Haemostasis And Blood Groups Lecture 2024 PDF

Sphinx University Faculty of Physical Therapy Haemostasis and Blood Groups First year Physical Therapy Dr. Rasha Mohammed Ali Lecturer of Medical Physiology, Faculty of Med...

Sphinx University Faculty of Physical Therapy Haemostasis and Blood Groups First year Physical Therapy Dr. Rasha Mohammed Ali Lecturer of Medical Physiology, Faculty of Medicine, Assiut University 2024-2025 Steps of Haemostasis. Mechanism of blood coagulation. Prevention of blood coagulation inside the blood vessels. Abnormalities of haemostasis. Objectives Blood groups. Complications of blood transfusion. Q. Enumerate steps of Haemostasis Hemostasis means prevention of blood loss from blood vessels. Bleeding is stopped by several mechanisms which are: Local Vasoconstriction: Immediately after injury: a) Liberation of serotonin and other vasoconstrictors from platelets. b) Local myogenic contraction of the blood vessel. 2) Formation of the Platelet Plug: The second event in hemostasis is an attempt by the platelets to plus the rent in the vessel. 3) Blood Coagulation: The third mechanism for hemostasis is the formation of the blood clot.  Blood clotting takes place in three essential steps: First: Formation of a prothrombin Second: The activator prothrombin activator Third: The thrombin substance in catalyzes the acts as an enzyme to response to conversion of convert fibrinogen rupture of the prothrombin into into fibrin threads, vessel or thrombin. that enmesh damage to the platelets, blood cells, blood itself. and plasma to form the clot itself.  There are two basic ways in which prothrombin activator can be formed: The extrinsic pathway: that begins with trauma to the vascular wall or to the tissues outside the blood vessels. The intrinsic pathway: that begins in the blood itself. 1 1 2 2 3 3 4 4 Calcium  Lysis of Blood Clots:- The plasma proteins contain plasminogen which, when activated, becomes a proteolytic enzyme called plasmin. - Plasminogen is activated by thrombin and tissue plasminogen activator. - Plasmin digests the fibrin threads, fibrinogen, factor V, factor VIII, prothrombin, and factor XII. (Factors 1,2,5,8,12) Therefore, it prevents excessive fibrin formation and causes lysis of the clot within a day or two after blood leakage. Q. Mention TWO intravascular anticoagulants 1 2 3  Q. Mention TWO Extra-vascular anticoagulants (outside the body) -Collection of blood in siliconized containers which have a ery smooth inner surface. Silicone prevents contact ctivation of factor XII. Q. Enumerate 4 differences etween heparin and oumarins. Abnormalities Of Hemostasis A) Bleeding Tendencies Abnormalities of Blood Platelets: Defect in the Clotting Mechanism B-Intravascular Thrombosis  Abnormalities of Blood Platelets Thrombocytopenia 2- Thrombasthenia (Thrombocytopenic Purpura) It is a state in which the very low level of platelets i.e. platelets are normal in below 50.000/cubic millimeter. quantity but defective in a) Idiopathic thrombocytopenia: function which may result which means: the cause is in a bleeding tendency. unknown. It may be primary or b) Secondary thrombocytopenia: secondary e.g. in severe occurs in association with aplasia uremia and exposure to of the bone marrow e.g. exposure certain drugs as aspirin. to X ray, radioactive substances, neoplastic deposits, very severe fevers and drug sensitivity.  Defect in the Clotting Mechanism 1-Hemophilia: 2-Vitamin K Deficiency: Prothrombin (factor - It is inherited sex-linked disease II) and factors, VII, IX and X require vitamin transmitted by females (mothers) to K for synthesis by the liver. males (infant) but females themselves show no symptoms. Causes of vitamin K deficiency: 1- Sterility of intestine (no bacteria). a) In - There are three types of hemophilia: newly born infants. Hemophilia A (85%) (classical b) Prolonged use of antibiotics. hemophilia) due to deficiency of factor 2- Failure of absorption of vitamin K as in: VIII. a) Obstructive jaundice - Hemophilia B (10%) (Christmas b) Fatty diarrhea. disease) due to lack of factor IX. 3- Liver diseases. - Hemophilia C (5%) due to absence of 4- Competitive inhibition with vitamin K as factor XI. with dicumarol. In hemophilia, only the intrinsic pathway In vitamin K deficiency, both the intrinsic and extrinsic pathways are defective. is defective.  B-Intravascular Thrombosis: It is the formation of blood clot inside blood vessels. Contributing Factors: Slowing of blood, e.g., after delivery and operation. Atherosclerosis Complications: 1- Obstruction of arterial supply which leads to ischaemia. 2- Obstruction of venous supply which leads to edema. 3- Embolic formation, i.e., dislodgment of small pieces of the blood clot. e.g., pulmonary emboli. Prevention: - Avoidance of prolonged recumbence. - Use of anticoagulant in susceptible patients. Blood Groups  The sites of danger in blood transfusion is that the RBCs of the donor which may be agglutinated by the agglutinins in the plasma of the recipient. The RBCs of the recipient are not usually affected by the agglutinins in the plasma of the donor. This is because the agglutinins in the injected plasma of the donor are very small and immediately will be diluted by the plasma of the recipient. Group “O” is “Universal Donor” because RBCs of group “O” contain no agglutinogens (A or B), so agglutination cannot take place. Group “AB” is “Universal Recipient” because group “AB” has no agglutinins in its plasma.  Rh Factor This is an agglutinogen which was discovered in the RBCs of Rhesus monkeys (hence the name “Rh”). - It is present in the RBCs of 85% of people who are thus called “Rh positive” The remaining 15% have no Rh factor in their RBCs and are called “Rh negative”. - In Egypt,“Rh positive”people are higher, about 92%. Remarks on Rh Factor: There are no anti-Rh antibodies in normal blood whether Rh positive or Rh negative. No agglutination on the first incompatible Rh transfusion. Only anti-Rh antibodies are formed. Rh negative blood can be transfused to both Rh positive and Rh negative persons antiRh antibodies  Importance of Rh Factor: RH+ fetal blood is transmitted to maternal circulation during delivery except during delivery Rh antibodies  Prevention: - Rh negative female should never receive an Rh positive blood. - When an Rh negative female delivers Rh positive foetus, an anti- D anti-bodies are given to neutralize the D antigen of the Rh positive fetal cells and prevent sensitization of the mother. Treatment: Replacement of the blood of the baby with Rh negative Group O blood.  Complications of Blood Transfusion 1- Effect on Donor: a- Shock. b- Anaemia if repeated withdrawal. 2- Effect on Recipient: a) Mechanical effect: i ) air and fat embolism. ii) displacement of clot. b) Infective complications: e.g., infective hepatitis, syphilis, malaria and AIDs. c) Physical complications: i) Overloading (excessive transfusion) leading to heart failure. ii) Pyrogenic reaction (fever and allergy) 3% of cases. d) Haemolytic complication, caused by: Incompatible transfusion. Results in: 1) Clumping of cells which block the capillaries® severe pain in chest and loin. 2) Haemolysed cells liberate (A,B,C and D): Q. What will happen if HB set free in the plasma ? A) Haemoglobulin if free in plasma: 1- It will be converted to bile pigments (jaundice). 2- It will pass through the glomeruli of kidneys, precipitate as acid haematin in their tubules blocking them leading to anuria. 3- It will increase the viscosity and colloidal osmotic pressure of the plasma. The work of the heart must be increased markedly. This leads to heart failure. B) Potassium which leads to arrhythmia. C) Toxic substances which produce powerful vasoconstriction of the blood vessels of the kidney, which lead to rapid renal failure (anuria), and death. D) Histamine which leads to hypotension.  Dehydration: It is a condition resulting from excessive loss of body fluid (usually H2O + NaCl). 1)Pure H2O Loss: e.g. due to inability to drink as during loss of consciousness. 2) Pure NaCL Loss: e.g. due to very deficient intake or excessive excretion of NaCl in urine. 3.Mixed H2O and NaCl Loss: This is much more common than pure H2O or pure NaCl loss. It may be due to, e.g. excessive sweating, vomiting diarrhea.