Cells and Non-Specific Body Defenses

Cells Involved in Immunity

• Lymphocytes, created in bone marrow, are responsible for producing a high quantity of T and B cells.
• T lymphocytes are responsible for reproducing and creating an army for cell-mediated immunity.
• Helper T cells direct the entire immune response.
• Cytotoxic T cells destroy damaged cells in the body.
• Suppressor T cells are responsible for limiting immune response.
• Memory T cells remember antigens for future encounters.
• B cells are humoral/antibody-related, and they act on bacteria and viruses.
• B cells produce plasma cells after exposure to an antigen, with the help of helper T cells.
• Natural killer cells use granzymes to shut everything down.
• Natural killer cells identify self-cells that lack MHC -1 and initiate apoptosis.

Non-Specific Body Defenses

• Non-specific body defenses react equally to all external threats, without recognition.
• They have no memory of threats for future encounters.
• Non-specific body defenses include both first and second line defenses.
• They include natural killer cells and interferons.
• Interferon is a protein produced by the body's cells as a defensive response to viruses.
• Interferon works to inhibit the replication of viral and other pathogens

Cell Mediated and Humoral Immune Response Definition

• Cell-mediated immunity does not involve antibodies but relies on the activation of specific immune cells to defend against pathogens, specifically T cells.
• Humoral/antibody immunity involves antibody production by B cells; this protects the body from pathogens and foreign substances in extracellular fluids.

HIV and AIDS Definition

• HIV is a retrovirus that infects and destroys helper T cells of the immune system, impairing their function.
• HIV is transmitted via body fluids: blood, semen, vaginal fluid, and breast milk.
• AIDS is a viral disease caused by HIV; it depletes T-helper cells and makes humans susceptible to life-threatening infections and malignancies.
• AIDS is diagnosed when CD4 counts (helper T cells) are low and opportunistic infections/malignancies occur.

HIV Mode of Transmission

• HIV is transmitted via unprotected sex, contact with infected blood and bodily fluids, sharing needles, and from infected mothers to infants during birth, breastfeeding, or pregnancy.

HIV & AIDS Signs and Symptoms

• HIV-related symptoms include memory loss, disorientation, persistent headaches, high fever, white patches on the tongue, swollen lymph nodes in the neck, armpits, and groin, heavy night sweats, loss of appetite, severe weight loss, chronic diarrhea, fatigue, and muscle weakness.
• AIDS-related symptoms include cryptococcal meningitis (inflammation in and around the brain and central nervous system), cytomegalovirus (CMV) retinitis (leads to blindness), herpes simplex (around the mouth and genitals), oral candidiasis (white fungal growth on the tongue), fever, shortness of breath, cough, pulmonary tuberculosis, severe diarrhea, weight loss, and purplish-brown skin lesions.

HIV Pathophysiology

• Initial infection (window period): the time of entry of HIV into the body before antibodies appear.
• Acute retroviral syndrome: initial flu-like illness as the body produces antibodies to HIV, often mistaken for the flu.
• Seroconversion: when antibodies first appear in the blood; the formation of antibodies takes 3-7 weeks.
• Latent period: 2-10 years
• Immunodeficiency: opportunistic infections (serious infections caused by pathogens).

Titre

• Titre measures the concentration and strength of a substance, such as an antiserum or antibody, in a solution.

Herd Immunity

• Herd immunity is indirect protection that only applies to contagious diseases.
• It requires a sufficient number of people in a group or area to achieve immunity against a virus or other infectious agent.

Allergies

• An allergy is defined as an abnormal immune response to a substance.
• An antigen is a substance the immune system recognizes as foreign and potentially harmful, this triggers an immune response, leading to the production of antibodies to neutralize or destroy the antigen.
• An antibody is a protein produced by the immune system in response to an antigen; antibodies target and bind to antigens to neutralize or destroy them.
• Pruritus is itching.
• Urticaria, also known as hives, is characterized by raised, red, itchy welts.
• Anaphylactic shock: A severe and potentially life-threatening allergic reaction that occurs rapidly.
• Anaphylactic shock symptoms include difficulty breathing, swelling, a drop in blood pressure, and loss of consciousness (LOC).

Pathophysiology of an Allergic Reaction

• Exposure to an allergen is the first event.
• An antigen-presenting cell phagocytizes the antigen and presents fragments on its surface.
• A helper T cell recognizes the non-self and activates B cells.
• Plasma cells produce IgE antibodies.
• IgE antibodies attach to the surface of mast cells.
• The antigen enters the body a second time.
• The allergen attaches itself to the IgE antibody on the mast cell.
• Mast cells degranulate, releasing histamine.
• Eosinophils accumulate at the site of allergen exposure.
• Eosinophils release pro-inflammatory mediators, which contribute to symptoms such as itching and swelling.
• Allergic rhinitis symptoms like a cold are caused by pollens, grasses, trees, molds, dust mites, foods, and animal dander, causing inflammation of the mucous membranes in the nose, throat, and airways.
• Allergic rhinitis results in frequent sneezing, copious watery secretions from the nose, itching, and red, watery and pruritic eyes.
• Food Allergies involve inflammation of the mucosa of the digestive tract.
• Food allergies result in nausea, diarrhea, and may cause rash or hives on the skin; in severe cases, hives can occur on the pharyngeal mucosa and obstruct the airway.
• Atopic dermatitis (eczema) is a chronic skin condition associated with genetic factors, commonly seen in children and linked to soaps, detergents, foods, fabrics, and dry air; this may reoccur in adulthood.

Allergic Reactions

• During the first exposure, antigen-presenting cells process the allergen and present it to helper T-cells.
• The helper T cells activate B cells to produce IgE antibodies specific to the allergen.
• The IgE antibodies bind to receptors on the surface of mast cells and basophils, sensitizing these cells to the allergen.
• No allergic symptoms occur because the allergen is just preparing the immune system for future encounters.
• During the second exposure, the allergen binds to the IgE antibodies on the surface of the sensitized mast cells and basophils.
• This binding triggers the release of inflammatory mediators, such as histamine, from the mast cells.
• These mediators cause the symptoms of an allergic reaction.

Respiratory Tracts

• The upper respiratory tract includes: the nose and nasal cavity which warms, moistens, and filters air, the pharynx (throat), which is the passageway for air and food, and the larynx (voice box) containing vocal cords that function in speech.
• The lower respiratory tract includes: the trachea (windpipe) which connects the larynx to the bronchi, the bronchi and bronchioles, which are air passages that branch into the lungs, the lungs, and the alveoli, where oxygen is absorbed into the blood and carbon dioxide is expelled.
• Chemoreceptors regulate breathing and monitor levels of carbon, oxygen, and pH in the blood and cerebrospinal fluid, and they send signals to the respiratory centers to adjust the rate and depth of breathing.
• When CO2 levels rise and pH decreases, chemoreceptors stimulate an increase in breathing.
• Lung receptors regulate breathing by responding to mechanical and chemical stimuli within the lungs.
• Stretch receptors are found in the smooth muscle of airways and respond to the stretch of lung tissues during inhalation; when the lungs are overstretched, these receptors send signals to the Hering-Breuer reflex to prevent over-inflation.
• Irritant receptors located in the epithelial lining of airways respond to chemical and physical irritants like smoke and dust, leading to coughing, bronchoconstriction, and rapid shallow breathing.
• J receptors (juxtapulmonary capillary receptors) in the alveolar walls near pulmonary capillaries respond to changes in lung tissue, such as congestion and edema; they induce rapid shallow breathing to help regulate lung field balance and maintain gas exchange.
• The Hering-Breuer reflex regulates breathing and prevents over-inflation involving stretch receptors in the bronchi and bronchioles of the lungs.

Hypoxic Drive

• Hypoxic drive for respirations regulates breathing in response to low levels of oxygen (hypoxia) in the blood, primarily seen in people with COPD.
• In individuals with COPD, the body becomes accustomed to high levels of carbon dioxide (hypercapnia).
• High levels of carbon dioxide cause the central chemoreceptors to become less sensitive to CO2 levels.
• When oxygen levels in the blood decrease, peripheral chemoreceptors are stimulated, which send signals to the respiratory centers in the brainstem to increase the rate and depth of breathing.
• Administering high levels of oxygen to people with hypoxic drive can suppress their respiratory drive.
• Peripheral chemoreceptors will detect the increased oxygen levels and reduce the signals to the respiratory centers, which lead to decreased breathing effort.
• In healthy individuals, breathing is regulated by the levels of carbon in the blood.

Mucociliary Clearance Mechanism

• The mucociliary clearance mechanism protects the respiratory tract by trapping and removing inhaled contaminants (dust, bacteria, viruses and allergens).
• It ensure efficient gas exchange and prevents various respiratory infections.
• Goblet cells produce mucus which traps inhaled particles.
• Cilia moves the mucus upward toward the pharynx

Etiology and Pathophysiology of Diseases

• Etiology of cold and flu is caused by variety of viruses, spread through droplets, direct contact with infected surfaces, or person to person contact.
• Pathophysiology of cold and flu is when the virus enters the upper respiratory tract and infects the nasal and throat mucosa. The body's immune response to the virus causes inflammation to mucosa membranes.
• Etiology of sinusitis is caused by infectious agents, allergies, anatomical factors such as deviated septum, environmental factors, medical conditions like asthma and cystic fibrosis.
• Pathophysiology of sinusitis is when the initial trigger causes inflammation of the nasal mucosa, in response, the mucous membranes of the nasal passages and sinuses produce excess mucus. The mucus can become thick and sticky, making it difficult for cilia to move it out of the sinuses.
• Trapped mucus leaves an environment to the growth of bacteria (breeding ground for infection).
• Sinusitis symptoms include nasal congestion, facial pain/pressure, fever, and headache.
• Etiology of bronchitis includes viral infections, bacterial infections, and irritants.
• Pathophysiology of bronchitis is the inflammation of the bronchi.
• Inflammatory mediators increase mucus production in the bronchial tubes, while swelling of the bronchial walls leads to narrowing airways and impaired cilia function.
• Mucus and narrowed airway trigger cough reflex.
• Manifestations of bronchitis include cough, sputum production, wheezing, chest discomfort, and shortness of breath.
• Etiology of Covid is transmitted through respiratory droplets when an infected person coughs, sneezes, or talks.
• Pathophysiology of Covid is when the virus enters the body and binds to receptors on host cells; the virus replicates leading to cell damage and death.
• Covid causes the body to releases cytokines and other inflammatory mediators.
• Covid can affect many organ systems and even cause death.

Disease Manifestations

• Manifestations of Covid include fever, dry cough, body aches, loss of taste and smell, runny nose, nausea, and confusion.
• Pneumonia is an inflammatory condition in the lungs affecting the alveoli, caused by bacterial (streptococcus is most common), viral (flu or COVID), fungal, or non-infectious agents (aspiration, chemical inhalation, or radiation).
• Primary pneumonia is a direct result of infection by pathogens that infect the alveoli, causing inflammation. Inflammatory cells migrate to the infection site, leading to consolidation of lung tissue. The alveoli fill with exudate, impairing gas exchange.
• Secondary pneumonia develops as a complication of another condition such as a viral infection, chronic lung disease, or immune-compromising condition such as HIV, with symptoms that may be more severe than those of primary pneumonia.

Pneumonia Pathophysiology

• Pneumonia Pathophysiology includes a release of inflammatory mediators and inflammation that causes the alveolar capillaries to become more permeable, which leads to the leakage of fluid into the alveoli.
• The alveoli fill with a protein-rich exudate containing immune cells, dead pathogens, and cell debris.
• Lung consolidation occurs and the exudate and immune cells within the alveoli lead to the affected lung tissue becoming solidified or consolidated, impairing the alveoli's ability to facilitate gas exchange, creating hypoxemia, SOB, and cyanosis.
• In severe cases of Pneumonia, the infection can spread beyond the lungs, which leads to sepsis.
• Asthma etiology includes genetics, environmental factors, lifestyle, physical activity, cold air, stress and medications.
• Pathophysiology of Asthma involves airway inflammation, increased mucus production with goblet cells secreting mucus, and bronchoconstriction/contraction of smooth muscle.
• Signs and symptoms of asthma include cough, dyspnea, wheezing, tight feeling in chest, and cyanosis.
• Asthma can also cause orthopnea, which is shortness of breath when lying down.

Asthma & Tuberculosis

• Asthmaticus is a medical emergency.
• Asthmaticus is a persistent severe attack of asthma that does not respond to therapy.
• Asthmaticus may be fatal as a result of severe hypoxia acidosis.
• Asthma improvement requires avoiding triggers, management of inflammation, rescue medication, and identification of triggers with skin tests.
• Tuberculosis is an infectious bacterial disease caused by mycobacterium tuberculosis, which commonly affects the lungs.
• Tuberculosis is a gram-positive, rod-shaped, acid-fast, aerobic bacteria.
• Tuberculosis is transmitted person to person via droplets from the throat and lungs of people with the active disease.
• Factors contributing to TB transmission include close proximity with infectious TB, poverty and overcrowding, suppressed immune systems (HIV, malnutrition), and bacillus.
• Bacillus can survive in dried sputum for weeks and it has developed multiple drug resistance; its cell wall protects it from destruction.
• Primary TB is an early infection where bacteria enter the body via the respiratory tract and are engulfed by alveolar macrophages.
• About 5% of persons may develop active TB, while most develop an immune response and test positive on TB tests in several weeks.
• Latent infection exits in a Ghon tubercle.
• Ghon tubercle is where macrophages and lymphocytes cluster together around the bacillus forming a granuloma (walled off area of bacteria).
• The center of the Ghon tubercle undergoes necrosis, which produces a pasty, yellow, cheese-like substance.
• Ghon complex: The lesion becomes walled off by fibrous tissue and eventually calcifies; it is visible in chest x-ray.

Secondary TB

• Secondary TB (latent after primary infection) occurs if the immune system becomes compromised and the latent bacteria are allowed to again proliferate so the infection becomes active.
• Active TB is aggressive and destructive cavitation are areas of necrosis that erode surrounding structures of the lungs, including the bronchioles, bronchi, and surrounding blood vessels.
• The events during mycobacterium Tuberculosis infection, the mycobacterium is inhaled into the lungs.
• Alveolar macrophages engulf the bacteria and trigger a cell-mediated immune response.
• Lymphocytes cluster around the macrophages, creating a Ghon tubercle.
• The center of the Ghon tubercle undergoes necrosis and forms a caseous substance.
• Granulation tissue around the lesion becomes fibrous and calcifies, forming a Ghon complex.
• Signs and symptoms of TB includes 95% of primary infections that are asymptomatic. Active TB will have insidious and vague symptoms.
• Other Active TB symptoms include anorexia, malaise, fatigue, weight loss, afternoon low-grade fever, night sweats, purulent sputum with blood as disease progresses, and chest pain if disease spreads to the pleurae.
• Tuberculin is a purified protein derivative (PPD) used in diagnostic testing to detect exposure to the bacteria of mycobacterium tuberculosis.
• The Tuberculin skin test (aka Mantoux test) involves injecting a small amount of tuberculin PPD into the skin.
• The injection site is examined for induration (a raised, hardened area) 48-72 hours after, and the size is measured to determine a positive or negative measure.
• A positive reaction means the person has been exposed to Tuberculosis bacteria and has developed an immune response.
• Additional testing, such as chest x-ray or sputum tests, is needed to confirm active infection because a positive reaction does not necessarily mean the disease is present.
• A false positive TB test may occur in persons who have been vaccinated with bacille Calmette-Guérin (BCG).
• The BCG vaccine contains a live strain of mycobacterium bovis, which is closely related to mycobacterium Tuberculosis.
• Antigens in the BCG vaccine can cross-react with the antigens in the PPD.
• The cross-reactivity can cause the immune system to recognize and respond to the test as if it were a TB infection.

COPD

• Chronic Obstructive Pulmonary Disease (COPD) is a lung disease that has progressive tissue degeneration and obstruction in the airways of the lungs.
• The Etiology for COPD stems from genetic disposition (alpha antitrypsin deficiency), occupational dusts and chemicals, smoking exposure, and frequent lung infections as a child.
• Bronchitis presents as increased mucus glands and secretions, inflammation, infection, and obstruction; Early, constant cough, some dyspnea, and large amounts of purulent sputum; a complication is cor pulmonale.
• Emphysema: destruction of alveolar walls, loss of elasticity, impaired expiration, barrel chest, and hyperinflation; presents as some coughing, severe dyspnea with little sputum, and late stages risk for cor pulmonale.
• Cor pulmonale presents is from pressure in lungs that increased, due to swollen airways, increased mucus, and alveolar damage leading to right-sided heart failure. Types of wounds include.
• Types of wounds are made by Incision, Contusion, Abrasion, Puncture, and Laceration.

Wounds: Type & Healing

• An Incision is a surgical cut often made with a sharp instrument like a scalpel; Ex, an abdominal incision for surgery.
• A Contusion is a region of injured tissue/skin in which blood capillaries have been ruptured, commonly known as a bruise; ex, a dark contusion on the cheek caused by a a fall.
• An Abrasion is the removing or scraping away of something; ex.a grazed knee from falling on rough pavement.
• A Puncture is a small hole in something such as the skin, that's caused by a sharp object; ex, puncture wound that is caused from stepping on a nail.
• A Laceration is a tear or ragged cut in skin or flesh; ex, Laceration on an arm from broken glass.
• A Penetrating wound is able to make a way through or into something, often enters deeper tissues; ex, Penetrating injury that is caused from a knife stab.
• A Contaminated wound is made impure by exposure or addition of a poisonous or polluting substance, ex. contaminated water that contains harmful bacteria.
• Resolution restores tissue without significant changes or scarring.
• Regeneration replaces damaged cells with identical cells, which restores normal structure and function.
• Repair Involves scar formation, with the new tissue differing from the original structure and function.

Resolution

• Resolution is where the tissue returns to its normal state after injury without significant structural changes or scarring.
• Also involves the removal of inflammatory cells, cellular debris, and the regeneration of cells that replace the damaged ones.
• Resolution promotes complete restoration of tissue structure and function
• An example of Resolution is a mild sunburn where the skin heals and returns to its normal state without scarring.
• Regeneration is the replacement of damaged or lost tissue with new cells that are identical in structure and function to the original cells
• It occurs through the proliferation of cells that are capable of dividing and differentiating which restores the tissues normal architecture.
• Restored tissue has the same structural and functional characteristics as the original
• An example of regeneration is liver regeneration after partial hepatectomy where the liver cells proliferate to restore the liver mass
• Repair is the that occurs when tissue damage is too extensive for resolution or regeneration alone, and involves the formation of scar tissue
• Injury would include inflammation, formation of granulation tissue, deposition of extracellular matrix proteins, and lead to scar formation
• The repaired tissue may not have the same structure and function as the original tissue which results in scar tissue formation
• An example of repairing by deep cut or laceration is where a scar forms due to the deposition of collagen and other extracellular matrix proteins.
• Healing by primary intention, occurs when a wounds edges are brought together and held in place, typically by sutures, staples, or adhesive tape; this is often used for clean, surgical wounds with minimal tissue loss.
• In the Inflammation phase, it begins immediately after injury and lasts for a few days, and blood clotting occurs to stop the bleeding, then afterwards, inflammatory cells migrate to the wound site.

Phases of Wound Healing

• In the proliferative phase of wound healing, it starts around 2-3 days after injury and can last up to 2-3 weeks.
• Granulation tissue forms when fibroblasts produce collagen with angiogenesis is occurring and new blood vessels grow to supply nutrients and oxygen to the healing tissue and epithelialization occurs where epithelial cells proliferate
• The wound starts to close and fill with new tissue, and is also less red and swollen.

Wound Maturation and Intention

• In the maturation (remodeling) phase, it begins around 3 weeks after injury and can last for months to years.
• Collagen fibers are reorganized, strengthened and aligned along tension lines.
• The wound contracts, and a scar forms. The scar tissue gradually becomes stronger and more flexible.
• The wound appears more like normal skin, with reduced redness and a flatter scar.
• Healing by secondary intention occurs when a wound is left open to heal naturally, without surgical closure.
• This method is used for wounds with extensive tissue loss, infection, or those that can't be approximated.
• The inflammatory phase usually lasts longer than primary intervention due to the larger wound size and potential for infection.
• Outcome is scar formation
• In the proliferation phase, has granulation tissue formation, wound contraction, and epithelialization.
• In the maturation phase, collagen fibers are recognized and the wound gradually strengthens.
• Healing by tertiary intention occurs with a combination of primary and secondary intention healing.
• It is used for wounds that are left open initially to manage infection or other complications and are later closed surgically once the risk of infection is reduced.
• In the initial phase of tertiary intention, the wound is left open and managed as if healing through secondary intention, which allows for drainage, cleaning, and a reduction in infection.
• A delayed closure occurs where surgical closure of the wound is performed after several days to weeks after the infection risk is minimized and granulation tissue is present.
• Healing phases follow surgical closure, where the wound undergoes the typical healing phases (inflammatory, proliferative, and maturation).

Wound Healing

• Tertiary intention promotes reduced risk of infection and improved healing.
• Factors that promote wound healing include youth, nutrition (protein and vitamins), hemoglobin, perfusion of tissue, clean wound, absence of other trauma
• Factors that delay would include age, poor nutrition, anemia, decreased perfusion ,co-morbidities, irritation, infection, chemotherapy, and steroids.
• Factors that delay wound healing in older adults include vascular changes/impaired blood flow, collagen tissue less flexible, scar tissue less elastic, an immune system that is less active, nutritional deficiency, and comorbidities.
• Risk factors for developing a pressure injury include decreased, after effects of trauma, presence of cast ,secondary to illness, impaired sensory perception ,impaired mobility.
• Additional risk factors for pressure injuries include shear, friction, moisture, nutrition, tissue perfusion of oxygen fuels, and infections since wound infection prolongs inflammation phase delays collagen synthesis that leads to tissue destruction.
• Pressure injuries are known as bedsores, pressure ulcers occur due to prolonged pressure on the skin and underlying tissues.
• Occurrences can caused by pressure on bony prominences compresses blood vessels which reduces blood flow and oxygen supply to the tissues.

Pressure Injury

• Pressure injury pathophysiology stems from shear forces occur where the skin moves in one direction while the underlying bone moves in another. Friction between the skin and external surfaces can damage the epidermis.
• Moisture that is made from sweat, urine, or feces can weaken the skins protective barrier, increasing the risk of injury.
• Stage 1, a Non-blanchable erythema of intact skin, this skin appears red and does not turn white when pressed.
• The area may be painful, firm, soft, warmer, or cooler for a stage 1.
• Stage 2 pressure injury has partial thickness skin loss with exposed dermis with a wound bed that is moist, pink or red with an intact and ruptured blister.
• Stage 3 is a full-thickness skin loss where adipose tissue is visible in the ulcer, but the surrounding bone, tendon, or muscle are not exposed and the wound may have slough or eschar.
• Stage 4 is another type of full thickness and tissue loss; exposed or directly palpable fascia, while tendon, ligament, cartilage, or bone with slough or eschar that can be present.
• Unstageable pressure injuries are full thickness with tissue loss to which the extent of tissue damage cannot be confirmed due to the presence of slough or eschar.
• Deep tissue injury shows Persistent non-blanchable deep red, maroon, or purple discoloration with skin intact or non intact, with revealing a dark wound bed or blood filled blister.

Venous & Arterial Ulcers

• Venous ulcers are superficial and have irregular shape, they are caused by where poor venous return where blood pools in the veins due to incompetent valves, and then leads to increased pressure which causes fluid leakage into the tissues
• Symptoms of Venous woulds include edema in the lower leg, brownish hemosiderin staining and Lipodermatosclerosis.
• Arterial Ulcers are caused by insufficient blood flow to the tissues due to arterial occlusion or reduced arterial blood supply, they are commonly associated with conditions like peripheral artery disease
• Characteristics of arterial wounds: smaller and deeper than venous, a punched out appearance, related to inadequate blood flow to legs.
• Look for legs that are pale, cool, and hairless, skinny (no edema)
• Legs becoming Redder in color when dependent with a round apperance and it will cause dependent rubor.
• Granular tissue: the new connective tissue and microscopic blood vessels that form on the surface of a wound during the healing process that appears red or pick and has granular or bumpy texture due to the presence of new capillaries

Wound Characteristics

• Epithelial tissue: is thetissue that forms the outer layer of the bodies surfaces and lines internal cavities and organs, serves as a protective barrier and is involved in absorption, secretion, and sensation.
• Necrotic eschar: a dry, drack scab or piece of dead tissue that develops over a wound, typically by burns, pressure injuries, or infections.
• Necrotic slough: the yellow or white, soft, dead tissue that can accumulate in a wound and is often seen in the later stages of wound healing or chronic wounds with a moiset and stringy feel.
• Gangrene: the death of body tissue is due to lack of blood supply often complicated by bacterial infection.
• Affected tissue in gangrene may appear black, green, or dark purple, and accompanied by a foul odor.
• Debridement: medical removal of dead, damaged or infected tissue to improve the healing potential of the remaining healthy tissue.
• Dead tissue harbors bacteria that may lead to infection.
• Autolytic debridement: is a natural process that uses the body to break down necrotic tissue by using moist wound dressings to apply to create moist wound environment that promotes enzymes to digest dead tissue, but it is a slower process for infected wounds.
• Mechanical debridement: involves physical removal of necrotic tissue like the usage of wet to dry dressings, wound irrigation that is used for large amounts tissue, can be painful and may damage healthy tissue.

More About Debridement

• The application of topical enzymes that are used for Enzymatic debridement requires a prescription for the removal of dead tissue.
• The removal of necrotic tissue that is used during Surgical debridement is quick and effective, which allows precise removal of necrotic tissue.
• Biological (maggot) debridement: is used through live maggots to consume dead tissue.
• Wound contamination: an element that has non replicating microorganisms on the wound surface without any host reaction ,that does not cause any symptoms , but microorganism are present but not proliferate
• Wound colonization:is the presence of replicating microorganisms on the wound surface without causing tissue damage or a host immune response but the microorganisms can be fully grown and multiply with no signs of infection
• Wound infection is defined as the invasion and multiplication of pathogenic microorganisms in the wound.
• Wound infection leads to leading to tissue damage and an immune response. Microorganisms proliferate and invade surrounding tissue.