Nutritional Anaemia Flashcards

1
Q

What is the definition of anaemia?

A

WHO definition: Anaemia is a condition in which the number of red blood cells (and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiologic needs.

In real life/ practice: Insufficient oxygen carrying capacity due to reduced haemoglobin concentration as seen with insufficient RBC.

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2
Q

What is Haemoglobin?

A

Iron containing oxygen transport metalloprotein within RBCs, essential for oxygen carrying properties of red blood cells and is where iron lives in RBCS.

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3
Q

What three main types of cells does blood contain?

A
  • Red blood cells, normal blood film has round cells with pale centre in the middle. Ring around it should be about 1/3 of the diameter. Redness is the Hb.
  • White blood cells – neutrophils, monocytes, lymphocytes, eosinophil, basophil
  • Platelets
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4
Q

What does normal erythropoiesis (maturation of RBC) require?

A
  • Vitamin B12 and folic acid – helps in DNA synthesis
  • Iron for Haemoglobin synthesis
  • Other vitamins
  • Cytokines (erythropoietin)
  • Healthy bone marrow environment needs to be working healthily
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5
Q

Why might anaemia occur?

A

Failure of production: hypoproliferation reticulocytopenia.

Ineffective erythropoiesis

  • You’ve got ingredients but not right instructions, seen in red cell disorders like thalassemia
  • Bone marrow can’t use ingredients – B12, folate etc, and so doesn’t make enough red blood cells

Decreased survival – blood loss, haemolysis, reticulocytosis

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6
Q

Why might you see increased reticulocytes in anameia? Why might you have reticulotyopenia (decreased)?

A
  1. If there isn’t enough Hb the bone marrow goes into overdrive to try to catch up, causing lots of reticulocytes. - reticulocytosis (seen in decreased survival)
  2. If BM can’t make enough RBC due to lack of right ingredits/instructions, peripheral blood lacks reticulocytes too.

Reticulocytes tell you if its failure of production or decreased survival of RBC.

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7
Q

What can cause microcytic anaemia?

A
  • Iron deficiency (heme deficiency)
  • Thalassaemia (Globin deficiency)
  • Anameia of chronic disease
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8
Q

What causes macrocytic anaemia?

A
  • B12 deficiency
  • Folate deficiency
  • Myelodysplasia
  • Alcohol induced
  • Drug induced
  • Liver disease
  • Myxoedma
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9
Q

What causes normocytic anaemia?

A
  • Anaemia Chronic Disease
  • Aplastic anaemia
  • Chronic Renal Failure
  • Bone Marrow infiltration
  • Sickle cell disease
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10
Q

What is nutritional anaemia?

A

Anaemia caused by a lack of essential ingredients that the body acquires from food sources

  • Iron deficiency
  • Vitamin B12 deficiency
  • Folate deficiency
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11
Q

What is iron important for?

A
  • Essential for O2 transport
  • Most abundant trace element in body
  • Daily requirement for iron for erythropoiesis
  • Varies depending on gender and physiological needs e.g are you pregnant, a child, menstruating
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12
Q

At 14 years old why is there a difference in iron requirements between males and females?

Why is iron from meat more readily available?

A
  1. Because females menstruate, so need more iron. Iron levels equal after menstration, 51+
  2. Meat sources contain blood, better absorption of iron. Non-heme iron absorption lower, need twice as much.
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13
Q

Where is iron absorbed? How is the iron transported in the body?

A

From duodenum, 1-2mg per day.

Body produces transferrin, transports iron to where it’s needed.

  • Most iron sits in RBC and BM in reticular endothelial system, macrophages and spleen
  • Iron in liver and muscles too

Iron lost by sloughed mucosal cells in GIT, menstruction and blood loss.

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14
Q

What are the stable forms of iron? What are the storage proteins?

A

More than 1 stable form of iron:

  • Ferric states (3+) and ferrous states (2+)
  • Most iron is in the body as circulating Hb

Hb: 4 haem groups, 4 globin chains able to bind to 4 O2

Storage proteins:

  • Ferritin and haemosiderin
  • Found in cells of liver, spleen and bone marrow
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15
Q

How is iron absorption regulated? How does iron absorption happen?

A
  • Regulated by GI mucosal cells and hepcidin (negative feedback)
  • Duodenum and proximal jejunum
  • Via ferroportin receptors on enterocytes
  • Transferred into the plasma, iron binds to plasma and then plasma with iron binds to transferrin , taking iron to where it is needed
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16
Q

What does hepcidin, its receptor and the iron channel ferroportin control?

A

Controls dietary absorption, storage and tissue distribution of iron.

  • Hepcidin causes ferroportin internalisation and degradation, decreasing iron transfer into blood plasma from duodenum
  • from macrophages recycling senescent erhtrocytes
  • and from iron-storing hepatocytes.
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17
Q

What regulates hepcidin feedback?

A

Iron concentrations in plasma and liver, and by erthropoietic demand for iron.

As you become more iron replete and there is enough iron, hepcidin falls.

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18
Q

Where is iron transported to and stored?

A

Iron is transported from enterocytes, either into plasma or if excess iron stored as ferritin.

In plasma: attaches to transferrin and then transported to bone marrow , binds to transferrin receptors on RBC precursors

In iron deficiency will see reduced ferritin stores and then increased transferrin.

19
Q

What can you get from iron binding studies?

A
  • Serum Fe
  • Ferritin
  • Transferrin saturation
  • Transferrin (sometimes)
  • Total iron binding capacity

relatively unreliable tests.

20
Q

What is fertitin?

A

Primary storage protein and providing reserve, water soluble.

21
Q

What does ferritin below the normal range mean? What might cause high ferritin?

A
  • There is iron deficiency
  • Ferritin also part of inflammatory response, if you’re unwell ferritin may be high.
22
Q

What is transferrin?

A

Made by liver. Production inversely proportion to Fe stores. Vital for Fe transport.

in iron deficiency:

  • low transferring saturation - no iron to bind to transferrin
  • raised transferrin - increases when iron is low
  • raised iron binding capacity
23
Q

What is total iron binding capacity?

A

Measurement of the capacity of transferrin to bind iron. It is an indirect measurement of transferrin.

24
Q

What is transferrin satuation?

A

Ratio of serum iron and total iron binding capacity - reveal % of transferrin binding sites that have been occupied by iron.

25
Q

What are the lab results in iron deficiency anaemia?

A

Ferritin = low

TF saturation = low

TIBC = high

Serum iron = low/normal

26
Q

What can cause iron deficiency?

A

Not enough in:

  • Poor diet
  • Malabsorption e.g coeliac disease
  • Increased physiological needs

Losing too much

  • Blood loss
  • Menstruation, GI tract loss, parasites
27
Q

What investigations do you carry out to diagnose iron deficiency?

A

Full blood count:

  • Hb conc,
  • MCV,
  • MCH (mean cell haemoglobin is the amount of Hb in each cell, that’s reduced so cells are pale)
  • reticulocyte count (low as bone marrow doesn’t have enough iron to make reticulocytes.

Iron studies: Ferritin, Transferrin saturation

Blood film

BMAT, bone marrow biopsies but this is invasive test and iron stores

28
Q

What are the symptoms and signs of IDA?

A

Symptoms:

  • Fatigue
  • Lethargy
  • And dizziness

Signs

  • Pallor of mucous membranes
  • Bounding pulse
  • Systolic flow murmurs, problems with cardiovascular system as you become more anaemic
  • Smooth tongue, koilonychias
29
Q

What anaemia do you have if you’re decicient in B12/Folate?

A

Macrocytic anaemia.

  • Low Hb
  • high MCV
  • normal mean cell Hb concentration / MCHC
30
Q

What is megaloblastoic macrocytic anaemia?

A

Megaloblastic: low reticulocyte count

  • Due to vitamin B12/ folic acid deficiency
  • Or because of drug related (interference with B12/FA metabolism pathway)
31
Q

What is non-megaloblastic macrocytic anaemia?

A
  • Alcoholism ++
  • Hypothyroidism
  • Liver disease
  • Myelodysplastic syndromes
  • Reticulocytosis (haemolysis)

Still macrocytic , still have high MCV and low Hb but don’t have problem with b12 and folate pathways

32
Q

What are sources of B12 and folate?

A
33
Q

What is the difference between megaloblast and non-megaloblast?

A

Megaloblastic changes of RBC seen in B12 and folic acid deficiency.

Megaloblasts:

  • RBC big and oval, more uniform
  • Changes in neutrophils, are segmented. Nucleus of neutrophil has lots of lobes
  • macroovalocytes and hypersegmented

Non megaloblast:

  • RBC big but not the same
  • In this picture myelodysplastic, bone marrow is producing abnormal red blood cells
34
Q

How do you diganose folate deficiency? And why is folate necessary?

A
  • Not enough reticulocytes due to not enough ingredients
  • Folate low
  • B12 a little low

Necessary for DNA synthesis; adenosine, guanine and thymidine synthesis

35
Q

What can cause folate deficiency/.

A

Increased demand for folate

  • Pregnancy/breast feeding
  • Infancy and growth spurts
  • Haemolysis and rapid cell turniver
  • Disseminated cancer
  • urinary losses e.g heart failure

Decreased intake

  • Poor diet
  • elderly
  • chronic alcohol intake

Decreased absorption

  • Medication (folate antagonists)
  • coeiliac
  • jejunal resection
  • tropical sprue
36
Q

What is needed for the absorption of vitamin B12 in the terminal ileum?

A

Intrinsic factor, made in parietal cells in stomach.

Vitamin B12 binds to it and is absorbed.

Transcobalamin I and Transcobalamin II transport vitamin B12 to tissues

37
Q

What is pernicious anaemia?

A
  • Autoimmune disorder
  • Lack of IF
  • Lack of b12 absorption

Body makes antibodies either against gastric parietal cell or IF - therefore you don’t have enough IF and are not able to absorb B12, no matter how much you eat

38
Q

What are some causes of b12 deficiency?

A
39
Q

How can you identify pernicious anaemia and treat it?

A

Identify antibodies against IF or gastric parietal cells and diagnose pernicious anaemia.

Treated with injections of B12 that goes straight into blood because orally it won’t be absorbed

40
Q

What are the clinical consequences of nutritional anaemia?

A
  • Brain: cognition, depression, psychosis
  • Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)
  • Infertility
  • Cardiac myopathy
  • Tongue: Glossitis, taste impairment
  • Blood: Pancytopenia – problems with WBC and platelets
41
Q

How do you treat nutritional anaemia?

A

Treat the underlying cause

Iron – diet, oral, parenteral iron supplementation, stopping bleeding

Folic acid – oral supplements

B12 – oral vs intramuscular treatment

42
Q
A
43
Q
A