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path3500 Hemophilic disease notes
- Course
- Path3500
- Institution
- University Of Western Ontario (UWO )
Hemophilic lecture notes
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PATH3500HEMATOLYMPHOID PATHOLOGY 2
Normal blood cells
- Peripheral blood smears are done when patients get CBCs
o Neutrophils are paler, eosinophils brighter red, basophils dark
Blood cell components: bone marrow origin
- Have pluripotential stem cell that can differentiate into different lines
o 2 main ones are myeloid stem cells + lymphoid stem cells; how you end up w/ RBCs,
WBCs, neutrophils, etc.
Blood cells – normal function
- RBC
o Oxygen transport
- WBCs
o Infections: bacteria, viruses, fungi, parasites
o Normal response to tissue injury, e.g. infarction
o Allergic, autoinflammatory diseases
- Platelets
o Preservation of blood vessel integrity (platelet plug formation) & participation in
coagulation
Blood abnormalities
- Few questions you ask:
o (1) what cell line(s) is affected?
o (2) what is abnormality? Too much? Too little?
- If result is outside of normal range, can infer if too much or too little
RBCs abnormalities
- Measured by hemoglobin concentration
- Too little = anemia (more common)
o Too much = polycythemia (less common)
- Bc of decreased hemoglobin concentration, have reduced oxygen transport ability of blood
- Can be asymptomatic (patient doesn’t feel anything, usually found through routine check ups) or
symptomatic
o Symptoms: headache, fatigue, light-headedness
o Signs: increased HR, palor
Anemia – causes
- 2 ways to classify anemia:
- (1) pathophysiologic
o Decreased RBC production – not enough RBCs produced in bone marrow
, ▪ Issues w/ production/maturation
▪ E.g. aplastic anemia, vitamin deficiency like in iron, B12, or folic acid, drugs,
thalassemia (inherent production problem), myelodysplasia (malignancy
affection bone marrow precursor cells), infiltration by other malignancies
o Increased blood loss
▪ Acute blood loss, e.g. trauma
▪ Chronic blood loss, e.g. colorectal tumours/lesions (many patients develop
polyps bc if they progress, can become cancerous mass); polyps + malignant
tumours can bleed
o Increased RBC destruction
▪ Decreased RBCs from destruction
▪ Can be due to RBC defects (intrinsic) that make it weaker than normal RBCs or
destruction by factors outside of RBCs (extrinsic)
• E.g. sickle cells often shear + tear apart that can cause destruction
within vessels – intrinsic
• E.g. can develop immune response against antibodies where antibody-
mediated destruction is initiated – extrinsic
• E.g. mechanical heart valves function in place of normal valve, RBCs that
go through can get destroyed bc of different material – extrinsic
▪ Intrinsic destruction
• Hemoglobinopathy: sickle cell disease
• Globin synthesis: thalassemia syndromes
• Membrane abnormalities: hereditary spherocytosis
▪ Extrinsic destruction
• Immune (antibody) mediated
• Non-immune mediated (e.g. heart valve)
- (2) morphologic
o Based on appearance (morphology) of RBCs
o Classification based on:
▪ (i) RBC size (measured by mean corpuscular volume)
• Microcytic – smaller than normal
• Normocytic – less RBCs
• Macrocytic – larger than normal
▪ (ii) decreased of hemoglobinization (measured by mean corpuscular hemoglobin
concentration)
• Normochromic – normal hemoglobin content
• Hypochromic – less than hemoglobin content
o Can have different situations when combined:
▪ (i) normocytic normochromic (less RBC in system but nothing abnormal)
• E.g. acute blood loss, many chronic diseases + malignancies
▪ (ii) microcytic hypochromic
• E.g. iron deficiency anemia, thalassemias (hereditary disorders w/ ↓
production of Hb due to Hb gene deletions)
▪ (iii) macrocytic (always normochromic)
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