporin.

72
Q

What type of inheritance is glucose-6-phosphate dehydrogenase deficiency?

A

X-linked recessive. Mainly affects men.

73
Q

What is an evolutionary advantage of glucose-6-phosphate dehydrogenase deficiency?

A

Protects against falciparum malaria.

74
Q

What is the pathophysiology of glucose-6-phosphate dehydrogenase deficiency?

A

G6PD vital in hexose monophosphate shunt which maintains glutathione in reduced state. Glucathione protects the RBC from oxidative crisis.

75
Q

When does glucose-6-phosphate dehydrogenase deficiency become symptomatic?

A

When exposed to oxidative stressor.

76
Q

What are symptoms of glucose-6-phosphate dehydrogenase deficiency?

A

Neonatal jaundice due to excess bilirubin.
Chronic haemolytic anaemia.
Acute haemolysis: rapid anaemia, jaundice. Caused by ingestion of fava beans and common drugs (quinine, sulphonamides, quinolones and nitrofurantoin).
Back pain.
Dark urine.

77
Q

What shows on a blood film with glucose-6-phosphate dehydrogenase deficiency?

A

Heinz bodies and bite and blister cells.

78
Q

What confirms the diagnosis of glucose-6-phosphate dehydrogenase deficiency?

A

Enzyme assay.

79
Q

What is the reticulocyte count in glucose-6-phosphate dehydrogenase deficiency?

A

Raised.

80
Q

What is the treatment for glucose-6-phosphate dehydrogenase deficiency?

A

Avoid precipitants and transfuse if severe.

81
Q

Where in the adrenal gland is aldosterone produced?

A

Zona glomerulosa.

2a Medicine (11 decks)

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