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MEH * > 4.1 - Introduction To Anaemia > Flashcards

4.1 - Introduction To Anaemia Flashcards

1
Q

What are the signs of anaemia?

A
  • kilonychia = nails bend upwards (iron deficiency)
  • glossitis = inflamed tongue (vit b12)
  • angular stomatitis = inflamed corners of the mouth (iron deficiency)
  • abnormal facial bone developement = thalassaemia
  • oesophageal webs (iron deficiency)

Then

  • pallor
  • tachycardia
  • tachypnea
  • hypotension
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2
Q

How can anaemia develop from reduced erythropoiesis?

A
  • lack of response to haemostasis loop e.g. in chronic kidney disease kidney stops making erythropoietin hormone which stimulates formation of RBC in the bone marrow
  • empty bone marrow unable to respond to EPO after toxic insult
  • marrow infiltrated by cancer cells or fibrous tissue (myelofibrosis) means normal haemopoietic stem cells are reduced
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3
Q

What is dyserythropoiesis and how does it arise?

A

Anaemia of inflammation or of chronic disease.

  • iron is not released for use in bone marrow
  • reduced lifespan of red cells
  • the marrow shows a lack of response to erythropoietin
  • seen in: renal disease, inflammatory conditions, chronic infections, etc.
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4
Q

How can defects in haemoglobin synthesis lead to anaemia?

A
  • lack of iron = deficiency in haem synthesis. Could be a result of anaemia of chronic disease (functional lack of iron)
  • lack of b12/folate: deficiency in the building blocks for DNA synthesis = megaloblastic anaemia
  • mutations in proteins encoding the globin chains = thalassaemia, sickle cell disease
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5
Q

How can defects in RBC membrane structure be inherited?

A

Abnormalities of proteins making RBC membrane lead to haemolytic anaemia and cells are less flexible and are damaged more easily and break up/ are removed more quickly from the circulation

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6
Q

How can defects in RBC membrane structure be acquired?

A

Mechanical damage to RBC

  • heart valves
  • vasculitis (inflammation of blood vessels)
  • MAHA (migroangiopathic haemolytic anaemia
  • disseminated intravascular coagulopathy - small blood clots develop in blood vessels reducing platelet count
  • heat damage through burns
  • osmotic change e.g drowning
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7
Q

What is the reticuloendthelial system?

A
  • the spleen removes damaged or defective red cells
  • it will do this in anaemias
  • in haemolytic anaemias, red cells are destroyed more quickly as they are abnormal or damaged
  • this can occur within the blood vessels (= intravascular) to outside within RES macrophages in the spleen, liver, bone marrow, etc (extravascular).
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8
Q

Why is autoimmune haemolytic anaemia a thing?

A

To remove excess RBC by res
In this condition antibodies bind to RBC membrane proteins
Cells in res recognise part of the antibody, attach to it and remove it and the red cells from the circulation

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9
Q

Why would RBC look like tear drops?

A

Myelofibrosis means there’s little space in bone marrow for synthesis of RBC === tear drop shaped

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10
Q

What is mean corpuscular volume?

A

The volume of a red blood cell

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11
Q

When would you get anaemia with reticulocytosis?

A
  • acute blood loss
  • splenic sequestration (with sickle cell disease, get splenomegaly)
  • haemolysis, either immune or non immune (mechanical e.g. heart valves/microangiopathic haemolytic anaemias, haemoglobinpathies or enzyme defects)
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12
Q

What are the traits of a low mean corpuscular volume (microcytic anaemia)?

A
  • Thalassaemia trait
  • Anaemia of chronic disease
  • Iron deficiency
  • Lead positioning
  • Sideroblastic anaemia (ringed RBC instead of normal cells produced)

TAILS = traits of microcytic anaemia

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13
Q

Why would you get macrocytic anaemia with a low reticulocyte count?

A
  • vitamin b12 and folate deficiency
  • liver disease
  • hypothyroidism
  • alcohol
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14
Q

Why would you get a low reticulocyte with a normal MCV?

A
  • primary bone marrow failure
  • aplastic anaemia (stem cells in bone marrow damaged)
  • red cell aplasia (bone marrow stops making red cells)
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15
Q

How can you get secondary bone marrow failure?

A
  • HIV
  • Anaemia of chronic disease
  • uraemia
  • endocrine abnormalities
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16
Q

Why is vitamin b12/folate important??

A

Building blocks for DNA synthesis. Without, get megaloblastic anaemia.
They’re converted to methylTHF which is the functional form, and is essential for purine synthesis, thymidylate synthesis and serine glycine conversions

17
Q

What is megaloblastic anaemia?

A

Anaemia that results from inhibition of dna synthesis during RBC production. When dna synthesis is impaired, the cel cannot progress from g2 growth stage to the mitosis stage of the cell cycle

18
Q

What are the causes of low b12?

A
  • dietary deficiency e.g vegan
  • lack of intrinsic factor IF = pernicious anaemia (an autoimmune disease affecting gastric parietal cells and causing a lack of intrinsic factor)
  • disease of the ileum (Crohn’s disease, etc.)
  • lack of transcobalamin = congenital deficiency
19
Q

How is vit b12 absorbed?

A
  • bind to haptocorrin from salivary glands and goes to stomach
  • then binds to Intrinsic factor (IF) made by parietal cells in the stomach in the small intestine
  • is absorbed into bloodstream in terminal ileum and binds to plasma protein transcobalamin which delivers b12 to tissues.
20
Q

What could deficiency’s in folate result from?

A
  • dietary deficiency.
  • increase use: pregnancy, increased erythropoiesis e.g in haemolytic anaemia, severe skin disease e.g. psoriasis
  • disease of duodenum and jejunum e.g. coeliac disease, crohns
  • lack of methylTNF e.g. by drugs that inhibit dihydrofolate reductase enzyme or alcoholism; urinary loss of folate in liver disease and heart failure
21
Q

What is the specific function of vitamin b12?

A
  • transfer a methyl group from L methylmalonyl coA to form succinyl CoA
  • transfers of a methyl group from FH4 to homocysteine to form methionine
  • lack of b12 traps folate in stable methyl - FH4 form amusing a functional folate deficiency
22
Q

How do vit b12 and folate deficiency cause megaloblastic anaemia?

A
  • lack = thymidylate deficiency
  • no thymine = uracil incorporated into dna instead
  • dna repair enzymes detect error and dna strands are destroyed
  • nucleus of RBC lacking dna doesnt fully mature = large RBC precursors with large nuclei and open chromatin.
23
Q

What are the features of a megaloblastic blood film?

A
  • macrocytic red cells
  • anisopoikilocytosis with tear drops
  • hypersegmented neutrophils
  • can see white cell precursors also
24
Q

Why is important to take b12/folate supplement when pregnant??

A
  • neural tube defects

- focal demyelination affecting the spinal cord

25
Q

What would you look for when investigating megaloblastic anaemia?

A
  • low Hb
  • high MCV
  • blood film
  • high bilirubin
  • check b12 and serum folate
26
Q

How would you treat a b12 and folate deficiency?

A

Folate
- folic acid orally

B12

  • hydroxycobalamine (beware of hypokalaemia)
  • transfusions (beware as high output = cardiac failure)

MEH * (21 decks)

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