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.

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

Plasma proteins

o Are produced by livero Transports lipids

• Gamma globulins o Are produced by

lymphatic tissueso function as antibodies

3. Fibrinogen• 4% of plasma proteins• Primary role in blood coagulation

Plasma proteins

• 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

Plasma Gasses & Nutrients

• About 7% is dissolved in plasma

• Nutrients:

• Amino acids

• Simple sugars

• Nucleotides

• Lipids

• Hydrophobic lipids are bound to plasma proteins

within the plasma

• 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

Nonprotein Nitrogenous Substances

• 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

• 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

Plasma Electrolytes

• Calcium

• Magnesium

• Chloride (most abundant with sodium)

• Bicarbonate

• Phosphate

• Sulfate

• Hemostasis refers to the stoppage of bleeding

• Actions that limit or prevent blood loss include:

1. Blood vessel spasm (vasospasm)

2. Platelet plug formation

3. Blood coagulation

Hemostasis

• 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

hemostasis, step 1: vasospasm

•Vasospasm reduces blood loss almost immediately, and may close small blood vessels completely.

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 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.

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.forms a mesh surrounding the damaged vessel.

• The cascade is divided into three events1. Extrinsic mechanism2. Intrinsic mechanism3. Common pathway

• 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

Coagulation

•Factor III initiates a cascade reaction that, in the

presence of Calcium, activates factor X.

•Activation of factor X initiates the common

pathway

• 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

Coagulation

of reactions in the presence of Calcium

to activate factor X.

•Activation of factor X initiates the

common pathway.

•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.

Coagulation

•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.

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.

hemostasis: review

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• Plasmin digests the blood clots

•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

Blood Clot Disorders

•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.

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.

Blood Clot Disorders

Ultrasound image of stenosis within the internal carotid artery.

• 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.

Blood TypingBlood typing is the process of identifying an individual’s blood group. (eg. Type A, B, AB or O)

• 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

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.

antigens

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

Blood Typing

antibodies

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.

ABO Blood Group

• 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

Rh Blood Group

• 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).

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+.

•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.