Nutritional anaemias Flashcards

1
Q

Define anaemia

A

A condition in which the number of RBCs (and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiological needs

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2
Q

Why does the concentration of Hb required to diagnose anaemia change?

A
  • Depends how old you are
  • At birth you have an increased number of RBCs
  • Then have a slightly lower Hb in first five years
  • By about 12, you reach adult levels
  • Degree of anaemia depends on Hb levels
  • Women are more likely - due to MC and pregnancy etc
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3
Q

What does normal erythropoeisis require?

A
  • maturation of RBCs requires:
  • Vit B12 and folic acid for DNA synthesis
  • Iron for Hb synthesis
  • Vitamins
  • Cytokines (erythropoeitin)
  • Healthy bone marrow environment
  • Need the right environment and building blocks
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4
Q

What can cause anaemia?

A
  • Failure of production - hypoproliferation, reticulocytopaenic - cannot make RBCs because they don’t have the right supplies
  • Ineffective erythropoiesis - have got all the right things (iron, B12, folate etc), but because they are ill,
    they cannot make it in the right way
  • Decreased survival - blood loss, haemolysis, reticulocytosis (make enough RBCs, but cannot keep hold of them)
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5
Q

What are the three different types of anaemia (in reference to MCV)?

A
  • Microcytic
  • Normocytic
  • Macrocytic
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6
Q

What are the 3 deficiencies of essential ingredients that will cause nutritional anaemias?

A
  • iron deficiency
  • Vitamin B12 deficiency
  • Folate deficiency
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7
Q

Why do we need iron?

A
  • Essential for O2 transport
  • Most abundant trace element in body
  • Daily requirement of iron for erythropoeisis varies depending on gender an physiological needs
  • requirements differ at various stages of development, between men and women and between pregnant and non-pregnant women
  • Most iron will come from haem sources from things like meats and seafood
  • Non-haem absorption is lower for those consuming vegetarian diets
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8
Q

How is iron distributed in adults?

A
  • We eat it
  • most iron in the blood as Hb
  • Quite a lot in liver and a bit in muscle
  • We have iron in the blood bound to transferrin
  • We have some stored in the bone marrow
  • The body doesnt excrete iron in a controlled way, we lose it through menstruation or sloughing of the gut wall
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9
Q

How is the iron absorbed?

A
  • Absorbed from duodenum via enterocytes into plasma and binds to transferrin, then transported to bone marrow to make RBCs
  • Excess absorption of iron is stored as ferritin
  • The amount absorbed is dependent on type ingested haem and ferric forms
  • Other foods, GI acidity, state of iron storage levels and bone marrow activity affect absorption
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10
Q

How does hepcidin regulate iron?

A
  • Causes ferroportin internalisation and degradation, thereby decreasing iron transfer into the blood plasma from the duodenum, from macrophages and from iron-storing hepatocytes
  • Feedback regulated by iron concentration in plasma and the liver and by erythropoeitic demand for iron
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11
Q

What iron studies lab tests are there?

A
  • Serum Fe (hugely variable)
  • Ferritin (primary storage protein and providing reserve)
  • Transferrin saturation (ratio of serum iron and total binding capacity - gives % of transferrin binding sites that have been occupied by iron)
  • Transferrin/ transferrin receptors - made by liver, production is inversely proportional to Fe stores - when we need more iron, we produce more transferrin to get iron to the places that need it
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12
Q

What is total iron binding capacity?

A
  • measurement of the capacity of transferrin to bind iron
  • It is an indirect measurement of transferrin
  • TIBC is technically easier to measure in the lab than transferrin levels directly
  • In iron-deficiency anaemia, TIBC is high
  • More transferrin produced aiming to transport more iron to tissues in nedd
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13
Q

What are the causes of iron deficiency?

A
  • Not enough in - poor diet, malabsorption increased physiological needs (pregnancy)
  • Losing too much - blood loss, menstruation GIT loss parasites
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14
Q

What blood tests would we do for iron deficiency?

A
  • FBC - Hb, MCV, MCH, reticulocyte count
  • Iron studies - ferritin, transferrin saturation
  • Blood film
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15
Q

What are stages in development of IDA?

A
  • Before anaemia develops, iron deficiency occurs in several stages.
  • Serum ferritin is the most sensitive laboratory indicators of mild iron deficiency. Stainable iron in tissue stores is equally sensitive, but is not performed in clinical practice.
  • The percentage saturation of transferrin with iron and free erythrocyte protoporphyrin values do not become abnormal until tissue stores are depleted of iron.
  • A decrease in the haemoglobin concentration occurs when iron is unavailable for haem synthesis.
  • MCV and MCH do not become abnormal for several months after tissue stores are depleted of iron.
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16
Q

What lab results would you expect to see in IDA?

A
  • Ferritin = low
  • TF saturation = Low
  • TIBC = high
  • Serum iron = low/normal
17
Q

What are the signs and symptoms of IDA?

A
  • Symptoms - fatigue, lethargy and dizziness

- Signs - pallor of mucus membranes, bounding pulse, systolic flow murmurs, smooth tongue, koilonychias

18
Q

What would B12 and folate deficiency show?

A
  • Both have very similar lab findings and clinical symptoms
  • Can be found together or as isolated pathologies
  • Macrocytic anaemia
  • Low Hb and high MCV with normal MCHC
19
Q

Where do we get Vit B12 and folate?

A
  • B12 = animal and dairy produce - absorb in the ileum via intrinsic factor
  • Folate = vegetables and liver - absorb in the duodenum and jejunum
20
Q

Do these deficiencies cause megaloblastic or non-megaloblastic anaemia?

A
  • Megaloblastic changes of blood cells are seen in both B12 and Folic acid deficiency
  • They are characterised on the peripheral smear by macroovalocytes and hypersegmented neutrophilsme
21
Q

What causes folate deficiency?

A
  • Increased demand (pregnancy, infancy and growth spurts, haemolysis, urinary losses)
  • Decreased intake (poor diet, elderly, chronic alcohol intake)
  • Decreased absorption (medication, coeliac, jejunal resection)
22
Q

Why do we need vit B12?

A
  • Essential cofactor for methylation in DNA and cell metabolism
  • IC conversion to 2 active coenzymes is necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine
23
Q

Where can we get B12 from?

A
  • Fish, meat, dairy

- Hard for vegans to get enough

24
Q

What is intrinsic facotr?

A
  • Required for the absorption of Vit B12 in the terminal ileum
  • Made by parietal cells in the stomach
25
Q

Give some causes of B12 deficiency

A
  • Impaired absorption - pernicious anaemia, ileal resection of gastrectomy, Zollinger-ellison syndrome, parasites
  • Decreased intake - malnutrition, vegan
  • Congenital causes - IF receptor deficiency, Mutation in CG1 gene
  • Increased requirements - haemolysis, HIV, pregnancy, growth spurts
  • Medication - alcohol, NO, PPI/H2 antagonists, metformin
26
Q

What will blood results show?

A
  • MCV = normal or high - megaloblastic anaemia from ineffective erythropoeisis
  • Hb = normal or low
  • reticulocyte count = low
  • Blood film = macrocytes, ovalocytes, hypersegmented neutrophils
27
Q

What are the clinical consequences of a B12 deficiency?

A
  • Brain - cognition, depression, psychosis
  • Neurology - myelopathy, sensory changes, ataxia, spasticity
  • Infertility
  • Cardiomyopathy
  • Tongue - glossitis, taste impairment
  • Blood - pancytopaenia
28
Q

What is pernicious anaemia?

A
  • Autoimmune disorder
  • Lack of IF and B12 absorption
  • gastric parietal cell antibodies
  • IF antibodies
29
Q

How do we treat anaemias?

A
  • Treat the underlying cause
  • Iron = diet, oral, parenteral iron supplementation, stopping the bleeding
  • Folic acid = oral supplements
  • B12 = oral vs IM treatment