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NURB 340

by: Kelsey Forbeck

NURB 340 NURB 340

Kelsey Forbeck

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These notes cover the Inflammatory lecture
Class Notes
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This 12 page Class Notes was uploaded by Kelsey Forbeck on Wednesday September 14, 2016. The Class Notes belongs to NURB 340 at University of Indianapolis taught by Moore in Fall 2016. Since its upload, it has received 21 views. For similar materials see Pathophysiology in NURSING at University of Indianapolis.

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Date Created: 09/14/16
NURB340:Pathophysiology Inflammation  First Line of Defense: o Innate (natural) (native) immunity o Physical:  Skin  Lining of the gastrointestinal, genitourinary, and respiratory tract o Epithelia cell-derived chemical barriers:  Secretes salvia, tears, ear wax, sweat, and mucous  Antimicrobial peptides o Normal microbiome (aka normal flora)  Each surface colonized by bacteria and fungi that is unique to the particular location and individual  EX: If you take antibiotics it will disrupt flora in vagina. This will cause an abundance of yeast  EX: if you disrupt normal flora of your gut you will get diarrhea.  A disruption in flora will cause a super infection  Second Line of Defense: o Inflammatory response (FIRST RESPONSE TO INJURY) o Nonspecific o Can be caused by numerous materials:  Infection  Tissue necrosis  Trauma  Physical or chemical injury o Inflammatory response:  Vascular response to inflammation is  Blood vessels dilate  Increase vascular permeability and leakage  White blood cell adherence to the inner walls of the vessels and migration through the vessels o Benefits of inflammation  Limit and control the inflammatory process  Prevent and limit infection and further damage  Initiate adaptive Immune response  Initiate healing  Plasma Protein Systems o Complement system  Produces biologically active fragments that recruit phagocytes, activate mast cells, and destroy pathogens  Activate C3 and C5  Once the C3 and C5 are stimulated we will get:  Opsonins  Chemotactic factors 2  Anaphylatoxins  Pathways:  Classical  Lectin o Activated by several plasma proteins o Independent of antibodies  Alternative o Activated by substances found on the surface of an infectious organism o Coagulation (clotting) system  A group of plasma proteins that when activated forms a fibrous meshwork at an injured or inflamed site (forms blot clot)  Prevents the spread of infection  Localizes foreign bodies and microorganisms  Forms a clot that stops bleeding  Provides a framework for repair and healing  Main substance is an insoluble protein called fibrin  Can be activated either extrinsically or intrinsically o Kinin System  It interacts with coagulation system  Both kinin and coagulation system can be activated by factor 12  Functions to activate and assist inflammatory cells 3  Primary kinin is bradykinin  Once bradykinin is released it causes: o Dilation of blood vessels o Pain o Smooth muscle contraction o Increases vascular permeability (moves fluid out to protect injury) o Control and interaction of plasma protein systems  Tight regulation is essential  Multiple mechanisms are available to either activate or inactive (regulate) these plasma protein systems  Cellular Components of Inflammation o Erythrocytes o Platelets o Leukocytes  Granulocytes  Basophils  Eosinophils  Neutrophils  Monocytes  Lymphocytes 4  Cytokines o They activate other cells and regulate inflammatory response o Chemokines  Synthesized by many cells (macrophages, fibroblasts, endothelial cells) in response to proinflammatory cytokines  Induce chemotaxis to promote phagocytosis and wound healing  EX: o Monocyte/macrophage chemotactic proteins o Macrophage inflammatory proteins o Neutrophils o Interleukin (type of cytokine)  Produced primarily by macrophages and lymphocytes in response to stimulation of pattern recognition receptors or by other cytokines  Many types  EX:  IL-1 is proinflammtory  IL-10 is anti-inflammatory o Tumor necrosis factor alpha  Secreted by macrophages in response to pathogen-associated molecular patterns (PAMP) and toll-like receptor (TLR) recognition  Induces fever by acting as an endogenous pyrogen  Increases synthesis of inflammatory serum proteins 5  Causes muscle wasting and intravascular thrombosis  VERY HIGH LEVELS CAN BE LETHAL o Interferon (IFN)  Protects against viral infections  Produced and released by virally infected host cells in response to viral double stranded RNA  Usually given to organ transplant recipients to help protect them from viruses  Mast Cells and Basophils o Mast cells:  Cellular bags of granules located in the loose connective tissues close to blood vessels  EX: skin, digestive lining, and respiratory tract  Contain histamine, cytokines, and chemotaxic factors o Basophils:  Found in blood and probably function in the same way as mast cells o Chemical release in two ways:  Degranulation  Release of contents of mast cell granules  Synthesis  The new production and release of mediators in response to a stimulus 6  Histamine o Vasoactive amine that causes temporary, rapid constriction of the large blood vessels and the dilation of the post capillary venules o Retraction of endothelial cells lining the capillaries o Receptors:  H1 Receptor  Proinflammatory  Present in smooth muscle cells of the bronchi  H2 Receptor  Anti-inflammatory  Present on parietal cells of the stomach mucosa o Induces the secretions of gastric acid  Synthesis of Mediators o Leukotrienes:  Product of arachidonic acid from mast cell membranes  Similar effects to histamine in later stages o Prostaglandins  Similar effect to leukotrienes; they also induce pain  Aspirin and some other nonsteroidal anti-inflammatory drugs (NSAIDs) block the synthesis of prostaglandins, thereby inhibiting inflammation and pain o Platelet-activating factor 7  Similar effect to leukotrienes and platelet activation  Platelets o Activated by tissue destruction and inflammation o The activation leads to interaction with coagulation cascade to stop bleeding o TXA2 (tranexamic acid)  Studying to stop excess bleeding  Post-surgical or trauma bleeding  Phagocytes o Neutrophils  MOST COMMON  Predominate in earl inflammatory responses  Ingest bacteria, dead cells, and cellular debris  Cells are short lived and become part of the purulent exudate (pus) o Eosinophils  Mildly phagocytic  Defends against parasites and regulation of vascular mediators o Basophils  Least prevalent of the granulocytes  Role unknown 8 o Monocytes and Macrophages  Monocytes are produced in the bone marrow, then they enter into the circulation, and migrate to the inflammatory site where they develop into macrophages  Macrophages arrive at the inflammatory site around 24 hours after neutrophils o Dendritic cells  In peripheral organs and skin  Migrate through lymph vessels to lymph tissue and interact with T lymphocytes to generate an acquired immune response  Perform a more SPECIFIC response  Phagocytosis o Defined: Process by which a cell ingests and disposes of foreign material o Production of adhesion molecules o Margination (pavementing)  Adherence of leukocytes to endothelial cells o Diapedesis  Emigration of cells through endothelial junctions o Steps of phagocytosis:  Adherence  Engulfment  Phagosome formation 9  Fusion with lysosomal granules  Destruction of the target  Exudative Fluids o Serous exudate  Watery: indicates early inflammation o Fibrinous  Thick, clotted: indicates more advanced inflammation o Purulent  Pus: indicates a bacterial infection o Hemorrhagic  Contains blood: indicates bleeding  Systemic Manifestations of Acute Inflammation o Fever o Leukocytosis  Increased number of circulating leukocytes o Increased plasma protein synthesis  Acute phase reactants  C reactive protein  Fibrinogen  Haptoglobin  Amyloid  Ceruloplsmin 10  Causes of Chronic Inflammation o High lipid and wax content of a microorganism o Ability to survive inside the macrophage o Toxin o Chemicals, particulate matter, or physical irritants  Chronic Inflammation Characteristics o Dense infiltration of lymphocytes and macrophages o Granuloma formation o Epithelioid cell formation o Giant cell formation 11 12


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