Acute and Chronic Inflammatory Disease PDF

Inflammatory Disease ACUTE & CHRONIC Reported by: Nicole Mica P. Horca, RPh  Topic Outline 1 INTRODUCTION OF ACUTE AND CHRONIC INFLAMMATION 4 SUMMARY 2 ACUTE INFLAMMATORY DISEASE 5 CONCLUSION 3 CHRONIC INFLAMMATORY DISEASE INTRODUCTION ...

Inflammatory Disease ACUTE & CHRONIC Reported by: Nicole Mica P. Horca, RPh  Topic Outline 1 INTRODUCTION OF ACUTE AND CHRONIC INFLAMMATION 4 SUMMARY 2 ACUTE INFLAMMATORY DISEASE 5 CONCLUSION 3 CHRONIC INFLAMMATORY DISEASE INTRODUCTION  Two types of Inflammation Inflammation is the body's immune response to injury, infection, or harmful stimuli. It is a protective mechanism designed to eliminate the initial cause of cell injury, clear out dead cells, and initiate tissue repair. The classic signs of inflammation: redness, heat, swelling, and pain. Feature Acute Inflammation Chronic Inflammation Onset Immediate (minutes to hours) Delayed (weeks to months) Duration Short-term (few days) Long-term (months to years) Predominant cells Neutrophils Macrophages, lymphocytes Healing, develops abcess or Tissue damage, fibrosis, scarring, Outcome progression to chronic inflammation loss of function  CARDIOVASCULAR ALLERGIC AUTOIMMUNE DISEASE METABOLIC CHEMICAL REACTION DISEASE DISORDER IRRITANTS BONE & JOINT DISEASE INFECTION ACUTE CHRONIC PULMONARY INFLAMMATION INFLAMMATION DISEASE TRAUMA & INJURY NEUROLOGICAL DISEASE BURNS LACERATION, CANCER CUTS, WOUNDS  Acute Inflammation 2 MAJOR COMPONENTS: Vascular Cellular It is critical for delivering cellular events of acute immune cells and proteins to inflammation involve the the affected area and occurs recruitment and activation of through a series of white blood cells (leukocytes) coordinated events. at the site of injury or infection. These cells eliminate pathogens, remove dead tissue, 1. Vasodilation and initiate healing. 2. Vascular permeability 1. Cellular recruitment and 3. Increase adhesion of activation of neutrophils white blood cells  1.Vasodilation Inflammatory Response Purpose: Allows increased volume of the blood, induce stasis (slows the blood flow) Mechanism: Activated macrophages release inflammatory lipid mediators (leukotrienes, prostaglandins, and platelet-activating factor) and NO. These inflammatory mediators will act on the smooth muscle cells to Causes: redness (erythema) and heat at the site of induce vasodilation. inflammation. The slower movement of blood, called stasis, allows white blood cells, primarily neutrophils, to adhere to the endothelial walls (margination).  2. Vascular Permeability Purpose: Permits immune cells, plasma proteins, and fluids to leave the bloodstream and enter the tissue. Mechanism: Endothelial cell contraction caused by (histamine, bradykinin, leukotrienes) and NO widens the gaps between endothelial cells leading to the movement of protein-rich fluid ,and even blood cells, to the extravascular tissues. Causes: swelling (edema) and pain at the site.  3. Increase WBC adhesion Purpose: Prepares immune cells for transmigration (movement into the tissue). Mechanism: Circulating immune cells have to interact with the endothelium to move into tissues. Adhesion molecules (selectins and integrins) on endothelial cells and leukocytes are upregulated in response to inflammatory signals, facilitating leukocyte adhesion.  Cellular Events 1. Leukocyte recruitment Margination Rolling Adhesion Diapedesis 2. Chemotaxis 3. Phagocytosis & Inflammatory mediators Purpose: movement of leukocytes towards the site of injury or infection in response to a chemical gradient. Mechanism: Phagocytosis is the process by which leukocytes Mechanism: engulf and destroy pathogens, debris, and dead Chemotactic agents bind to receptors on leukocytes, cells. It is enhanced by opsonization and thus the triggering intracellular signaling pathways that central action of the cellular response. It also cause the cell’s cytoskeleton to reorganize, includes leukocyte release of pro-killing effectors allowing the leukocyte to move toward higher such as lysozyme, granzyme B, NO, and concentrations of the chemotactic factor. interferon-gamma. Cellular Events Mediators of Adhesion  Resolution of Inflammation The final stage of the cellular phase is resolution. After the elimination of the inciting cause, the body must return to homeostasis: Clearance of dead cells, pathogens, and debris by macrophages. Anti-inflammatory signals (such as lipoxins, protectins, maresins, and resolvins) Healing Angiogenesis  ACUTE INFLAMMATORY DISEASES BURNS CONJUNCTIVITIS ALLERGIC RHINITIS MECHANISM: Burn injuries are characterized by aka pink eye, is the swelling or inflammation inflammation of the inside of the nose, which significant local swelling (edema) and redness of the conjunctiva causes redness and swelling. (erythema) around the injury site, indicating acute inflammation. Immediately following a MECHANISM: Inflammatory mediators, MECHANISM: Within minutes of coming into burn, hemostasis and coagulation occur including histamine, prostaglandins, and contact with an allergen, mast cells release through the formation of a blood clot made up leukotrienes, contribute to the substances like histamine, leukotrienes (LTC, of platelets, cross-linked fibrin, and fibronectin, manifestations of ocular allergy. LTD4, and LTE4), and prostaglandins. These which quickly acts to prevent excessive fluid substances can increase blood vessel loss from the wound site. CAUSE: - Infectious: Viral, Bacterial permeability, which causes blood vessels to CAUSE: Thermal sources (fire, hot liquids, - Non-Infectious: Eye injury, Allergens, widen, and promote mucus production. steam and contact with hot surfaces), Toxic substances Chemicals (cement, acid, drain cleaners), CAUSE: Allergens (Dust mites, Pollen, Pet Electricity, Sun (UV light) SIGNS/SYMPTOMS: Redness in white of the dander, Mold spores, Cockroaches) eye, Eye discharge, Dry/watery eyes, Itchy SIGNS/SYMPTOMS: Blisters, pain, swelling, eyes, Blurred vision, Eye pain, Swollen SIGNS/SYMPTOMS: pruritus, sneezing, white or charred skin, and peeling skin Eyelids rhinorrhea, and nasal congestion. TREATMENT/MANAGEMENT: TREATMENT/MANAGEMENT: TREATMENT/MANAGEMENT: - Run cool water over the burn. - Viral Conjunctivitis: Usually doesn't require - Antihistamines (Loratidine, Cetirizine) - Don’t apply ice. treatment unless it's caused by herpes - Decongestants (Phenylephrine nasal spray) - For sunburns, apply aloe vera gel. simplex, varicella-zoster or STI. - Corticosteroid nasal spray - For thermal burns, apply antibiotic cream and cover lightly with gauze. - Bacterial Conjunctivitis: Antibiotics - Leukotriene inhibitors (Montelukast) - Patients may also take OTC pain - Allergic conjunctivitis: OTC antihistamines medication. & decongestants (Tetrahydrozoline) - Non-Medication treatments: OTC eye drops, Warm/Cool compress  ACUTE INFLAMMATORY DISEASES DERMATITIS APPENDICITIS PEPTIC ULCER DISEASE Dermatitis refers to conditions causing skin Inflammation of the appendix. It can cause Involves inflammation that damages the inflammation, such as eczema, contact sudden, intense pain in the lower abdomen. stomach or duodenal lining, leading to dermatitis, and seborrheic dermatitis. Blockages or infections from feces can lead to ulcers. inflammation, causing the appendix to swell MECHANISM: Histamine activates eosinophils, and potentially burst. CAUSE: H. pylori bacteria and long-term use mast cells, basophils, and Th2 cells through of nonsteroidal anti-inflammatory drugs the histamine H4 receptor. It also regulates MECHANISM: Cytokines, chemokines, and (NSAIDs) the expression of pruritic factors, such as adhesion molecules are the inflammatory nerve growth factor and semaphorin 3A, in mediators involved. SIGNS/SYMPTOMS: dull, burning pain in skin keratinocytes via histamine H1 receptor. CAUSE: their stomach, difficulty swallowing food, - Fecaliths appendicoliths, or appendix stones, nausea, vomiting, feeling bloated or full, CAUSE: black, sticky stool - Atopic dermatitis: the immune system can block the opening of the appendix, overreacts to small irritants or allergens, trapping bacteria inside. causing inflammation. - Lymphoid hyperplasia: lymphatic system TREATMENT/MANAGEMENT: - Genetics: Family history of dermatitis produces more white blood cells, causing - H2 blockers - Environmental factors: tobacco smoke, swelling in the appendix. - PPIs fragrances in skin products or soap - Colitis: inflammation in the colon due to - Triple therapy with two antibiotics and a infection or inflammatory bowel disease, can PPI SIGNS/SYMPTOMS: Blisters, red rashes, dry irritate the appendix and potentially spread skin, and itchiness. infection to it. - Surgery may be needed for bleeding cases TREATMENT/MANAGEMENT: SIGNS/SYMPTOMS: Abdominal pain, nausea - Avoiding triggers and reduce stress and loss of appetite. - Prescribed medications (corticosteroid creams, calcineurin inhibitors, or TREATMENT/MANAGEMENT: antihistamines) - Antibiotics - Skin hydration - Surgery  ACUTE INFLAMMATORY DISEASES INFLUENZA ACUTE OTITIS MEDIA Flu, or influenza, is an infection that affects This middle ear infection occurs abruptly the nose, throat, and lungs. causing swelling and redness. Fluid and mucus become trapped inside the ear. MECHANISM: pro-inflammatory cytokines are produced, including IL-6 and TNF-α. These MECHANISM: The presence of live viruses in proteins play a key role in triggering the middle ear, along with bacteria, leads to inflammation in the body. higher levels of inflammatory substances and cytokines like histamine, leukotriene B4, and IL- CAUSE: 8. Influenza is caused by viruses that spread CAUSE: through the air in tiny droplets when It is usually caused by viral infections like cold someone coughs, sneezes, or talks. or flu, or by bacterial infections like strep throat. SIGNS/SYMPTOMS: Fever, cough, headache, muscle aches, SIGNS/SYMPTOMS: fatigue, sweating and chills Tugging or pulling at one or both ears, fever, TREATMENT/MANAGEMENT: fluid draining from ear(s), loss of balance, - Antiviral drugs (Oseltamivir) hearing difficulties, and ear pain - Phenylephrine (Neozep) - Pain relievers (Paracetamol, Ibuprofen) TREATMENT/MANAGEMENT: - Drink plenty fluids - Analgesic - Rest - Antibiotics (Amoxicillin, Co-Amoxiclav)  CHRONIC INFLAMMATION Mechanism Causes Clinical Manifesation Continuous release of 1. Persistent infections 1. Ulceration of epithelial inflammatory mediators. 2. Autoimmune disorders cells 3. Uric acid deposits 2. Sinus & Fistula formation Failure to remove 4. Unregulated immune 3. Loss of function harmful agents or repair response 4. Wall thickening of hollow tissues. 5. Hypersensitivity reaction organs Activation of the immune 6. Prolonged exposure to 5. Distortion of organ response leading to irritants (e.g., smoking, tissue destruction and industrial pollutants). repair (fibrosis). 7. Organ transplant rejection  Chronic Inflammatory Diseases NEUROLOGICAL DISEASE MULTIPLE SCLEROSIS ALZHEIMER’S DISEASE Multiple sclerosis (MS) is a chronic inflammatory disease where Alzheimer's disease is a progressive brain disorder that worsens the immune system attacks the central nervous system. over time. It is the leading cause of dementia, which involves a gradual decline in memory, thinking, behavior, and social skills. MECHANISM: Patients with multiple sclerosis have higher levels of pro-inflammatory cytokines in their blood and cerebrospinal MECHANISM: Certain cells in the brain contribute to ongoing fluid (CSF). These cytokines include TNF-α, IL-17, CXCL8, IL-23, inflammation in Alzheimer's by releasing cytokines, chemokines, and CXCL-13. and neurotoxins. CAUSE: CAUSE: Autoimmune disorders, The exact causes of Alzheimer's disease are not fully Infectious agents, such as viruses, understood, but it involves brain proteins not functioning Environmental factors, properly, which disrupts neurons and leads to their damage and Genetic factors death. For most people, Alzheimer's is likely caused by a mix of genetic, lifestyle, and environmental factors. SIGNS/SYMPTOMS: Fatigue, Eye/Vision Problems, Numbness/Tingling, Loss of balance SIGNS/SYMPTOMS: Memory loss, increasing confusion and disorientation, Hallucinations and delusions TREATMENT/MANAGEMENT: - There is currently no cure for multiple sclerosis (MS). TREATMENT/MANAGEMENT: Steroid medication to reduce swelling and improve nerve - Cholinesterase Inhibitors function. - Memantine Disease-modifying therapies to lower the frequency and - New Medications approved by FDA (Lecanemab, severity of relapses. Donanemab) Muscle relaxants to ease muscle spasms, cramps, or - Creating a safe and supportive environment stiffness. Medications to manage pain, vision issues  Chronic Inflammatory Diseases PULMONARY DISEASE BRONCHIAL ASTHMA COPD A common lung disease characterized by airflow limitation. It is A chronic inflammatory disease of the airways which includes both chronic and progressive and is associated with an variable expiratory airflow limitation. abnormal inflammatory response of the lungs to noxious particles or gases. MECHANISM: Various cells such as mast cells, eosinophils, T- lymphocytes, macrophages, neutrophils, and epithelial cells, all MECHANISM: Major cell types present are macrophages, play a role in the condition. neutrophils and CD8+ lymphocytes. CAUSE: CAUSE: a.) Environmental factors (Smoking, Farm living, Urban living) Tobacco smoke, Occupational dust and chemicals, Indoor and b.) Genetic factors (family history, C-section) outdoor pollution SIGNS/SYMPTOMS: SIGNS/SYMPTOMS: SOB, Chest tightness, Wheezing, Trouble sleeping caused by Chronic cough, Chronic sputum production, Dyspnea, Barrel SOB or cough chest, Quiet Chest, Hoover sign TREATMENT/MANAGEMENT: TREATMENT/MANAGEMENT: Inhaled corticosteroids LABA + LAMA + ICS Bronchodilators (SAMA, LAMA, SABA, LABA) LABA + LAMA Anti-inflammatory medicines Bronchodilators  Chronic Inflammatory Diseases BONE & JOINT DISEASE RHEUMATOID ARTHRITIS OSTEOARTHRITIS A degenerative joint disease that impacts various tissues in the Rheumatoid arthritis (RA) leads to inflammation and pain in the joint. It is the most common type of arthritis. OA can affect any joints. It occurs when the immune system malfunctions and joint, it most often involves the hands, knees, hips, lower back, attacks the synovium, the lining of the joints. This condition and neck. commonly affects the hands, knees, and ankles, often impacting the same joints on both sides of the body. MECHANISM: The main inflammatory mediators includes: cytokines, chemokines, growth factors, adipokines, and MECHANISM: Cytokines such as TNF, IL-1, and IL-6 that are neuropeptides. released synovial microenvironment are responsible for many systemic manifestations of the disease CAUSE: Joint injury, Overuse of joints, Obesity, Weak muscle, Genetics, CAUSE: Gender, Environmental factors (occupation, diet, bone density, They believe that individuals with certain genes may have these level of physical activity) genes activated by environmental triggers, such as a virus or bacteria, physical or emotional stress, or other external factors. SIGNS/SYMPTOMS: SIGNS/SYMPTOMS: Joint pain, joint stiffness, swelling around a joint, muscle Joint pain, Morning stiffness, Fatigue, same joint on both weakness, and joint instability sides are affected, low-grade fever TREATMENT/MANAGEMENT: - Acetaminophen TREATMENT/MANAGEMENT: - NSAIDs - NSAIDS (Ibuprofen, Naproxen) - Duloxetine - Corticosteroids - Physical therapy/Occupational therapy - DMARDs (Methotrexate, Sulfasalazine) - Cortisone/Lubrication injections - BRMs (Adalimumab, Etanercept) - Joint Replacement  Chronic Inflammatory Diseases METABOLIC DISORDER TYPE 2 DIABETES FATTY LIVER DISEASE Type 2 diabetes occurs when the body cannot use insulin Fatty liver disease occurs when fats accumulate in the liver, effectively. If left untreated, it can lead to serious health issues potentially harming the organ and leading to serious such as heart disease, kidney problems, and stroke. complications. MECHANISM: Inflammatory mediators like IL-1β, IL-6, TNF-α, MECHANISM: The levels of cytokines are often higher in people and (CRP), are contributing factors in the development and with type 2 diabetes. Excess body fat, particularly around the progression of fatty liver disease. abdomen, leads to ongoing low-level inflammation, which disrupts how insulin works and plays a role in the development of the disease. CAUSE: Eating excess calories, obesity, diabetes, alcohol abuse, rapid CAUSE: weight loss Insulin, resistance, Genetics, Excess body fat, Physical inactivity, and Long term corticosteroid use SIGNS/SYMPTOMS: Fatty liver usually doesn't cause symptoms, so many SIGNS/SYMPTOMS: people only find out they have it through tests done for Increased thirst (polydipsia), Frequent urination, fatigue, other reasons. slow healing of cuts, dry skin, tingling/numbness of feet Non-alcoholic fatty liver disease can harm the liver for years without showing any signs. TREATMENT/MANAGEMENT: If the condition worsens, symptoms like tiredness, - Healthy diet - Thiazolidinediones weight loss, belly pain, weakness, and confusion may appear. - Regular exercise - DPP-4 inhibitors - Weight loss - GLP-1 agonist TREATMENT/MANAGEMENT: - Insulin - SGLT2 inhibitors - Losing weight - Metformin - Controlling diabetes - Sulfonylureas - Avoid alcohol - Lower cholesterol and triglyceride levels  Chronic Inflammatory Diseases CARDIOVASCULAR DISEASE HYPERTENSION HEART FAILURE Hypertension, or high blood pressure, happens when the Heart failure occurs when the heart is unable to pump blood pressure in your blood vessels is 140/90 mmHg or higher. effectively. Congestive heart failure (CHF) is a specific form of heart failure that requires prompt medical attention. MECHANISM: Certain immune cells, like CD8+ T cells, T helper MECHANISM: Key cytokines involved in the progression of CHF cells, regulatory T cells, monocytes, macrophages, and B cells, include tumor TNFα, IL-1, and IL-6. along with chemokines and cytokines (IL-17, IL-18, interferon-γ, TNF) play important roles in the immune processes that contribute to high blood pressure. CAUSE: Myocardial infarction, Abnormal heart valves, Any damage to CAUSE: the heart muscle (drug/alcohol abuse, infections), congenital Old age, Genetics, Being obese/overweight, physically inactive, heart defects high salt diet, alcohol abuse SIGNS/SYMPTOMS: SIGNS/SYMPTOMS: SOB, Persistent coughing/wheezing, Edema, Fatigue, - Headaches, blurred vision , chest pain Increased heart rate, lack of appetite TREATMENT/MANAGEMENT: TREATMENT/MANAGEMENT: - HACEi (enalapril and lisinopril) - ACEi (enalapril and lisinopril) - ARBs (losartan and telmisartan) - ARBs (losartan and telmisartan) - CCBs (amlodipine and felodipine) - Beta blockers (metoprolol) - Diuretics (hydrochlorothiazide) - Potassium-sparing diuretics (spironolactone)  Chronic Inflammatory Diseases AUTOIMMUNE DISORDER SYSTEMIC LUPUS ERYTHEMATOSUS TYPE 1 DIABETES Long-lasting autoimmune disease that can affect many parts of Type 1 diabetes (T1D) is an autoimmune disease that involves the body. In lupus, the immune system mistakenly attacks the chronic inflammation of the pancreatic islets of Langerhans. body’s own tissues, leading to inflammation and sometimes This inflammation is usually caused by both adaptive and innate permanent damage. immune cells. MECHANISM: Inflammation of pancreatic beta cells in T1D are MECHANISM: Cytokines (IL-1β, IL-8, IL-12 ) are associated with caused by IFN-gamma, TNF-a, and IL-1beta the activity and severity of SLE. CAUSE: CAUSE: Genetics, exposure to viruses and other environmental factors The cause of lupus in most cases is unknown. Some potential triggers include: Sunlight, Infections, Medications (blood SIGNS/SYMPTOMS: pressure medications, anti-seizure medications and antibiotics) - Polydipsia - Polyphagia SIGNS/SYMPTOMS: - Frequent urination Joint pain/swelling, butterfly-shaped rash on the face, skin - Fatigue lesions, SOB, chest pain, dry eyes - Blurred vision - Unexplained weight loss TREATMENT/MANAGEMENT: TREATMENT/MANAGEMENT: - NSAIDs - Losing weight - Antimalarial drugs - Controlling diabetes - Corticosteroids - Avoid alcohol - Immunosuppressants - Lower cholesterol and triglyceride levels - Biologics  Summary Acute inflammation is a short-term event that ends when the pathogen or foreign particles are removed. Chronic inflammation involves both innate and adaptive, or specific, immune cell types, and is generally distinguished by a situation where the insult cannot be removed. The vascular stage of acute inflammation is primarily concerned with preparing the blood vessels for the delivery of immune components. The sequence of events-vasodilation, increased permeability, stasis, and leukocyte migration-sets the stage for the cellular phase, where immune cells actively combat infection or clear debris. The cellular events of acute inflammation are essential for clearing infections and initiating tissue repair. Neutrophils are the primary first responders, followed by monocytes and macrophages. These cells work together to eliminate harmful agents, degrade dead tissue, and set the stage for healing. These processes result in the classic signs of inflammation: redness, heat, swelling, and pain.  CONCLUSION Inflammation is a critical immune response that can be beneficial when acute. However, when inflammation becomes chronic, it can lead to serious diseases and health complications. 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