Physiology Flashcards

Question

what are the functions of plasma proteins?

Answer 1

1. production of effective osmotic pressure - by their Colloidal osmotic pressure - 25 mmHg 2. blood viscosity - Fibrinogen helps maintain peripheral resistance and therefore diastolic blood pressure - RBCs are more important for blood viscosity 3- Clotting factor: as fibrinogen, prothrombin 4- Defense as: gamma globulin 5-Buffering function:15% of the buffering capacity of the blood. 6- Carrier: carry lipophilic substances as some hormones, metals as iron and calcium and other molecules (fatty acids, amino acids..) 7- carry carbon dioxide 8-Protein reserve: Reserve proteins are used by the body in cases of fasting or decreased food intake. 9- Maintain capillary permeability - close the pores of capillaries

Answer 2

Plasma proteins form carbamino compounds with CO2 CO2 (10%) + amino group (NH2) of plasma proteins >>carbamino compounds >> release CO2 to be expired (CO2 + proteins in lung capillaries)

Answer 3

 Formed in the bone marrow  Lifespan 120 days  RBCs are the most abundant cells in the blood ➢ 4-5 million/mm3 in females 5-6 million/mm3 in males -Higher in male and newly born

Answer 4

A-60% water b- chief cation: k+, chief anion: cl c- 34% hemoglobin: D-The average normal hemoglobin concentration in blood is 15 gm/dl: 15-17 g/dL in men and 13-15 g/dL in women, all of it in red cells

Answer 5

1- Concave to increase surface area available for gas exchange and diffusion 2- Maintain the shape and flexibility of the cell membrane: _The integral proteins Band 3 (the negative ion exchanger) _The linker protein ankyrin _The cytoskeleton protein spectrin ==Genetic mutations in these proteins leads to hereditary spherocytosis== 3-Plasticity The ability of the red blood cells (8 microns) to change their shape to cross through the narrow capillaries (3 microns) 4- Semipermeability allows anions to pass easily in or out of the RBC, but not cations. - It contains Na-K ATPase pump to maintain cell volume 5-Blood grouping Conatins agglutinogens to determine blood groups 6-Keep Hemoglobin (Hb) inside RBCs and prevents loss in urine

Answer 6

A) To avoid increase in: ➢ Blood viscosity, which may increase work of the heart ➢ Osmotic pressure, which interfere with filtration at capillaries B) To avoid Hb loss in urine where it will react with HCL, forming acid haematin that block renal tubules leading to renal failure

Answer 7

The red, oxygen carrying pigment in human red blood cells. It is composed of four polypeptide chains, each with a heme moiety attached to it.

Answer 8

➢ Hemoglobin binds O2 to form oxyhemoglobin  O2 attaches to the Fe2+ in the heme leading to hemoglobin oxygenation (not oxidation), iron remains in the ferrous state.  Each Hb molecule carry 4 O2 molecules  1 gm of blood Hb carry 1.33 ml of oxygen15 gm Hb in 100 ml blood,  Each 100 ml blood can carry 15 X 1.33 = 19.95ml which is the oxygen carrying capacity of the blood. ➢Hemoglobin binds CO2 to form carbaminohemoglobin  CO2 binds to amino group of hemoglobin ➢Hemoglobin acts as a buffer in the blood as it contains many amino acids eg histidine

Answer 9

HbA - 98% a2,B2 HbF - ~1% a2,y2 HbA2 - <3.5%

Answer 10

➢ The fetus has HbF (α2 y2) ➢ Fetal Hb is replaced by adult hemoglobin 2-3 months after birth. It has a higher oxygen affinity than adult Hb which facilitates O2 transport across the placenta

Answer 11

1-Normal functioning bone marrow: Bone marrow is the site where erythropoiesis takes place. 2-Normal functioning kidneys: Kidneys secrete 85% of erythropoietin hormone. 3-Normal functioning liver: Liver stores iron and vitamin B12. It also synthesizes the globin part of hemoglobin and secretes 10 % of erythropoietin. 4-Hormones: Androgens, thyroxine and glucocorticoids stimulate erythropoiesis, while estrogen inhibits it 5-Dietary substances  Proteins: Proteins of high biological value (especially animal proteins) to build up the globin part of Hb.  Iron: It is the principle constituent of Hb molecule.  Vitamin B12 and folic acid: Vitamin B12 and Folic acid are called “Maturation factors” as they are essential for normal formation of DNA and cell division during red blood cell maturation. Deficiency of vitamin B12 and Folic acid results in megaloblastic or macrocytic anemia.  Other trace elements as Copper and cobalt: They are required as cofactors for the formation of Hb Tissue oxygenation is the most important regulator of erythropoiesis

Answer 12

It is a glycoprotein that comes from: 85-90% : kidneys 10-15% : liver

Answer 13

1) Hypoxia 2) Hormones: androgens (testosterone), catecholamines, corticosteroids, growth hormone, and thyroxin increase erythropoietin secretion 3) Alkalosis as in high altitudes

Answer 14

➢ Renal failure is associated with anemia that can be treated only by erythropoietin. ➢ In aplastic anemia the stem cells do not respond to erythropoietin.

Answer 15

1-Iron intake is 15-20 mg% ➢ Absorbed iron (3-6%of the intake) ➢ iron lost by cells sloughing 2-Iron homeostasis depends on control of iron absorption from the intestine (Duodenum). Iron losses are generally unregulated. Absorption is also increased by increasing demand -Females need more iron absorption because of the periodically loss of iron in menstrual blood flow - pregnancy, lactation, growing children and blood loss

Answer 16

hemoglobin synthesis myoglobin synthesis cytochrome oxidase, peroxidase and catalase

Answer 17

hemoglobin - 65% stored iron (ferritin and hemosiderin) - 15-30% myoglobin - 4% cytochrome oxidase, peroxidase and catalase - 1% In plasma (transferrin) - 0.1%

Answer 18

1- Heme absorption:  Through the enterocyte Heme carrier protein (HCP-1)  Iron is released from heme by Heme oxygenase enzyme 2- Non- Heme absorption:  Diet iron is ferric  Ferric is reduced by ferric reductase helped by HCL and vitamin C to ferrous iron  Ferrous iron is transported into the enterocyte with a proton via a divalent metal transporter (DMT-1).  Fe2+ is transported out of the enterocyte by the basolateral membrane protein (ferroportin)

Answer 19

Hepcidin is a hormone released by the liver when iron levels are high. It inhibits ferroportin transporter Its deficiency causes tissue iron overload

Answer 20

Factors that increase iron absorption:  Gastric acidity and vitamin C aid iron reduction  Increased erythropoietic activity e.g. bleeding, hemolysis, high altitude.  Increased demand in Infancy and adolescence Factors that decrease iron absorption:  Phytic acid, oxalates and phosphates form insoluble salts  Iron overload  Calcium in dairy food

Answer 21

➢Heme iron is absorbed better than inorganic iron. ➢Ferrous iron is absorbed better than ferric iron

Answer 22

 Iron is transported as transferrin, normally 35% saturated. - Fe2+ is changed to Fe3+ and bound to apotransferrin forming transferrin - Transferrin is a glycoprotein synthesized in the liver. -Binds to receptors in cell membrane of erythroblasts in the bone marrow. - Ingested by endocytosis and iron is delivered to the mitochondria where heme is synthesized.

Answer 23

Iron is stored mostly in hepatocytes and to a lesser extent the reticuloendothelial cells of the bone marrow and skeletal muscle cells. Ferritin is the predominant storage form. It keeps iron in a soluble and non-toxic form. It is present in most cells especially intestinal mucosa, liver, spleen and bone marrow. Excess iron is stored as hemosiderin - iron deposition adjacent to ferritin spheres

Answer 24

Ferritin -Iron binds apoferritin to form ferritin -It is water soluble -It represents 2/3 of stored iron -If plasma iron is decreased, iron in ferritin is transported easily to replenish ferritin in plasma -It is easily mobilized for Hb synthesis Hemosiderin -It is water insoluble -It represents 1/3 of stored iron -Excess hemosiderin can be found in iron overload due to frequent blood cell destruction and trnasfusions

Answer 25

Can result in microcytic hypochromic anemia due to decreased hemoglobin synthesis and RBC size.

Answer 26

 Both vitamin B12 and folic acid are essential for normal formation of DNA and hence for nuclear maturation. - VB12 is important in myelin sheath formation  Vitamin B12 is absent from plant sources, formed exclusively by microorganisms  The minimum requirement is 1-3 microgram/day - Liver and yeast are good sources  Absorbed in terminal ileum by endocytosis

Answer 27

 Malabsorption (lack of the intrinsic factor) due to atrophy of gastric mucosa, achlorhydria, or after total gastrectomy.  Vegetarian peopleare most likely to be infected. If plants are contaminated with microorganisms, supply of B12 will be sufficient.  Deficiency Leads to a condition called pernicious anemia or megaloblastic anemia (macrocytic anemia). This occurs due to Impaired DNA synthesis and prevention of cell division with the accumulation ofimmature erythrocytes in the circulation.  Neurological disorders are due to progressive demyelination of nervous tissue.

Answer 28

 Large immature erythrocytes

Answer 29

Definition: Polycythemia, or erythrocytosis, refers to an increase in the RBC mass, usually with a corresponding increase in hemoglobin level.

Answer 30

Increase in RBCs number → increase in blood viscosity → sluggish blood flow → increased Work load on the heart→ increase peripheral resistance → high blood pressure

Answer 31

 Primary polycythemia (Polycythemia rubra vera): It is considered as a neoplastic disease  B. Secondary polycythemia: Hypoxia: as in high altitudes, cyanotic congenital heart disease and chronic pulmonary disease. Renal disease: due to secretion of an erythropoietin-like substance.

Answer 32

 Definition of anemia  It is a decrease or deficiency of RBCs number or decrease in Hb concentration or decrease in both RBCs and Hb. in a unit volume of blood in the presence of a low or normal total blood volume  It can be caused either by too rapid loss or too slow production of RBCs.

Answer 33

1-Aplastic anemia -Due to Bone marrow failure -causes: X-ray,chloramphenicol, chemotherapy, idiopathic (primary) -Aplastic anemia results in Pancytopenia 2-Deficiency anemia: A) Iron deficiency -Due to Less Hb formation -Deficient iron intake - Causes: Excess demand, puberty, pregnancy -Poor iron absorption -> chronic bleeding Iron deficiency results in Microcytic hypochromic anemia B) Vitamin B12 deficiency -Due to Erythroblast failure to proliferate or mature into RBCs -Causes: Malabsorption, Atrophic gastritis - Vitamin B12 deficiency results in Pernicious anemia, Macrocytic hyperchromic anemia + Neurological defects C- Folic acid deficiency -Due to Erythroblast failure to proliferate or mature into RBCs -Cause:Nutritional defect -Folic acid deficiency results in Macrocytic hyperchromic anemia 3- Renal anemia -due to insufficient RBCs production - cause: defect in erythropoeitin - results in : Normocytic normochromic anemia

Answer 34

Microcytic hypochromic anemia:  Small size RBCs  Less Hb Macrocytic hyperchromic anemia (megaloblastic anemia)  Large size, immature odd shaped, fragile RBCs  Severe number reduction

Answer 35

corpuscular:  Hereditary spherocytosis  Sickle cell anemia  Thalassemia  Glucose 6 p dehydrogenase deficiency extracorpuscular:  Incompatible blood transfusion  Rh incompatability  Malaria infection  Sulfonamide  Snake venum  Lead

Answer 36

Spherocytes That rupture easily (Haemolysis)

Answer 37

 Genetic defect in RBCs membrane proteins  RBCs are spherocytic and hemolyze more readily than normal cells

Answer 38

Inherited genetic defect in Hb formation  Hb A: 4 polypeptide chains:2 alpha, 2 beta  Hb S: Normal glutamic acid aa in position 6 on the chain is substituted by Valine aa.  Oxygenated: Soluble  Deoxygenated: insoluble, precipitates into long crystals leading to sickled cells which are fragile and liable to hemolysis

Answer 39

Severe pain that affects the bones of the hands, the feet, or both. It's often the first symptom of sickle cell disease in babies. Dactylitis is caused by blocked blood circulation. Symptoms include extreme pain and tenderness, usually with swelling.

Answer 40

 Glucose 6 phosphate enzyme is an enzyme that : ➢ Is coded by gene on X chromosome ➢ helps in producing the antioxidants

Answer 41

-X-linked recessive disorder -Leads to acute intravascular hemolysis on exposure to oxidizing agents - The oxidizing agents include: fava beans, sulfonamides

Answer 42

defect or absence of one or more of the genes responsible for synthesis of α or β chains

Answer 43

Acute: RBCs loss Cause: Wound bleeding Results in: Normocytic normochromic anemia Chronic: iron loss Cause: Bleeding piles, excessive mensis Microcytic hypochromic anemia

Answer 44

RBCs size: normal Hb content per cell: normal Cause : -Aplastic anemia -Renal failure -Acute haemorrhage -Acute haemolysis

Answer 45

RBCs size: small Hb content per cell: decreased Cause : -Iron Deficiency anemia -Thalassemia

Answer 46

RBCs size: large Hb content per cell: normal or increased Cause : - Vitamin B12, folic acid deficiency anemia

Answer 47

Tiredness. Weakness. Shortness of breath. Pale or yellowish skin, which might be more obvious on white skin than on Black or brown skin. Irregular heartbeat. Dizziness or lightheadedness. Chest pain. Cold hands and feet. Headaches yellowing eyes (hemolytic anemia)

Answer 48

1-Decreased tissue oxygenation: especially during exercise. 2-Increased work load on the heart due to: Decreased blood viscosity due to decrease number of RBCs will decrease the resistance to blood flow so that greater quantities of blood flow through the tissues and then return to the heart

Answer 49

Antigen is any substance recognized by the body as foreign, causing the body to form antibodies that specifically react with it. The antigen must be a complex molecule. The more the complex the molecule , the more its antigenicity.

Answer 50

* Everybody has a blood type. * Blood groups or types are a classification of blood based on the presence or absence of antigens (agglutinogens) on the surface of RBCs * The most common system blood type classification is the ABO system According to the ABO system, there are 4 major groups (types): 1. A 2. B 3. AB 4. O

Answer 51

A & B antigens are found on RBC membrane as well as many other tissues e.g. salivary glands, kidney, liver lung & pancreas.

Answer 52

Antibodies against red cell agglutinogens are called agglutinins and they are present in plasma. Agglutinins against A and B‐agglutinogens [anti‐A ( α) and anti‐B (β )] occur naturally. Thus, types A individuals develop anti‐B antibodies, type B‐individuals develop antiA antibodies, type O‐individuals develop both antibodies type AB‐individuals develop neither antibody.

Answer 53

Blood Group A: -41% frequency -Agglutinogen on RBC membrane: A -Agglutinin in plasma: B B: -10% frequency -Agglutinogen on RBC membrane: B -Agglutinin in plasma: A AB: -4% frequency -Agglutinogen on RBC membrane: A & B -Agglutinin in plasma: None O: -45% frequency -Agglutinogen on RBC membrane: None -Agglutinin in plasma: A & B

Answer 54

When A or B antigen meet its corresponding antibody agglutination reaction occurs. In agglutination reaction , RBC clump and stick to each other then hemolyse A& B antigens are called agglutinogens, while their corresponding antibodies are called A and B agglutinins

Answer 55

-Agglutination occurs when antigen and its corresponding antibody come together.  The agglutinins attach themselves to the RBCs.  Because agglutinins have many binding sites, a single agglutinin can attach to different red cells at the same time.  This causes the cells to clump, then these clumps plug small blood vessels, then destroyed by phagocytic cells and the reticuloendothelial system, releasing Hb.

Answer 56

* Plasma compatibility is the inverse of red blood cell compatibility. * Type AB plasma carries neither anti‐A nor anti‐B antibodies and can be transfused to individuals of any blood group * but type AB patients can only receive type AB plasma. * Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group, * but type O plasma can be used only by type O recipients. * In addition to donating to the same blood group; plasma from type AB can be given to A, B and O; * plasma from types A, B and AB can be given to O.

Answer 57

* The "Rh" factor named for the Rhesus monkey because it was first studied using the blood of this animal. * This system has not been found or detected in tissues other than red cells. * "D" is the most important antigenic component. * The population are divided according to presence of D‐Antigen into Rh‐positive and Rh‐negative "Rh‐positive" means that the individual has agglutinogen D (function is unknown). Never produce anti‐D antibodies and it was found in 85 90% of population. "Rh‐negative" means that the individual has no D‐antigen and forms the anti‐D agglutinin when injected with D +ve cells. * The anti‐D‐antibodies (agglutinin) are not naturally present in Rh‐ negative individuals.

Answer 58

ABO system: Antigens: -A and B -Present on RBC membrane and many tissues Antibodies: -Naturally occurring -Mostly IgM -Can not cross the placenta Rh system: Antigens: -many antigens -Only restricted to red blood cells Antibodies: -Not naturally occurring -Mostly IgG -can cross the placenta and cause hemolytic disease of the newborn

Answer 59

1. Ensure compatible blood transfusion. 2. Used in pre‐marriage counseling to avoid Rh incompatibility.

Answer 60

(Hemolytic disease of the New‐born): -It is a condition due to Rh‐incompatibility between mother and fetus blood. -It occurs when a Rh‐negative mother carries a Rh‐positive fetus. -During the labor of the first baby, small amounts of fetal blood pass into the maternal circulation leading to formation of anti‐Rh agglutinins in mother's circulation during the postpartum period (mother becomes sensitized). -The first baby is usually normal because sensitization of Rh‐ negative mother carrying a Rh‐positive fetus generally occurs at birth. -If the second fetus blood is Rh‐positive, this results in agglutination and then hemolysis of fetus red cells.

Answer 61

* If hemolysis is severe, the infant may die inside the mother uterus (Intrauterine death). * Less severe form causes hemolysis of fetus RBCs causing anemia and increased bilirubin resulting in severe jaundice, and edema of fetus (Hydrops fetalis). * If bilirubin concentration is very high it deposited in the basal ganglia causing brain damage, a serious condition called Kernicterus.

Answer 62

To prevent sensitization of a Rh‐negative mother, she is given a single dose of anti‐Rh antibodies (Anti‐D immune globulin) in the first 48 hours after delivery starting from first delivery. Also, be careful when giving blood transfusion to females (even very young girls) who may be Rh‐negative and are transfused with Rh‐positive blood.

Answer 63

Exchange transfusion - replace newborn blood with Rh-ve blood

Answer 64

It is the process of transferring blood or blood products from one person into the circulatory system of another.

Answer 65

1. Hemorrhage: from severe trauma or after surgical operation (to restore blood volume) and bleeding attacks due to disturbances in clotting mechanisms or platelet function (transfusion of clotting factors). 2. Severe anemia: (to restore Hb level) people suffering from hemophilia or sickle-cell disease may require frequent blood transfusions. 3. Erythroblastosis fetalis.

Answer 66

1- Blood typing: the donor's blood should be compatible with that of the recipient regarding ABO system and Rh factor. 2- Cross matching test: should be done "The donor's cells are added to the recipient plasma and the donor's plasma tested with the recipient cells" This test is done to avoid incompatibility due to any subgroup, or due to increased concentration of agglutinins in the donor's plasma. 3- A healthy donor must be carefully chosen with no history of serious diseases such as: Hepatitis, HIV (human immunodeficiency virus) or AIDS, Malaria and Syphilis. 4- Good storage of the blood with the addition of  acid citrate (to prevent its clotting) and  glucose (as a nutrient to the RBCs).  The blood should be kept at a temperature of 4º C in the blood banks and not frozen, otherwise the RBCs will be destroyed.  The blood should not be used after 5 weeks

Answer 67

 Hemolytic transfusion reactions occur when blood is transfused to an individual with incompatible blood group i.e. when the recipient has agglutinins against the RBCs in the donor's blood.  The transfused plasma (donor's plasma) is usually so diluted in the recipient that it rarely causes agglutination.

Answer 68

1. Agglutinated RBCs form clumps which block capillaries leading to pain and tightness of the chest immediately. The clumps are then hemolyzed, releasing Hb into plasma causing jaundice. 2. The cells hemolyze. Free Hb is liberated into the plasma. The severity of the transfusion reaction may vary from minor asymptomatic rise in plasma bilirubin to severe jaundice (hemolytic jaundice), renal tubular damage and renal failure and may be death. 3. Histamine release from the hemolyzed RBCs causing vasodilatation and resulting in hypotension.

Answer 69

There are three causes: a- The antigen-antibodies reaction of the transfusion reaction releases toxic substances from the hemolyzing RBCs and causes powerful renal vasoconstriction with reduction in the glomerular filtration rate. b- Circulatory shock from the loss of RBCs and the production of toxic substances decreasing the glomerular blood flow and urine output. c- Renal tubular blockage due to Precipitation of Hb which passes through the glomeruli by the acidic urine in the form of acid hematin which obstruct the lumen of the tubules decreasing the flow of urine. Thus, renal vasoconstriction, circulatory shock, and renal tubular blockage together cause acute renal shutdown. Due to renal failure there is uremia and hyperkalemia. If the shutdown is complete and fails to resolve, the patient dies within a week to 12 days. summary: Acute kidney shut down.due to a-Ag-Ab reaction -> release of toxic substances from hemolysed RBCs -> renal V.C. -> dec GFR b- circulatory shock -> toxic substances -> dec GBF and urine output c- renal tubular blockage by precipitated hemoglobin ( acidic urine + HB -> acid hematin)

Answer 70

1. Acute hemolytic (Incompatibility) reactions as pain, jaundice and acute renal shut down. 2. Febrile Reactions: fever is body’s response to the white blood cells in the transfused blood (white cell antibodies in a recipient react with white blood cells in a transfused blood). 3. Allergic Reactions: They arise from recipient antibody response to donor plasma proteins. 4. Mechanical overloading of the circulation particularly in patients with cardiac diseases 5. Hyperkalemia: With storage there is increased amount of K+ in the plasma due to its release from old hemolyzed cells that may lead to ventricular fibrillation and sudden death. 6. Citrate intoxication with massive transfusion due to excessive citrate infusion: this may produce decreased ionized calcium (hypocalcemia) and acidosis. 7. Bacterial infection: due to contamination of blood by bacteria specially with cold-growing gram-negative bacilli. After a latent period, it produces shock associated with fever. N.B. Prolonged storage at room temperature (more than 4 hours) encourages the growth of contaminating bacteria

Answer 71

1. Transmission of diseases e.g. AIDs, hepatitis, malaria and syphilis. 2. Iron overload: Most common in patients that receive repeated transfusions due to too much iron from donor blood. This can produce damage to organs as liver (developing liver cirrhosis), pancreas (diabetes mellitus) and heart

Answer 72

It is the spontaneous prevention of blood loss by physiological processes. Effective in stopping bleeding from small blood vessels.

Answer 73

1) Local vasoconstriction 2) Formation of temporary platelet plug 3) Formation of definitive blood clot 4) Repair of injured blood vessel

Answer 74

1) Nervous reflexes: induced by pain impulses due to trauma 2) Local myogenic spasm: induced by direct damage to vascular wall 3) Chemicals released by endothelial cells and platelets

Answer 75

occurs through: 1) platelet adhesion 2)platelet activation 3)platelet aggregation 1) damage to blood vessel disrubts endothelium exposing underlying collagen. 2) The platelets adhere to the collagen and such adhesion is potentiated by Von Willebrand factor 3) Platelet binding to collagen induces platelet activation 4) The activated platelets swell, become irregular in shape with pseudopods and become sticky. 5) They secrete ADP and thromboxane A2 which act on nearby platelets causing platelet activation. 6) formation of platelet plug effective in preventing blood loss from small blood vessels

Answer 76

1) physically seals the break in the vessel 2) Actin myosin protein complex contracts to compact and strengthen the originally loose plug 3) Platelets release vasoconstrictors (serotonin, epinephrine, thromboxane A2) - induce constriction 4) Release of other chemical substances to enhance blood coagulation

Answer 77

1) causes surface of platelets to become sticky 2) Continuous aggregation of platelets by positive feedback

Answer 78

- secreted by endothelial cells - forms bridge between the vessel wall and first layer of platelets. - binds to collagen facilitating adherence of platelets to damaged vessel walls

Answer 79

Platelet adhesion causes conversion of arachidonic acid to thromboxane A2. - stimulates platelet aggregation and secretion of platelet granules.

Answer 80

Inhibits platelet aggregation, avoid spread along endothelium

Answer 81

Factor I - fibrinogen Factor II - prothrombin Factor III - tissue thromboplastin (tissue factor) Factor IV - ionized calcium ( Ca++ ) Factor V - labile factor or proaccelerin Factor VI - unassigned Factor VII - stable factor or proconvertin Factor VIII - antihemophilic factor Factor IX - plasma thromboplastin component, Christmas factor Factor X - Stuart-Prower factor Factor XI - plasma thromboplastin antecedent Factor XII - Hageman factor Factor XIII - fibrin-stabilizing factor

Answer 82

Proteolytic enzymes called clotting factors undergo a series of chemical reactions resulting in: 1) Formation of prothrombin activators 2) Catalyze conversion of prothrombin to thrombin 3) converts fibrinogen to fibrin Fibrin is converted to a dense tight aggregate stabilized by activated factor XIII and requires Ca++

Answer 83

1) Begins with trauma to the vascular wall and surrounding tissues 2) Traumatized tissues release tissue factor (Factor III) 3) Tissue factor activates Factor VII (proconvertin) 4) Tissue Factor + Proconvertin + Ca++ activate Factor X (Stuart Prower factor) 5) Xa + Factor V (proaccelerin) + tissue phospholipids form prothrombin activator 6) Prothrombin activator splits prothrombin into thrombin in the presence of Ca++ and platelet phospholipids and the clotting process proceeds

Answer 84

It begins with: 1) In vivo with: a) exposure of blood to collagen from traumatized vascular wall or damaged endothelial cells b) Trauma to the blood In vitro with: c) blood coming in contact with wettable surface such as glass 2) These cause activation of Factor XII (Hageman, glass factor) 3) XIIa activates factor XI - this reaction requires HMW kininogen and is accelerated by prekallikrein 4) XIa activates factor IX in presence of calcium 5) IXa acting with VIIIa, platelet phospholipids and calcium activate factor X 6) Xa combines with Va and phospholipids to form prothrombin activator as the last step of the extrinsic pathway

Answer 85

1) Clotting occurs by both pathways simultaneously 2) The extrinsic pathway is much more rapid than the intrinsic pathway 3) The extrinsic pathway potentiates the intrinsic pathway through: - The trace amount of thrombin formed by the extrinsic system activates factors V and VII which are involved in the intrinsic system - Activated factor VII share in the activation of factor IX

Answer 86

- fat-soluble vitamin - requires bile for its absorption from the small intestine and absorbed in blood along with the fats

Answer 87

- bacteria including human intestinal normal flora - diet

Answer 88

Necessary for liver formation of prothrombin, factor VII, IX and X and protein C and protein S. - deficiency leads to bleeding tendency

Answer 89

1. Engulfing and digesting the foreigner. 2. Initiation of the immune response. 3. Removal of injured or dead cells and help healing 4. Destruction of cancer cells. Tumor cells produce proteins that are not normally produced by normal cells. T lymphocytes can recognize these antigens presented on the surface of tumor cells, thereby mediating cancer regression

Answer 90

1) Diapedesis 2) Ameboid motion 3) chemotaxis 4) phagocytosis

Answer 91

-The white blood cell leaves the blood stream to the tissues (i.e. a small portion of the cell is momentarily constricted and slides through the capillary pore). -This happens by interaction between endothelial cells and leukocytes

Answer 92

It is the movement of leucocytes which starts by protrusion of pseudopodium from one end, then movement of the remainder of the cell towards this pseudopodium.

Answer 93

It is the attraction of white blood cells towards some chemical substances which include: A. Some of the bacterial or viral toxins. B. Degenerative products of the inflamed tissues. C. Leukotrienes and polypeptides from WBCs (lymphocytes, mast cells and basophils). D. Several components of the "complement complex (C5a).

Answer 94

It is the ingestion of foreign particles and microorganisms by white blood cells.

Answer 95

Mechanism of Phagocytosis 1. Opsonization: coating of bacteria or virus by opsonins like Immunoglobulins (IGg) and some components of the complement proteins (C3b) to render them tasty for phagocytes. 2. Binding: of the coated bacteria to receptors on the cell membrane of neutrophil. 3. Pseudopodia from neutrophils protrude around the bacteria and fuse to form a phagosome. 4. Fusion of lysosomes with the phagosome creates phagolysosome to digest bacteria. 5. Expulsion of waste materials

Answer 96

Functions of thrombin: 1. Causes conversion of fibrinogen to fibrin. 2. Acts in a positive feedback to facilitate its own formation through the activation of factors VIlI & V. 3. Enhances platelet aggregation, which is essential to clotting process. 4. Activates factor XIlI to stabilize the resulting fibrin meshwork. 5. Activates plasminogen to plasmin (anticlotting).

Answer 97

Within few minutes after the fibrin clot is formed it begins to contract and a clear non coagulable fluid called serum is squeezed out. As the clot retracts it pulls the edges of the broken vessel together.

Answer 98

-bond the fibrin fibers together - release fibrin stabilizing factor (XIII) which causes more linking bonds between fibrin fibers. •activate thrombosthenin, actin and myosin, which are all contractile proteins

Answer 99

• Clot dissolution (Fibrinolysis): Few days later, after the clot has stopped the bleeding, clot lysis occurs and allows blood flow to be reestablished and allows tissue repair to take place.

Answer 100

It is the eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.

Answer 101

Functions of platelets: 1. Formation of a hemostatic plug that seals the injured vessel by aggregated platelets 2. Platelet plug release chemicals (platelet release reaction), such as: -ADP which causes the platelets aggregation. - Serotonin, epinephrine and thromboxane A2 which are potent vasoconstrictors which induce profound constriction of the affected vessel to reinforce the initial vascular spasm. - • Release platelet factor 3 (PF3) which enhances blood clotting mechanism. 3. Stabilization of blood clot as platelets have cytoplasmic granules, which contain fibrin stabilizing factor (factor XIII) 4. Induce clot retraction. 5. Release of platelet-derived growth factor (PDGF) that stimulates wound healing.

Answer 102

Definition: These are mechanisms that prevent clotting inside blood vessels, breakdown any clots that do form, or both. Include : 1) Anticoagulation system 2) Fibrinolytic system

Answer 103

it facilitates the removal of activated clotting factors by the circulating blood and their inactivation by the liver.

Answer 104

1. Intact smooth endothelium It prevents contact activation of the intrinsic clotting system and platelets. 2. Layer of glycocalyx on endothelium It repels clotting factors & platelets. 3. Balance between prostacyclin (PGI2) and thromboxane A2 -It keeps clot formation at site of injury only and rest of vessel lumen free of clot. -PGI2 is produced by healthy endothelium and inhibits platelet aggregation and phospholipid release that initiate coagulation and thus opposes the aggregating effects of thromboxane A2. 4. Thrombomodulin It is a protein present in the endothelium and binds thrombin to prevent clot formation. Thrombomodulin-thrombin complex activates protein C that act as an anticoagulant. 5. Tissue factor pathway inhibitor (TFPI) - It is made by the endothelial cell. It inactivates tissue factor / factor VIla complex and active factor X.

Answer 105

1. Protein C (PC) -It is a naturally occurring anticoagulant plasma protein. -Protein C is activated by thrombomodulin-thrombin complex and the activation is enhanced by protein S which acts as a cofactor. Activated protein C (APC) causes: • Inactivation of active factors VIII, V •Inactivation of inhibitors of plasminogen activators. •Increase of the formation of plasmin which helps lysis of fibrin. 2. Protein S - It is vitamin K-dependent hemostatic protein, and it is PC cofactor. 3. Anti-thrombin III (heparin cofactor !) It causes inactivation of thrombin and active factors IX, X, XI, XII. Its action is facilitated by heparin.

Answer 106

Thrombin removal from blood is mediated by: 1. Fibrin fibers (antithrombin action of fibrin) 2. Antithrombin III - 85 -90% of thrombin is bound to fibrin, which prevents spread of thrombin. Remaining amount is bound to antithrombin-Ill.

Answer 107

-Heparin is a powerful anticoagulant but is present in small amounts in blood. -When heparin combines with antithrombin III (Heparin + Antithrombin III complex), the effectiveness of antithrombin III for removing thrombin increases 100-1000 folds, and thus it acts as an anticoagulant. -Heparin + Antithrombin III complex causes removal of thrombin and active factors XII, XI, X, IX.

Answer 108

A fibrin clot is a transitory device until permanent repair of the vessel occurs. The fibrinolytic system is the physiological process for: -Clot removal. -Restriction of clotting to a limited area, thereby preventing excessive intravascular coagulation.

Answer 109

1. Plasminogen (profibrinolysin) is an Inactive globulin produced by the liver and circulates in the plasma as a plasma protein. 2. Plasminogen is converted to plasmin (fibrinolysin) by: • Thrombin. Tissue plasminogen activator (1-PA), which is released very alowly from damaged tissues and vascular endothelium. • Urokinase plasminogen activator (u-PA). 3. Plasmin is a proteolytic enzyme that digests: Fibrin and fibrinogen, with the production of degradation products (FDP) that inhibit thrombin. • Prothrombin, factor V, factor VIlI and factor XII. 4. FDP inhibits the interaction between fibrinogen and thrombin and inhibits platelets activation and aggregation.

Answer 110

1. Thrombomodulin-thrombin complex activates protein C. 2. Activated protein C along with its cofactor protein S inactivates: Active Factor V and Factor VIII. Inhibitors of tissue plasminogen activator, increasing the formation of plasmin.

Answer 111

These are a group of diseases characterized by an increased tendency to bleeding after trauma or spontaneously. Vessel wall defects and platelet disorders - superficial bleeding Clotting disorders - deep bleeding

Answer 112

It is prolonged bleeding time due to weak fragile vascular wall Causes: 1) Hereditary 2) Acquired: - Nutrient deficiency (scurvy) -Drug induced (steroids) -Aging -Certain Infections -Malignancies -

Answer 113

Decreased Platelet count - Clot retraction is deficient and there is poor vessel constriction - tendency to bleed from many small capillaries and venules, causing small punctuate hemorrhages. -- Bleeding occurs when platelet count is below 50,000uL Lethal - <10,000uL Normal range 150,000 - 410,000

Answer 114

- petechiae - subcutaneous hemorrhages small, purplish blotches on skin - prolonged bleeding time

Answer 115

1) Autoimmune disease in which platelets are destructed by antibodies (Idiopathic thrombocytopenia purpura) 2) Secondary thrombocytopenia purpura due to : - Hypersplenism -Severe bone marrow destruction

Answer 116

- weak platelet function It gives the same picture as thrombocytopenia

Answer 117

1) Prolonged use of aspirin leads to defective platelet aggregation 2) Renal failure 3) Von WillebrandT factor deficiency

Answer 118

- Platelet transfusions - Fresh whole blood transfusions containing large number of platelets

Answer 119

Deficient clotting due to lack of any of the clotting factors -Tendency to bleed from large vessels - Coagulation tests are prolonged while bleeding time is normal

Answer 120

1) Liver diseases - almost all clotting factors are formed by the liver 2) Vitamin K deficiency - insufficiency of clotting factors II, VII, IX and X. 3) Congenital deficiency of clotting factor - hemophilia congenital deficiency of factor VIII or IX or XI

Answer 121

1) Parahemophilia - deficiency of factor V 2) Afibrinogenemia - deficiency of fibrinogen 3) Hypothrombinemia - decreased prothrombin synthesis by the liver, usually in Vitamin K deficiency

Answer 122

1) Liver disease - failure to secrete bile 2) Failure of absorption in case of: - obstruction of bile ducts so no bile reaches the intestine - chronic diarrhea - GIT disease as a result of poor absorption of fats 3) Deficient intestinal bacteria in case of - prolonged use of antibiotics - newly born infant 4) Anticoagulant drugs

Answer 123

Inherited sex-linked anomaly, transmitted by females -females show no symptoms, males manifest signs of the disease - symptoms usually begin early in life -slight injury causes severe hemorrhage

Answer 124

1) Hemophilia A (classical): - It is due to deficiency of factor VIII - represents 85% of hemophilic patients 2) Hemophilia B - due to factor IX deficiency (Christmas disease) 3) Hemophilia C - due to factor XI deficiency

Answer 125

1) Bleeding either from natural orifices or after injury or incisions 2) Recurrent hemarthrosis - bleeding in joints, preceded by minor injury leading to crippling deformity due to fibrous adhesions

Answer 126

supplying the patient with the deficient clotting factor

Answer 127

Abnormal clot formation inside the blood vessel is called thrombus

Answer 128

1. Sluggish blood flow: It allows activated clotting factors to accumulate instead of being washed away. 2. Damaged or roughened endothelial surface of a vessel as in atherosclerosis. 3. As a complication of septicemia or extensive tissue damage. 4. Imbalance between clotting-anticlotting systems. 5. Factor V Leiden: an inherited disorder which is an abnormal form of factor V caused by mutation in the gene that makes clotting factor V. Factor V Leiden is resistant to the action of activated protein C (APC), so it leads to increased risk of developing blood clots in legs (DVT) or lungs (PE). These blood clots can be life-threatening.

Answer 129

1) blood vessel occlusion due to thrombus enlargement 2) formation of embolus in distant sites 3) block of vessel prevents blood flow and oxygen to tissues and organs - leads to organ damage and failure

Answer 130

Heredity Hemophilia: congenital Purpura: not congenital Sex Hemophilia: males Purpura: males + females Cause Hemophilia: lack of clotting factors purpura: diminished platelets PT Hemophilia: normal Purpura: normal aPTT Hemophilia: prolonged Purpura: normal Bleeding time Hemophilia: normal Purpura: prolonged

Answer 131

1) Neutrophils produced by bone marrow leave bloodstream by diapedesis 2) They are attracted by chemotaxis to: - C5a - leukotrienes and polypeptides from lymphocyrtes 3) Neutrophils migrate towards site of inflammation via ameboid movement 4) phagocytosis of bacteria

Answer 132

- a single neutrophil can phagocytize 3-20 bacteria before death - contain proteases and antimicrobial molecules that kill ingested organism - synthesize toxic oxygen metabolites like superoxide radical and hydrogen peroxide and hypochlorous acid. These are strong oxidants formation of killing zone that destroys organism

Answer 133

- First line of defense against parasites - Exhibit diapedesis, chemotaxis, and weak phagocytosis - Target certain tissues such as skin, lungs, urinary tract and GIT - secrete lysozymes, ROS, interleukins and leukotrienes

Answer 134

- Contain IgE and are involved in allergic reactions a. release histamine and other mediators to initiate inflammation b. release heparin which prevents blood coagulation by acting as a cofactor for anti-thrombin II. Heoarin may also exert anti-inflammatory effects c. involved in type 1 hypersensitivity which range from mild urticaria to severe anaphylactic shock

Answer 135

- form the core of immune system - 2% found in peripheral blood and the rest in the lymphoid tissues functions: - B lymphocytes are responsible for humoral immunity. Each B-cell produces immunoglobulins with a single antigenic specificity. - T-lymphocytes are responsible for cell mediated immunity. They attack and kill virus-infected cells as well as malignant cells. They facilitate antibody production by B-cells.