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Clinical Pathology > 4. Nutritional Anaemias > Flashcards

4. Nutritional Anaemias Flashcards

1
Q

What is anaemia?

A
  • Number of red blood cells (and consequently their oxygen-carrying capacity) is insufficient to meet body’s physiological needs; can also be less than normal quantity of haemoglobin in blood
  • Insufficient oxygen carrying capacity is due to reduced haemoglobin concentration as seen with insufficient RBC
  • Hb in g/L
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2
Q

What is haemoglobin? and what is expected on the blood film?

A
  • Haemoglobin – iron containing oxygen transport metalloprotein within RBCs
  • Varying normal concentration according the age, menstrual cycle, gender, pregnancy.
  • On a blood film, if the RBC has sufficient levels of Hb, there would be a clear ring of colour
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3
Q

What is required for normal erythropoiesis?

A

• Maturation of red blood cells require:

  • Vitamin B12 and folic acid for DNA synthesis
  • Iron for Haemoglobin synthesis

• Also need other vitamins, cytokines (erythropoietin), healthy bone marrow environment

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4
Q

What mechanisms cause anaemia?

A

1) Failure of production: hypoproliferation -> reticulocytopoenic (decreased number of reticulocytes)
2) Ineffective erythropoiesis: (red blood cell production)

3) Decreased survival:
- > blood loss, haemolysis, reticulocytosis (increased number of reticulocytes/immature RBCs)

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5
Q

How is anaemia classified?

A

Microcytic, normocytic, macrocytic anaemia - MCV

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6
Q

Expand on microcytic

A
  • Iron deficiency (haeme deficiency)
  • Thalassaemia (globin deficiency)
  • Anaemia of chronic disease
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7
Q

Expand on normocytic

A
  • Anaemia chronic disease
  • Aplastic anaemia
  • Chronic renal failure
  • Bone marrow infiltration
  • Sickle cell disease
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8
Q

Expand on macrocytic

A
  • B12 and folate deficiency
  • Myelodysplasia – deficiency in the bone marrow where it makes abnormal RBCs
  • Alcohol induced
  • Drug induced
  • Liver disease
  • Myxoedema
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9
Q

What are the different measurements to allow anaemia classification?

A
  • MCV (mean cell volume) – of RBC, part of complete blood count
  • Reticulocyte count – caused by failure of production (reticulocytopoenic) or increased losses?
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10
Q

What are the key players in nutritional anaemia?

A
  • Iron deficiency
  • vitamin B12 deficiency
  • folate deficiency
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11
Q

Expand on iron.

A
  • Essential for O2 transport (haemoglobin synthesis)
  • Daily requirement for iron for erythropoiesis varies depending on gender (little bit more in a menstruating women) and physiological needs, increases in pregnancy and lactation
  • Recommended intake assumes 75% of iron is from heme iron sources (meats, seafood). Non heme iron absorption is lower (applies to those with vegetarian diets, for whom iron requirement is approx.. 2-fold greater)
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12
Q

What is the distribution of iron within adults body? - inc, regulation and transport/storage

A
  • Dietary iron -> plasma transferrin, mainly absorbed in duodenum
  • MAJORITY of iron is in circulating erythrocytes (also a lot utilised in bone marrow and muscle myoglobin), storage iron in liver
  • Iron levels are REGULATED by hepcidin ~ tells your body how to regulate it at absorption level

• TRANSPORT:
- transferrin and lactoferin
•STORAGE ~ most in hepatocytes and reticuloendothelial macrophages.
- Ferritin = short-terM
- Haemosiderin = long-term
- (found in cells of liver, spleen and bone marrow)

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13
Q

Describe iron metabolism.

A
  • Iron metabolism controlled by absorption (rather than usual excretion); only lost through blood loss or loss of cells as they slough
  • More than 1 stable form of iron: Ferric states (3+) and Ferrous states (+2); these are two different oxidation states
  • Reticuloendothelial macrophages ingest senescent RBCs, catabolise Hb to scavenge iron and load the iron onto transferrin for reuse
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14
Q

Describe iron absorption

A
  • Regulated by GI mucosal cells and hepcidin
  • Most absorption in duodenum and proximal jejunum
  • Via FERROPORTIN receptors on enterocytes
  • Amount absorbed depends on the type ingested ~ heme, ferrous iron-containing proteins GREATER absorption than non-heme, ferric forms which is bound to other substances
  • Other factors that affect absorption: other foods, GI acidity, state of iron storage levels, bone marrow activity
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15
Q

How is iron concentration regulated?

A

HEPCIDIN

  • Inhibits iron transport by binding to iron export channel ferroportin located on the BASOLATERAL surface of enterocytes and membrane of reticuloendothelial cells (macrophages), and hepatocytes
  • Hepcidin causes ferroportin internalisation and degradation (lysosomal) -> decreased iron transfer into the blood plasma, from macrophages involved in recycling senescent erythroyctes and from iron-storing hepatocytes
  • Hepcidin is feedback-regulated by iron concentrations in plasma and the liver and by erythropoetic demand for iron.
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16
Q

Describe iron transport and storage.

A
  • From duodenum into mucosal cells ~ Iron transported from enterocytes and then either into plasma or if excess iron stored as ferritin
  • Combine with apoferritin (unbound ferritin) -> ferritin
  • Or cross to plasma where it binds to transferrin and enter cells via transferrin receptor (e.g. in erythroid precursors)
17
Q

How can you carry out iron deficiency investigations?

A
  • Full blood count (red blood cells): Hb, MCV, MCH, reticulocytes and blood film
  • Iron studies: ferritin, transferrin saturation, TIBC (total iron binding capacity)
  • Other studies: BMAT, iron stores
18
Q

What are the different lab iron studies?

A
  • SERUM Fe - Hugely variable during the day.
  • BLOOD TEST: FERRITIN – measures amount of iron stored; primary storage protein, provides reserve, water soluble ~ high levels can indicate iron storage disorder,
  • BLOOD TEST: TRANSFERRIN – made by liver, inversely proportional to Fe stores, vital for Fe transport,
  • URINE TEST: HAEMOSIDERIN – water insoluble, Fe- protein complex/iron-storage complex in cells; haemodiserinuria (brown urine) is secondary to excess intravascular haemolysis
  • BLOOD TEST: IRON BINDING CAPACITY – shows capacity to bind iron with transferrin (indirectly reflects transferrin levels)
  • BLOOD TEST: TRANSFERRIN SATURATIONS – Ratio of serum iron and total iron binding capacity – revealing % of transferrin binding sites that have been occupied by iron
19
Q

What would you see in a state of iron deficiency?

A
  • Reduced Hb levels
  • Reduced MCV
  • Reduced MCH
  • Reduced serum Fe
  • Reduced ferritin
  • Increased TIBC (reflecting transferrin)
  • Reduced transferrin saturation
  • Reduced/absent bone marrow iron studies
20
Q

What are the causes of iron deficiency?

A
  • Not enough: poor diet, malabsorption, increased physiological needs (e.g. pregnancy)
  • Losing too much: blood loss, menstruation, GI tract loss, parasites
21
Q

Iron deficiency occurs in several stages before anaemia develops. What are they?

A
  • Initially normocytic and normochromic
  • Moderate: microcytic (low MCV), hypochromic (low MCHC), reticulocytopoenic?
  • Serum ferritin most sensitive indicator for mild iron deficiency
  • Percentage saturation of transferrin with iron and free erythrocyte protoporphyrin (high levels indicate disruption of heme production?) values do not become abnormal until tissue stores are depleted of iron
  • Decrease in Hb concentration -> when iron unavailable for haem synthesis
  • MCV and MCH do not become abnormal for several months after tissues stores are depleted of iron.
22
Q

What is the prevalence of iron deficiency?

A
  • World’s most common nutritional deficiency
  • Blood loss from GI tract – most common causes of IDA in adult men and postmenopausal women
  • Excessive menstrual losses – 1st cause in premenopausal women
23
Q

What are the symptoms of iron deficiency?

A
  • Symptoms: fatigue, lethargy, dizziness

- Signs: pallor of mucous membranes, bounding pulse, systolic flow murmurs, smooth tongue, koilonychias (‘spoon nails’)

24
Q

Expand on clinical results of vitamin B12 and folate deficiency.

A
  • Both have very similar lab findings and clinical symptoms
  • Can be found together or as isolated pathologies
  • Cause of macrocytic anaemia – low Hb, high MCV, normal MCHC
25
Q

Expand on folate

A
  • Folate necessary for DNA Synthesis:
    Adenosine, guanine and thymidine synthesis
  • absorbed in the Jejunum and the body
26
Q

Causes of folate deficiency

A

=> Increase demand - e.g. pregnancy/breast feeding, infancy and growth spurts, haemolysis and rapid cell turnover (e.g. SCD), disseminated cancer and urinary losses (e.g. heart failure)

=> Decreased intake - e.g. poor diet, elderly and chronic alcohol intake

=> Decreased absorption - e.g. medication (folate antagonists), coeliac, jejunal resection and tropical sprue

27
Q

Expand on vitamin B12.

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
  • Animal sources: Fish, meat, dairy
  • 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
28
Q

What are the causes of B12 deficiency?

A

=> Impaired absorption - e.g. pernicious anaemia, gastrectomy/ileal resection, Zollinger-Ellison syndrome and parasites

=> Decreased intake - e.g. malnutrition, vegan diet

=> Congenital causes - intrinsic factor receptor deficiency, Cobalamin mutation, C-G-1 gene

=> Increase requirements - e.g. Haemolysis, HIV, pregnancy, growth spurts

=> Medication - e.g. alcohol, NO, PPI H2 antagonists, metformin

29
Q

What are haematological consequences?

A
  • Normal/raised MCV ~ megaloblastc anaemia ineffective erythropoeisis
  • Normal/low Hb
  • Low reticulocyte count
  • Raised LDH ~ intramedullary haemolysis
  • BLOOD FILM: macrocytes, ovalocytes, hypersegmented neuts
  • BMAT: hypercellular, megaloblastic, giant metamyelocytes ~ unusual to need
  • Increased MMA ~ not standard lab test
30
Q

Clinical consequences

A
  • Brain: cognition, depression, psychosis
  • Neurology: myelopathy, sensort changes, ataxia, spasticity (SACDC)
  • Infertility
  • Cardiac cardiomyopathy
  • Tongue: glossitis, taste impairment
  • Blood: Pancytopenia (reduction in the number of red blood cells, white blood cells and platelets)
31
Q

What is pernicious anaemia?

A
  • Autoimmune disorder
  • Lack of IF -> lack of B12 absorption
  • From gastric parietal cell autoantibodies or IF autoantibodies
32
Q

Treatments for iron, folate/B12 deficiency:

A
  • Treat the underlying cause
  • Iron – diet, oral, parenteral iron supplementation, stopping the bleeding
  • Folic acid – oral supplements
  • B12 – oral vs intramuscular treatment
33
Q

Macrocytic anaemia: causes

A 
• MEGALOBLASTIC: low reticulocyte count
- Vitamin b12/folic acid deficiency
- Drug-related
- Any interference with B12/folic acid metabolism
• NONMEGALOBLASTIC:
- Alcoholism ++
- Hypothyroidism
- Liver disease
- Myelodysplastic syndromes
- Reticulocytosis (haemolysis)
34
Q

Megaloblastic vs. non Megaloblastic

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.

Clinical Pathology (62 decks)

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