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Inflammation & Infection
OCCURS BECAUSE CELLS HAVE BEN INJURED IN SOME WAY. THERE ARE TWO TYPES OF INJURY. ©SKUBALA
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The Dust Mite OH, see how they itch!
Quietly lurking under our beds, inside sofas and carpet are creatures too small to see without a microscope or strong magnifying glass. OH, see how they itch! ©SKUBALA
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Antigen The dust mite deposits antigens on our skin surface and are immune system system reacts ©SKUBALA
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Inflammatory Response
Antigens stick to the mast cell IgE antibodies, causing granules in the mast cell to fire their contents into the surrounding tissue. ©SKUBALA
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Response to Injury ADAPTIVE Hypertrophy – increased size
Hyperplasia – increased number Atrophy – decreased size Metaplasia – change in type of cell; reversible MALADAPTIVE Dysplasia – reversible if stimulus is removed Anaplasia – often characteristic of malignant tumors ©SKUBALA
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Inflammation vs. Infection
Inflammation can be caused by non-living agents Inflammation is always present with infection A superimposed infection can occur with inflammation Infection is caused by the invasion of cells by microorganisms Infection is not always present with inflammation Important to realize there is a difference between inflammation and infection. ©SKUBALA
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Iatrogenic vs Nosocomial
Iatrogenic: Caused by the treatment of a physician, resulting in an adverse condition Nosocomial: Caused by exposure to an organism in the hospital setting ©SKUBALA
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Clinical Manifestations Localized
Redness Heat Pain Swelling Loss of Function ©SKUBALA
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Clinical Manifestations Systemic
Leukocytosis Malaise Nausea Anorexia Increased pulse Increased respiratory rate Fever ©SKUBALA
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Primary Defense Mechanisms
Skin and mucous membranes Mononuclear phagocyte system Inflammatory response Immune system ©SKUBALA
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Mononuclear Phagocyte System
MPS is made up of monocytes, macrophages and their precursor cells. Located in various tissues and organs Originate in bone marrow Function: Phagocytosis and participation in the immune response ©SKUBALA
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Inflammatory Response Vascular
Vasoconstriction Release of histamine/chemicals Vasodilation Increased capillary permeability Fluid exudate THE VASOCONSTRICTION OF THE ARTERIOLES IN THE AREA. IF CELL DEATH OCCURS BECAUSE OF THE INJURY THERE IS A RELEASE OF HISTAMINE/CHEMICALS LEADS TO LOCAL VASODILATION – CAUSING HYPEREMIA OR INCREASED BLOOD FLOW INCREASED CAPILLARY PERMEABILITY – MOVEMENT OF FLUID FROM CAPILLARIES INTO TISSUE SPACES FLUID EXUDATE FORMED CAUSES RISING ONCOTIC PRESSURE ©SKUBALA
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Inflammatory Response Cellular
Margination and diapedesis Chemotaxis to attract leukocytes Neutrophils Pus formation WBC’s (bands) Monocytes Lymphocytes Eosinophils and basophils ©SKUBALA
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Mediators in Inflammatory Response
Histamine Serotonin Kinins Complement components Fibrinopeptides Prostaglandins and leukotrienes Lympokines ©SKUBALA
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Stages of Febrile Response
Prodromal Chill Flush Defervescence ©SKUBALA
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The Healing Process Regeneration – replacement of lost cells and tissue with cells of the same type Repair – healing as a result of lost cells being replaced by connective tissue Primary intention Secondary intention Tertiary intention ©SKUBALA
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Primary Intention Wound margins well approximated Phases:
Surgical incisions Paper cuts Phases: Initial Granulation Scar contraction and maturation- ©SKUBALA
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Secondary Intention Wide, irregular wound margins Wound classification
Trauma Ulceration Infection Wound classification Red Yellow Black ©SKUBALA
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Tertiary Intention Delayed primary intention Larger deeper scar
Delayed suturing Infection Larger deeper scar ©SKUBALA
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Complications of Healing
Keloid formation Contracture Dehiscence Adhesions Complications of Healing Hypertrophic Scars and Keloid formation occurs when the body produces to much collagen tissue. It results in a very large, red, raised and hard. Hypertrophic Scars regress with time but Keloid formation protrudes over the wound edge, may appear like a tumor and are permenent. Dark skinned people, particularly african americans are predisposed to keloid formation. Contracture of a wound is a normal process but when there is excessive contracture it can result in deformity or contracture. It is caused by excessive fibrous formation. Usually occurs in burns. Dehiscence is the separation and disruption of previously joined wound edges. Primary healing site ruptures. Adhesions: are bands of scar tissue between or around organs. Abdominal surgery ©SKUBALA
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Factors that Delay Wound Healing
Nutritional deficiencies Inadequate blood supply Corticosteroid drugs Infection Mechanical friction on wound Advanced age Diabetes Mellitus Anemia NUTRITIONAL DEFICIENCIES: Vitamin C – delays formation of collagen Protein – supplies amino acid Zinc – impairs epithelialization INADEQUATE BLOOD SUPPLY DECREASED NUTRIENT TO AREA DECREASED REMOVAL OF DEBRIS INHIBITS INFLAMMATORY RESPONSE CORTICOSTEROIDS IMPAIRS PHAGOCYTOSIS, DEPRESSES FORMATION OF GRANULATION TISSUE, INHIBITS WOUND CONTRACTURE INFECTION – INCREASES INFLMMATORY RESPONSE AND TISSUE DESTRUCTION MECHANICAL FRICTION ON WOUND DISRUPTS REPAIR THAT HAS ALREADY TAKEN PLACE ADVANCED AGE DIABETIS…………….CIRCULATORY CHANGES ASSOCIATED WITH, NEUROPATHIES ANEMIA; LESS O2 AT TISSUE LEVEL ©SKUBALA
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Health Promotion Prevention Adequate nutrition Early recognition
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Interventions Observation of symptoms Assess wound and document Fever
Consistency Color Odor Drainage ©SKUBALA
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Rest and immobilization Elevation Oxygenation Heat/Cold
Wound management Prevent infection ©SKUBALA
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Wound Classifications
Red wound Yellow wound Black Wound ©SKUBALA
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Red Wound Treatment PURPOSE: Protection and gentle atraumatic cleansing Dressing: Transparent film dressing Gauze dressing with antimicrobial ointment or solution Telfa dressing with antibiotic ointment ©SKUBALA
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Yellow Wound PURPOSE: Wound cleansing to remove nonviable tissue and absorb excess drainage Wound irrigation Wet to dry dressings With or without antimicrobial agent Hydrocolloidal dressing (Duoderm) ©SKUBALA
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Black Wound PURPOSE: Debridement of eschar and nonviable tissue
Topical enzyme debridement Surgical debridement Hydrotherapy Chemical debridement Moist gauze dressing Hydrogel covered with gauze ©SKUBALA
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Show the difference colors…………..
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Antibiotic Resistant Organisms
Methicillin-resistant Staphylococcus aureus (MRSA) Vancomycin-resistant enterococci (VRE) Penicillin-resistant Streptococcus pneumoniae (PRSP) ©SKUBALA
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The Immune Response Immunity is a state in which the body is capable of responding to microorganisms such as bacteria, viruses, and tumor proteins. ©SKUBALA
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Immunity Functions of immune response
Defense Homeostasis Surveillance Properties of the immune response Specificity Memory Self-recognition Self-limitation Specialization The immune response serves three functions: Defense: Protects against invasions by microorganisms and prevents the development of infection Homeostasis: Damaged cels, cellular debris and digested and removed. Cells remain uniform and unchanged by this process Surveillance: Mutations continually arise in the body but are normally recognized as foreign cells and destroyed ©SKUBALA
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Specificity Antigen – introduced into body Cellular reaction
Antibody formed Sensitized lymphocytes Antigen/antibody complex ©SKUBALA
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Types of Immunity Natural Immunity Not produced by an immune response
Innate Acquired Immunity Active acquired Passive acquired Activ ©SKUBALA
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Components - Immune System
Thymus Bone marrow Tonsils Gut – Genital – Bronchial Lymph nodes Spleen Figure 12-1 Key points: The Thymus is important in the differentiation and maturation of T-lymphocytes necessary for cell-mediated immune response. Lymph Nodes are responsible for filtration of foreign material brought to the site and the circulation of lymphocytes. Spleen: Primary site for filtering foreign substances from the blood. It is the major site of immune response to blood-borne antigens. Monomuclear Phagocyte System: Moncytes in blood and macrophages found throughout the body. Critical role in immune response……………..Responsible for capturing, processing and presenting the antigen to the lymphcyte, stinulating a humoral or cell-mediated immune response. Via phagocytosis. ©SKUBALA
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Humoral Immunity Antibody-mediated immunity
Antigen-antibody interactions Immunoglobulins IgG IgA IgM IgD IgE Humoral Immunity Antibody-mediated immunity. B-cells Produce antibodies – (Immunoglobulins) Pathogens such as bacteria enters the body. B-lymphocyte recognizes the antigen because it has receptors specific for that antigen. Once there is contact the B-cell is activated and differentiates eventually producing immunoglobulins. ©SKUBALA
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Cell Mediated Immunity
Immunity from pathogens that survive inside of cells such as viruses/bacteria Immunity from fungal infections Rejection of transplanted tissues Contact hypersensitivity reaction Tumor immunity ©SKUBALA
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Cell Mediated Immunity Cell Types
T- lymphocytes (CD3) T-cytotoxic T-helper (CD4) T-suppressor (CD8) Natural killer cells Cytokines Macrophages T-cytotoxic cells attack antigens on cell membrane of foreign pathogens releasing cytolytic substances that destroy it. Like B lymphocytes some sensitized T-cells do not attack but remain as memory T-cells. T-helper and T-Suppressor cells are involved in the regulation of the humoral antibody response and cell mediated immunity. They are known as IMMUNOREGULATORY cell. In many autoimmune disease the number of T-suppressor cells decrease in proportion to the number of T-helper cells resulting in an overaggressive immune response. In HIV the virus invades %-helper cells, decreasing their number and function…………decreasing the immune response leaving them at an increased risk for opportunistic infections and malignancies. Natural killer cells are neither T or B lymphocytes. Cytokinees act as messengers between the cell types. Cytokines instruct cells to alter their proliferation, differentiation, secretion or activity. They are large granular lymphocytes that do not require prior sensitization for their generation. ©SKUBALA
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Altered Immune Response
Hypersensitivity reactions Allergic disorders Immunodeficiency Autoimmune Disorders Altered immune resonse First an overhiew and review of hypersensitivity reactions Then we will discuss allergice disorders Followed by immunodeficiency And autoimmune disorders ©SKUBALA
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Hypersensitivity Reactions
Immediate – humoral immunity Types I, II, III Delayed – cell mediated immunity Type IV Immunoglobulins ©SKUBALA
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Type I: Anaphylactoid Reactions
Sensitized IgE Localized Wheal and flare Systemic Anaphylactic shock Clinical significance ©SKUBALA
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Anaphylactic Shock Bronchial constriction Airway constriction
Airway obstruction Vascular collapse Target organs affected (Fig 12-7) MUST REACT QUICKY TO INSURE AIRWAY ©SKUBALA
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Initial Symptoms Edema Uticaria ©SKUBALA
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Symptoms of Shock Rapid, weak pulse Hypotension Dilated pupils Dyspnea
Possible cyanosis Bronchial edema Angioedema ©SKUBALA
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Type II: Cytotoxic and Cytolytic Reactions
IgG or IgM Complement system Cytolisis/Enhanced phagocytosis Clinical significance – transfusion reactions Type II Hypersensitivity reactions involves IgG or IgM antibodies which activate the Complement system which mediates the reaction Cellular tissue is destroyed by cytolysis or enhanced phagocytosis which is activated by the complement system Clinical importance: Transfusion reaction ©SKUBALA
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Type III: Immune-Complex Reactions
Antigen IgG and IgM Complement system Chemotactic factors Clinical significance Examples of antigen involved in Type III reations are extracellular fungal, viruses and bacteria They comine with s IgG, and IgM antibodies and form complexes too small to be effectively removed by the phagocyte system. These complexes are deposited in tissue or small blood vessels and cause fixation of complement and the release of chemotactic factors leading to inflammation and destruction of the tissue involved. Clinical signficance: Serum sickness (horse antitoxin), autoimmune disorders such as systemic Lumpu erythematosus, rheumatoid arthritix ©SKUBALA
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Type IV: Delayed Hypersensitivity Reaction
Intracellular or extracellular antigens No immunoglobulins involved T-lymphocytes Clinical significance Intracellular or extracellular antigens are attacked or destroyed by the relese of cytokines which attract macrophages to the area. No immunoglobulins are involved Rather sensitized T-lymphokines mount the attack Clinical significance: Contact dermatitis, hypersensitivity reactions to bacterial, fungal and viral infections and transplant rejection. Some drug reactions fit this category. ©SKUBALA
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Allergic Disorders Health history Family history
Past and present allergies Physical exam Allergies or Type I hypersensitivity reactions are seen frequently. A HEALTH HISTORY which includes family allergies. Should ask about the clinical manifestations and the various treatments prescribed. What social and environmental facts are involved. Ask about past and present allergies. Question about pets, trees and plants on property. Their cooling and heating systms in home and workplace. Have them keep a food diary. Ask about their lifestyle and stress levels and what connection they have with the symptoms they are experiencing. PHYSICAL EXAM should be head to toe with particular attention focused on the site of allergic manifestations. ©SKUBALA
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Allergic Disorders Diagnostics
Lymphocyte count < 1200/µl Eosinophil count RAST (radioallergosorbent test) Sputum/nasal/bronchial secretions PFT’s Skin Tests ©SKUBALA
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Skin Tests Types Results: Cutaneous scratch Intracutaneous injection
A + reaction - implies sensitivity ©SKUBALA
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Nursing Care/Therapy Therapy: Be prepared: Reduce exposure
Treat symptoms Desensitization Be prepared: Anaphylactic reactions List allergies Shell fish ©SKUBALA
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Anaphylaxis Sudden onset Therapeutic Management
antibiotics blood products insect bites Therapeutic Management Recognize signs/symptoms Maintain patent airway Prevent spread Administer drugs: Epinephrine Benadryl O2 Establish IV: IVF’s/Dopamine ©SKUBALA
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Chronic Allergies Allergen recognition and control Stress management
Environmental controls Bee-sting kits Medic alert bracelets ©SKUBALA
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Drug Therapy Antihistamines Epinephrine Corticosteroids Antipruritics
Mast-cell stabilizers ©SKUBALA
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Immunotherapy Anaphylactic reactions to insect venom
Unavoidable exposure Drug therapy ineffective ©SKUBALA
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