Anaemia 1

Question 1

Describe the RBC on a blood film in IDA?

Answer 1

hypochromic and microcytic.

Question 2

List causes of a hypochromic and microcytic appearance of RBCs on a blood film?

Answer 2

• IDA: not enough haem
• Thalassemia: not enough globin
• Anaemia of chronic disease
• Sideroblastic anaemia, particularly congenital.

Question 3

What is the normal Tf saturation?

How does this compare to IDA? Why?

Answer 3

• normally TF is 30% saturated with iron.

- In IDA, the liver makes more Tf to try pick up any circulating iron so is 15% saturated.

Question 4

How does serum ferrtin compare to RES iron stores?

Answer 4

Serum ferritin directly reflects RES stores.

So low serum ferritin = low RES stores.

Question 5

Describe serum ferritin, RES iron store and Hb in latent IDA and IDA?

Answer 5

Latent: Low serum ferritin, low RES iron and normal Hb (RBCs take up all the iron)
IDA: Low serum ferritin, low RES stores and low Hb.

Question 6

Why would IDA be missed in a patient with RA or IBD?

Answer 6

As serum ferritin can can be raised as it is an acute phase protein and is raised in tissue damage.

Question 7

List clinical signs of IDA?

Answer 7

Koilonicia
Atrophic glossitis
Angular stomatitis
Oesophageal web

Question 8

List causes of IDA?

Answer 8

1. Dietary
2. Malabsorption e.g. coeliax
3. Blood loss (GI blood loss, period)

Question 9

Describe oral iron replacement therapy? How much iron is in them?

Answer 9

Ferrous sulphate: 200mg = 60mg of iron

Ferrous gluconate: 300mg = 36g of iron. Give these to reduce iron intake if patient is having GI upset.

Question 10

When would IV iron replacement therapy be used? What is the dose?

Answer 10

When patient is intolerant of oral therapy or has poor complience.
Give 1g over 2-3h

Question 11

Describe (briefly) the reason patients with chronic disease get anaemia?

Answer 11

Elevated IL-6 which stimulates hepcidin production so there is reduced ferroportin. Iron becomes trapped in RES stores.
Also reduced Epo response and depressed bone marrow activity due to cytokines and chemokines.

Question 12

Why do patients with chronic kidney disease get anaemia?

Answer 12

due to anaemia of chronic disease + decreased Epo production.

Question 13

What is the role of B12?

Answer 13

Needed for methylation of homocystine to methionine.

Also for isomerisation of methylmalmonyl-CoA.

Question 14

What are dietary sources of B12/

Answer 14

Meat such as liver and kidney.

Small amount in dairy products.

Question 15

What is the daily requirement of B12?

Answer 15

1 microgram.

Question 16

How is B12 absorbed?

Answer 16

Gastric parietal cells make intrinsic factor.
Stomach acid and enzyme breakdown food and release B12 which binds to IF.
IF-B21 complex binds to cubilin receptor in the termial ileum.

Question 17

How much and where is B12 lost daily?

Answer 17

1-2 micrograms in urine/faeces.

Question 18

How long do normal B12 stores last?

Answer 18

3-4 years.

Question 19

Where do you get folate from?

Answer 19

Dietary from green veg.

Question 20

Where is folate absorbed from?

Answer 20

Most of small bowel.

Question 21

How long do folate stores last?

Answer 21

Only a few days.

Question 22

What can speed up the rate of folate store depletion?

Answer 22

Quick cell turnover e.g. pregnancy or increased cell turnover.

Question 23

Describe the pathophysiology of anaemia due to B12/folate deficiency?

Answer 23

Not enough B12/folates you get problems with triphosphates and DNA is fragile and bad at dividing causing abnormal cell division.
Causes ineffective erythropoiesis and red cells are broken down in the marrow as they dont pass quality control.

Question 24

Describe histology on blood film in B12/folate deficiency?

Answer 24

Get nuclear and cytoplasm dissociation as cytoplasm matures but the nucleus is fragmented.
May see large oval RBC’s.
Macrocytic Megaloblastic Anaemia.
May also get leukopenia and thrombocytopenia.

Question 25

What neurological manifestations may be seen in B12/folate deficiency?

Answer 25

Bilateral peripheral neuropathy.
Get demyelination of the posterior and pyramidal tracts of spinal cord.
Problems with join position, walking and sensation.

Question 26

Why is there neurological manifestations in B12/folate deficiency?

Answer 26

Due to problem with converting homocystine to methionine.

Question 27

What tissues are affected in B12/folate deficiency?

Answer 27

All rapidly growing tissues

• epithelial surfaces
• pregnancy
• bone marrow
• spinal cord

Question 28

Why is raise LDH a useful marker in anaemia?

Answer 28

As LDH is abundant in RBC’s so is raised in haemolysis.

Question 29

What are the signs of B12/folate deficiency?

Answer 29

• SOB due to decreased O2 carrying capacity.
• Tired.
• Pale
• May have bruising due to thrombocytopenia
• May have jaundice due to haemolysis
• May have neurological problems due to degeneration of lateral and dorsal columns
• Painful tongue

Question 30

What are the causes of anaemia due to B12 deficiency?

Answer 30

• Dietary intake
• Malabsorption - problem with terminal ileum, following surgery, crohns
• ## Pernicious anaemia: Autoantibodies against gastric parietal cells so unable to make intrinsic factor.

Question 31

What are causes of folate deficient anaemia?

Answer 31

• Dietary
• Extensive small bowel disease
• Increased cell turnover: Haemolysis, skin disorders, pregnancy.

Question 32

What are causes of macrocytosis?

Answer 32

1. Reticulocytosis: e.g. after a bleed and the BM makes lots of reticulocytes.
2. Cell wall abnormalities e.g. due to liver problems or hypothyroidism. Cells have poor architecture and may be larger.
3. In bone marrow failure: Causing abnormal cells to be produced e.g. after chemotherapy.