Nutritional anaemia Flashcards

1
Q

What is anaemia? (3)

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
  • Anemia is a decrease in number of red blood cells (RBCs) or less than the normal quantity of haemoglobin in the blood
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2
Q

What is Hb?

A
  • Iron containing oxygen transport metalloprotein

* Within RBCs

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3
Q

Can we use Hb levels to diagnose anaemia?

A

Yes

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4
Q

What does maturation of RBCs require?

A

• Maturation of red blood cells require
o Vitamin B12 & folic acid; DNA synthesis
o Iron; Haemoglobin synthesis

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5
Q

What are vitamins needed for?

A
o	Cytokines (erythropoeitin)
o	Healthy bone marrow environment
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6
Q

What are the mechansism of action of anaemia?

A

• Failure of Production: hypoproliferation (bone marrow can make RBC but doesn’t have right ingredients)
o Reticulocytopenic
• Ineffective Erythropoiesis (cannot make it properly)
• Decreased Survival
o Blood loss, haemolysis, reticulocytosis

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7
Q

Give types of nutrional anaemia

A

o Iron deficiency
o Vitamin B12 deficiency
o Folate deficiency

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8
Q

What is the function of iron?

What’s our daily requirement and why do women need more?

A
  • Essential for O2 transport
  • Most abundant trace element in body
  • Daily requirement for iron for erythropoeisis varies depending on gender and physiolgical needs
  • Women need more iron due to blood loss from menstruation
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9
Q

What are the daily iron requirements?

A
  • Daily dietary iron requirements differ at various stages of development, between men and women, and between pregnant and nonpregnant women.
  • The data reported in this table assume an average dietary iron absorption of 10%.
  • 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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10
Q

How is iron distributed in the body?

A
  • Iron is an essential component of cytochromes, oxygen-binding molecules (i.e., haemoglobin and myoglobin), and many enzymes.
  • Dietary iron is absorbed predominantly in the duodenum.
  • Fe+++ ions circulate bound to plasma transferrin and accumulate within cells in the form of ferritin. Stored iron can be mobilized for reuse.
  • Adult men normally have 35 to 45 mg of iron per kilogram of body weight. Premenopausal women have lower iron stores as a result of their recurrent blood loss through menstruation.
  • More than two thirds of the body’s iron content is incorporated into haemoglobin in developing erythroid precursors and mature red cells.
  • Most of the remaining body iron is found in hepatocytes and reticuloendothelial macrophages, which serve as storage deposits.
  • Reticuloendothelial macrophages ingest senescent red cells, catabolise haemoglobin to scavenge iron, and load the iron onto transferrin for reuse.
  • Iron metabolism is unusual in that it is controlled by absorption rather than excretion. Iron is only lost through blood loss or loss of cells as they slough.
  • Men and nonmenstruating women lose about 1 mg of iron per day. Menstruating women lose from 0.6 to 2.5 percent more per day.
  • An average 60-kg woman might lose an extra 10 mg of iron per menstruation cycle, but the loss could be more than 42 mg per cycle depending on how heavily she menstruates.
  • Average values in a 70-kg man. Values in women are lower
  • Only lose iron from blood loss- very little excreted
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11
Q

What are the forms of stable iron?

What is it used for?

A

• >1 stable form of iron:
• Ferric states (3+) and Ferrous states (2+)
• Most iron is in body as circulating Hb
o Hb: 4 haem groups, 4 globin chains able to bind 4 O2
• Remainder as storage and transport proteins
• ferritin and haemosiderin
• Found in cells of liver, spleen and bone marrow

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12
Q

What absorbs iron?

What transports it into the blood?

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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13
Q

How is iron-regulated by hepcidin?

How is hepacin regulated?

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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14
Q

How is iron transported?

How is iron deff identified

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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15
Q

Read over Laboratory iron studies

A

On image

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16
Q

What are the causes of ID?

A

NOT ENOUGH IN
• Poor Diet
• Malabsorption
• Increased physiological needs

LOSING TOO MUCH
• Blood loss
• menstruation, GI tract loss, paraistes

17
Q

How can we investigate ID?

A
  • FBC: Hb, MCV, MCH, Reticulocyte count
  • Iron Studies: Ferritin, Transferrin Saturation
  • Blood film
  • ?BMAT and Iron stores
18
Q

Describe the initial stages of ID?

A
  • As you start to run out or iron stores ferritin respond very quickly
  • 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.
19
Q

What are the symptoms and signs of anaemia?

A
Symptoms 
•	fatigue, lethargy, and dizziness
Signs
•	pallor of mucous membranes, 
•	Bounding pulse, 
•	systolic flow murmurs, 
•	Smooth tongue, koilonychias
20
Q

Describe B12 and folate deficiency

A
  • Both have very similar laboratory finding and clinical symptoms
  • Can be found together or as isolated
  • pathologies
  • Macrocytic Anaemia
  • Low Hb and high MCV with normal MCHC
21
Q

What causes macrocytic anaemia?

A
  • Megaloblastic : Low reticulocyte count
  • Vitamin B12/Folic acid deficiency
  • Drug-related
  • (interference with B12/FA metabolism)
22
Q

Define Nonmegaloblastic

What is folic acid needed for?

A

Anaemia causes by:

  • Alcoholism ++
  • Hypothyroidism
  • Liver disease
  • Myelodysplastic syndromes
  • Reticulocytosis (haemolysis)
  • Vitamin B12 = cobalamin
  • Folic acid
  • Both important for the final maturation of RBC and for synthesis of DNA
  • Both needed for thymidine triphosphate synthesis
23
Q

Describe the differences in a blood film between megablastic and nonmegablastic anaemia

A
  • Megaloblastic changes of blood cells are seen in B12 and Folic Acid deficiency
  • They are characterized on the peripheral smear by macroovalocytes and hypersegmented neutrophils.
24
Q

What are the causes of megablastic and nonmegablastic?

A

Diagnosis: Folate Deficiency
• Reticulocytes: 20
• Folate 0.9 (5-15)
• B12 163 (180 – 350)
• Folate necessary for DNA Synthesis:
• Adenosine, guanine and thymidine synthesis
• Folate comes from most foods with 60-90% lost in cooking. It is absorbed in the Jejunum and the body has enough stores usually for 3-5 months

25
Q

What are the causes of Causes of Folate Deficiency?

A

On table

26
Q

What is VB12 needed for?

A
  • 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
  • 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
  • Requires the presence of Intrinsic Factor for absoprtion in terminal ileum
  • IF made in Parietal Cells in stomach
  • Transcobalamin II and Transcobalamin I transport vitB12 to tissues
27
Q

Give some causes of causes of B12 Deficiency

A

On table

28
Q

What are the clinical and haematological consequences of VB12 deficiency?

A

Clinical consequences
• Brain: cognition, depression, psychosis
• Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)
• Infertility
• Cardiac cardiomyopathy
• Tongue: glossitis, taste impairment
• Blood: Pancytopenia

29
Q

What is Pernicious Anaemia and the treatments available?

A
  • Autoimmune disorder
  • Lack of IF
  • Lack of
  • B12 absorption
  • Gastric Parietal cell antibodies
  • IF antibodies
Treatments
•	Treat the underlying cause ****
•	Iron – diet, oral, parenteral iron supplementatin, stopping the bleeding
•	Folic Acid – oral supplements
•	B12 – oral vs intramuscular treatment
30
Q

Look at summary table

A

On image