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Phase 2 Metabolic > Anaemia & Bleeding Disorders > Flashcards

Anaemia & Bleeding Disorders Flashcards

1
Q
  1. What is anaemia?

2. Name the 4 overall causes of anaemia

A
  1. decrease in Hb (leading to reduced oxygen carrying capacity of blood)
  2. blood loss
    hypervolaemia
    inadequate RBC production
    excessive RBC destruction
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2
Q

Name 4 causes of microcytic anaemia

A
  • Iron deficiency
  • thalassaemia
  • anaemia of chronic disease
  • sideroblastic anaemia
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3
Q

Name 7 causes of normocytic anaemia

A
  • acute blood loss
  • anaemia of chronic disease
  • CKD
  • autoimmune rheumatic disease
  • marrow infiltration
  • endocrine disease
  • haemolytic anaemias
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4
Q

What is the difference between megaloblastic and normoblastic macrocytic anaemia

A

MEGALOBLASTIC - presence of megaloblasts (RBCs with delayed nuclear maturation due to defective DNA synthesis) in the bone marrow

NORMOBLASTIC - bone marrow is normal

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5
Q

Name 2 causes of megaloblastic macrocytic anaemia

A

folate deficiency

B12 deficiency

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6
Q

name 4 causes of normoblastic macrocytic anaemia

A
  • alcohol
  • liver disease
  • hypothyroidism
  • drug therapy (azathioprine)
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7
Q
  1. What is the name given to the nail change seen in anaemia?
  2. What type of heart murmur can anaemia cause?
  3. What kind of symptoms does anaemia exacerbate?
A
  1. koilonychia (spoon shaped nails)
  2. systolic flow murmur
  3. cardiorespiratory symptoms (breathlessness, angina, claudication)
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8
Q
  1. What is sideroblastic anaemia?
  2. What is the blood film of sideroblastic anaemia?
  3. Name 4 causes of acquired sideroblastic anaemia
A
  1. INHERITED OR ACQUIRED condition whereby iron is not incorporated into haem, leading to the formation of SIDEROBLASTS. Iron accumulates in mitochondria
  2. dimorphic - sideroblasts and hypochromic microcytic cells
  3. myeloproliferative disorders
    myeloid leukaemias
    alcohol use
    lead poisoning
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9
Q

Name 6 factors that can lead to B12 deficiency

A
  1. veganism
  2. pernicious anaemia
  3. congenital deficiency in intrinsic factor
  4. ileal disease/resection
  5. bacterial overgrowth
  6. gastrectomy
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10
Q

Name 6 factors that can result in folate acid deficiency

A
  1. starvation
  2. alcohol excess
  3. GI disease - IBD, gastrectomy
  4. antifolate drugs - methotrexate, trimethoprim, pheytoin
  5. haematological/malignant disease
  6. metabolic disease
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11
Q
  1. What is pancytopenia?
  2. What does it occur due to?
  3. What is another name for pancytopenia?
  4. What is the name of the inherited cause of aplastic anaemia?
  5. What are the majority of cases caused by?
A
  1. deficiency of all three cellular components of blood with hypocellularity/aplasia of the bone marrow
  2. bone marrow failure
  3. aplastic anaemia
  4. fanconi’s anaemia
  5. idiopathic acquired
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12
Q
  1. What is the inheritance pattern of spherocytosis?
  2. What is the disease characterised by? (2)
  3. How might a patient present?
  4. how is the condition managed? (2)
A
  1. autosomal dominant
  2. red cell membrane defects and increased permeability to sodium
    - cells become spherocytic (rigid and less deformable); cells are unable to pass through spleen or become damaged as they pass through spleen so are destroyed
3. jaundice
    splenomegaly
    leg ulcers
    aplastic/haemolytic/megaloblastic crises
    pigment gallstones
  1. splenectomy and lifelong penicillin prophylaxis
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13
Q
  1. What is thalassaemia?

2. In which populations is thalassaemia more common?

A
  1. Condition characterised by defective globulin chains. Leads to imbalanced globin chain production, causing precipitation of chains, thus resulting in ineffective erythropoiesis and haemolysis
  2. mediterranian, middle easter, indian and SE asian
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14
Q
  1. What is the defect of beta thalassaemia?

2. How is it clinically divided?

A
  1. no normal or significantly reduced beta chain production leading to an excess of alpha chains
  2. minor - asymptomatic heterozygous carriers
    intermedia - moderate anaemia
    major - homozygous. severe anaemia requitring regular transfusions. Most sufferers present in first year of life with FTT
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15
Q
  1. how many genes normally code for alpha globulin?
  2. what is the defect of alpha thalassaemia?
  3. Describe the severity classification of alpha thalassaemia based on defect
A
  1. 4 (2 on each chromosome 16)
  2. deletion of gene for alpha globulin
  3. 4 gene deletion - incompatible with life
    3 gene deletion - thalassaemia intermedia
    2 gene deletion - microcytosis with or without mild anaemia
    1 gene deletion - blood picture is usually normal
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16
Q
  1. What is the abnormal Hb formed in sickle cell anaemia?

2. What is the consequence of this mutation?

A
  1. HbS

2. when deoxygenated, it is insoluble. and thus the chains aggregate, making the RBCs in which it is found rigid.

17
Q
  1. Name 2 consequences of the sickling of red blood cells

2. Name conditions in which sickling is precipitated

A
  1. shortened red cell survival (haemolysis)
    impaired passage of cells through the microcirculation leading to obstruction of small vessels and tissue infarction
2. infection
    dehydration
    cold
     acidosis
     hypoxia
18
Q

Why do patients with sickle cell generally feel well despite being anaemic?

A

because HbS releases oxygen into tissues more readily than normal Hb

19
Q
  1. Describe the presentation of vaso-occlusive crises

2. How are vaso-occlusive crises managed? (3)

A
  1. acute pain in hands and feet (due to occlusion of small vessels)
    severe pain in bones occurs in older children and adults
  2. rest
    IV fluids
    analgesia
20
Q
  1. What is acute chest syndrome?
  2. How do patients present?
  3. What are the long term complications of Acute Chest Syndrome?
  4. How is it managed? (4)
A
  1. A type of vaso-occulsive crisis whereby sickled cells become sequestered in the small vessels of the lung, resulting in pulmonary infarction/emboli or viral/bacterial pneumonia
  2. SOB, chest pain, hypoxia and new CXR changes
  3. pulmonary hypotension and chronic lung disease
  4. analgesia
    treatment of sepsis (if present)
    oxygen therapy
    red cell change if patient hyperaemic
21
Q
  1. What is the biggest cause of mortality in sickle cell disease?
  2. What neurological disease are patients with sickle cell disease more at risk of?
A
  1. sepsis - underlying immune dysfunction due to hyposplenism
  2. stroke
22
Q
  1. What is the pathogenesis of autoimmune haemolytic anaemia?
  2. What is the auto-antigen in autoimmune haemolytic anaemia?
  3. What is the name of the test for the autiantibodies against these antigens?
A
  1. increased red cell destruction due to the presence of red cell autoantibodies
  2. globin
  3. Coomb’s test
23
Q

What are the 2 common presentations of autoimmune haemolytic anaemias?

A
  1. short episode of anaemia and jaundice

2. remiting and relapsing course of anaemia and jaundice, progressing to an intermittent chronic pattern

24
Q
  1. Name 2 instances (relating to blood groups) in which haemolytic disease of the newborn can occur
  2. Describe the pathogenesis of haemolytic disease of the newborn.
A
  1. mother is blood group O (thus has anti A and B antibodies) and foetus is group A
    Mother is Rh- and foetus is Rh + (and mother is exposed to foetal blood during first pregnancy)
  2. maternal alloantibodies against foetal red cell antigens pass from the maternal circulation via the placenta and destroy foetal FBCs
25
Q

How does splenic failure occur in sickle cell disease?

A

splenic sequestration (blockage of splenic vasculature by sickled cells) leads to splenic cell death

26
Q

Why is low haptoglobin a marker of intravascular haemolysis?

A

haptoglobin binds to free Hb (following haemolysis) and is involved in the recycling of Hb
It is therefore low following intravascular haemolysis because it is bound to free Hb

27
Q

Describe the 3 phases of haemostasis?

A
  1. vascular spasm
  2. platelet plug formation
  3. coagulation
28
Q

Name 3 things that are promoted by Thromboxane A2

A
  • vasoconstriction
  • platelet activation
  • platelet aggregation
29
Q

Which clotting factors are involved in:

  1. Extrinsic Pathway
  2. Intrinsic Pathway
  3. Common Pathway
A
  1. XII, XI, IX, VIII, X
  2. III, VII, X
  3. X, V, thrombin, fibrin, XIII
30
Q

Which clotting factors are affected in:

  1. Haemophilia A
  2. Haemophilia B
  3. Von Willebrand’s Disease
A
  1. Loss of Factor VIII (impaired extrinsic pathway)
  2. Loss of Factor IX (impaired extrinsic pathway)
  3. Loss of VWF leading to factor VIII deficiency
31
Q
  1. Which clotting factors are vitamin K dependent?

2. What is the clinical relevance of this?

A
  1. II, XII, IX and X

2. Liver disease > vitamin K deficiency > bleeding

32
Q
  1. What is Disseminated Intravascular Coagulation?
  2. What is its pathogenesis
  3. Name 6 causes of Disseminated Intravascular Coagulation
A
  1. formation of blood clots throughout the body which obstruct small vessels
  2. exposure to cytokines > release of factor III (tissue factor) > activation of extrinsic pathway
    widespread stimulation of the coagulation cascade leads to the consumption and depletion of clotting factors and platelets
  3. sepsis, infection, major trauma, burns
    malignancy
    obstetric disorders
    severe organ dysfunction
    vascular disorders
    severe toxic or immunological reaction (e.g. haemolytic reaction, organ transplant rejection)

Phase 2 Metabolic (12 decks)

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