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Molecular basis of disease > Nutritional Anaemias > Flashcards

Nutritional Anaemias Flashcards

1
Q

What is anaemia?

A

A condition where the number of red blood cells (or oxygen carrying capacity) is insufficient to meet the body’s physiologic needs

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2
Q

What is haemoglobin?

Haemoglobin structure?

A

iron containing oxygen transport metalloprotein within RBCs.

4 iron-containing haem groups
4 globin chains able to bind 4 O2

reduction in Hb = anaemia

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3
Q

Where are the blood cells made?

A

Bone marrow

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4
Q

Normal Erythropoiesis

A
  • Erythropoiesis begins in the bone marrow
  • the cells go through multiple processes of maturation
  • lose their nucleus and then are transferred into the peripheral blood where they are considered circulating RBCs.
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5
Q

What does maturation of red blood cells require?

A
  • Vitamin B12 & folic acid
  • DNA synthesis
  • Iron
  • Haemoglobin synthesis
  • Vitamins
  • Cytokines (erythropoietin)
  • Healthy bone marrow environment
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6
Q

Causes of anaemia

A

Failure of production :
hypoproliferation or reticulocytopenic

Ineffective Erythropoiesis

Decreased Survival:
Blood loss, haemolysis , reticulolysis

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7
Q

How to investigate the underlying CAUSE of anaemia?

A

Investigate the SIZE of RBC

Reticulocyte count then adds further clue as to failure of production or increased loss.

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8
Q

Function of iron

A

essential for O2 transport

The daily requirement for iron for erythropoiesis varies depending on gender and physiological needs

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9
Q

Nutritional anaemia

A

Nutritional anaemia is anaemia that is 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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10
Q

Which gender needs more daily iron?

A

Women need more daily iron than men (e.g. due to menstruation).

When pregnant, a lot more iron is needed.

Women reach male iron levels post-menopause

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11
Q

Where is dietary iron absorbed?

A

predominantly in the duodenum and the proximal jejunum via ferroportin receptors on enterocytes

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12
Q

Types of iron in food

A

Haem (meat, chicken, fish)
-easily absorbed

Non-haem (plant foods)
-not as easily absorbed

Recommended intake assumes 75% of iron is from haem iron sources

Non-haem iron absorption is lower for those consuming vegetarian diets, for whom iron requirement is approximately 2-fold greater.

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13
Q

Amount of iron absorbed depends on…

A

TYPE of iron ingested

-more haem iron and ferrous iron (e.g. red meat) is absorbed than non-haem and ferric forms

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14
Q

What is iron absorption regulated by?

What happens after iron is absorbed?

How is iron lost?

A

GI mucosal cells and hepcidin

iron is transferred into plasma and binds to transferrin

through sloughed mucosal cells and Desquamination/menstruation. You can’t excrete it or lose it by urination

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15
Q

How does Fe3+ circulate?

A

bound to plasma transferrin and accumulates within the cells as ferritin (stored)
-stored iron can be mobilised for reuse

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16
Q

Hepcidin

Stable iron forms

A

a hormone which regulates the absorption of iron in circulation

Ferric state- Fe3+
Ferrous state- Fe2+

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17
Q

Iron stores in men and women

A

Adult men normally have 35 to 45mg of iron per kg of body weight. Premenopausal women have lower iron stores as a result of their recurrent blood loss through menstruation.

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18
Q

Distribution of iron in the body

A

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 storage and transport proteins found in hepatocytes and reticuloendothelial macrophages in liver, spleen and bone marrow:

  • Ferritin
  • Haemosiderin
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19
Q

Function of reticuloendothelial macrophages

A

Ingest senescent red cells, catabolise haemoglobin to scavenge iron, and load the iron onto transferrin for reuse

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20
Q

Iron metabolism

A

Controlled by absorption rather than excretion, as we don’t have a natural excreting method for iron.

If you take in an excess of iron, the body doesn’t have a natural way of losing it. Some is lost through:

  • Blood loss/Menstruation
  • Mucosal cells desquamation
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21
Q

How does hepcidin function in iron homeostasis?

A

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

  • duodenum
  • macrophages involved in recycling senescent erythrocytes
  • iron-storing hepatocytes.
22
Q

Regulation of hepcidin

A

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

23
Q

Excess iron is stored as…

State of iron store…

A

Ferritin (protein)

reduce Ferritin stores and increase transferrin

24
Q

What happens to iron when absorbed in plasma?

A

Iron attaches to transferrin and transported to bone marrow, binding to receptors on RBC precursors

25
Q

Laboratory Iron studies

A 
Serum Fe
Haemoglobin levels
Ferritin
Transferrin Saturation
Total Iron Binding Capacity
26
Q

Laboratory investigations of iron deficiency anaemia

A

Ferritin - low
TF saturation - low
TIBC - high
Serum iron - low/normal

27
Q

Iron deficiency causes

A

Not enough in:

  • poor diet
  • Malabsorption (celiac disease)
  • increased physiological needs (e.g. pregnancy)

Losing too much:
- blood loss (menstruation, GI tract loss, parasites)

28
Q

Stages in the development of iron deficiency anaemia

A

Before anaemia develops, iron deficiency occurs in several stages:

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 (mean corpuscular volume) and MCH (mean corpuscular haemoglobin) do not become abnormal for several months after tissue stores are depleted of iron.

29
Q

What is the most sensitive laboratory indicator of mild iron deficiency?

A

Serum Ferritin

30
Q

Signs and symptoms of iron deficiency anaemia

A

Symptoms:

  • fatigue
  • lethargy
  • dizziness

Signs:

  • smooth tongue
  • systolic flow murmurs
  • pallor of mucous membranes
  • bounding pulse
  • koilonychias (thin,concave nails)
31
Q

Vitamin B12 and Folate Deficiency

A

· Both have very similar laboratory finding and clinical symptoms.
· Can be found together or as isolate pathologies

32
Q

What causes B12 and folate deficiency?

A

Macrocytic Anaemia

33
Q

Laboratory findings of B12 and folate deficiency

A 
[Hb] = low
[MCV] = high
[MCHC] = normal
34
Q

Macrocytic Anaemia

A

Macrocytic anaemia can be subdivided into megaloblastic and non-megaloblastic anaemia depending on their cause.

35
Q

Macrocytic anaemia: Megaloblastic

A

Megaloblastic: low reticulocyte count
>Vitamin B12/Folic acid deficiency
>Drug-related (interference with B12/Folic acid metabolism)

36
Q

Characteristics of megaloblastic anaemia on peripheral smear

A
  • macroovalocytes

- hypersegmented neutrophils

37
Q

Macrocytic anaemia: Non-megaloblastic

A 
Non-megaloblastic: if patient has macrocytic anaemia but not B12/Folic acid deficient
>Alcoholism
>Hypothyroidism
>Liver disease
>Myelodysplastic syndromes
>Reticulocytosis (haemolysis)
38
Q

Where do we get vitamin B12 from?

Where is vitamin B12 absorbed?

Where do we get Folate from?

Where is folate absorbed?

A

animal and dairy produce

Ileum via intrinsic factor

Vegetables, Liver

duodenum and jejunum

39
Q

Role of vitamin B12 and folate

A

Final maturation of RBC and synthesis of DNA

Both are need for thymidine triphosphate synthesis

40
Q

function of folate

A

DNA synthesis:

-adenosine, guanine, and thymidine synthesis

41
Q

Causes of folate deficiency

A

Increased Demand

  • pregnancy/breast feeding
  • infancy and growth spurts
  • haemolysis & rapid cell turnover (e.g. SCD)
  • disseminated cancer
  • urinary losses (e.g. heart failure)

Decreased Intake

  • poor diet
  • elderly
  • chronic alcohol intake

Decreased Absorption

  • medication (folate antagonists)
  • coeliac
  • jejunal resection
  • tropical sprue
42
Q

Folate stores

A

usually has enough stores for 3-5 months

43
Q

Role of vitamin B12

A

co-factor for methylation in DNA and cell metabolism

intracellular conversion of vitamin B12 to 2 active coenzymes is necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine

44
Q

What does vitamin B12 require for absorption?

A

Presence of intrinsic factor for absorption in terminal ileum

45
Q

Where is the intrinsic factor found?

How is vitamin B12 transported to tissues?

A

parietal cells in stomach

Transcobalamin II and Transcobalamin I transport vit B12 to tissues

46
Q

Causes of vitamin B12 deficiency

A

see picture

47
Q

Clinical consequences of Vitamin B12/Folate Deficiency

A

· Brain: Cognition, Depression, Psychosis
· Neurology: Myelopathy, Sensory changes, Ataxia, Spasticity (SACDC)
· Infertility
· Cardiac cardiomyopathy
· Tongue: glossitis, taste impairment
· Blood: Pancytopenia

48
Q

Pernicious anemia

A

an autoimmune disorder which causes vitamin B12 deficiency.

> antibodies are made against the cells which make the intrinsic factor (gastric parietal cells), or against the intrinsic factor itself

> lack of intrinsic factor therefore causes lack of B12 absorption

49
Q

Treatment of pernicious anaemia

A

If oral B12 given to patient, they still won’t be able to absorb it. To treat, patients are given injections of vitamin B12.

50
Q

Treatment of iron deficiency

A

Diet, oral, parenteral iron supplementation, stopping the bleeding

51
Q

treatment of folate deficiency

A

Oral supplements

52
Q

Treatment of vitamin B12 deficiency

A

oral vs intramuscular treatment

Molecular basis of disease (31 decks)

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