Nutritional Anaemia 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

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2
Q

Describe the structure of haemoglobin in RBCs

A
  • One iron group per heme.
  • one heme group per subunit
  • 4 subunits make up oner molecule of haemoglobin
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3
Q

What is needed for normal erythropoiesis to take place

A
  • Vitamin B12
  • Folic acid
  • Iron
  • Vitamins
  • Cytokines
  • Healthy bone marrow environment
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4
Q

why may a patient be anaemic

A
  • Failure of production
  • Ineffective erythropoiesis
  • Decreased survival
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5
Q

How would we investigate low Hb levels

A

Do a full blood count

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6
Q

What can we see about the mean cell volume in a full blood count

A
  • Microcytic RBC
  • Normocytic RBC
  • Macrocytic RBC
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7
Q

What can cause microcytic anaemia

A
  • Iron deficiency
  • Thalassamia
  • Anaemia of chronic disease
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8
Q

What can cause Normocytic anaemia

A
  • Anaemia chronic disease
  • Aplastic anaemia
  • Chronic renal failure
  • Bone marrow infiltratrion
  • Sickle cell disease
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9
Q

What can cause microcytic anaemia

A
  • B12 deficiency
  • Folate deficiency
  • Myelodysplasia
  • Alcohol induced
  • Drug induces
  • Liver disease
  • Myxoedema
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10
Q

Define nutritional anaemia

A

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

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11
Q

How is iron used in the body

A
  • Essential for O₂ transport
  • Most abundant trace element in body
  • Daily requirement for iron for erythropoeisis varies depending on gender and physiolgical needs
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12
Q

How is iron distributed in adults

A
  • The duodenum takes in 1-2gm per day via the diet
  • Plasma transferrin (3mg)
  • Bone marrow (300mg)
  • Muscle myoglobin (300mg)
  • Liver (1000mg)
  • Circulating erythrocytes (1800mg)
  • Reticuloendothelial macrophages (600mg)
  • Iron loss 1-2mg per day
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13
Q

How is Iron metabolised

A
  • Ferric states (3+) and Ferrous states (2+)
  • Most iron is in the body as circulating Hb
  • Remainder as storage and transport proteins; ferritin and haemosiderin
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14
Q

How is iron absorbed in the body

A
  • Regulated by GI mucosal cells and hepcidin
  • Duodenum & proximal jejunum
  • Via ferroportin receptors on enterocytes
  • Transferred into plasma and binds to transferrin

The amount absorbed depends on type ingested: red meat> than non-heme

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15
Q

What is the role of hepcidin in the regulation of iron

A

Hepcidin causes ferroportin internalisation and degradation, thereby decreasing iron transfer into blood plasma from the duodenum

Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron

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16
Q

How is iron transported and stored

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
17
Q

What does the laboratory iron tests tell us

A
  • Serum Fe: Hugely variable during the day
  • Ferritin: Primary storage protein & providing reserve, Water soluble
  • Transferrin Saturation: Ratio of serum iron and total iron binding capacity – revealing %age of transferrin binding sites that have been occupied by iron
  • Transferrin: Made by liver, Production inversely proportional to Fe stores. Vital for Fe transport.
  • Total Iron Binding Capacity: Measurement of the capacity of transferrin to bind iron It is an indirect measurement of transferrin
18
Q

What do the laboratory tests show for iron deficient anaemia

A
  • Ferritin: LOW
  • TF Saturation: LOW
  • TIBC: HIGH
  • Serum Iron: LOW/NORMAL
19
Q

What are the causes for iron deficiency

A
  • Poor diet
  • Malabsorption
  • Increased physiological needs
  • Blood loss
  • GI tract loss
  • Parasites
20
Q

What are some symptoms and signs of iron deficient anaemia?

A

Symptoms:

  • Fatigue
  • Lethargy
  • Dizziness

Signs:

  • Pallor of mucous membranes
  • Bounding pulse
  • Systolic flow murmurs
  • Smooth tongue, koilonchias
21
Q

What are the causes of megaloblastic: low reticulocyte count

A
  • Vitamin B12/Folic acid deficiency
  • Drug-related (interference with B12/FA metabolism)
22
Q

What are the causes of nonmegaloblastic low reticulocyte count

A
  • Alcoholism
  • Hypothyroidism
  • Liver disease
  • Myelodysplastic syndromes
  • Reticulocytosis (haemolysis)
23
Q

What is B12 and folic used for

A
  • Both are important for the final maturation of RBC and for the synthesis of DNA
  • Both needed for thymidine triphosphate synthesis
24
Q

What is the difference between megaloblastic and non-megaloblastic

A

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

25
Q

What can cause folate deficiency

A
  • Increased demand
  • Decreased intake
  • Decreased absorption
26
Q

how does increased demand cause folate deficiency

A
  • Pregnancy/Breastfeeding
  • Infancy and growth spurt
  • Haemolysis & rapid cell turnover
  • Disseminated cancer
  • Urinary losses e.g: heart failure
27
Q

How does a decreased intake lead to folate deficiency

A
  • Poor diet
  • Elderly: eat less
  • Chronic alcohol intake
28
Q

How does decreased absorption lead to folate deficiency

A
  • Medication (folate antagonist)
  • Jejunal resection
  • Tropical sprue
29
Q

How is Vitamin B12 absorbed in the ileum

A
  • Requires the presence of Intrinsic Factor for absorption in terminal ileum
  • IF made in Parietal Cells in the stomach Transcobalamin II and Transcobalamin I transport vitB12 to the tissue
30
Q

What are some causes of B12 deficiency

A
  • Impaired absorption
  • Decreased intake
  • Congenital causes
  • Increased requirements
  • Medication
31
Q

what can cause impaired absorption of B12

A
  • Pernicious anaemia
  • Gastrectomy or ileal resection
  • Zollinger-ellison syndrome
  • Parasites
32
Q

What can cause decreased intake of B12

A
  • Malnutrition
  • Vegan diet
33
Q

What congenital causes led to B12 deficiency

A
  • Intrinsic factor receptor deficiency
  • Cobalamin mutation C-G-1 gene
34
Q

How can increased requirements cause b12 deficiency

A
  • Haemolysis
  • HIV
  • Pregnancy
  • Growth spurts
35
Q

What medications can cause b12 deficiency

A
  • Alcohol
  • NO
  • PPI, H2 antagonists
  • Metformin
36
Q

What are the clinical consequences?

A

Brain: Cognition, depression, psychosis

Neurology: myelopathy, sensory changes, ataxia, spasticity

Infertility

Cardiac cardiomyopathy

Tongue: Glossitis, taste impairment

Blood: Pancytopenia

37
Q

What is pernicious anaemia

A
  • Autoimmune disorder
  • Lack of IF
  • Lack of B12 absorption
  • Gastric Parietal cell antibodies IF antibodies
38
Q

What are the treatments for nutritional anaemias?

A
  • Treat the underlying cause
  • Iron – diet, oral, parenteral iron supplementation, stopping the bleeding
  • Folic Acid – oral supplements
  • B12 – oral vs intramuscular treatment