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Flashcards in Chapter 9 (Blood) Deck (30):

Blood Introduction

8% of total body weight
Average volume
- 5 L for women
- 5.5 L for men
Three elements of the plasma 55%
1. Erythrocytes (RBC), important in O2 and CO2 transport to body tissue. 45%
2. Leukocytes (WBC), immune system's mobile defense units (antibodies) <1%
3. Platelets, important in hemostasis (blood clotting)


Hematocrit Definition

99% of cells in centrifuged test tube is composed of RBCs. It is called hematocrit/ packed cell volume.
Hematocrit values
- Women have 42%
- Men have 45%
Average pleura volume in blood
- Women have 58%
- Men have 55%
WBC and platelets are colorless and less dnese
These cells represents 1%.


Plasma and it's Proteins

Plasma is 90% water
1. Transports and distribute substances
2. Removes metabolic wastes
Plasma proteins compose 6-8% of plasma's total weight.
1. Albumins
2. Globulins
3. Fibrinogens



1. Most abundant plasma protein
2. Contributes to colloid osmotic pressure
3. Transports many substances (bilirubin, penicillin, bile salts etc. )



1. Composed of 3 units (a, B & ɣ)
2. These units bind and transport number of substances (TH, iron, cholesterol) in the plasma
3. Factors involved in blood-clotting process
4. a Globulins activates conversion of angiotensinogen into angiotensin
5. Gamma (ɣ) globulins are antibodies (defence mechanisms). Produced by B cells.



Blood clotting



- 1 ml of blood has 5 billion RBCs
- There's no nucleus, organelles, or ribosomes
Biconcave discs
- provide larger sruface area for diffusion of O2 across the membrane
- thinness of cell enables rapid O2 to diffuse
Flexible membrane
- allows RBCs to travel through narrow capillaries without rupturing in the process.



- Found only in RBC
Pigments contains iron
- Reddish when oxygenated
- Appears bluish when deoxygenated
2 parts
1. Globin portion.
- Protein composed of four highly folded polypeptide chains
2. Heme groups
- Four iron-containing non protein groups
- Each is bound to one of the polypeptides
Structure and Function
1. Carries O2 (98.5 % of O2 is bound to Hb)
2. Binds with
a. CO2
b. Acidic H+ ion, helps maintain pH
c. CO can cause CO poisoning
d. NO. In the lungs, NO binds with sulphur within Hb molecule to form SNO.
i) is a vasodilator to arterioles
ii) helps stabilize blood pressure by vasodilation and vasoconstriction


Erythrocyte Key Enzymes

Glycolytic enzymes
- Necessary for generating the energy needed to fuel active transport mechanisms involved in maintaining proper ionic concentrations within the cells.
- Relies on glycolysis for ATP formation.
Carbonic Anhydrase
- Critical in CO2 transport
- Catalyzes reaction that leads to conversion of metabolically produced CO2 into bicarbonate ion (HCO3-)
- HCO3- is the primary form in which CO2 is transported in the blood.


Erythrocytes' Short Life Span

RBCs survive 120 days
- the nutrient that the nucleus produces lasts 120 days. After the nucleus/nutrient supply is used up, the cell dies. there's no DNA or RNA.
- spleen removes most of the old erythrocytes from ciruclation



A hormone secreted by the kidneys that stimulates RBC production.
- Synthetic version is available.
1. The kidneys detect reduced O2 carrying capacity of the blood
2. When less O2 is delivered to the kidneys, they secrete the hormone erythropoietin into the blood
3. Erythropoietin stimulates erythropoiesis (RBC production) by the bone marrow
4. The additional circulating erythrocytes increase the O2-carrying capacity of the blood
5. The increased O2 carrying capacity relieve the initial stimulus that triggered erythropoietin secretion.



Refers to a below-normal O2 carrying capacity of the blood, characterized by low hematocrit.
3 types:
1. Nutritional anemia
2. Pernicious anemia
3. Hemolytic anemia
3 causes:
1. Decreased rate of erythropoisesis
2. Excessive loss of RBC
3. Deficiency in the Hb content of the RBC


Nutritional Anemia

- Caused by a diet deficient in iron; iron is essential for the production of Hb
- RBC are produced but contains less Hb than normal, since they can't transport O2 in a greater quantity


Pernicious Anemia

Caused by:
1. An inability to absorb an adequate amount of ingested vitamin B12 from the digestive system
2. Deficiency in intrinsic factor (secreted from the stomach lining) prevents the absorption of B12 from digestive system into the blood.
This leads to impairment of RBC production and matruation


Hemolytic Anemia/ Sickle-cell Anemia

Caused by
1. Rate of RBC rupture exceeds the rate of erythropoiesis
2. Defects in RBC or rupture induced by external factors
3. Various hereditary abnormalities of erythrocytes
4. Defective type of Hb polymerizes
5. Deformed RBCs clump together and can block the blood flow through small blood vessels, leading to tissue damage



Characterized by too many circulation RBC's and elevated hematocrit. (normally 42 for males, 38 for females)
- Caused by tumourlike condition of the bone marrow
- Erythropoiesis proceeds at an uncontrolled rate.
- Erythropoietin-induced adaptive mechanism to improve blood's oxygen-carrying capacity in response to prolonged reduced oxygen delivery to the tissues
- occurs normally in people living in high altitudes



- Mobile units of the body's immune defence system
- Colorless: lack hemoglobin
5 types
1. Neutrophils
2. Monocytes
3. Basophils
4. Eosinophils
5. Lymphocytes


Leukocyte Production

- Originates from undifferentiated multipotent stem cells in red bone marrow.
- Granulocytes and monocytes are produced only in the bone marrow.
- Most new lymphocytes are actually produced by lymphocytes already in the lymphoid tissues (lymph nodes and tonsils)
See figure 9-9 on page 394.



Haemostasis prevents blood loss from a broken blood vessel.
1. Vascular spasm
- Reduces blood flow through a damaged vessel
2. Formation of a platelet plug
- Platelets aggregate on contact with exposed collagen in damaged wall of the blood vessel
- Platelets release ADP which causes surface of nearby circulating platelets to become sticky in order to adhere to the first layer of aggregated platelets
3. Blood coagulation (clotting)
- Transformation of blood from liquid into a solid gel.



A hormone produced by liver increases number of megakaryocytes and therefore increases platelet production


Formation of a Platelet Plug

1. Platelets adhere to and are activated by exposed collagen at the site of vessel injury
2. Activated platelets release ADP and thromboxane A2.
3. Theses chemical messengers work together to activate other platelets passing by.
4. Newly activated platelets aggregate onto growing platelet plug and release even more platelet-attracting chemicals.
5. Normal (uninjured) endothelium releases prostacyclin and nitric oxide, which inhibit platelet aggregation, so platelet plug is confined to the site of injury.

Positive feedback cycle


Role of the Platelet Plug

1. The actin-myosin complex within the aggregated platelets contract to compact and strengthen the loose plug
2. Platelet plug releases powerful vasoconstrictors (serotonin, NE, and thromboxane A2)
3. These substances cause profound vasoconstriction
4. Release other chemical that enhance blood coagulation.


Process of Clot Formation

1. Fibrinogen, a large, soluble pl. protein (produced by the liver)
2. Thrombin, at the injured site
3. Fibrin, insoluble, thread-like molecule
- Adheres to the damaged vessel surface
- This attracts other blood cellular elements (aggregated platelets)
- This forms a clot (red due to trapped RBCs)
4. Factor XIII, fibrin-stabilizing factor (plasma)
- Causes cross-linkage and strengthens fibrin strands.


Role of Thrombin in Hemostasis

1. Thrombin, a component of the clotting cascade, plays multiple roles in haemostasis
a. It stimulates conversion of fibrinogen to fibrin
b. it activates the factor that stabilizes the fibrin meshwork of the clot
c. it enhances activation of more prothrombin into thrombin through positive feed back
d. it enhances platelet aggregation
2. through positive feedback, aggregated platelets secrete PF3, which stimulates the clotting cascades that results in thrombin activation


Clotting Cascade (Intrinsic)

1. Inactive factor XII is activated by damaged vessel surfaces. This turns it into active factor XII (Hageman factor)
2. Active factor XII stimulates inactive factor XI and activates it.
3. Active factor XI (with Ca 2+ [factor IV]) stimulates inactive factor IX and activates it.
4. Active factor IX (with Ca 2+, factor VIII, and PF3) stimulates inactive factor X and activates it.
5. Active factor X (with Ca 2+, factor V and PF3) stimulates prothrombin (factor II) and changes it into thrombin.
5. Thrombin converts Fibrinogen (factor I) into fibrin.
6. Thrombin also converts loose meshwork fibrin into stabilized meshwork fibrin (through factor XIII)
7. Clot is formed

12 --- 11 -4- 9 -8- 10 --- 2(prothrombin-thrombin) -13- stabilized fibrin


Clot Pathways (Extrinsic)

1. Tissue damage stimulates tissue thromboplastin (factor III)
2. Ca 2+ and factor VII activates active factor X.
Active factor X (with Ca 2+, factor V and PF3) stimulates prothrombin (factor II) and changes it into thrombin.
3. Thrombin converts Fibrinogen (factor I) into fibrin.
4. Thrombin also converts loose meshwork fibrin into stabilized meshwork fibrin (through factor XIII)
5. Clot is formed

- Requires contact with tissues factors external to the blood


Clot Retraction and Dissolution

- Contraction of platelets shrinks fibrin mesh, squeezing fluid from the clot
- Enzyme plasmin dissolves clot
- Plasmin formed from plasminogen


Cerebrovascular Accident

- An abnormal or excessive clot formation within blood vessels can compromise flood flow to vital organs
- The body's clotting and anticoagulant systems function in check-and-balance manner.
- abnormal intravascular clot attached to a vessel wall
- Can eventually completely occlude the vessel
- Freely floating clots
- Can suddenly block flood flow



1. Roughened vessel surfaces associated with atherosclerosis
2. Imbalances in the clotting-anticlotting systems
3. Slow-moving blood
4. Occasionally release of tissue thromboplastin into blood from large amounts of traumatized tissue



Excessive bleeding caused by deficiency of one of the factors in the clotting cascade (inability to produce factor VIII)