Medically Fit For Exams
Medically Fit For Exams




  • Reduction in haemoglobin levels, usually as a result of fewer red blood cells
  • Normal Hb: male: 235-175 g/l, female: 115-160 g/l
  • Microcytic: MCV <80 fL
  • Normocytic: MCV 80-96 fL
  • Macrocytic: MCV >96 fL


Risk factors

  • Iron deficiency
    • Diet low in iron
    • Heavy periods
    • Malabsorption (including IBD and coeliac disease)
  • Family history
  • Chronic disease


Differential diagnoses

  • Cancer (fatigue)
  • Diabetes (fatigue)
  • Angina
  • Peripheral arterial disease (intermittent claudication)
  • Any of the other types of anaemia



  • About 25% of global population has anaemia
    • 47% pre-school age children
    • 25% school age children
    • 42% pregnant women
      • NB a certain degree of anaemia is physiological in pregnancy, as the increased blood volume dilutes RBCs, and does not need treating
    • 30% non-pregnant women
    • 12% men
    • 24% elderly
  • Severe anaemia is most prevalent in Africa, also in eastern Mediterranean and SE Asia
  • Sickle cell anaemia is more common in those from Africa, South America
  • Alpha thalassemia is most highly prevalent in SE Asian population
  • Beta thalassemia is most common in SE Asian and eastern Mediterranean
  • In general: tropical and sub-tropical regions are at highest risk



  • Microcytic – anything that results in lack of haemoglobin
    • 95% is iron deficiency
      • Insufficient intake
      • Malabsorption
      • Blood loss
    • Anaemia of chronic disease may cause microcytic, though more commonly causes normocytic
    • Thalassaemia (abnormalities in haemoglobin)
    • Congenitial sideroblastic anaemia (acquired sideroblastic anaemia is likely to give macrocytic)
  • Normocytic – generally result of damage to another body system or acute blood loss
    • Anaemia of chronic disease
      • Rheumatoid arthritis
      • Lupus
      • Lung and breast carcinoma
      • Hodgkin disease
    • Acute blood loss
    • Renal failure
    • Bone marrow failure – aplastic anaemia
    • Hypothyroidism
    • Pregnancy
    • Sickle cell
    • Haemolysis
      • RBC broken down faster than they are made
      • Extravascular vs intravascular
      • Innate vs acquired
      • Immune vs non-immune (subset of acquired)
  • Macrocytic – generally caused by problem with DNA
    • Megaloblastic – RBC in bone marrow develop slowly, with late DNA maturation, so that cells have grown large by the time DNA is ready to divide, and nucleus is lost
    • Vitamin B12 deficiency – B12 produces a form of folate needed to make DNA, so deficiency delays DNA maturation as above
      • Pernicious anaemia – autoimmune disorder in which gastric mucosa atrophy prevents intrinsic factor production by parietal cells, which prevents B12 absorption in the gut
    •  Folate deficiency – causes megaloblastic
    • Reticulocytosis
    • Hypothyroidism (also can cause normocytic)


Clinical features

  • Non-specific
    • Fatigue
    • Headache/faintness
    • SOB
    • Angina
    • Pallor
      • Palmar creases
      • Conjunctiva
    • Intermittent claudication
    • Palpitations
    • Tachycardia
    • Cardiac failure
  • Iron deficiency
    • Brittle nails and hair
    • Koilonychia (spoon shaped nails)
    • Angular stomatitis
    • Glossitis
    • Blue sclerae
  • Pernicious anaemia
    • Lemon-yellow jaundice (pallor + mild jaundice)
    • Glossitis
    • Angular stomatitis
    • Neurological symptoms
      • Peripheral neuropathy, symmetrical
      • Ataxia
      • May result in paraplegia
      • Dementia, hallucinations, confusion etc
  • Sickle cell
    • Sickle cell crises – systemic pain, including joints and bones, where sickle complexes get stuck
    • Pulmonary hypertension – 30-40% of patients – sickle cells consume NO, so less for vasodilation
    • Frequent infections – sickle cells can damage spleen
    • Hand-foot syndrome – swollen hands and feet where sickle cells get stuck in small vessels
  • Thalassaemia
    • Enlarged spleen, and frequent infections
    • Slow growth and delayed puberty
    • Brittle bones – bone marrow expansion causes bones to be wider and weaker, especially in face, osteoporosis
    • Jaundice, including dark urine



  • Iron deficiency
    • Reduction in available haemoglobin causes cells to become microcytic because they divide/get smaller in an attempt to conserve Hb concentration
  • Anaemia of chronic disease
    • Chronic inflammatory condition à increased cytokines
    • Increased hepcidin production
      • Decreased iron absorption in small intestine
      • Decreased breakdown and recycling of iron in spleen/liver
      • à low iron levels
    • This occurs because bacteria causing infection (major cause of inflammation) need iron to survive
      • Attempt to reduce iron to help combat infection
  • Pernicious anaemia
    • Autoimmune response destroying parietal cells in gastric mucosa
    • Lack of intrinsic factor production
    • Inability to absorb vitamin B12
    • Inability to produce folate to make DNA
    • RBD grow large while DNA is maturing slowly
  • Sickle cell
    • HbS causes sickle cell trait (carrier) or sickle cell disease (double hit)
    • Causes some RBC to become sickle shaped
    • Abnormal shape causes damage and haemolysis
    • Abnormal proteins on RBCs attract immune response which also causes haemolysis
  • Alpha thalassemia
  • Beta thalassemia




  • Full blood count
  • Iron studies
    • Iron deficiency
      • Low ferritin
      • High total binding capacity (transferrin à compensatory mechanism)
    • Anaemia of chronic disease
      • High ferritin (lots of iron stored away)
      • Low total binding capacity (to prevent iron availability to bacteria)
  • Blood film
  • Genetic testing (for suspected haemoglobinopathies)
  • Hb electrophoresis for beta thalassaemia
  • PR to rule out rectal bleeding
  • Endoscopy/colonscopy to check for GI bleed/malignancy



  • Iron deficiency
    • Identify cause
    • Treat bleed
    • Hormonal therapies for heavy periods
    • Increased oral intake/supplements
    • Treat malabsorption
  • Anaemia of chronic disease
    • Never treated with supplementation
      • Isn’t too little iron in body
      • Adding extra iron will increase liver storage and cause liver damage
    • Treating the underlying condition
  • Pernicious anaemia
    • Intramuscular B12 injections
  • Sickle cell
    • Transfusion therapy
    • Monitoring
  • Thalassaemia
    • Transfusion therapy, especially in beta thalassaemia



  • Thalassaemia can be fatal – more so in beta thalassemia, have reduced life expectancy
  • Sickle cell crises can be fatal, increases risk for stroke and ACS
  • GI bleed (causing iron deficiency) can be fatal, especially if not picked up early
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