Skin, mucous membranes and blood clotting

Organisms (Interaction and interdependence) · Defence against disease · note 2 of 8

Spec C3.2.2, C3.2.3Download all Defence against disease notes (PDF)Download all notes (PDF)11 pages

Skin, mucous membranes and blood clottingSpec C3.2.2, C3.2.3

In short

Skin and mucous membranes are the primary defence against pathogens. The skin acts as both a physical and a chemical barrier, and mucous membranes trap pathogens in sticky mucus. Cuts are sealed by blood clotting: platelets release clotting factors that start a cascade, ending with thrombin rapidly converting fibrinogen into fibrin, which traps erythrocytes to form a clot.

Primary defence

The primary defence stops pathogens entering the body in the first place.

Skin as a physical barrier: the outer layer is made of tough, dead cells packed with keratin, which pathogens cannot easily penetrate. Dead cells are constantly shed, taking microorganisms with them.
Skin as a chemical barrier: secretions from sebaceous and sweat glands contain fatty acids and lactic acid, making the skin surface acidic, and contain antimicrobial chemicals that inhibit the growth of many bacteria and fungi.
Mucous membranes line the airways, gut, urinary and reproductive tracts. They are thinner than skin but secrete sticky mucus that traps pathogens. In the airways, cilia sweep mucus up to the throat to be swallowed. Mucus, tears and saliva contain lysozyme, an enzyme that digests bacterial cell walls.

Sealing of cuts by blood clotting

A cut in the skin breaks the primary barrier, so it must be sealed quickly. Blood clotting does this.

Platelets at the site of the cut release clotting factors.
The clotting factors start a cascade pathway: a series of reactions, each activating the next, which amplifies the signal.
The cascade produces active thrombin, an enzyme.
Thrombin rapidly converts soluble fibrinogen (a plasma protein) into insoluble fibrin.
Fibrin forms a mesh of fibres that traps erythrocytes, forming a clot that seals the cut.

Flow chart of blood clotting: cut in blood vessel, platelets release clotting factors, cascade pathway, thrombin; thrombin converts soluble fibrinogen into insoluble fibrin; a fibrin mesh with trapped erythrocytes forms a clot that seals the cut. — Blood clotting: a cascade produces thrombin, which converts soluble fibrinogen into insoluble fibrin.

Exam tip:

Students are not required to draw or label diagrams of skin, and no further clotting details beyond platelets, clotting factors, the cascade, thrombin, fibrinogen, fibrin and trapped erythrocytes are required.

Written and checked against the IB Biology SL specification · Updated October 2026

Frequently asked questions

How do vaccines work?

Vaccines contain antigens, or DNA or RNA coding for antigens, from a specific pathogen. They trigger a primary immune response in which B-cells are activated and memory cells are produced, without causing the disease. If the real pathogen infects later, memory cells respond quickly, producing antibodies before the person becomes ill.

Why can't antibiotics kill viruses?

Antibiotics work by blocking processes found in bacteria but not in eukaryotic cells, such as cell wall synthesis or protein synthesis by 70S ribosomes. Viruses have no metabolism of their own, so there is nothing for antibiotics to block. They replicate using the host cell's processes, which antibiotics do not target.

What is the difference between innate and adaptive immunity?

The innate immune system responds to broad categories of pathogen and does not change during an organism's life; phagocytes are part of it. The adaptive immune system, based on lymphocytes, responds specifically to particular pathogens and builds up a memory of pathogens encountered, so later responses are faster and more effective.

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