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SEM 4: Haematology > The Nutritional Anaemias > Flashcards

The Nutritional Anaemias Flashcards

1
Q

What is the most common definition of anaemia?

A

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

What causes insufficient oxygen carrying capacity?

A

Due to reduced haemoglobin concentration as seen with insufficient RBC.
Most pts are diagnosed before it is severe.

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3
Q

What is haemoglobin?

A
  • Iron containing oxygen transport metalloprotein
  • Within RBCs
  • Carries Fe and O2
  • Used to measure anaemia: reduction in Hb causes anaemia
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4
Q

Where are RBC made?

A
  • Made in the bone marrow

- Dependent on environment, structure and cytokines available

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5
Q

What do RBC look like on a normal blood film?

A

RBC usually round and have a central pallor.

1/3 diameter

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6
Q

Difference between anaemia in the UK and in the USA

A

UK is based on Hb levels and USA relies on RBC count.

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7
Q

Describe the normal Hb levels

A 
Normal: g/L
> 120 teens 
> 110 children up to 5 years 
> 115 children up to 12 
> 110 pregnant women 
> 120 non-pregnant women 
> 130 men

Less than this will cause anaemia and there can be mild, moderate or severe anaemia

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8
Q

Why do women have lower Hb levels than men?

A

Due to menstruation and pregnancy

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9
Q

What does the maturation of RBC require?

A
  • Vitamin B12
  • Folic Acid
  • DNA synthesis
  • Iron
  • Haemoglobin synthesis
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10
Q

Describe the simple life cycle of a RBC

A
  • RBC (in bone marrow)
  • Rounds of maturation
  • Loss of nucleus
  • Released into peripheral blood
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11
Q

Why is erythropoeitin needed?

A

It induces bone marrow to produce RBC.

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12
Q

What conditions does normal erythropoeisis require?

A
  • Working bone marrow
  • Correct environment to structure
  • Correct Genetics
  • Vitamin B12 and Folic Acid = DNA synthesis
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13
Q

Why does someone become anaemic?

A
  • Failure of production (of RBC): hypoproliferation; Reticulocytopenic
  • Ineffective Erythropoiesis: Problem with bone marrow
  • Decreased Survival: Blood loss, haemolysis, reticulocytosis - anaemic due to blood loss
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14
Q

What are reticulocytes?

A

Immature RBCs are seen in peripheral blood.

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15
Q

Why is the size of RBC important?

A

It is used to decide underlying cause of anaemia

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16
Q

What is microcytic anaemia? What causes microcytic anaemia?

A

Smaller Hb sizes

  • Iron deficiency (haem deficiency)
  • Thalassemia (globin deficiency)
  • Anaemia of Chronic Disease
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17
Q

What is normocytic anaemia? What causes normocytic anaemia?

A

Mixtured MCV

  • Anaemia Chronic Disease
  • Aplastic anaemia
  • Chronic Renal Failure
  • Bone marrow infiltration
  • Sickle cell disease
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18
Q

What is macrocytic anaemia? What causes macrocytic anaemia?

A 
Bigger Hb sizes 
- B12 deficiency 
- Folate deficiency 
The above are key causes of macrocytic anaemia 
- Myelodysplasia: deficiency of bone marrow 
- Alcohol-induced 
- Drug-induced 
- Liver disease 
- Myxoedema
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19
Q

WHat causes nutritional anaemia?

A

Anaemia caused by lack of essential ingredients that the body acquires from food sources e.g. iron deficiency, V12 deficiency, Folate deficiency

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20
Q

What is the function of iron?

A
  • Essential for O2 transport
  • Most abundant trace element in body
  • Daily requirement for iron for erythropoiesis varies depending on gender and physiological needs
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21
Q

Why do maternal iron stores decrease quickly?

A

A child requires a lot of iron for growing etc. As well as this, women need more iron than men due to menstruation etc. Pregnancy require a lot more iron due to the growth of the baby.

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22
Q

What are the two sources of iron?

A

Haem (meat) -> better absorption

Non-haem (non-meat) -> 50% absorption rate

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23
Q

Describe the absorption and storage of iron

A
  1. Iron enters and absorbed by the duodenum
  2. It is absorbed by the plasma
  3. In plasma, proteins required to metabolize and also tested for in labs.
  4. If too much iron is absorbed, the protein transferrin enters the duodenum and is the storage protein.
  5. Iron is regulated by hepcidin which tells the body how to regulate the absorption level.
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24
Q

What are the forms of iron?

A

> 1 stable form of iron: Ferric states (3+) and Ferrous states (2+)
Most iron is in the body as circulating Hb and the remainder as storage and transport proteins - ferritin and haemosiderin. This is found in cells of liver, spleen and bone marrow.

25
Q

Which cells regulate the absorption of iron?

A
  • GI mucosal cells and hepcidin
26
Q

Which parts of the body absorb iron?

A

Duodenum and proximal jejunum via ferroportin receptors on enterocytes

27
Q

What happens when the iron is transferred to plasma?

A

It binds to transferrin

28
Q

What affects the absorption of iron?

A
  • The 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.
29
Q

What is hepcidin?

A

It is an iron-regulatory hormone (as well as ferroportin) that control the dietary absorption, storage, and tissue distribution of iron.

30
Q

How does hepcidin work?

A
  • It 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.
31
Q

What regulates hepcidin?

A

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

32
Q

Describe the transport of irons

A
  • 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 or iron deficiency means there are reduced ferritin stores and then increased transferrin
33
Q

Describe the action of transferrin

A
  1. Takes it to storage in the RBC and the reticuloendothelial system in the bone marrow to RBC production.
  2. Some are put into myoglobin in muscles and some in the liver.
  3. The iron that is not needed is stored as ferritin.
34
Q

What is measured to look at iron deficiency?

A
  • Transferrin levels are measured as there is an increase in transferrin to increase levels of iron. The levels are transient. Transferrin has low saturation; if transferrin cannot bind, ferritin will still be in the normal range but still iron deficiency due to low transferrin saturation.
  • Ferritin; when looking at low iron = low ferritin - also part of the immune system increasing levels so other tests need to be done.
35
Q

Why is serum Fe not measured when looking at iron deficiency?

A

Not as good as hugely variable during the day

36
Q

What are the lab results in iron deficiency anaemia?

A

Ferritin: Low
Tf Saturation: Low
TIBC: High
Serum Iron: Low/Normal

37
Q

What are the iron deficiency investigations?

A

FBC: Hb, MCV, MCH, Reticulocyte count (likely to be low)
Iron studies: ferritin, transferrin saturation
Blood film
BMAT and Iron stores: take liquid from bone and stain for iron stores

38
Q

What does FBC show initially in iron deficiency anemia?

A

Normocytic and normochromic

- Ferritin is the first measurement that changes and done early on to show anaemia

39
Q

Hypochromic Microcytic Anaemia

A
  • Area of central pallor is thinner so low Hb = Hypochromic

- Low MCV: smaller RBC = microcytic

40
Q

What is the normal ferritin levels?

A

Between 30-400

41
Q

Signs and Symptoms of IDA

A

Symptoms
Fatigue, lethargy and dizziness

Signs 
Pallor of mucous membranes 
Bounding pulse 
Systolic flow murmurs
Smooth tongue, koilonychias
42
Q

What type of anaemia does B12 and Folate Deficiency cause?

A

Macrocytic anaemia

- Low Hb and high MCV with normal MCHC

43
Q

What are the two types of macrocytic anaemia and how are they different?

A

Megaloblastic - interferes with the DNA pathway = vitamin B12 and folate deficiency or drug-related

Non-megaloblastic - anything else that causes macrocytic anaemia such as alcoholism, hypothyroidism, liver disease etc

44
Q

Why is vitamin B12 and Folic acid important?

A

VB12 = cobalamin and folic acid are required for AA production.
Both important for the final maturation of RBC and for the synthesis of DNA.
Both needed for thymidine triphosphate synthesis

45
Q

The blood film of megaloblastic anaemia

A
  • Macrovalocytes and hypersegmented neutrophils
  • Ovalocytes still with haemoglobin
  • Whereas in Non-megaloblastic - abnormal RBCs
46
Q

How to diagnose folate deficinecy?

A

Low reticulocyte count
Low folate levels
Low B12 levels - chaotic RBC production

47
Q

What synthesis for folate deficiency needed for?

A

Needed for adenosine, guanine and thymidine synthesis

48
Q

What are the causes of folate deficiency?

A
  • Common in the elderly population - so gradual development
  • Poor diet
  • Chronic alcohol intake: direct toxic or interferes with folate pathway
  • Medication such as folate antagonists
  • Coeliac disease
  • Jejunal resection
  • Tropical Sprue
  • Pregnancy/Breastfeeding
  • Infancy and growth spurts
  • Haemolysis and rapid cell turnover e.g. SCD
  • Disseminated Cancer
  • Urinary losses e.g. heart failure
49
Q

Where is folate lost?

A

When cooking most foods - 60-80%

50
Q

What is vitamin B12 a co-factor for?

A

It is a co-factor for methylation in DNA and cell metabolism
It converts 2 active coenzymes for homeostasis of methylmalonic acid (MMA) and homocysteine

51
Q

Foods that contain vit B12

A

Animal sources: Fish, meat and dairy

recommended intake is 1.5 mcg/day etc

52
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum which requires the presence of intrinsic factor

53
Q

Where is IF made?

A

It is made in parietal cells in the stomach without it Vit B12 cannot be absobred

54
Q

How is vit B12 transported to tissues?

A

By transcobalamin II and Transcobalamin I

55
Q

What are some causes of B12 deficiency?

A

Impaired Absorption: pernicious anaemia, gastrectomy or ileal resection and Zollinger-Ellison syndrome and Parasites
Decreased intake: malnutrition and vegan diet
Congenital causes: intrinsic factor receptor deficiency and cobalamin mutation C-G-1 gene
Increased requirements: Haemolysis, HIV, Pregnancy and Growth spurts
Medication: Alcohol, NO, PPI, H2 antagonists and metformin

56
Q

Which cell is used to gauge the size of RBC?

A

Lymphocyte

57
Q

What are the clinical (neurology- specifically) consequences of vit B12 deficiency?

A

*Neurology: Myelopathy, sensory changes, ataxia, spasticity (SACDC - subacute combined degeneration of cord)
Brain: cognition, depression, and psychosis
Infertility
Cardiac cardiomyopathy
Tongue: glossitis, taste impairment
Blood: Pancytopenia

58
Q

What is pernicious anaemia?

A

An autoimmune disorder where antibodies are developed against IF or cells that produce IF = vitamin B12 deficiency as no absorption if no IF.

59
Q

What are the treatments of deficiency anaemias?

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

SEM 4: Haematology (8 decks)

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