WEEK 4 Flashcards
(72 cards)
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
RED BLOOD CELLS (ERYTHROCYTES) Structure
- Anucleate, circular, biconcave discs
- Diameter; 7-8μm
- Nucleus shed before cell matures
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
RED BLOOD CELLS (ERYTHROCYTES) Function
Transport oxygen and carbon dioxide
BLOOD CELL COUNTS AND INDICES: RBCC
- Red blood cell count→ Number of cells/ volume
BLOOD CELL COUNTS AND INDICES: Hb
Haemoglobin concentration→ Weight hb/ volume
BLOOD CELL COUNTS AND INDICES: HCT
Haematocrit→ % of rbc/ volume
BLOOD CELL COUNTS AND INDICES: RDW
Red cell distribution width→ variation in cell size
BLOOD CELL COUNTS AND INDICES: MCV
Mean cell volume→ Volume of each rbc
BLOOD CELL COUNTS AND INDICES: MCH
Mean cell haemoglobin→ amount of haemoglobin in each rbc
BLOOD CELL COUNTS AND INDICES: MCHC
Mean cell haemoglobin→ concentration of haemoglobin in each RBC
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
ABNORMAL VARIATIONS IN BLOOD
- May be due to disease processes
- Hypoxia
- Neoplasia
- Infection
- Haemolysis
- Metabolic disorders
- Trauma
2 common conditions affecting variations;
- Anemia
- Polycythaemia
ANEMIA: CAUSE
- Any abnormality of/reduction in Haemoglobin leads to HYPOXIA as rbc cannot transport oxygen efficiently
- Quality→ Abnormal Haemoglobin (Hb)
- Quantity→ of RBC
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)
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
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
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
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
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
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
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)
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
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