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
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
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
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)
5
Q
What are the three different types of anaemia (in reference to MCV)?
A
- Microcytic
- Normocytic
- Macrocytic
6
Q
What are the 3 deficiencies of essential ingredients that will cause nutritional anaemias?
A
- iron deficiency
- Vitamin B12 deficiency
- Folate deficiency
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
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
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
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
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
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
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
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
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.
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
