1. Plasma is the liquid portion of blood
2. Makes up 55% of blood volume
3. Straw colored
4. Components include Plasma proteins, Dissolved gasses, Wastes, Electrolytes,
Chapter 14, Section 2 of 2.
• 60% of plasma proteins
• Synthesized in liver
• Creates an osmotic that helps
maintain blood pressure
• 36% of plasma proteins
• Alpha & Beta globulins
o Are produced by liver
o Transports lipids
• Gamma globulins
o Are produced by
o function as antibodies
• 4% of plasma proteins
• Primary role in blood coagulation
Plasma Gasses & Nutrients
• Blood Gasses:
•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
• Amino acids
• Simple sugars
• Hydrophobic lipids are bound to plasma proteins
within the plasma
Nonprotein Nitrogenous Substances
• These are molecules containing nitrogen but are not proteins
• In plasma they include:
• Urea – product of protein catabolism; about 50% of nonprotein
• 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
• Plasma contains a variety of these ions called electrolytes
• They are absorbed from the intestine or released as by-products of
• They include:
• Sodium (most abundant with chloride)
• Chloride (most abundant with sodium)
• 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, step 1: vasospasm
• 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 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
3. In addition, platelets secrete
thromboxanes, which attract
additional platelets to the site of
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.
cascade is divided into three events
• 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
• 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
•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.
Figure 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.
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
Blood Clot Disorders
•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
Figure 14.20 Artery cross sections.
(a) light micrograph of a normal
(b) The inner wall of an artery
changed as a result of atheroclerosis.
Ultrasound image of stenosis within the internal carotid artery.
Blood typing is the process of identifying an individual’s blood group.
(eg. Type A, B, AB or O)
• Terms to become familiar with:
•Antigen – a chemical (or membrane protein) that stimulates cells to
• 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.
Type B blood contains B-antigens on the
surface of its RBCs. and anti-A antibodies in its
Type AB blood contains A-antigens and Bantigens on the surface of its RBCs. and has
Type O blood contains neither A or B antigen
on the surface of its RBCs
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.
Rh 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
• 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 Dantigen (Rh sensitization).
•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.
End of Section 2 of 2.