Lecture notes

Comprehensive Year 2 Haematology Lecture Notes

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Module
Haematology (BIOL21361)

Institution
The University Of Manchester (UOM)

These detailed Haematology notes cover all key concepts from my second-year university lectures, offering a clear and concise understanding of blood-related topics, including blood cell formation, clotting mechanisms, blood disorders, and diagnostic techniques. Perfect for students looking to reinf...

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Uploaded on October 13, 2024
Number of pages 150
Written in 2022/2023
Type Lecture notes
Professor(s) Dr michelle keown
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Different sickle cells
1. Sickle cells: iden ed by their elongated form without central pallor. They are also characterised
by sharp ends along with a curved shape. This is the result of a muta on that replaces
nucleo de base A to nucleo de base T, forming sickle haemoglobin (HbS). As a result,
nega vely charged glutamic acid on the 6th posi on of beta globin chain is replaced by neutral
valine. As valine is not charged, it promotes hydrophobic interac ons between the adjacent
haemoglobin molecules. Deoxygenated sickle haemoglobin then polymerises into linear chains
that distort the red cell into a long form with sharp ends.

2. Boat shaped cells: appear to have sharp ends like sickle cells but present a canoe appearance,
as they are broader and are not curve-shaped as sickle cells. The cell body is also more dense
and a central pallor can be observed. Similar to sickle cells, boat shaped cells are formed due to
sickle cell disease (HbSS) where haemoglobin solubility is altered and linear globin chains are
formed when cells are deoxygenated . Other causes of this kind of cells might be Compound
heterozygote with beta-thalassaemia (HbS-beta thalassaemia) and compound heterozygote with
beta-thalassaemia (HbS-beta thalassaemia).

3. Dehydrated/contracted cells: characterised by a distorted shape and irregular outline and
therefore they can present a broad spectrum of shapes in the blood lm. Because they lack a
central pallor or have it diminished, haemoglobin staining may be irregular. This is the result of
damaged or altered haemoglobin within the red cell which is caused by sickle cell disease and
thalassemias. The repeated cycles of sickling and then reversal, eventually causes damage to the
red cell’s membrane, impairing ion pumps and causing s dehydra on.

4. Target cells: iden ed by a central pallor that presents an abnormal accumula on of
haemoglobin. Target cells are associated with thalassemia and iron de ciency where the
haemoglobin concentra on is lower than normal. These anaemias are classi ed as microcy c.

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, Disorders of haemostasis
Defective haemostasis with abnormal bleeding may be caused by:

1. Abnormalities of the vessel wall (vascular system)
2. Thrombocytopenia
3. Disordered platelet function (thrombocytopathy)
4. Defective blood coagulation

• Vessel wall abnormalities:
• characterized by easy bruising and purpura (bleeding into the skin or mucous
membranes)

• Vascular and platelet bleeding disorders:
• associated with bleeding from the mucous membranes and into the skin

• Coagulation disorders:
• bleeding is often into joints or soft tissues

Vascular bleeding disorders

Characteristics
• Easy bruising
• Spontaneous bleeding from small vessels

Pathology
• Abnormality in blood vessels
• Bleeding and other haemostasis tests usually normal

Inherited vascular disorders - Hereditary haemorrhage telangiectasia

Hereditary haemorrhage telangiectasia
- Uncommon: a ects 1.2 million worldwide
- A ects men and women equally
- It’s an autosomal dominant disease
- It’s caused by defect in 3 genes but only 1 gene is the cause in any one family.
- It causes abnormally formed blood vessels = arterovenous malformations.
- 90-95%: at least a few telangiectasia on the skin of the face and/or hands by
middle age.
- 90-95%: nosebleeds by adulthood.
- 20-25%: bleeding in the stomach or intestines, but rarely before 50 years old

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, Symptoms:
- Telangiectases = dilated microvascular swelling; easy to rupture
- Nose, tongue, lips
- Nosebleeds and gastrointestinal blood loss.
- Chronic iron de ciency is frequent

Treatment:
- Embolization
- Laser treatment
- Tranexamic acid

Acquired Vascular Defects

• Wide variety of causes: infections, drug reactions, trauma, old age and steroid use.

• Vascular purpura can be categorized as such:
• Purpura simplex
• common benign disorder, women of child bearing age.
• Senile purpura
• old age, due to the loss of skin elasticity and atrophy of vascular collagen.
Mainly on the forearms and hands.
• Infection associated purpura
• Bacterial and viral infections, e.g. measles can cause purpura from
vascular damage by the organism.

Thrombocytopenia

• De ciency in platelet numbers
• De ned as a low platelet count with values less than 150 x 109/L

3 main causes of thrombocytopenias:
1. Failure of platelet production
2. Increased destruction of platelets
3. Sequestration (abnormal distribution) of platelets

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, 1. Failure of platelet production

• Most common cause of thrombocytopenia

• Usually part of bone marrow failure.
• aplastic anaemia or leukaemia.
• Drug/viral induced toxicity

• Diagnosis
• clinical history, peripheral blood count, blood lm and bone marrow
examination

2. Increased destruction of platelets

• Primary cause: autoantibodies attaching to the platelet surface

• Autoimmune (idiopathic) thrombocytopenia purpura (ITP)

• Two disease categories: chronic ITP and acute ITP.

Chronic ITP

• Relatively common
• Common between young women 15-50 years old
• Asymptomatic or insidious onset of bleeding
• Autoantibodies in their plasma and on their platelets.
• Platelets sensitised with autoantibodies (mostly IgG): destroyed by macrophages
in spleen and liver.
• Antibodies : glycoprotein IIb/IIIa or Ib.
• Platelet lifespan considerably reduced: as little as a few hours!

Acute ITP

• Children under 10
• Majority, onset is abrupt following vaccination or a viral episode (chicken pox,
measles).
• Post viral cases:
• likely IgG antibody attaches to viral antigen absorbed onto the platelet
surface
• dramatic fall in platelet count to less than 20 x 109/L.
• Spontaneous remissions usual
• Minority of cases develop chronic ITP

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