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Year 3 Clinical > Macrocytosis and Macrocytic Anaemia > Flashcards

Macrocytosis and Macrocytic Anaemia Flashcards

1
Q

What is macrocytosis?

A

Increased in rbc size

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2
Q

What is macrocytic anaemia?

A

Anaemia in which the rbcs have a larger volume than normal (MCV)

NOTE - macrocytosis and macrocytic anaemia are not the same

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3
Q

Units of MCV?

A

Mean Corpuscular Volume

Units are femtolitres (fL)

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4
Q

Results with a macrocytic anaemia?

*EXAMS*

A

Reduced Hb and RBC count = anaemia

Raised MCV = macrocytosis

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5
Q

Results with macrocytosis? *EXAMS*

A

Normal Hb and RBC count

MCV raised

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6
Q

2 broad classifications of macrocytosis causes?

A

Genuine (true) macrocytosis:

  • Megaloblastic
  • Non-megaloblastic

Spurious (false) macrocytosis

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7
Q

What is an erythroblast?

A

AKA normoblast

Normal rbc precursor, with a nucleus

NOTE - rbc precursors, except the reticulocyte, have a nucleus and are usually marrow-based

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8
Q

Changes in developing erythroid cells in the marrow?

A

Accumulate Hb

Reduced size

Stop dividing and lose nucleus (enucleation)

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9
Q

Structure of a mature rbc?

A

Membrane surrounding soluble proteins and electrolutes

NO NUCLEUS

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10
Q

Differences between a reticulocyte and a mature rbc/erythrocyte?

A

Reticulocyte is larger

Reticulocyte retains some RNA (blue tint)

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11
Q

What is a megaloblast?

A

Abnormally LARGE red cell precursor with an IMMATURE NUCLEUS

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12
Q

Characteristics of megaloblastic anaemias?

A

Predominant effects in DNA synthesis and nuclear maturation

WITH

Relative preservation of RNA and Hb synthesis

This results in the more mature erythroblasts having reduced division and increased apoptosis

A few erythroblasts survive as megaloblasts and have normal cytoplasmic development and enucleation; however, the rbc is larger than normal and there are fewer rbcs overall, i.e: patient has a macrocytic anaemia

NOTE - the bone marrow is full of megaoblasts in this type of anaemia

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13
Q

Why are the red cells bigger in a megaloblastic anaemia?

A

Megaloblasts are abnormally large precursors and, as less cell division occurs, the red cells FAIL TO GET SMALLER and thus are larger than normal

In fact, the rbcs are termed MACRO-OVALOCYTES (due to their large, oval shape)

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14
Q

Why is there anaemia in a megaloblastic anaemia?

A

The end result is a low number of rbcs, due to increased apoptosis

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15
Q

Causes of megaloblastic anaemia?

A

B12 deficiency

Folate deficiency

Others:

  • Drugs
  • Rare, inherited abnormalities, e.g: in enzymes assoc. with B12 and folate
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16
Q

Why does B12 or folate deficiency cause a megaloblastic anaemia?

A

B12 and folate are essential co-factors for nuclear maturation; they enable chemical reactions that provide enough nucleosides for DNA synthesis

17
Q

Biochemical reactions of B12 and folate?

A

They are inter-linked:

  • Methionine cycle - produces s-adenosyl methionine, a methyl donor that has a potential impact on DNA, RNA, proteins, lipids, folate intermediates
  • Folate cycle - for nucleoside synthesis, e.g: uridine to thymidine conversion
18
Q

What is homocysteine a marker of?

A

Homocysteine is converted to methionine as part of the methionine cycle, which is linked to the folate cycle

If homocysteine accumulates, indicates a B12 or folate deficiency

19
Q

How is vitamin B12 absorbed?

A

Gastric parietal cells release intrinsic factor; this travels with B12 to the small bowel and the basic environment here allows them to bind and form a complex

Absorption occurs in the terminal ileum, into the bloodstream

20
Q

Issues with B12 absorption at different sites?

A

Inadequate dietary intake is an unlikely cause

Stomach:

  • Pernicious anaemia
  • Atrophic gastritis
  • Achlorohydria (PPIs, H2-receptor antagonists)
  • Gastrectomy, bypass

Pancreas:

• Chronic pancreatitis (less basic pancreatic juices entering the small bowel)

Small bowel:

  • Jejunum - coeliac disease (malabsorption), bacterial overgrowth (use B12)
  • Duodenum - resection, Crohn’s disease
21
Q

What is pernicious anaemia?

A

Autoimmune condition resulting in gastric parietal cell destruction; leads to intrinsic factor deficiency with B12 malabsorption and deficiency

Assoc. with atrophic gastritis and PMH or FH of other autoimmune disorders, e.g: Hypothyroidism, vitiligo, Addison’s disease

22
Q

How is folate absorbed?

A

Dietary folates are converted to monoglutamate and absorbed in the jejunum

23
Q

Compare the characteristics of folate and B12 diet and stores?

A

B12:

  • Source - animal
  • Body stores - 2-4 years
  • Absorbed - ileum
  • Daily requirement - 1-3 micrograms/day

Folate:

  • Source - leafy vegetables, yeast; it is destroyed by cooking
  • Body stores - 4 months
  • Absorbed - duodenum and jejunum
  • Daily requirement - 100 micrograms/day
24
Q

Causes of folate deficiency?

A

Inadequate intake more likely with folate than with B12, as there are less stores of folate

Malabsorption:

  • Coeliac disease
  • Crohn’s disease

EXCESS UTILISATION:

  • Haemolysis
  • Exfoliating dermatitis
  • Pregnancy
  • Malignancy

Drugs, e.g: anti-convulsants

25
Q

Clinical features that are common to both B12 and folate deficiency?

A

Symptoms/signs of anaemia

Weight loss, diarrhoea

Infertility

Sore tongue

Jaundive

Developmental issues

26
Q

Clinical features that are more common with vitamin B12 deficiency?

A

Neurological issues, e.g:

  • Posterior/dorsal column abnormalities (LOSS OF PROPRIOCEPTION AND VIBRATION SENSE is common)
  • Neuropathy
  • Dementia
  • Psychiatric manifestations
27
Q

Results with B12 or folate deficiency anaemia?

A

Macrocytic anaemia (low rbc number)

In some patients, pancytopenia (all cells are low in number)

Blood film shows macro-ovalocytes and hypersegmented neutrophils (normally, 2-5 nuclear segments)

EXAMS - what is the blood film appearance of B12/folate deficiency?

28
Q

Other methods of identifying B12/folate deficiency?

A

Assay B12 and folate levels in serum - however, low levels may not indicate a deficiency and normal levels may not indicate normalcy

Check for auto-antibodies:

  • Anti gastric-parietal cells (GPC)
  • Anti- intrinsic factor (IF)

Schilling’s test (not routinely used)

Bone marrow examination (not usually required)

29
Q

Flaws with auto-antibodies?

A

Anti-GPC is sensitive but not specific; other situations where they may be +ve include hypothyroidism

Anti-IF is more specific but not sensitive; if these are +ve, highly likely to be pernicious anaemia, but not sensitive

30
Q

Treatment of megaloblastic anaemia?

A

Treat the underlying cause if possible

For PA - life-long vitamin B12 injections

Folic acid tablets (5mg per day) PO

If potentially life-threatening anaemia, transfuse rbcs

31
Q

Causes of non-megaloblastic macrocytosis?

A

This is where the rbc membrane changes

The following may not be assoc. with anaemia:

  • Alcohol
  • Liver disease
  • Hypothyroidism

The following are assoc. with anaemia:

  • Myelodysplasia
  • Myeloma • Aplastic anaemia
32
Q

What is spurious (false) macrocytosis?

A

Size of the mature rbc is NORMAL but the MCV is measured as high

33
Q

Causes of spurious macrocytosis?

A

Haemolysis - increased reticulocytes as a marrow response to acute blood loss or rbc breakdown; as reticulocytes are larger than mature rbcs, they produce a high MCV result i.e: the reticulocytosis is causing a false macrocytosis

Cold-agglutins - autoimmune disease with IgM against rbcs; results in clumps of agglutinated rbcs being registered as 1 ‘giant cell’, increasing the MCV

34
Q

How to approach macrocytic anaemia?

A
35
Q

Why can patients with PA appear mildly jaundiced?

A

Intramedullary haemolysis, due to ineffective erythropoiesis:

  • Red cells die prematurely in the marrow
  • Hb and lactate dehydrogenase are released from dead red cells
  • Hb is converted to bilirubin
36
Q

Complications of severe megaloblastic anaemia?

A

Pancytopenia

NOTE - patient vitamin B12/folate megaloblastic anaemias often have a degree of pancytopaenia, as DNA synthesis is affected in all cells; problems occur with bone marrow first due to the high rate of cell division

Year 3 Clinical (100 decks)

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