Download - section 2, chapter 14: blood plasma
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PlasmaOverview1. Plasma is the liquid portion of blood2. Makes up 55% of blood volume3. Straw colored4. Components include Plasma proteins, Dissolved gasses, Wastes,
Electrolytes, Nutrients, Hormones
Chapter 14, Section 2 of 2.
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1. Albumin• 60% of plasma proteins• Synthesized in liver• Creates an osmotic that
helps maintain blood pressure
2. Globulins • 36% of plasma proteins • Alpha & Beta globulins
o Are produced by liver
o Transports lipids• Gamma globulins
o Are produced by lymphatic tissues
o function as antibodies
3. Fibrinogen• 4% of plasma proteins• Primary role in blood
coagulation
Plasma proteins
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Plasma proteins
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• Blood Gasses:• Oxygen
• Most is bound to hemoglobin. Less than 2% of oxygen is dissolved in plasma
• Carbon dioxide• Most CO2 is transported as bicarbonate (HCO3
-)• About 7% is dissolved in plasma
• Nutrients:• Amino acids• Simple sugars• Nucleotides• Lipids
• Hydrophobic lipids are bound to plasma proteins within the plasma
Plasma Gasses & Nutrients
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• These are molecules containing nitrogen but are not proteins
• In plasma they include:• Urea – product of protein catabolism; about 50% of nonprotein
nitrogenous substances
• Uric acid – product of nucleic acid catabolism
• Amino acids – product of protein catabolism
• Creatine – biproduct of creatine phosphate metabolism
• Creatinine – product of creatine metabolism
Common tests that evaluate kidney functions:• Creatinine test – measures creatinine• BUN – blood urea nitrogen; indicates health of kidney
Nonprotein Nitrogenous Substances
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• Plasma contains a variety of these ions called electrolytes
• They are absorbed from the intestine or released as by-products of cellular metabolism
• They include:• Sodium (most abundant with chloride)• Potassium• Calcium• Magnesium• Chloride (most abundant with sodium)• Bicarbonate• Phosphate• Sulfate
Plasma Electrolytes
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• Hemostasis refers to the stoppage of bleeding
• Actions that limit or prevent blood loss include:1. Blood vessel spasm (vasospasm)2. Platelet plug formation3. Blood coagulation
Hemostasis
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• Blood vessel spasm (vasospasm)• Cutting or breaking a vessel wall stimulates the
smooth muscles in its walls to contract.
• Vasospasm reduces blood loss almost immediately, and may close small blood vessels completely.
hemostasis, step 1: vasospasm
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hemostasis, step 2: platelet plug formation
1. Platelet adhesion – platelets adhere to collagen fibers that become exposed due to the damage in a vascular walls
2. Platelets undergo a shape change, producing several processes to which additional platelets bind.
3. In addition, platelets secrete thromboxanes, which attract additional platelets to the site of injury.
4. A platelet plug may control blood loss from a small break.
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hemostasis, step 3: coagulation
• Blood coagulation• Is triggered by cellular damage and blood contact with foreign surfaces
• Coagulation is a cascade reaction involving several biochemicals (clotting factors)
• The major event is formation of a blood clot when fibrin (a thread-like protein) forms a mesh surrounding the damaged vessel. • The cascade is divided into three events
1. Extrinsic mechanism2. Intrinsic mechanism3. Common pathway
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• Extrinsic clotting mechanism• A chemical released from tissue outside the blood
vessels trigger the extrinsic pathway
• Damaged tissues releases thromboplastin (also called factor III)
• Factor III initiates a cascade reaction that, in the presence of Calcium, activates factor X.
• Activation of factor X initiates the common pathway
Coagulation
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• Intrinsic clotting mechanism• An inactive clotting factor within the
blood (Hageman, or factor XII) is activated when foreign tissue, such as collagen enters the bloodstream.
• Factor XII proceeds through a cascade of reactions in the presence of Calcium to activate factor X.
• Activation of factor X initiates the common pathway.
Coagulation
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•Common Pathway • Is the point at which intrinsic & extrinsic pathways converge
• Activated factor X (with help of Calcium & factor V) leads to the release of prothrombin activator from platelets.
• Prothrombin activator converts prothrombin into thrombin.
• Thrombin, in turn converts fibrinogen into long threads of fibrin.
• Fibrin forms an insoluble clot at the site of injury.
Coagulation
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CoagulationFigure 14.19c. Schematic of the common pathway in the blood clotting mechanism
Figure 14.18 A scanning electron micrograph of fibrin threads. The insoluble fibers trap blood cells and platelets, which contribute to the blood clot formation.
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hemostasis: review
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Blood Clot Dissolution
• After a blood clot forms it retracts and pulls the edges of a broken blood vessel together while squeezing the fluid serum from the clot
• Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessel walls
• Plasmin digests the blood clots
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•A thrombus is an abnormal blood clot• Deep vein thrombosis – prolonged immobility causes blood to pool,
especially in the deep veins of the legs or pelvis.
• An embolus is a blood clot moving through the blood vessels• Pulmonary embolism – may occur when part of a thrombus breaks
away from the clot and lodges in a pulmonary artery. Rapidly fatal.
•Atherosclerosis – accumulation of fatty deposits along arterial lining• May cause inappropriate clotting• Most common cause of thrombosis in medium-sized arteries
•Arteriosclerosis – hardening of an artery.
•Stenosis – abnormal narrowing of a passage in a body• Atherosclerosis of an artery narrows the passage through which blood
flows in an artery, and increases the likelihood of an embolism at that site.
Blood Clot Disorders
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Figure 14.20 Artery cross sections.(a) light micrograph of a normal artery. (b) The inner wall of an artery changed as a result of atheroclerosis.
Ultrasound image of stenosis within the internal carotid artery.
Blood Clot Disorders
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• Terms to become familiar with:
• Antigen – a chemical (or membrane protein) that stimulates cells to produce antibodies
• Foreign antigens in the body stimulate the immune response.
• Antibodies – a plasma protein that reacts against a specific antigen
• Agglutination – clumping of red blood cells in response to a reaction between an antibody and an antigen
Blood TypingBlood typing is the process of identifying an individual’s blood group. (eg. Type A, B, AB or O)
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ABO Blood Group
• This blood group is based on the presence (or absence) of two antigens on red blood cell membranes: Antigen A & Antigen B
Type A blood contains A-antigens on the surface of its RBCs.
Type B blood contains B-antigens on the surface of its RBCs. and anti-A antibodies in its plasma.
Type AB blood contains A-antigens and B-antigens on the surface of its RBCs. and has neither antibody
Type O blood contains neither A or B antigen on the surface of its RBCs
antigens
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Blood Typingantibodies
Type A blood plasma contains anti-B antibodies.
Type B blood plasma contains anti-A antibodies.
Type AB blood plasma contains neither antibody
Type O blood plasma contains both anti-A and anti-B antibodies.
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ABO Blood Group
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• The Rh blood group was named for the rhesus monkey
•Rh positive (Rh+) indicates the presence of D-antigen (or other Rh antigen) on the red blood cell membranes
• Rh negative (Rh-) lacks the D-antigen
• When Rh- blood is exposed to the D antigen, it becomes sensitized and develops anti-D antibodies
• Anti-D antibodies are formed only after a person is exposed to D-antigen (Rh sensitization).
Rh Blood Group
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erythroblastosis fetalis • The seriousness of the Rh blood group is evident in a fetus that develops
the condition erythroblastosis fetalis or hemolytic disease of the newborn.• If the mother is Rh- and has been sensitized to the D-antigen, her own antibodies may attack the red blood cells of a fetus that is Rh+.
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•Erythroblastosis fetalis can be prevented for women at high risk by administering a serum that contains anti-D antibodies into the mother during the pregnancy and after birth (before she becomes sensitized to D-antigen).
•The injected antibodies quickly agglutinate any fetal red blood cells, thereby preventing her from becoming sensitized to the D-antigen.
erythroblastosis fetalis
End of Section 2 of 2.