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1

LYMPHATIC SYSTEM

- Structurally→ lymph nodes are part of lymphatic system
- Thousands of nodes are clustered around lymphatic veins→ collect interstitial fluid from tissues and transport it as a fluid (lymph) back into cardiovascular system near heart

2

RED BLOOD CELLS (ERYTHROCYTES) Structure

- Anucleate, circular, biconcave discs
- Diameter; 7-8μm
- Nucleus shed before cell matures

3

RED BLOOD CELLS (ERYTHROCYTES) Relate structure of cell to function

- Facilitates gaseous exchange across cell membrane by
- Maximising surface area
- Brining haemoglobin molecules closer to cell surface

4

RED BLOOD CELLS (ERYTHROCYTES) Function

Transport oxygen and carbon dioxide

5

BLOOD CELL COUNTS AND INDICES: RBCC

- Red blood cell count→ Number of cells/ volume

6

BLOOD CELL COUNTS AND INDICES: Hb

Haemoglobin concentration→ Weight hb/ volume

7

BLOOD CELL COUNTS AND INDICES: HCT

Haematocrit→ % of rbc/ volume

8

BLOOD CELL COUNTS AND INDICES: RDW

Red cell distribution width→ variation in cell size

9

BLOOD CELL COUNTS AND INDICES: MCV

Mean cell volume→ Volume of each rbc

10

BLOOD CELL COUNTS AND INDICES: MCH

Mean cell haemoglobin→ amount of haemoglobin in each rbc

11

BLOOD CELL COUNTS AND INDICES: MCHC

Mean cell haemoglobin→ concentration of haemoglobin in each RBC

12

NORMAL VARIATIONS IN BLOOD

Blood composition may be influenced by;
- Age (RBC and WBC is greater in infants than adults)
- Race (RBC + Hb + Hct is greater in Caucasians than Africans)
- Geography (RBC is greater living in mountains than sea level)
- Activity of patient/food intake
- Time of day
- Total body fluid

13

ABNORMAL VARIATIONS IN BLOOD

- May be due to disease processes
- Hypoxia
- Neoplasia
- Infection
- Haemolysis
- Metabolic disorders
- Trauma

2 common conditions affecting variations;
- Anemia
- Polycythaemia

14

ANEMIA: CAUSE

- Any abnormality of/reduction in Haemoglobin leads to HYPOXIA as rbc cannot transport oxygen efficiently
- Quality→ Abnormal Haemoglobin (Hb)
- Quantity→ of RBC

15

ANEMIA: CLINICAL MANIFESTATIONS

- Hypoxia and compensatory mechanisms
- Movement of fluid from interstitium to blood to restore volume; less viscous blood
- Increased cardiac output (increased stroke volume and heart rate)
- Increased rate and depth of breathing
- Redirection of blood from periphery to internal organs
- Increased erythropoiesis (RBC production)

16

ANEMIA: SYMPTOMS

- Pallor, fatigue, tachycardia, dyspnoea, lethargy, dizziness
- FBC test results→ Low Hb
- Jaundice (especially for haemolytic anemias)
- The presence and severity of symptoms is related to the decrease in Hb level; however some people with severe anemia may be asymptomatic

17

ANEMIAS CAUSED BY REDUCED Hb: Disorders of iron metabolism: The Iron deficiency anaemias

- Chronic blood loss: menorrhagia; or gastric or duodenal ulcers
- Malnutrition/eating disorders
- Increased demand: Infancy, adolescence, menstruating women, pregnancy, lactation

18

ANEMIAS CAUSED BY REDUCED Hb: Disorders of Haem Synthesis: The sideroblastic anaemias

- Characterised by “ring sideroblasts” : granules of iron arranged in a ring around the nucleus found in the bone marrow
- With defects in haem synthesis (such as the porphyrias) → Acquired causes in lead poisoning
- Porphobilinogen (PBG) is one of the precursors to haem that is readily filtratable in the kidneys and thus is detectable in urine.
- Testing for urinary PBG can be part of a screen for porphyria or acquired defects in haem synthesis

19

ANEMIAS CAUSED BY REDUCED Hb: Disorders of Globin Synthesis--> Review: Haemoglobin structure and genetics

- A molecule of Hb consists of 4 polypeptide chains each containing a haem group
- In the blood of a normal adult between 96-98% of the Hb is in the form of Hb A which consists of 2 a chains and 2 b chains
- There is a seperate gene for each chain
- The b chain gene is located on chromosome 11
- The a chain gene is duplicated. Located on chromosome 16 both genes (a1 and a2) are active

20

ANEMIAS CAUSED BY REDUCED Hb: Disorders of Globin Synthesis--> The Thalassaemias

- Inherited impaired rate of synthesis of either alpha or beta globin chains
- When one or more of the genes for a chain are defective: thalassaemia minor/trait
- When all genes for a chain are defective: thalassaemia major

21

ANEMIAS CAUSED BY REDUCED Hb: Disorders of Globin Synthesis--> Sickle Cell Anaemia

- Inherited defect in beta globin→ a valine type amino acid is substituted for a glutamic acid-type amino acid
- A decrease in pO2 causes the sickle cell- type beta chains to form aggregates leading RBC shape change
- Modified RBC are trapped in organs (reticuloendothelial organs such as the spleen and liver) hence: an anaemic presentation
- Person can experience an occlusive “sickling crisis” brought on by infection, acidosis, high altitudes, excessive physical activity, ischaemia
- Heterozygotes (sickle cell trait) are commonly asymptomatic
- The sickle cell gene has a high prevalence amongst people from or originating from West Africa

22

ANAEMIAS CAUSED BY REDUCED RBC NUMBERS: Defects in erythropoiesis: aplastic anaemia

- Inherited disorder in DNA repair: Fanconi anaemia
- Secondary: caused by a number of drugs (e.g. some chemotherapeutic drugs, and the antibiotic chloramphenicol)

23

ANAEMIAS CAUSED BY REDUCED RBC NUMBERS: Increased/ Premature Erythrocyte destruction: Haemolytic Anaemias

Congenital defects; For example;
- RBC membrane defects: Lead to shape changes
- Glucose- 6- Phosphate dehydrogenase deficiency: G6PD is the only source of NADP in RBC and so these cells have a reduced capacity to regenerate reduced glutathione and thus the RBC become more sensitive to oxidative destruction. People with G6PD deficiency may manifest favism

Acquired Haemolytic Anaemias
- Autoimmune disease, Drug coated RBC, Haemolytic transfusion reaction, Haemolytic disease of the newborn, - A blood type incompatibility

24

MEGALOBLASTIC ANAEMIA: A MACROCYTIC ANAEMIA

- Defects in erythropoiesis: development of the nucleus vs. the cytoplasm are not synchronised due to defects in DNA synthesis. The principal causes are;
- B12 malabsorption (or deficiency)
- Folate deficiency
- Autoimmune gastritis
- Incidence increases with age
- Higher prevalence in Northern European races
- As the disease mechanism is a defect in DNA synthesis, people with pernicious anaemia may also experience: gastrointestinal problems and loss of bone density

25

MEGALOBLASTIC ANAEMIA: A MACROCYTIC ANAEMIA B12 deficiencies

- Vegans as there is no adequate plant supply of B12
- Gastric surgery
- Congenital intrinsic factor deficiencies
- Pernicious anemia: is an autoimmune disorder in which your body can’t make enough health RBC because it can’t absorb enough Vit B12

26

MEGALOBLASTIC ANAEMIA: A MACROCYTIC ANAEMIA
Folate deficiencies

- Nutritional deficiencies
- Utilisation outstrips supply (e.g. pregnancy)
- Malabsorption

27

HEMATINIC AGENTS

- Haematinic → An agent that improves the quality of blood, increasing the haemoglobin level and the number of RBC, e.g. iron, liver extract, B complex vitamins
- EPO= erythropoietin, naturally occuring kidney hormone

28

POLYCYTHAEMIA→ TOO MANY RBC

- Erythrocytosis: elevated RBC
- Neoplastic disorder: hyperproliferation of RBC→ largely affects elderly males
- Secondary polycythaemia
- Response to hypoxia
- High altitude
- EPO→ blood doping
- Treatment→ phlebotomy

29

POLYCYTHAEMIA VERA→ TOO MANY RBC

- Too many RBC→ increased synthesis in overactive bone marrow
- Circulatory problems relating to increased viscosity and volume:
- Elevated BP
- Congestive cardiac failure
- Venous pooling
- Thrombus formation
- Pulmonary oedema

30

Summary→ RBC
Anaemia

- Microcytic hypochromic→ Fe deficiency and Thalassemia
- Bone marrow → Sideroblastic and Aplastic
- Sickle shape → Sickle cell
- Macrocytic→ Folate/B12 deficiency/intrinsic factor
- Normocytic normochromic, Poikilocytes→ Acute blood loss