Nutritional Anaemias Flashcards Preview

Sem 4: TI2 > Nutritional Anaemias > Flashcards

Flashcards in Nutritional Anaemias Deck (19):

Define anaemia.

WHO: a condition in which the amount of haemoglobin and consequently the oxygen-carrying capacity of RBCs is insufficient to meet the body's physiologic needs. 


Name the nutritional causes of microcytic and macrocytic anaemia. 

  • Microcytic - iron deficiency 
  • Macrocytic - B12/folate deficiency 


Outline the absorption and distribution of iron. 

  • Iron is absorbed from duodenum via enterocytes into plasma, where it binds to transferrin. 
  • Transported via transferrin to bone marrow to make RBCs. 
  • Excess iron absorbed is stored as ferritin. 
  • The hormone hepcidin decreases absorption from the duodenum and release from macrophages and iron-storing hepatocytes - this process is driven by ferroportin (iron channel) internalisation and regulated by negative feedback mechanisms. 


What happens to ferritin and transferrin during a state of iron deficiency?

  • Ferritin stores are depleted. 
  • Increased transferrin levels, but low saturation. 
  • Transferrin saturation calculated by ratio of serum iron to total iron binding capacity (TIBC). 
  • In iron deficiency, TIBC is very high compared to serum iron > low saturation. 


Name the main causes of iron deficiency anaemia (IDA). 

Not enough in:

  • Poor diet
  • Malabsorption
  • Increased physiological needs

Losing too much:

  • Blood loss - menstruation, GI tract loss, parasites


What tests are likely to diagnose iron deficiency anaemia at an earlier stage and why?

  • IDA initially normocytic and normochromic.
  • FBC will show microcytic RBCs and low Hb but not until later on. 
  • Ferritin levels fall before other markers, so ferritin test is good for early diagnosis. 


A patient presents with moderate anaemia, microcytic and hypochromic erythrocytes, reticulocytopenia and a ferritin level of 8. What is the diagnosis and why?

  • Microcytic and hypochromic RBCs consistent with iron deficiency anaemia. 
  • Reticulocytopenia - reduced reticulocyte count indicates poor erythrocyte production from the bone marrow. 
  • Ferritin < 20, 8 is very low - severe depletion of iron stores - confirms iron deficiency. 
  • High TIBC and low transferrin saturation would corroborate the findings. 


What is the most common cause of iron deficiency anaemia in adult men and postmenopausal women?

  • Blood loss from the GI tract
  • Menstrual blood loss is the most common cause in premenopausal women 


Describe the common signs and symptoms of iron deficiency anaemia. 

  • Symptoms - fatigue, lethargy, dizziness 
  • Signs - pallor of mucous membranes, bounding pulse, systolic flow murmurs, smooth tongue, koilonychias



Outline the different causes of megaloblastic and nonmegaloblastic macrocytic anaemia. 

  • Megaloblastic - caused by B12/folate deficiency or drug-related interference with B12/folate metabolism.
  • Nonmegaloblastic - alcoholism, liver disease, hypothyroidism, myelodysplastic syndromes, reticulocytosis. 


In B12/folate deficiency, which of these nutrients is likely to be depleted from the body's stores more quickly and why?

  • B12: 2-3mg stored over 2-4 years, easy to obtain sufficient amounts from animal and dairy products. 
  • Folate: 10-12mg stored over 3-4 months, found in vegetables and animal liver and harder to obtain in diet. 
  • Folate stores depleted quicker because required daily intake is higher, stores are short-term, harder to obtain in typical Western diet and cooking produces 60-90% loss. 


Outline the role of vitamin B12 (cobalamin) and folic acid (folate) in erythrocyte production. 

  • Both important for final RBC maturation and DNA synthesis. 
  • Both needed for thymidine triphosphate synthesis. 


Describe the characteristic changes seen on a peripheral blood smear in B12/folate deficiency anaemia. 

  • Changes are megaloblastic. 
  • Macroovalocytes - large oval RBCs. 
  • Hypersegmented neutrophils. 


Describe the main causes of folate deficiency. 

  • Increased demand - pregnancy/breast feeding, growth spurts, haemolysis/rapid cell turnover, disseminated cancer, urinary loss. 
  • Decreased intake - poor diet, elderly, chronic alcohol intake. 
  • Decreased absorption - medication (folate antagonists), coeliac, jejunal resection, tropical sprue. 


How is folate absorbed and stored?

  • Absorbed in the jejunum. 
  • Body stores enough folate for 3-5 months. 


Outline the cellular role of vitamin B12 (cobalamin). 

  • Essential co-factor for methylation in DNA and cell metabolism. 
  • Co-factor in metabolism of methylmalonic acid (MMA) - thus high MMA may indicate B12 deficiency. 
  • Co-factor in homocysteine metabolism - producing methionine. 


Describe the absorption and transport of vitamin B12. 

  • Absorbed in the terminal ileum - requires intrinsic factor (IF) which is made in gastric parietal cells. 
  • Transcobalamin I and II transport vitB12 to tissues. 


What is pernicious anaemia?

  • Anaemia caused by impaired vitB12 absorption. 
  • Intrinsic factor/IF receptor deficiency. 
  • May be congenital or autoimmune - e.g. anti-parietal cell antibodies. 
  • Most common cause of vitB12 deficiency anaemia. 


Outline the clinical consequences of vitamin B12 deficiency. 

  • Brain - cognition, depression, psychosis. 
  • Neurology - myelopathy, ataxia, sensory changes.
  • Infertility. 
  • Cardiomyopathy. 
  • Tongue - glossitis. 
  • Blood - pancytopenia.