Hemoglobin

Blood is more than just a red liquid; it is a complex, life-sustaining tissue composed of a liquid matrix (plasma) and three types of blood cells ( $\text{BCs}$ ): red blood cells (

\text{RBCs}

), white blood cells (

\text{WBCs}

), and platelets. The continuous formation and regulation of these components are essential for health.

I. Hemopoiesis: The Birth of Blood Cells

Hemopoiesis (or Hematopoiesis) is the continuous process by which blood cells are formed. Blood cells are not created in the bloodstream itself but originate from specialized cells within the bone marrow.

In adult humans:

All $\text{RBCs}$ .
$60\%-70\%$ of $\text{WBCs}$ .
All platelets.

These are produced in the bone marrow to replenish the components that are constantly depleted through use and aging.

II. Hemoglobin and Oxygen Transport

The primary function of $\text{RBCs}$ is to carry oxygen, a task performed by the protein hemoglobin ( $\text{Hb}$ ).

Structure of Hemoglobin:

Hemoglobin is composed of:

Globin: A globular protein component.
Haem: A pigmented, iron-containing complex.

Each hemoglobin molecule has four chains, and each chain contains one iron atom. This structure allows a single $\text{Hb}$ molecule to carry up to four oxygen ( $\text{O}_2$ ) molecules (one per iron atom). With approximately 280 million $\text{Hb}$ molecules per $\text{RBC}$ , each red blood cell has the capacity to carry billions of oxygen molecules.

Iron Transport

Iron is vital for $\text{Hb}$ production. In the bloodstream, iron is bound to a protein called transferrin, which transports it to the liver for storage and to the bone marrow for $\text{RBC}$ production. Since the body's absorption of dietary iron is slow, iron deficiency can occur easily if loss exceeds intake.

III. Anemia: Oxygen Deficiency Disorders

Anemia is a condition defined by a lack of $\text{RBCs}$ or an insufficient amount of hemoglobin within them, resulting in reduced oxygen-carrying capacity.

Type of Anemia	Cause/Mechanism	Key Characteristics
Iron-Deficiency	Lack of dietary iron for $\text{Hb}$ production.	Hemoglobin level is below normal, but $\text{RBC}$ count may appear normal.
Pernicious	Lack of Vitamin $\text{B}12$ (often due to poor absorption).	$\text{RBCs}$ are large, misshapen, and fragile.
Sickle-Cell	Genetic disorder causing abnormal $\text{Hb}$ synthesis.	$\text{RBCs}$ become rigid and "sickled," leading to capillary clogging and rupture.
Aplastic	Suppression of red bone marrow activity.	Leads to lower counts of $\text{RBCs}$ , $\text{WBCs}$ , and platelets; can be triggered by radiation or chemicals.
Hemolytic	Premature rupture/destruction of $\text{RBCs}$ before the end of their normal lifespan.	Associated with jaundice (due to increased bilirubin production). Examples: Sickle-cell, $\text{Rh}$ disease, Malaria.

IV. Coagulation: The Mechanism of Clotting

Coagulation is the complex, multi-stage process of blood clotting, vital for stopping blood loss after injury. It involves a cascade of protein factors (clotting factors) and is an example of positive feedback.

Clotting Factors and the Common Pathway

There are $\mathbf{13}$ numbered clotting factors ( $\text{I}$ through $\text{XIII}$ , excluding $\text{VI}$ ). Their numbers reflect the order of their discovery, not their order of action.

Vitamin $\text{K}$ is essential for the synthesis of factors $\text{II}$ , $\text{VII}$ , $\text{IX}$ , and $\text{X}$ .

The cascade involves factors sequentially activating one another, culminating in the formation of prothrombin activator, which initiates the common pathway:

Prothrombin ( $\text{Factor II}$ ) is converted into the active enzyme thrombin by prothrombin activator.
Thrombin then catalyzes the conversion of inactive fibrinogen ( $\text{Factor I}$ ) into insoluble protein threads called fibrin.

The fibrin threads form a strong, three-dimensional mesh within the existing platelet plug, trapping $\text{BCs}$ to form a strong, stabilizing blood clot.

Initiating the Pathway

The common pathway can be initiated by two distinct mechanisms:

Extrinsic Pathway: Triggered very quickly (seconds) by tissue damage. Damaged tissue releases Tissue Factor ( $\text{Factor III}$ ), which starts the coagulation cascade.
Intrinsic Pathway: Triggered more slowly ( $\mathbf{3-6}$ minutes) by damage to the lining of the blood vessel (endothelium).

Clot Resolution

Once formed, the clot shrinks (retracts) as platelets contract. This action squeezes out a sticky fluid called serum (plasma minus the clotting factors) and pulls the edges of the damaged vessel together, sealing the hole and reducing further bleeding.