Innate Immunity, Inflammation, and Wound Healing: Key Concepts for Nursing

Innate Immunity

Present at birth, before any exposures; non-specific and immediate.

Nonspecific Immune Response

A type of immune response that does not target specific pathogens.

Inflammatory Response

A biological response to harmful stimuli, aimed at removing damaged cells and pathogens.

Adaptive/Acquired Immunity

A specific immune response developed after exposure to pathogens.

Physical Barriers

Structures such as skin and mucous membranes that prevent pathogen entry.

Biochemical Barriers

Substances like saliva, tears, and sweat that help to inhibit pathogen growth.

Normal Flora

Non-pathogenic microorganisms that reside in our body and compete with pathogens.

Vascular Response

The first stage of the inflammatory response characterized by increased blood flow and permeability.

Cardinal Signs of Inflammation

Heat, redness, swelling, pain, and loss of function.

Cellular Stage of Inflammatory Response

The second stage involving white blood cells and other cellular components.

Mast Cells

Cells that live in tissues and release histamine and other substances during inflammation.

Neutrophils

Phagocytes that engulf pathogens and are the primary white blood cells in early inflammation.

Macrophages

Large phagocytic cells that remove debris and pathogens.

Monocytes

A type of white blood cell that differentiates into macrophages and dendritic cells.

Platelets

Cell fragments that help stop bleeding and initiate scab formation.

Phagocytosis

The process by which cells engulf and digest foreign particles or pathogens.

Chemotaxis

The movement of cells towards the site of injury in response to chemical signals.

Lysosomes

Organelles that contain enzymes to break down cellular waste and pathogens.

Antimicrobial Peptides

Small proteins that can kill bacteria and fungi.

pH of Certain Areas

The acidity or alkalinity of body areas that can inhibit pathogen growth.

Cilia

Hair-like structures that help move mucus and trapped pathogens out of the respiratory tract.

Phagocytes

Programmed to destroy foreign cells.

Interferons

Chemicals that keep the inflammatory response local and eventually stop it.

Natural killer lymphocytes

Elimination of viral and cancer cells.

Mast cells and basophils

Degranulate to release chemotactic factors and to direct WBC to kill pathogens.

Lymph system

Bone marrow, spleen, lymph nodes- drain extra fluids and cellular waste out of the area.

Complement System

Leads to increased phagocytosis, mast cell release of histamine, and neutrophil migration.

Clotting System

Leads to blood clot formation and attracting neutrophils to the area.

Kinin System

Primary substance bradykinin; leads to dilation of blood vessels and interacts with prostaglandins to create pain through stimulation of nerve endings.

Vasodilation

Clinical manifestation resulting in warmth.

Increased vascular permeability

Clinical manifestation resulting in swelling.

Increased RBC concentration

Clinical manifestation resulting in redness and warmth.

WBC migration

Clinical manifestation may see drainage or exudate.

Plasma Protein System activation

Clinical manifestation resulting in pain and loss of function.

Acute Inflammation

Self-limiting, short duration, starts immediately to 24 hours after injury.

Chronic Inflammation

Lasts two weeks or longer (years), usually happens due to unsuccessful acute response.

Causes of chronic inflammation

Ability of microorganism or other insult to survive in macrophage, irritation from toxins or physical contact.

Increased serum WBC count

Systemic response in inflammation.

Increased plasma protein synthesis

Systemic response in inflammation.

Fever

Systemic response where pyrogens tell the hypothalamus to increase temperature.

Detrimental effects of fever

If too high, causes denaturation of vital proteins, leading to disruption of biological processes.

White Blood Cell Count Differential

A test that includes CBC with differential and fibrinogen to assess inflammation.

Neutrophil

A type of white blood cell that may indicate bacterial infections or stress when elevated.

Erythrocyte Sedimentation Rate (ESR)

A non-specific indicator of inflammation.

Lymphocyte

A type of white blood cell that may indicate viral infections when elevated.

Monocyte

A type of white blood cell that may indicate fungal infections, malaria, or TB when elevated.

C-Reactive Protein (CRP)

A non-specific indicator of inflammation.

Eosinophil

A type of white blood cell that may indicate allergic reactions, parasitic infections, or autoimmune diseases when elevated.

Basophil

A type of white blood cell that may indicate cancers when elevated.

Bands (immature neutrophils)

Indicates an overwhelming infectious process.

Culture and Sensitivity

A test where a sample of the pathogen is taken and allowed to grow in the lab to identify it and test which antibiotics are most effective against it.

Inflammation Resolution

The ideal progression includes regeneration, debridement, and healing.

Wound Healing Phase 1

Inflammation phase where clotting and cleaning occur.

Wound Healing Phase 2

Proliferation and new tissue formation (granulation) phase.

Wound Healing Phase 3

Remodeling and maturation phase.

Clotting and Cleaning

The initial response in the inflammatory phase of wound healing.

Fibrin

A component that stops bleeding and provides a framework for clot with platelets.

Neutrophils and macrophages

Cells that remove foreign materials and pathogens during the inflammatory phase.

Tissue Growth Factor

A biochemical mediator that promotes healing.

Angiogenesis Factor

A biochemical mediator that promotes new blood vessel growth.

Collagen Synthesis

The process of producing collagen, the most abundant protein in the body and a major component of skin, ligaments, tendons, and teeth.

Epithelialization and granulation

The process of new tissue growing in during wound healing.

Wound Dehiscence

A condition where a wound that was once closed has edges that are pulled open.

Dysfunctional Wound Healing

A condition characterized by impaired collagen matrix assembly, hypertrophic scars, keloids, and impaired epithelialization.

Hypertrophic Scar

A dark, raised scar that may regress over time.

Keloid

A larger scar that will not go away and may return if removed.