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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

what is anaemia classified as according to Hb conc.? how is Hb conc measured in the lab? how is HCT measured?

A

Men: Hb<130g/l (HCT 0.38-0.52)
Women: Hb<120g/l (0.37 - 0.47)

RBC lysed to create a Hb solution, Hb stabilised and optical density measured which is proportional to Hb conc.

HCT is the ratio of whole blood that is RBCs, machines do this by adding calculated volume of RBC it counts

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2
Q

Which two situations is Hb/HCT not a good marker for anaemia?

A

When a patient has had an acute bleed and plasma has expanded

when a patient has been given IV fluids which ‘dilute’ blood

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3
Q

What are the two responses the body has to anaemia?

A
  • EPO is released from kidney to increase erythropoeisis

- peripheral blood reticulocytosis (up regulation of bone marrow to reticulocytes may take a few days)

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4
Q

What different blood analyses are important in anaemia?

A

measured red cell indices: Hb conc., RBC count, MCV (size of cells)
calculated red cell indices: HCT, mean cell Hb/HCT

Blood film: morphology

Reticulocyte count - assess bone marrow response

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5
Q

What two mechanisms of anaemia would result in a low reticulocyte count?

A
  • hypoproliferative = reduced amount of erythropoeisis e.g. cancer
  • maturation abnormalities = ineffective erythropoeisis
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6
Q

What are the two main pathophysiologies for maturation abnormalities in RBCs, what types of anaemia would this cause?

A

-Cytoplasmic defects: impaired haemoglobinisation = hypochromic, microcytic
(haemoglobin is synthesis occurs in cytoplasm and needs haem and globins)

-Nuclear defects: macrocytic

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7
Q

What are the three causes of haem deficiency?

A
  • Iron deficiency
  • anaemia of chronic disease (normocytic)
  • lack prorphyrin synthese RARE (lead poisoning/pyridoxine responsive anaemias/congenital sideroblastic anaemias)
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8
Q

What is the cause of globin deficiency?

A

Thalassaemia:

  • trait
  • intermediate
  • major
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9
Q

What mechanism of anaemia would result in a high reticulocyte count?

A

increased loss/destruction of RBC’s

  • bleeding
  • haemolysis
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10
Q

What is macrocytosis?

A

increase in the number of large cells

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11
Q

What is macrocytic anaemia?

A

anaemia and RBCs have larger than normal cell volume (MVC)

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12
Q

what are the two causes for genuine macrocytosis and what are the two causes for spurious macrocytosis?

A

Genuine:

  • megaloblastic anaemia
  • non-megaloblastic anaemia

Spurious:

  • reticulocytosis (reticulocytes look bigger, this is the marrows response to bleeding or haemolysis)
  • cold agglutins (clumps of agglutinated RBC’s registered as 1 big cell)
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13
Q

What is a megaloblast?

A

-abnormally large nucleated red cell precursor with an immature nucleus

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14
Q

Describe what happens to cells as they advance through erythropoeisis?

A

Pronormoblast: no Hb and lots of nucleus

Then the nucleus becomes condensed and cytoplasm matures and produces Hb

When the cytoplasm is fully matured it ‘throws’ out nucleus (enucleation) = reticulocyte (RNA still present)

Reticulocytes start to appear in blood

Then RNA is lost = erythrocyte

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15
Q

what causes a megaloblastic anaemia?

A

normal cytoplasmic maturation and haemoglobin synthesis but defects in DNA synthesis and nucleus maturation

(cytoplasm has developed and became big enough to divide but nucleus lags behind and remains immature so the cell doesn’t actually divide. Then the cytoplasm senses it has enough Hb and throws out the nucleus without dividing and cytoplasm remains big as nucleus hasnt condensed
=bigger than normal red cell precursor
=small number of big cells)

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16
Q

what are the 3 causes for megaloblastic anaemia?

A
  • B12 deficiency: B12 produces chemical that methylates DNA
  • Folate deficiency: folate responsible for DNA/nucleoside synthesis
  • others: rare inherited abnormalities/drugs
17
Q

B12 deficiency:

  • small bowel causes
  • pancreas causes
  • stomach causes
A

Small bowel causes:

  • jejunum: bacterial overgrowth/coeliac disease
  • Duodenum: crohn’s/resection

Pancreas:
-chronic pancreatitis

Stomach:

  • atrophic gastritis
  • pernicious anaemia
  • PPI’s/H2 receptor antagonists
  • Gastrectomy/bypass
18
Q

What is pernicious anaemia caused by?

A

autoantibodies to parietal cells in stomach that release intrinsic factor

  • CD4 mediated response
  • assoc. with gastritis/PMH or FH autoimmune disorders
19
Q

B12 or folate deficiency:

  • what type of anaemia is seen?
  • what is seen on blood film?
  • what other tests are important? 2
  • What can be done to look for megaloblasts?
A

Macrocytic anaemia (pancytopenia in some)

  • hypersegmented neutrophils (usually 3-5segments)
  • Macro-ovalocytes (oval macrocytes)

Other test:

  • Assay of B12 and folate in serum (not sensitive/specific)
  • check autoantibodies (anti-gastric parietal cell/anti-intrinsic factor)

Bone marrow examination can be used as a last resort to look for megaloblasts

20
Q

What are the four general causes of folate deficiency?

A

Drugs: anticonvulsants

Excess utilisation: haemolysis, pregnancy, malignancy, exfoliating dermatitis

Malabsorption: crohn’s / coeliac

Inadequate intake

21
Q

What are the clinical signs and symptoms of B12 and folate deficiency? 7

A
  • s/s anaemia
  • wt loss
  • diarrhoea
  • infertility
  • sore tongue
  • jaundice (ineffective erythropoeisis and RBC’s prematurely die in marrow releasing Hb)
  • developmental problems
22
Q

What irreversable complication is there for B12 deficiency?

A

Myelin sheath abnormalities = neuro. problems

  • posterior/dorsal column abnormalities
  • neuropathy
  • dementia
  • psych. manifestations
23
Q

What is the management of megaloblastic anaemia:

  • pernicious anaemia
  • folate deficiency
  • if life threatening
A

treat cause

Pernicious anaemia: vitamin B12 injections for life (high dose oral hydroxycobalamine may be effective - passive diffusion)

Folate deficiency: folic acid 5g/day tablets

If life threatening: transfuse red cells

24
Q

What are some causes for non-megaloblastic macrocytosis?

A

Alter the red cell membrane (may not be anaemic)

  • Alcohol
  • Liver disease
  • hypothyroid

With anaemia as well (marrow failure)

  • myelodysplasia
  • myeloma
  • aplastic anaemia
25
Q

If a patient has a microcytic, hypochromic anaemia: what is the main problem and what are the causes?

A

Problem with Haemoglobin

Causes:
-Iron deficiency
-Thalassaemia
Rare - lead poisoning, pyroxidane responsive anaemias, sideroblastic anaemia

26
Q

If a patient has a macrocytic, normochromic anaemia: what is the main problem and what are the causes?

A

Main problem is the nucleus if megaloblastic or other if not

Causes:

  • Megaloblastic is B12 or folate deficiency
  • myelodysplasia
  • myeloma
  • aplastic anaemia
  • spurious (cold agglutins or reticulocytosis)
  • often no anaemia (alcohol/hypothyroid/liver disease)
27
Q

If a patient has a normocytic normochromic anaemia: what is the main problem and what are the causes?

A

not enough normal RBCs

Causes:

  • blood loss/early iron deficiency
  • hypoproliferative (chronic inflammatory, infective, malignant, renal failure, anaemia chronic disease, hypometabolic states e.g. hypothyroid, marrow failure
28
Q

What is anaemia of chronic disease?

A

Cant access iron

Inflammatory stimulus causes an increase of hepcidin from the liver, inhibits erythroid proliferation, inhibits EPO release, augments haemophagocytosis
=micro/macro/normocytic anaemia
=mixed picture

29
Q 
How is:
serum iron
serum transferrin
transferrin saturations
ferritin
MCV 
different in iron deficiency and anaemia of chronic disease?
A

Iron deficiency:

  • serum iron is low
  • serum transferrin is normal or high
  • Transferrin saturation is low
  • Ferritin levels low
  • MCV low or normal

Chronic disease:

  • serum iron is low
  • serum transferrin is normal or low
  • transferrin saturations are low
  • ferritin is high (lots of iron but cant get to it)
  • MCV is normal

USE FERRITIN TO DISTINGUISH

Haematology (19 decks)

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