Nutritional anaemias Flashcards

1
Q

What is anaemia?

A

“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.”

→ Insufficient oxygen carrying capacity is due to reduced haemoglobin concentration as seen with insufficient RBC

→ WHO: Haemoglobin concentrations for the diagnosis of anaemia and assessment of severity.

Anaemia caused by lack of essential ingredients that the body acquires from food sources:
→ Iron deficiency
→ Vitamin B12 deficiency
→ Folate deficiency

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2
Q

What does the Maturation of red blood cells require?

A

→ Vitamin B12 & folic acid; important for DNA synthesis
Iron; important for Haemoglobin synthesis
→ Vitamins
→ Cytokines (erythropoietin)
→ Healthy bone marrow environment

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3
Q

Why is there not enough haemoglobin? (what factors play a role in that to investigate in someone with anaemia?)

A

→ Failure of Production(of Hb by the bone marrow) hypoproliferation
→ Reticulocytopenic - you see a reduction in the number of reticulocytes (slightly premature red blood cells) so if anaemic there will be even a lack of the ‘baby red blood cells’ as bone marrow cant even produce to try compensate

    → Ineffective Erythropoiesis
    → Decreased Survival 
    → Blood loss, haemolysis, reticulocytosis
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4
Q

Using the MCV- mean cell volume, what can be some of the causes of anaemia?

A

MICROCYTIC: (RBCs smaller than normal)
→ Iron deficiency (heme deficiency)
→ Thalassamia (globin deficiency)
→ Anaemia of Chronic Disease

NORMOCYTIC:
→ Anaemia Chronic Disease
→ Aplastic Anaemia
→ Chronic Renal Failure
→ Bone marrow infiltration
→ Sickle Cell Disease

MACROCYTIC:
→ B12 Deficiency
→ Folate Deficiency
→ Myelodysplasia
→ Alcohol induced
→ Drug Induced
→ Liver Disease
→ Myxoedema
→ Reticulocyte count then adds further clue as to failure of production or increased losses

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5
Q

What is iron essential 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

→ Recommended intake assumes 75% of iron is from heme iron sources (meats, seafood).
→ Non-heme iron absorption is lower for those consuming vegetarian diets, for whom iron requirement is approximately 2-fold greater.

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6
Q

Where does your iron come from/what do you do with it etc?

A

→ Iron comes from diet, absorb it into your duodenum, body then produces protein called transferrin- transport takes iron where needed, most iron in your body sits within your red blood cells, quite a bit in liver and muscle too

→ Only main ways of losing iron is from menstruation or GI tract, you cant naturally get rid of iron easily (unlike vitamin c where you pee out excess) so your body chooses how much to absorb from intake

→ So iron regulation is within absorption

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7
Q

What is iron absorption regulated by?

A

→ Regulated by GI mucosal cells and hepcidin
→ Duodenum & proximal jejunum
→ Via ferroportin receptors on enterocytes
→ Transferred into plasma and binds to transferrin
→ Amount absorbed depends on type ingested
→ Heme, ferrous (red meat, > than non-heme, ferric forms Heme iron makes up 10-20% of dietary iron
→ Other foods, GI acidity, state of iron storage levels and bone marrow activity affect absorption

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8
Q

What is hepcidin and and what does it do?

A

“the iron-regulatory hormone hepcidin and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron…
Hepcidin causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes.
Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron.”

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9
Q

Where is iron transported from and where does it go?

A

→ Iron transported from enterocytes and then 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

→ A state of iron deficiency will see reduced ferritin stores and then increased transferrin

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10
Q

What are some symptoms and signs of Iron Deficiency Anaemia?

A

Symptoms:
→ Fatigue
→ Lethargy
→ Dizziness

Signs:
→ Pallor of mucous membranes,
→ Bounding pulse,
→ Systolic flow murmurs,
→ Smooth tongue, koilonychias

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11
Q

What do you find with regards to rbc size with b12 and folate deficiency?

A

Macrocytic anaemia-Low Hb and high MCV with normal MCHC (mean cell Hb conc) so fewer red cells and bigger essentially

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12
Q

What is macrocytic anaemia?

A

Megaloblastic : Low reticulocyte count
Causes:
→ Vitamin B12/Folic acid deficiency
→ Drug-related (interference with B12/FA metabolism)

Nonmegaloblastic
Causes:
→ Alcoholism ++
→ Hypothyroidism
→ Liver disease
→ Myelodysplastic syndromes
→ Reticulocytosis (haemolysis)

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13
Q

Why is it more common to have a folate deficiency in comparison to a b12 deficiency? - looking at the average western diet
(excluding vegan diets)

A

→ B12 source - animal and dairy produce
→ Folate source: vegetables and liver

→ When cooking, there is more nutritional loss of folate (60-80%) in comparison to B12(10-30% loss)

→ Also we get an abundance of b12 (7-30mcg) in comparison to the daily requirement for it (1-2mcg)

→ Whereas we get just about what is required of folate - less in excess, we get about 200-250mcg whereas the daily requirement is 100-150mcg.

→ Also the average body stores of folate is much shorter (3-4 months, 10-12mg) so needs replenishing more often, hence it is more common to find a folate deficiency.

→ We store b12 for 2-4 years on average (2-3mg)

→ The absorption site of b12 is the ileum via the intrinsic factor

→ The absorption site of folate is the duodenum and jejunum

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14
Q

What is vitamin b12 also known as and what, along with folic acid, are they important for?

A

→ Vitamin B12 = cobalamin
→ Folic acid
→ Both important for the final maturation of RBC and for synthesis of DNA
→ Both needed for thymidine triphosphate synthesis
→ Folate necessary for DNA Synthesis:
→ Adenosine, guanine and thymidine synthesis
→ Essential co-factor for methylation in DNA and cell metabolism
→ Intracellular conversion to 2 active coenzymes necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine

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15
Q

What foods contain b12 and what are the recommendations with regards to intake?

A

Foods containing vit B12:
→ Animal sources: Fish, meat, dairy
→ UK intake recommendations are 1.5mcg/day
→ EU: 1mcg/day and USA: 2.4mcg/day
average western intake 5-30mcg/day
→ Body (liver) storage: 1-5mg so many years for deficiency

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16
Q

What does vitamin b12 require for absorption?

A

→ Requires the presence of intrinsic factor (IF) for absorption in terminal ileum

→ IF made in Parietal Cells in stomach

→ Transcobalamin II and Transcobalamin I transport vitB12 to tissues

17
Q

What is pernicious anaemia?

A

Essentially, no matter how much vitamin b12 you are eating, you cannot absorb it.
→ Autoimmune disorder
→ Lack of Intrinsic factor
→ Lack of B12 absorption
→ Gastric Parietal cell antibodies
→ Intrinsic factor antibodies

18
Q

What do clinical consequences of anaemia include?
What treatments are there for this?

A

Brain: cognition, depression, psychosis

Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)

Infertility

Cardiac cardiomyopathy

Tongue: glossitis, taste impairment

Blood: Pancytopenia

Treatment:
→ Treat the underlying cause **
→ Iron – diet, oral, parenteral iron supplementatin, stopping the bleeding
→ Folic Acid – oral supplements
→ B12 – oral vs intramuscular treatment