22. Review of Anaemia Flashcards

1
Q

What is anaemia? (Give values)

How is the total body erythrocyte mass measured?

Describe the pathophysiology of anaemia.

A
  • *Low Hb** concentration (< 120g/L) due to decrease in total body erythrocyte mass (haematocrit < 37%) or increased plasma volume -> hypoxia. (pic)
  • All damage to body from any pathologic state in the end is caused by hypoxia at some level*.

Requires special radiolabelling techniques. Daily measure: FBC - Hbg and HTC (haematocrit).

Normally balanced production (bone marrow) and destruction of RBC, retics 2%. Anaemia = unbalanced. Due to:
a) destruction/loss (e.g. bleeding, haemolysis, retics >2%) OR
b) low/no production (aplastic anaemia, retics 0%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the clinical classification of anaemia? Include the different types.

A

(pic)

MCV: Low: <76fl. Not making Hb so cells smaller.
Norm: 76-96fl. Incl. renal failure and pregnancy.
High: >96fl. Normally problems with DNA prod and maturation. Incl myelodysplasia. Reticulocytosis = increase in retics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Identify A-C on this blood film.

How many L is one ft?

How many cubic micrometers (μm3) is one ft?

What is the normal volume of 1 RBC?

A

A) reticulocyte
B) Neutrophil
C) Platelet

10-15L

1μm3

80-100fl. (femtolitre)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe 3 things that happen in acute compensation (e.g. if you suddenly start bleeding).

A
  • *1) Right shift of 2,3 DPG curve** (pic) - 2,3 DPG in RBC at approximately 5 mmol/L, binds with greater affinity to deO2 Hb (e.g. in respiring tissue) than oxygenated (e.g. in lungs). Decreases beta subunit affinity for oxygen thus promoting release of remaining O2.
  • 2) Increased cardiac output** (via increased stroke volume and/or increased HR*) b/c Hb amount decreases -> tachycardia
  • *3) Redistribution of blood flow** - e.g. during heavy exercise muscle get’s more O2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the chronic compensation methods for e.g. chronic severe anaemia.

Distinguish between syndrome and disease.

What does this blood film show? What are some possible causes for this?

A

(pic) - NB: peripheral vasodilation to maximise perfusion. Cycle.

Syndrome: constellation of symptoms.
Disease: specific pathopysiological basis.

Hypochromic microcytic anaemia. Causes: Iron deficiency anaemia. Haemoglobinopathies (thalassaemia). Congenital sideroblastic anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 3 types of macrocytic anaemia are these blood films showing?

A

Top: hypersegmented neutrophils => folate/B12 deficiency (Crohn, Pernicious - autoimmune attack on gastric patietal cells so less IF which binds B12…)
Middle: target cells => alcohol liver disease (excess of cholesterol in CM) (also sometimes see in thalassaemia + splenectomy)
Bottom: hypogranular neutrophil (normally 3-5 lobes), abnormally shaped RBC => myelodysplastic syndrome (group of cancers - immature blood cells in bone marrow don’t mature and become healthy blood cells).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Identify the following syndromes and diseases/ cellular features in these pathogenomic blood films (various MCV).

A

Top L: sickle cell
Top R: splenectomy - arrow = Howell–Jolly body, basophilic nuclear remnants (clusters of DNA) in circulating erythrocytes. Usually signifies damaged/absent spleen b/c healthy spleen would normally filter this type of RBC.
Middle: G6PD (also in liver disease) (Heinz body (pic)) - inclusions within RBCs composed of denatured Hb - from damage to Hb component molecules. Damaged cells cleared by macrophages in spleen, where the precipitate and damaged membrane are removed, leading to characteristic “bite cells”.
Bottom L: roleaux and agglutination - roleaux - red cells stacked = raised ESR, in chronic inflammation, paraproteinaemia, myeloma. Agglutination - clumping RBCs by own serum due to RBCs surface coating of antibodies. Seen in immune mediated haemolytic anaemia.
Bottom R: malaria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Case 1

30 yo, normally fit and well, caucasian lady presents to GP with tiredness. She reports a normal diet. How will you approach this clinical scenario and what do you expect to find?

A

FBC. Expect to find iron deficiency anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Case 2

28 yo, normally fit and well, woman of Asian origin presents to GP for general check-up. Hb 100g/L, MCV 62fl. Iron studies normal. She is asymptomatic. How will you approach this clinical scenario and what do you expect to find?

A

Hb low = mild anaemia. MVC low = microcytic. Normal Fe. May be thalassaemia trait, not full blown. Do haemoglobinopathy screen to look at type of Hb. Don’t need to do anything unless she wants to have a baby - need to see dad isn’t carrier too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Case 3

24 yo man presents with a few months hx of RLQ pain, low grade fever, and prolonged hx of intermittant diarrhoea with some mild wt loss. His Hb is 102g/L with an MCV of 105fl. What could be the reason for this presentation?

A

MCV slightly high - macrocytic anaemia. Deficiency from Crohn’s?

People with Crohn’s often have anemia due to vitamin B12, folate, iron deficiency, or due to anemia of chronic disease. The most common is iron deficiency anemia from chronic blood loss, reduced dietary intake, and persistent inflammation leading to increased hepcidin levels, restricting iron absorption in the duodenum. As Crohn’s disease most commonly affects the terminal ileum where the vitamin B12/intrinsic factor complex is absorbed, B12 deficiency may be seen. Involvement of duodenum and jejunum can impair the absorption of many other nutrients including folate. If Crohn’s disease affects the stomach, production of intrinsic factor can be reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly