2024_0814_1300_bracamonte_acute_inflammation_indep_learn_notes_final.pdf

ACUTE INFLAMMATION Block: Foundations Block Director: James Proffitt, PhD Session Date: Wednesday, August 14, 2024 Time: 1:00 – 2:00 pm Instructor: Erika Bracamonte, MD Department: Pathology Email: [email protected] INSTRUCTIONAL METHODS...

ACUTE INFLAMMATION Block: Foundations Block Director: James Proffitt, PhD Session Date: Wednesday, August 14, 2024 Time: 1:00 – 2:00 pm Instructor: Erika Bracamonte, MD Department: Pathology Email: [email protected] INSTRUCTIONAL METHODS Primary Method: IM10: Independent Learning ☐ Flipped Session ☐ Clinical Correlation Resource Types: RE18: Written or Visual Media (or Digital Equivalent) INSTRUCTIONS Please read lecture objectives, notes and watch the pre-recorded video attached to the session in MedLearn. READINGS RECOMMENDED Reading: Robbins and Cotran Pathologic Basis of Disease. 10E (2021) BOOK / E-BOOK: pp. 75 – 96. LEARNING OBJECTIVES: 1. Explain the three major components of acute inflammation. 2. Describe four common types of stimuli that trigger acute inflammation. 3. Describe the various types of extracellular fluid collections, including exudate, transudate, edema and pus. 4. Understand the two major results of the vascular response in acute inflammation to be vasodilation and increased vascular permeability, and describe the forces favoring fluid movement out of vessels. 5. Name the chemical mediator responsible for the primary, transient vascular permeability response and identify the type of blood vessel in which increased permeability primarily occurs. 6. Know the sequence of events in leukocyte extravasation, and explain how adhesion molecules are involved at various steps. 7. Explain the three main steps of phagocytosis, and describe four processes that are important in the third step (killing and degradation of microbes). 8. Name two diseases that occur due to defects in leukocyte function. 9. Know the two main types of vasoactive amines, their source and explain their main effects. 10. Know the two main pathways of the arachidonic acid cascade and describe where anti-inflammatory medications act in the cascade to inhibit the production of prostaglandins and leukotrienes. 11. Explain how nitric oxide acts as an endogenous regulator of inflammation. [1 of 11] Block: Foundations | BRACAMONTE ACUTE INFLAMMATION 12. Know two main cytokines involved in inflammation and describe their major effects. 13. Recognize the complement, kinin and clotting systems as enzyme cascades that can act to modify the inflammatory response. 14. Explain the four common morphologic patterns of acute inflammation in tissues, and be able to give an example of each pattern. 15. Describe the three main outcomes of acute inflammation and explain factors favoring each outcome. Explain why some types of ongoing or repeated injury responses may display a mixed (both acute and chronic) inflammatory picture. CURRICULAR CONNECTIONS Below are the competencies, educational program objectives (EPOs), disciplines and threads that most accurately describe the connection of this session to the curriculum. Related Related Competency\EPO Disciplines Threads COs LOs CO-02 LO #1 - 15 MK-05: The altered structure and Pathology H & I: Acute function (pathology & Care pathophysiology) of the body/organs in disease INFLAMMATION I GENERAL FEATURES: A) Definition and general description: Inflammation is a complex reaction of vascularized living tissue to injurious agents (such as microbes or damaged/necrotic cells) that consists of vascular responses, migration and activation of leukocytes, and systemic reaction. IMPORTANT: Inflammation is NOT synonymous with infection and can be due to multiple types of injury (although some types of inflammation may be secondary to injury by an infectious agent). Inflammation is closely tied to the process of repair. It is fundamentally a protective host response. However, if poorly regulated, inflammation and repair can be harmful to host tissues. Inflammation involves the actions of blood vessels, cells and chemical mediators. B) Patterns of inflammation: 1. Acute inflammation – Rapid onset, usually of short duration (minutes to days) [2 of 11] Block: Foundations | BRACAMONTE ACUTE INFLAMMATION a. In some types of ongoing or repeated injury, acute inflammation may occur over a longer time frame. 2. Chronic inflammation – Longer duration, variable time course a. Granulomatous inflammation (specialized form of chronic inflammation) ACUTE INFLAMMATION I GENERAL FEATURES A) Basic objectives: Rapid delivery of leukocytes and plasma proteins to site of injury, destruction of the offending agent, and amplification and regulation of the inflammatory response B) Major components: 1. Dilation of small vessels; leads to increased blood flow to affected area. 2. Increased permeability of microvasculature; leads to movement of fluid and plasma proteins from circulation into tissue (exudation). 3. Emigration of leukocytes (white blood cells) from microcirculation, with their accumulation at site of injury and activation to eliminate offending agent. a. Circulating cells - Neutrophils, monocytes, eosinophils, lymphocytes, basophils and platelets b. Cells in tissue – Mast cells, macrophages and lymphocytes C) Stimuli triggering acute inflammation: 1. Infections and microbial toxins 2. Tissue necrosis – May be due to ischemia, trauma, or physical/chemical agents (i.e. burns, frostbite, irradiation) 3. Foreign bodies 4. Immune reactions – Autoimmune diseases, hypersensitivity reactions D) Extracellular fluid collections 1. Exudate – Fluid with a high protein concentration, containing cellular debris, and specific gravity >1.020 2. Transudate – Fluid with a low protein content (mostly albumin), minimal cells, and specific gravity