Body Fluids and blood- HAP II ( B. Pharm)

 

Body fluid and blood

Body fluids: Blood, intracellular fluids(ICF) and Extracellular fluid( ECF)à plasma, lymph, and cerebral spinal fluid.

Blood:

Functions of Blood:

1.       Transportation: blood transports oxygen from the lungs to the cells of the body and carbon dioxide from the body cells to the lungs for exhalation. It carries nutrients from the gastrointestinal tract to body cells and hormones from endocrine glands to other body cells.

2.       Regulation: Circulating blood helps maintain homeostasis of all body fluids. Blood helps regulate pH through the use of buffers. It also helps adjust body temperature through the heat-absorbing and coolant properties of the water.

3.       Protection: Blood can clot (become gel-like), which protects against its excessive loss from the cardiovascular system after an injury. In addition, its white blood cells protect against disease by carrying on phagocytosis.

Components of blood:

                              

 

 

 

Hemopoiesis (Formation of Blood)

Definition: Hemopoiesis is the formation of blood cells from the hemopoietic stem cells in red bone marrow.

 

Red blood Cells

Concave disk like Structure, Non nucleated cells ,

There are 5 -6 million RBCs per microliter blood.

RBC formation (Erythropoiesis): Erythropoiesis is the process which produces red blood cells (erythrocytes), which is the development from erythropoietic stem cell for mature red blood cell.

The bone marrow of essentially all the bones produces red blood cells until a person is around five years old. The tibia and femur cease to be important sites of hematopoiesis by about age 25; the vertebrae, sternum, pelvis and ribs, and cranial bones continue to produce red blood cells throughout life.

 

Mechanism of Blood Coagulation

·       Definition: Blood coagulation or clotting is an important phenomenon to prevent excess loss of blood in case of injury or trauma. The blood stops flowing from a wound in case of   injury.

·       Blood coagulation pathway:

Vascular Spasm: When arteries or arterioles are damaged, the circularly arranged smooth muscle in their walls contracts immediately, a reaction called vascular spasm

Platelet Plug Formation:

1.        Initially, platelets contact and stick to parts of a damaged blood vessel, such as collagen fibers of the connective tissue underlying the damaged endothelial cells. This process is called platelet adhesion.

2.       Due to adhesion, the platelets become activated, and their characteristics change dramatically. They extend many projections that enable them to contact and interact with one another, and they begin to liberate the contents of their vesicles. This phase is called the platelet release reaction. Liberated ADP and thromboxane A2 play a major role by activating nearby platelets. Serotonin and thromboxane A2 function as vasoconstrictors, causing and sustaining contraction of vascular smooth muscle, which decreases blood flow through the injured vessel.

3.       The release of ADP makes other platelets in the area sticky, and the stickiness of the newly recruited and activated platelets causes them to adhere to the originally activated platelets. This gathering of platelets is called platelet aggregation. Eventually, the accumulation and attachment of large numbers of platelets form a mass called a platelet plug.

 

Clotting is a sequential process that involves the interaction of numerous blood components called coagulation factors. There are 13 principal coagulation factors in all, and each of these has been assigned a Roman numeral, I to XIII. Coagulation can be initiated through the activation of two separate pathways, designated extrinsic and intrinsic. Both pathways result in the production of factor X. The activation of this factor marks the beginning of the so-called common pathway of coagulation, which results in the formation of a clot.

The extrinsic pathway is generally the first pathway activated in the coagulation process and is stimulated in response to a protein called tissue factor, which is expressed by cells that are normally found external to blood vessels. However, when a blood vessel breaks and these cells come into contact with blood, tissue factor activates factor VII, forming factor VIIa, which triggers a cascade of reactions that result in the rapid production of factor X. In contrast, the intrinsic pathway is activated by injury that occurs within a blood vessel. This pathway begins with the activation of factor XII (Hageman factor), which occurs when blood circulates over injured internal surfaces of vessels. Components of the intrinsic pathway also may be activated by the extrinsic pathway; for example, in addition to activating factor X, factor VIIa activates factor IX, a necessary component of the intrinsic pathway. Such cross-activation serves to amplify the coagulation process.

The production of factor X results in the cleavage of prothrombin (factor II) to thrombin (factor IIa). Thrombin, in turn, catalyzes the conversion of fibrinogen (factor I)—a soluble plasma protein—into long, sticky threads of insoluble fibrin (factor Ia). The fibrin threads form a mesh that traps platelets, blood cells, and plasma. Within minutes, the fibrin meshwork begins to contract, squeezing out its fluid contents. This process, called clot retraction, is the final step in coagulation. It yields a resilient, insoluble clot that can withstand the friction of blood flow.