Acute Inflammation Presentation PDF

ACUTE INFLAMMATION BY DR MUHAMMAD ALI SOOMRO  WHAT IS INFLAMMATION? Response of vascular tissue to harmful stimuli such as foreign antigens, damaged cells, or irritants. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells an...

ACUTE INFLAMMATION BY DR MUHAMMAD ALI SOOMRO  WHAT IS INFLAMMATION? Response of vascular tissue to harmful stimuli such as foreign antigens, damaged cells, or irritants. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.  SIGNS The five classical signs of inflammation are: – Rubor (Redness). – Dolor (Pain) – Calor (Heat) – Tumor (Swelling) – Functio Laesa (Loss of Function)  CAUSES: Infection. Trauma. Physical injury from thermal extremes or ionizing radiation. Chemical injury. Immunologic injury. Tissue death.  TYPES: Inflammation can be classified as either acute or chronic.  ACUTE INFLAMMATION: Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially gran ulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue  ACUTE INFLAMMATION: Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus. It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation.  PROCESS OF ACUTE INFLAMMATION: The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells and mast cells. These cells possess surface receptors known as pattern recognition receptors (PRRs), which recognize (i.e., bind) two subclasses of molecules: pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).  PROCESS OF ACUTE INFLAMMATION: PAMPs are compounds that are associated with various pathogens, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related injury and cell damage. At the onset of an infection, burn, or other injuries, these cells undergo activation (one of the PRRs recognize a PAMP or DAMP) and release inflammatory mediators responsible for the clinical signs of inflammation.  PROCESS OF ACUTE INFLAMMATION: Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor). Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid into the tissue (edema), which manifests itself as swelling (tumor). Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor).  PROCESS OF ACUTE INFLAMMATION: The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury. The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain.  PROCESS OF ACUTE INFLAMMATION: In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated by necrosis, e.g. a burn or a trauma.  PROCESS OF ACUTE INFLAMMATION: Acute inflammation may be regarded as the first line of defense against injury. Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed.  COMPONENTS: Acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (Granulocytes).  VASCULAR PHASE: The vascular component of acute inflammation involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue. Characterized by marked vascular changes, including vasodilatation, increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators.  VASCULAR PHASE: Vasodilatation occurs first at the arteriole level, progressing to the capillary followed by venules, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood. Stasis allows leukocytes to marginate (move) along the endothelium, a process critical to their recruitment into the tissues.  CELLULAR PHASE: The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release  CELLULAR PHASE: Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. In general, acute inflammation is mediated by granulocytes, whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.  OUTCOMES: The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. The possible outcomes to inflammation are as follows: – RESOLUTION – FIBROSIS – ABSCESS FORMATION – CHRONIC INFLAMMATION THANKS THE END!