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Inflammation, Infection, and Tissue Healing - Coggle Diagram
Inflammation, Infection, and Tissue Healing
Diagnosis terminology in diseases cause by infection
Etiologic agent (bacteria, virus, fungi, parasite, prion), site of infection, signs and symptoms, severity (acute, chronic, asymptomatic), nosocomial infection, community-acquired infection, opportunistic infection
Clinical features of chronic inflammation (cardinal signs)
Definition and etiology of infection
Definition: invasion and growth of germs in the body
Causes: direct contact, indirect contact, airborne transmission, vector transmission, food and water contamination
Type of cells in inflammation and their mechanism
Acute inflammation
Neutrophils: first responders
Macrophages: cleans up dead cells and debris
Monocytes: mature into macrophages upon reaching the inflamed area
Chronic inflammation:
Lymphocytes: directly attacks damaged tissues
Plasma cells: produces antibodies
Macrophages: become the dominant cell, promotes inflammation
Mechanism of host-agent interaction
Pathogen can damage host tissues that trigger an immune response --> infection
The host's immune system can recognize and eliminate the pathogen through antibodies and immune cell activation
Types of inflammation
Acute inflammation: rapid onset, innate immunity, classic signs and symptoms, resolves in a few days
Chronic inflammation: slow onset, adaptive immunity, less prominent classic clinical signs, long duration (months-years)
Mechanism of cell and tissue regeneration in the sterile wound
Regeneration is the process of replacing destroyed tissue with new, similar tissue, with three levels: continuous, latent, and permanent
Wound healing relies on cells, including leukocytes, neutrophils, macrophages, platelets, and fibroblasts
Mediators in acute and chronic inflammation
Acute inflammation: vasoactive amines, eicosanoids, cytokines, acute-phase proteins
Chronic inflammation: cytokines, chemokines, growth factors, oxidative stress mediator
Definition, etiology of inflammation
Inflammation: immune system's response to harmful stimuli
Causes: infectious (pathogens, infections), non-infectious (physical injury/trauma, allergens, etc)
Histopathological features of acute and chronic inflammation
Acute inflammation: edema, hyperemia, exudation of liquids and living elements into the injured tissue
Chronic inflammation: fibrosis, granuloma formation, predominance of lymphocytes and macrophages
Exudate and transudate
Exudate: liquid that is secreted or leaked from the blood vessels in the adjoining tissues as a result of injury/inflammation
Transudate: ultrafiltered fluid secreted or leaked from the circulatory system due to underlying medical conditions that have altered the venous blood pressure
Factors that affect wound healing
Age
Nutrition
Blood supply
Types and severity of wound
How to recognize microorganism and cell damage due to inflammation
Clinical signs and symptoms, laboratory tests, imaging studies, histopathological examinations
Types of granulomatosa
Non-caseating: do not have necrosis, are often caused by foreign bodies, ex: sarcoidosis
Caseating: have necrosis, is a hallmark of bacterial/viral/fungal infections, ex: tuberculosis
Pathogenesis of acute and chronic inflammation
Acute inflammation: vascular phase -- cellular phase
Chronic inflammation: immune response -- phagocytosis -- necrosis -- repair
Mechanism and port d’entree microorganism in the body
Mechanism: direct penetration, breaches/wounds, natural openings, active invasion, enzymes, toxins, carrier entry, eukaryotic cells, professional carriers
Port d'entree: respiratory tract, GI tract, urogenital tract, skin and mucous membranes, bloodstream
Mechanism of cellular aging
Cellular senescence
Mitochondrial dysfunction
Epigenetic changes
Cellular stress and protein misfolding
DNA damage
Telomere shortening
Nasywa Azzahra S. - 2306173731
