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Clinical Teaching > Clinical Presentation, Diagnosis and Management of Anaemia > Flashcards

Clinical Presentation, Diagnosis and Management of Anaemia Flashcards

1
Q

What is anaemia?

A

The umbrella term which decribes either having fewer RBCs than is normal, or having an abnormally low amount of haemoglobin in each RBC.

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2
Q

What are the reference ranges for Hb in adult male and adult female?

A
  • Male = 135-175
  • Female = 120-155
  • But, a change in the Hb of one specific patient is more important than the absolute value, for that specific patient.
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3
Q

What is the referenc range of Hb for a new baby?

A
  • Reference range for a new baby is 160-200 Hb.
  • This drops considerably in the first 24-48 hours.
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4
Q

Give examples of some of the things which can cause anaemia.

A
  • Tired all the time - this needs to be unpacked.
  • Underactive thyroid
  • Symptoms relating to reduced O2 delivery:
    • Shortness of breath
    • Muscle pain on exertion
    • Dizziness
    • Angina
    • Can present as a change in exercise tolerance.
  • Symptoms relating to the cause of anaemia. For example:
    • Menorhhagia
    • Bleeding of the bowel
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5
Q

What are the clinical signs of anaemia?

A
  • Palor in skin and conjunctiva (changed from normal; some people are just pasty).
  • Tachycardia
  • Rapid breathing
  • Peripheral odema if severe asthma
  • Signs relating to cause of anaemia
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6
Q

Describe the body’s adaption to anaemia.

A
  • Mild anaemia is likely to cause no symptoms unless extreme exertion.
  • Cardiac output increases - rate and stroke volume.
  • Changes in distribution of blood flow:
    • If someone has a lot of blood volume or they are anaemic, the blood flow to the liver is reduced and the body tries to oxygenate brain, heart and also muscles according to need. Localised vasodilation.
  • Change in O2 dissociation curve - 2,3 DPG.
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7
Q

Describe how anaemia is classified.

A
  • Under-production or increased loss of RBC.
  • Congenital or acquired.
  • Acute or chronic.
  • By mean cell volume (MCV) - microlytic / normolytic / macrolytic. This measure gives a big help to establish the cause of the anaemia. Findings help to structure investigation and management.
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8
Q

Describe the classification of anaemia by mean cell volume (MCV).

A
  • MCV is calculated from RBC histogram:
    • Haematocrit (Hct) / RBC
  • MCH (mean cell Hb):
    • Hb / RBC
  • MCHC (mean cell Hb concentration):
    • Hb / Hct
  • RDW (red cell distribution width) - measure of spread of RBC size. Eg. retics / transfusion.
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9
Q

What are the values for microcytic, normocytic and macrocytic MCV?

A
  • Microcytic - MCV 60-80fl
    • Iron deficiency
    • Thalassaemia
  • Normocytic - MCV 80-100fl
    • Blood loss
    • Anaemia of chronic disease
    • Renal impairment
  • Macrocytic - MCV 100-120fl
    • Megaloblastic anaemia:
      • B12/folate deficiency
      • Myelodysplasia
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10
Q

Describe iron deficiency anaemia.

A
  • Commonest cause of anaemia worldwide.
  • Typically reduction in MCV (microcytic) to 65-80, then in Hb, low ferritin, low transferrin saturation with iron. Rest of FBC normal, but raised platelets if bleeding.
  • Caused by:
    • Poor intake
    • Blood loss:
      • Menstrual
      • GI tract - could be from peptic ulcer / cancer / angiodyslasia / hookworm
        • Haematemesis
        • Malaena
    • Malabsorption - coeliac disease
    • Increased need eg. growth spurt / pregnancy
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11
Q

What are the clinical signs of anaemia?

A
  • Palor
  • Tachycardia
  • Koilonychia
  • Hair loss
  • Pica - children who are iron deficient eat soil and their own hair. Their taste changes and they eat odd things.
  • Glossitis / angular stomatitis
  • Features relating to the cause:
    • Weight loss
    • Abdominal pain
    • Bowel change
    • Heavy periods
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12
Q

Describe the investigation of a patient with suspected iron deficiency.

A
  • Be guided by the history - recent and past clinical findings.
  • Confirm iron deficiency by low ferritin and typical FBC.
  • Screen for coeliac disease (IgA tissue transglutaminase or tGA).
  • Upper and lower endoscopy for all except pre-menopausal women.
  • Consider other imaging/capsule endoscopy.
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13
Q

Describe the oral treatment of iron deficiency.

A
  • Oral replacement with sufficient iron for long enough period.
    • Eg. ferrous sulphate 200mg 2 or 3 per day - 65mg elemental iron per dose.
  • Side effects:
    • Nausea
    • Abdominal pain
    • Constipation
  • Side effects are dose related - may improve if changed to ferrous gluconate or fumarate.
  • Typically patients need 3 months of iron after correction of anaemia to build up iron stores.
  • Treat the underlying cause.
  • Rise in Hb generally 10g/L per week if not bleeding.
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14
Q

Describe the parenteral treatment of iron deficiency.

A
  • Intramuscular - not used now. Painful, multiple doses, stains skin.
  • Intravenous:
    • Ferric carboxymaltose (ferinject) - over 15-30 minutes. Often needs 2 doses.
    • Iron dextran (cosmofer) - over 4-6 hours aftr a test dose.
  • All IV iron preparations can cause flu-like symptoms and a small risk of hypersensitivity reaction or anaphylaxis.
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15
Q

Describe B12 deficiency.

A
  • Typically a macrocytic anaemia - MCV 100-120 and later a pancytopaenia. Often bilirubin and LDH raised.
    • This is as a result of ineffective haematopoiesis.
  • Can also cause peripheral neuropathy - demyelination and posterior column damage.
  • B12 result can be falsely low in pregnancy / oral contraceptive / on metformin.
  • Can be caused by:
    • Pernicious anaemia
    • Strict vegan or terminal ileal disease also possible.
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16
Q

What is pernicious anaemia?

A

Gastric atrophy and auto antibodies to parietal cells and intrinsic factor in the stomach preventing absorption.

17
Q

Describe the treatment of B12 deficiency.

A
  • Hydroxocobalamin 1mg IM alternate days for 5 doses, then 3 monthly if confirmed ongoing need (eg. in the case of pernicious anaemia).
  • Cyanocobalamin available orally but not available on prescription.
18
Q

Describe folate deficiency.

A
  • Blood count and film appearance same as B12 deficiency.
  • Limited stores of folate so deficiency can develop in weeks.
  • Poor intake, increased use. For example:
    • Pregnancy / haemolysis
    • Malabsorption
    • Drugs (eg. antiepileptics or trimethoprim)
  • Replacement with oral folic acid 5mg per day.
  • Pre-conception folic acid reduces neural tube defects.
19
Q

Describe anaemia secondary to blood loss.

A
  • Hb immediately after blood loss will be normal.
  • Hb will drop after fluid replacement.
  • Each 500ml loss gives ~10-15g/L drop in Hb.
  • Retic response within hours/days.
  • May need blood transfusion to replace loss, eg. trauma/GI bleed/around delivery.
20
Q

Describe anaemia relating to chronic diseases.

A
  • Typically a normocytic anaemia associated with chronic inflammatory disease.
  • Plentiful iron stores but poor transfer to RBC due to hepcidin and cytokines.
  • History of chronic disease, inflammatory markers increased eg. CRP/ESR/plasma viscosity, exclusion of other causes.
  • Will responsd to treatment of underlying disease.
21
Q

Describe anaemia associated with renal failure.

A
  • Drop in Hb once creatinine clearance drops below 20-30 ml/min chronically.
  • Mainly due to lack of erythropoietin.
  • Contribution from blood loss at dialysis, inflammatory disease.
  • Responds well to erythropoietin eg. weekly or alternate weeks subcutaneously.
22
Q

Describe anaemia relating to haemolysis.

A
  • Haemolysis = blood cell breakdown.
  • Increased RBC destruction, marrow can increase production 5-10 fold.
  • Can be acute or chronic, congenital or acquired.
  • Issues to do with:
    • RBC membrane
    • RBC enzymes
    • Globin chains in Hb
23
Q

Describe the different types of haemolysis relating to the RBC membrane.

A
  • Congenital spherocytosis - autosomal dominant defect in spectrin causing spherical cells - less able to deform so shortened survival.
    • Not often anaemic at birth - often a chance finding in adult life. Options in the short term if the baby is anaemic at birth are transfusion, removing the spleen (because this is the major site of destruction).
  • Auto-immune haemolysis - auto antibodies against RBC surface antigens - Fc portions recognised by macrophages in the spleen.
    • Treated with steroids / splenectomy / rituximab.
24
Q

What are the the other causes of anaemia relating to the RBC membrane and enzymes?

A
  • Leaky heart valve where the red cells are being fragmented and destroyed within the circulation.
  • Disseminated intravascular coagulation - coagulation is activated in the circulation, fibrin is laid down, the cells are sliced up by passing across the fibrin strands. Eg. in prostate cancer or sepsis.
  • RBC enzyme deficiency, for example, G6PD or pyruvate kinase can cause shortened RBC survival.
25
Q

Describe anaemia relating to abnormal Hb.

A
  • Haemoglobinopathy (eg. sickle cell disease) - single point mutation causing Hb polymerisation in hypoxic cells in homozygotes.
  • Shortened RBC survival, reduced production.
  • Chronic anaemia and bone / liver / lung / brain ‘crisis’ ie. acute infarction.
  • Treated by supportive care, hydroxycarbamide to increase HbF production, potentially a stem cell transplant?
26
Q

Describe anaemia relating to thalassaemia.

A
  • Imbalance of globin chain production.
  • Beta thalassaemia - as HbF (2 alpha, 2 gamma chains) declines after birth - progressive anaemia.
  • Treated with supportive care, transfusion, possibly stem cell transplant?
  • Progressive iron overload.
  • Antenatal screen for Haemoglobinopathy and thalassaemia.
27
Q

Describe anaemia relating to marrow infiltration.

A
  • Myeloma
    • B cell malignancy of mature plasma cells - produce monoclonal immunoglobulin or light chains.
    • Presents as a chance finding, anaemia, renal failure, hypercalcaemia, bone pain or fracture.
    • Treated with supportive care, chemotherapy and radiotherapy.
  • Haematological malignancy eg. lymphoma, acute leukamia.
  • Diagnosed by sampling marrow - pelvis or sternum.
  • Treated by chemotherapy / immunotherapy.
  • Other ‘solid’ tumours can spread to marrow eg. prostate, breast, small cell lung.
28
Q

Describe anaemia relating to marrow failure.

A
  • Myelodysplastic disorders - progressive decline in Hb, neutrophils, platelets, macrocytosis. Tendency to progress to acute leukaemia. Treated by supportive care, chemotherapy or stem cell transplant in some.
  • Aplastic anaemia - pancytopaenia. Expected result post chemotherapy but can be drug induced eg. NSAIDs, chloramphenicol or idiopathic. Treated by supportive care, anti-thymocyte globulin, stem cell transplant.

Clinical Teaching (12 decks)

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