Inflammation Pathophysiology PDF

Pathophysiology Stress & Inflammation Steve Casarez RN, Paramedic Objectives ◼ Stress and it’s phases in the body ◼ The bodies three Defense Mechanisms ◼ Inflammation Response System and its progression ◼ Inflammation diseases and process ◼ Systemic Inflammatory Response Syndrome...

Pathophysiology Stress & Inflammation Steve Casarez RN, Paramedic Objectives ◼ Stress and it’s phases in the body ◼ The bodies three Defense Mechanisms ◼ Inflammation Response System and its progression ◼ Inflammation diseases and process ◼ Systemic Inflammatory Response Syndrome (SIRS) and its phases Stress is triggered by multiple factors ◼ Anxiety ◼ Depression ◼ Disease ◼ Insomnia ◼ Infections ◼ Cardiovascular Disease ◼ Trauma  Figure 02.F01: Physiological response to stress. Story, L. (2012). Pathophysiology: A practical approach. Jones & Bartlett Learning: Burlington, MA.  Stress Response ◼ General Adaptation Syndrome 1. Alarm phase 2. Resistance phase 3. Exhaustion phase Figure 02.F02: General adaptation syndrome. 1st Stage /Alarm Phase ◼ Stimulation of the sympathetic nervous system (fight or flight) ◼ Releasing catecholamine's ◼ Releasing cortisol “stress hormone” ◼ These are released from the adrenal glands 2nd Stage / Resistance Phase ◼ Body either adapts or alters ◼ If the stressor is prolonged then you move into the next phase 3rd Stage / Exhaustion Phase ◼ Final phase related to stress ◼ Body now becomes depleted and damaged ◼ Body’s defenses are utilized Protective Agents Against Stress ◼ Genetics ◼ Age ◼ Gender (male vs. female) ◼ Life experiences ◼ Dietary status ◼ Social support ◼ Exercise Effects Of Stress To The Body Figure 02.F03: Effects of stress. © Jones & Bartlett Learning The Human Body Three Defense Mechanisms 1. Physical Surface Barriers ▪ Skin is the first line of defense 2. Inflammation ▪ Triggered by damage to tissue ▪ Isolation of the invader ▪ Destruction and clean up. 3. Immune Response ▪ Antigen/Antibody response ▪ Production of lymphocytes (WBC) Inflammatory Responses The SWAT Team for your cells! Sickness / Infections / Trauma (SIT) What is the trigger for Hypotension? What is the trigger for Edema? What is the principal blood work to DX infection or cellular stress? What temp. does our clotting factors need to be? What is the cellular trigger to give oxygen? What is R.I.C.E? Figure 02.F04: Inflammatory Response. Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning. What is inflammation? ◼ A vascular and cellular response to cellular trauma ◼ Its to initiate the healing process ◼ The body’s attempt to dispose of foreign and dying material ◼ Protects the body by localizing the injury of infection Inflammation Concept Map The Inflammatory Process Mediators ◼ Mast Cells ◼ Histamine ◼ Vasodilation (vessel dilation) ◼ Hypotension ◼ Prostaglandins ◼ Stimulates pain receptors ◼ Biochemical mediators ◼ Stimulates fibrin and the clotting factors ◼ This is optimized at temperatures >35.5C Vascular Responses To Inflammation ◼ Increases Vascular (capillary) Permeability- ◼ The spreading of endothelial (whole) cells ◼ Vasodilation- ◼ Blood increasing causing redness and heat ◼ Increases Capillary Permeability- ◼ Fluid moves from IVF to ECF ◼ Leaking of fluid into tissue area ◼ Localized edema begins Cellular Response To Inflammation ◼ Neutrophil- ◼ The foot soldiers of the process ◼ They eat and destroy microorganisms, foreign materials, or dead cells ◼ Chemotaxis- ◼ The drawing in of neutrophils to the injured area ◼ Phagocytosis- ◼ The process of cell eating  Figure 03.F05: The role of neutrophils Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA. Figure 03.F04: Leukocyte movement Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Inflammatory Mediators ◼ Three factors that MUST be in place to support Acquired Immunity or Adaptive immunity ◼ If not in place may lead to Autoimmunity issues 1. Complement System ◼ Part of the immune system ◼ Destroy and remove microorganisms from the body 2. Clotting ◼ Promotes the cascade of clotting factors to repair and heal 3. Kinin ◼ Potent vasoactive mediator  Cellular Response “The SWAT team response” Chemotaxis “SWAT team members” = moving cells to the injury site Cellular adherence “SWAT team game plan” = inflammatory mediators = binding receptors Cellular migration “SWAT breaching the target” = Leukocyte (WBC) = Neutrophil = Macrophages = Erythrocyte (RBC) = Platelet Cardinal Signs of Localized Inflammation ◼ Heat ◼ Redness ◼ Swelling ◼ Pain ◼ Loss of function Cardinal Signs of Systemic Inflammation ◼ Fever ◼ Fatigue ◼ Weight loss ◼ Lethargy ◼ Increased leukocytes and plasma proteins ◼ Increased WBC Inflammatory Exudates ◼ Serous / Sanguineous- clear serum like fluid containing protein. ◼ Fibrinous- scab appearance. Indicates larger injury. ◼ Purulent- dead/dying cells, and pus forming bacteria. ◼ Pyogenic- pus filled ◼ Abscess- localized collection of pus ◼ Empyema- collection of pus in a body cavity  Treatment of Inflammation ◼ Reduce the blood flow ◼ Ex: ice packs ◼ R.I.C.E ◼ Decrease the swelling ◼ Ex: NSAID (ibuprofen) ◼ R.I.C.E ◼ Block the action of chemical mediators ◼ Ex: ABX Phases of the Inflammatory Process Healing Stages Phase 1: Acute Phase 2: Tissue Phase 3: Remodeling Inflammation stage Formation ▪ Adapt to original ◼ Early (acute): ◼ Proliferation tissue inflammatory ◼ Tissue rebuilding ▪ Continues for up response approximately 2-3 to 1 year post last 2-4 days weeks injury ◼ Late: usually ◼ This does not complete in 2 include chronic wks inflammation  Chronic Inflammation ◼ Recurrent or persistent inflammation lasting several weeks or longer ◼ Monocytes, macrophages and lymphocytes more prominently involved ◼ Formation of granulomas and scarring often occur  Complications of Healing ◼ Infection ◼ Ulceration ◼ Dehiscence ◼ Keloids ◼ Adhesions  Common Inflammation Problems ◼ Rheumatoid Arthritis (RA) ◼ Gastritis ◼ Inflammatory Bowel Disease (IBS) ◼ (SIRS) Systemic Inflammatory Response Syndrome ◼ Burns ◼ Sepsis ◼ Trauma  RA Pathophysiology ◼ Chronic inflammation of synovial membranes and synovial hyperplasia ◼ Etiology combines ◼ Genetics ◼ Triggering events ◼ Stress ◼ Autoimmunity  RA Pathophysiology (cont’d) ◼ Remissions and exacerbations ◼ “it comes and goes” ◼ Pannus formation ◼ Abnormal formation of fibrovascular tissue ◼ Cartilage erosion ◼ Fibrosis ◼ Excess fibrous connection tissue ◼ Ankylosis ◼ Stiffness or fixation of a joint  RA Clinical Manifestations ◼ Mild to debilitating ◼ Symmetrical joints ◼ Pain, stiffness ◼ Redness, heat, swelling ◼ Decreased mobility  RA Diagnostic Criteria ◼ No definitive test ◼ Increased likelihood with positive findings of: ◼ Erythrocyte sedimentation rate (ESR) ◼ C-reactive protein (CRP) ◼ Rheumatoid factor (IgG) ◼ Antinuclear antibodies (ANA)  RA Treatment ◼ Pharmacologic Drug TX ◼ NSAIDS ◼ COX-2 inhibitors (Celebrex) ◼ Non-pharmacologic: ◼ Rest/activity balance ◼ Physical therapy exercises ◼ Splints ◼ Surgery Inflammatory Lesions ◼ Broad term that includes wounds, ulcers, wheals, blisters, vesicles, pustules, or tumors. ◼ Abscesses- streptococcal and staphylococcal bacteria. Often will form a head causing an outpouring of pus, relief of pain, and onset of healing. Inflammatory Lesions ◼ Ulcer- crater like lesion resulting of an injury and the inflammatory process. ◼ Common sites are stomach, and pressure ulcers of the heel, sacrum, and elbow. The tissue becomes necrotic. Inflammatory Lesions ◼ Cellulitis- widespread acute inflammatory process. Usually seen on skin and subcutaneous tissues. General edema, redness, pain, and heat to the area. Systemic Inflammatory Response Systems SIRS ◼ SIRS is nonspecific and can be caused by ischemia, inflammation, trauma or several other insults combined. Thus, SIRS is not always related to infection or sepsis. Testing for Infection ◼ Leukocytosis- elevated WBC’s ◼ Septicemia- pathogens in blood ◼ Identification of infection: ◼ Culture and Sensitivity test either blood, urine tissue.