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Blood Analysis
- 1. Activity 6 Red Cell Fragility, Blood Typing, Bleeding Time and Clotting Time and Hyperemia
- 2. Discussion Outline • Red cell fragility • Blood typing • Cross-matching • Bleeding time • Clotting time • Hyperemia
- 3. Red Blood Cells Specialized aspects: • Biconcave shape – Approx 7.8 µm mean diameter; 2.5 µm thickness at the thickest point and 1.0 µm at the center – Due to cytoskeletal structure – Aids in movement through capillaries and allows them to maintain integrity even as osmotic pressures vary • Anucleate condition in mature RBCs – Implications: to contain hemoglobin – Life span: Ave. of 120 days
- 4. • Production and transport of hemoglobin (Hb) which accounts for 97% of the content of a mature rbc! – This comes to approximately 280 million hemoglobin molecules/cell! – Each Hb molecule carries 4 oxygen molecules – Increases the O2 carrying capacity of blood by about 70 times! Hemoglobin
- 5. Red cell fragility / Osmotic fragility • Osmotic fragility is a test to detect whether red blood cells are more likely to break down. • Additional water entry stretches the RBC membrane and it becomes leaky. Hemolysis • Hemoglobin in RBC leaks out down the concentration gradient leaving the intracellular concentration low.
- 6. • This test is performed to diagnose hereditary spherocytosis and thalassemia. – Hereditary spherocytosis makes red blood cells more fragile than normal (cytoskeleton does not link properly due to defective or deficient cytoskeletal proteins). – Some red blood cells in patients with thalassemia are more fragile than normal, but a larger number are less fragile than normal.
- 7. BLOOD TYPING Principle: •Blood groups (types) based on specific RBC surface antigens (= proteins) •A surface antigen = blood type A •B surface antigen = blood type B •both surface antigens = type AB •neither surface antigen = type O
- 8. . . . 2 - 8 months after birth: Anti-A and anti-B antibodies can be formed in plasma!
- 9. Blood typing Blood typing, showing agglutination of cells of the different blood types with anti-A and Anti-B agglutinins in the sera Red blood cell types Sera Anti-A Anti-B O - - A + - B - + AB + + A B AB O
- 11. Transfusion of incompatible blood can be fatal! Blood type O is universal donor; Blood Type AB is universal recipient. Universal Donor vs. Universal Recipient Only for emergencies - must be given slowly !
- 12. Bleeding time • From the deep prick, let bleeding without placing pressure on the finger. • After 1 minute, blot this drop of blood with a piece of filter paper • Continue blotting to the bleeding point at regular intervals of 30 seconds until no more blood oozes from the pricked finger. PATIENT’S VALUE NORMAL VALUE 2 MINUTES 1-4 MINUTES
- 13. Bleeding time Principle: •The bleeding time test is a useful tool to test platelet plug formation and capillary integrity. •Bleeding time is dependent upon: – The efficiency of tissue fluid in accelerating the coagulation process, – Capillary function – The number of blood platelets present and their ability to form platelet plug.
- 14. Platelet plug formation • Hemostasis: the prevention of blood loss • Most common source of bleeding – injuries in small blood vessels. • Two processes: – Formation of a platelet plug; – Blood coagulation (clotting)
- 15. Hemostasis Platelet Plug Formation • Platelets stick to damaged vessel – Release cytokines which initiate further vasoconstriction and additional platelet adhesion – Sets up a cascading effect – Leads to a loose plug being formed • The damaged vessel at the same time with collagen exposed and tissue factor released starts the coagulation cascade
- 16. Stopping blood loss • Pressure in the vessel must be decreased long enough to create a secure mechanical seal in the form of a blood clot. • Once the clot is in place and blood loss has been stopped, the body’s repair mechanism can take over. • As the wound heals, enzymes gradually dissolve the clot, while scavenger white blood cells ingest and destroy the debris.
- 17. Clotting Time • Blood clotting is an important mechanism to help the body repair injured blood vessels. • Objective: – To determine the clotting time of the subject and compare it to the normal values. PATIENT’S VALUE NORMAL VALUE SLIDE METHOD 3 minutes and 30 seconds 2-6 minutes CAPILLARY METHOD 2-6 minutes.
- 19. SIGNIFICANCE: • used to screen for problems in blood clotting or coagulation mechanism • This procedure tests the function of the blood vessels in blood clotting. • Delayed or lack of clotting can be due to a deficiency in one or more coagulation factors.
- 20. Hyperemia • Wind rubber band in second joint of finger and dipped in warm water. • Immerse the finger in the beaker with water (45°C) for a few minutes to note for sensations other than warmth that the finger was exposed to. Hyperemia - increase of blood flow to different tissues in the body. Erythema - redness of the skin or mucous membranes, caused by hyperemia of superficial capillaries.
- 21. Functional Hyperemia - a regulatory response • There is increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. • When tissue increases activity: • ↓partial pressure of oxygen and pH • ↑partial pressure of carbon dioxide • ↑temperature • ↑ concentration of potassium ions. • Vasodilation - precapillary sphincter opens
- 22. References •Guyton, A.C. and J.E. Hall.2006. Textbook of Medical Physiology. Elsevier and Saunders. PA, USA. •Widmaier, E.P., Raff, H. and K.T. Strang. 2004. Vander et al’s Human Physiology: The Mechanisms of Body Functions 9th Edition. The Mac Graw-Hill Companies. USA
Editor's Notes
- Guide questions: 1. What will happen to the cell volume and solute concentration if a cell that is normally in osmotic equilibrium was transferred to a more diluted concentration? 2. What will happen to the same RBC, if it was transferred to a more concentrated solution?
- Blood typing is performed in the following way: The red blood cells are first separated from the plasma and diluted with saline. One portion is then mixed with anti-A agglutinin and another portion with anti-B agglutinin. After several minutes, the mixtures are observed under a microscope. If the red blood cells have become clumped— that is, “agglutinated”—one knows that an antibody antigen reaction has resulted. * Explain the reaction of your blood to the anti-sera used?
- Bleeding time: From the deep prick, let bleeding without placing pressure on the finger. After 1 minute, blot this drop of blood with a piece of filter paper and continue blotting to the bleeding point at regular intervals of 30 seconds until no more blood oozes from the pricked finger. This is your bleeding time. Write your recorded time in your worksheet.
- - Capillary function - Bleeding time is a blood test that looks at how fast small blood vessels close to stop you from bleeding. - Ability to form platelet plug – mechanical and chemical action of platelets. Occasionally, the bleeding time test will be ordered on a patient scheduled for surgery. * What is the significance of determining bleeding and clotting before performing surgical operation?
- When a blood vessel is severed or otherwise injured, its immediate inherent response is to constrict (the mechanism is unclear). This short-lived response slows the flow of blood in the affected area. The staunching (stopping) of bleeding ultimately is dependent upon two other processes that are interdependent and occur in rapid succession: (1) formation of a platelet plug; and (2) blood coagulation (clotting). Fig. The involvement of platelets in hemostasis requires their adhesion to a surface. Injury to a vessel disrupts the endothelium and exposes the underlying connective tissue collagen molecules. Platelets adhere to collagen, largely via an intermediary called von Willebrand factor (vWF), a plasma protein secreted by endothelial cells and platelets. This protein binds to exposed collagen molecules, changes its conformation, and becomes able to bind platelets; thus vWF forms a bridge between the damaged vessel wall and the platelets. Binding of platelets to collagen triggers the platelets to release the contents of their secretory vesicles, which contain a variety of chemical agents. Many of these agents, including adenosine diphosphate (ADP) and serotonin, then act locally to induce multiple changes in the metabolism, shape, and surface proteins of the platelets, a process termed platelet activation. Some of these changes cause new platelets to adhere to the old ones, a positive feedback phenomenon termed platelet aggregation, which rapidly creates a platelet plug inside the vessel. Chemical agents in the platelets’ secretory vesicles are not the only stimulators of platelet activation and aggregation. Adhesion of the platelets rapidly induces them to synthesize thromboxane A2, a member of the eicosanoid family, from arachidonic acid in the platelet plasma membrane. Thromboxane A2 is released into the extracellular fluid and acts locally to further stimulate platelet aggregation and release of their secretory vesicle Contents. Fibrinogen, a plasma protein whose crucial role in blood clotting is described in the next section, also plays a crucial role in the platelet aggregation produced by the factors previously described. It does so by forming the bridges between aggregating platelets. The receptors (binding sites) for fibrinogen on the platelet plasma membrane become exposed and activated during platelet activation. The platelet plug can completely seal small breaks in blood vessel walls. Its effectiveness is further enhanced by another property of platelets—contraction. Platelets contain a very high concentration of actin and myosin, which are stimulated to contract in aggregated platelets. This results in a compression and strengthening of the platelet plug. (When they occur in a test tube, this contraction and compression are termed “clot retraction.”) While the plug is being built up and compacted, the vascular smooth muscle in the damaged vessel is being stimulated to contract (Figure 12–72), thereby decreasing the blood flow to the area and the pressure within the damaged vessel. This vasoconstriction is the result of platelet activity, for it is mediated by thromboxane A2 and by several chemicals contained in the platelet’s secretory vesicles.