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Redness (rubor) and Heat (calor) inflammatory mediators are powerful vasodilators includes blood vessels and capillaries
Hyperemia increased blood suply to area makes tissue appear red and feel warmer than surrounding body surface. redness (rubor) and heat (calor) due to fluid buildup
Swelling (tumor) Dilated capillaries cause increase in size of gaps in their walls Endothelial cells contract Increases size of gaps in capillary walls Blood components can now fit through gaps and migrate into tissue spaces (monocytes and neutrophils)
Inflammatory exudate Inflammatory change in vessel fluid escapes with large proteins into tissues = edema/swelling
Pain (dolar) and Loss of Function (f. laesa) Inflammatory mediators increase sensitivity of local nociceptors (pain) Lower depolarization threshold, make firing of action potential more likely with much less pressure than normally necessary Pulse pressure (throbbing) may be enough to cause pain pain inhibits use of body part - loss of function
Hyperalgesia increased pain response pain (dolor) due to bradykinin and histamine increasing sensitivity of area and loss of function (functio laesa)
Innate Immunity Inborn, non-specific immunity Short lived Uses cytokines, the complement system, and WBCs Activates the adaptive system by presenting antigens
Adaptive immunity Acquired, specific immunity (learned) Creates immunological memory to fight pathogens if met again Carried out by lymphocytes which recognize antigens and secrete antibodies Sometimes cannot distinguish non-self, hence allergies and autoimmune dz
Vascular Permeability (stage 1 - inflammation) Histamine and bradykinin dilate vessels and make them more permeable Fluids, WBCs, and platelets can then travel out to site of injury or infection Capillaries become permeable Fluid flows out of capillaries to injured tissues Protein rich, filled w/ WBCs to eat foreign material Dilutes toxins and lowers pH – microbes prefer acidic environments Associated with hyperemia and hyperalgesia Associated wtih fluid filtration of proteins and WBCs (phagocytosis, purulent exudate, transudate) Makes blood more basic to make basic hating bacteria go away
Phagocytosis (by WBCs) Consuming of foreign material by WBCs during acute vascular stage
Purulent Exudate (pus) Tissue continues to swell with fluid of protein, microbes, and cellular trash = dead WBCs and protein cause it to appear milky. Infected. tissue continues to swell (edema) with fluid of protein, microbes, and cellular debris
Transudate Little to no protein and mainly watery filtrate of blood. Blister has bacteria - needs neutrophils, brings good pus
Cellular Chemotaxis (stage 2 inflammation) Chemical signal to attract help to site of injury Emitted by microbes, WBCs, and endothelial cells to attract platelets and more WBCs to site of injury Neutrophils (polymorphonuclear leukocytes – PMNs) Primary responder of all the leukocytes; band or stab cells Margination Adhesion of the leukocytes to the wall of the endothelium near injury Release inflammatory mediators called cytokines and acute-phase proteins
Neutrophils First responders to chemotaxis call As mature cells dies bone marrow responds with immature - band and stab cells Dead cells make up most of pus Squeeze out of widened capillaries and into tissue towards wound (extravasation/diapedesis/transmigration) Polymorphonuclear leukocytes (PMNs)
Margination blood flow slows down Neutrophils line up along vessel wall nearest injury Rolling adhesion to firm adhesion Neutrophils sticking on vessel wall (extravasation/diapedesis/transmigration)
Transmigration of Neutrophil N’s wedge a pseudopod foot between endothelial cells and escape towards wound site AKA extravasion or diapedesis Neutrophils, platelets, monocytes, and lymphocytes are circulating in blood with RBCs Tearing of tissue releases von Willebrand factors to draw platelets Signals the neutrophils to become sticky inside the blood vessel walls and they slow down to a roll = Adherence Become very sticky and squeeze out between endothelial cells towards injury, also a form of transmigration through the capillary wall = Extravasation or Diapedesis
Inflammatory Mediators Inflammatory mediators released by WBCs when they arrive at the site of inflammation or injury Some amplify the inflammatory process Some attract more WBCs to the area Some attempt to stop the inflammation process Cytokines Acute-phase inflammatory proteins
Cytokines Modulate (control) inflammation by amplifying or deactivating the process Cause both local and systemic effects Tumor necrosis factor (TNF-alpha) Interleukins (ILs) stimulate liver to release APPs, which stimulate, modify, or deactivate the process of inflammation
TNF-alpha involved in systemic inflammation and makes up acute phase reaction Tumor necrosis factor Systemic effects: Lipid and protein mobilization, cachexia, fasting, wasting of body, Can enhance release of WBCs and corticosteroids. During sepsis, promotes hypotension, vasodilation, high HR, low BP
Interleukins (ILs) glycoproteins produced by leukocytes for regulating immune response
Acute-Phase Proteins Cytokines stimulate liver to release APPs, which stimulate, modify, or deactivate the process of inflammation C-reactive protein (CRP), fibrogen, serum amyloid A
C-reactive protein (CRP) Both pro-inflammatory and anti-inflammatory Identifies invaders of the immune system Activates the complement system and inflammatory cytokines Prevents WBCs from sticking to endothelium If elevated on blood test, indicates active inflammation
Erythrocyte Sedimentation Rate (ESR) Lab test that monitors Elevated CR-P and ESR for inflammation Influenced by fibrinogen levels in blood Imprecise because fibrinogen can now be measured directly, but still commonly used to monitor inflammatory diseases Measures rate at which red blood cells precipitate (fall out) of the plasma
Leukocytosis Elevated WBC count during cellular phase of acute inflammatory reaction >15,000
Normal WBC count 4,000-10,000 Cells/mL
Increased WBC count 15,000-20,000 cells/mL
Leukemoid reaction 50,000+ cells/mL Leukemia
Leukopenia too few WBCs
Bone marrow produces RBSs (erythrocutes, transport O2 and CO2), plateles (cell fragments without nuclei, that initiate blood clotting), and WBCs (leukocytes)
Red Blood cells Erythrocytes that transport O2 and CO2
Platelets Cell fragments without nuclei that initiate blood clotting
Immune cell: Granulocytes Nuetrophils, Eosinophol, basophil Contain obvious granules in cytoplasm when seen under microscope Granules contain enzymes and inflammatory mediators
Immune cell: Agranulocytes lymphocute (B or T cels) and monocytes (precuros to macrophage)
The Leukocytes 60% Neutrophils Acute bacterial infection 30% Lymphocytes Increase in the presence of a viral infection, giving the classic "inverted diff" -e.g. 60% Lymphocytes with 30% Neutrophils- seen with acute viral infections 8% Monocytes (become macrophages) Increase in the presence of chronic inflammation or TB 3% Eosinophils Increase in the presence of Parasitic infections and allergic reactions) 0% Basophils Increase in the presence of leukemia or Hodgkin's disease (alteration in bone marrow function), allergic reactions or acute infections
WBC Differential Total number of WBCs measured and percentages of each calculated Predominate type indicates etiology of inflammation Ex: elevated WBC of 16K cells/mL with 90% neutrophils = bacterial pneumonia Ex: elevated WBC and 90% lymphocytes = viral pneumonia Shift to left High numbers of bands indicates newly formed neutrophils b/c marrow trying to replaced used neutros. Acute inflammation
The Phagocytes Scavengers produced by bone marrow, that protect the body by ingesting and removing harmful foreign particles, bacteria, and dead or dying cells. called by chemotaxis Monocytes become macrophages
monocytes made in bone marrow Become macrophages once they reach the organs
Macrophages (from monocytes) found in organs, not blood larger than neutrophils become predominant at injury site Display antigens to lymphocytes on surface (must eat and digest the invader in order to display the invaders calling card or antigen) arrive after first 24-48 hours and phocytize debris long lived (months to years) Initiate immune responses as they display antigens from the pathogens to the lymphocytes, especially T-helper cells
Systemic response (acute inflammation) Effects: Fever Pain Lymphadenopathy Anorexia Guarding Sleepiness Anemia Lethargy Inflammatory mediators are responsible for much of the unpleasant effects
Inflammatory mediators chemicals released locally into tissues that cause inflammatory response Released from WBCs: Prostaglandins (PGs), histamine, leukotrienes, TNF-alpha, and Interleukins (ILs) responsible for much of the unpleasant systemic effects
Fever Increase in body temperature caused by pyrogens Keep below 102 deg. F using antipyretcs (acetaminophen, ibuprofen) Chills due to change in set point of hypothalamus Sweating (diaphoresis) d/t vasodilation when pyrogens stop stimulating PGs
Pyrogens Inflammatory mediators released by WBCs which cause fever (bacterial toxins, cytokines, viruses) Activate prostaglandins (PGs) to reset hypothalamic temperature reg. to a higher level Supposedly increases WBC efficiency against invaders causes Diaphoresis (sweating) when stop stimulating prostaglandins (PGs)
TNF-alpha, IL-1 and IL-6 (systemic effects) major cytokines produced by macrophages during inflammation Effects: fever, loss of appetite lethargy
Histamine release Inflammatory mediator released from basophils, platelets, and mast cells Arteriolar vasodilation, large artery vasoconstriction, and increased permeability of venules (in other words, tissue swelling and congestion) Physical injury, immune reactions, cytokines, etc. all stimulate histamine release, especially from MAST CELLS
Mast Cells Release histamine. specialized cells found in blood vessels, nerves, mucosa of mouth, digestive tract, lungs, and dermis of skin, that remain local to their tissue contain granules (vesicles) of histamine Tissue insult causes mast cells to degranulate, releasing: Histamine Heparin (anticoagulant) Nitric Oxide (vasodilator) Cytokines
Inflammatory Mediator Conversion Path cell membrane injured releases phospholipids into tissues phospholipids converted by phospholipase A into arachidonic acid Arachidonic acid converted in prostaglandins by cyclo-oxygenase (COX) and into leukotienes by leukooxygenase Free prostaglandins (pains) start inflammatory response and leukotrienes cause inflammation of bronchi and brain Mast cells (histamine) are also activated (at same time as prostiglandins) and release histamine
Step one: Inflammatory Mediator Conversion Path Phospolipids released into local tissues when phospholipid bilayer damaged. Phospholipase A converts phospholipids into Arachadonic acid
Step 2: Inflammatory Mediator Conversion Path Arachadonic acid converted into prostaglandins by cyclo-oxygenase (COX) and into leukotrienes by leukooxygenase
Step 3: Inflammatory Mediator Conversion Path Prosiglandins and leukotrines free prostaglandins generate an inflammatory response
Step 4.5: Inflammatory Mediator Conversion Path Mast cells activated at same time as prostiglandins which releasehistamine (sneezing, rhinorrhea, eye tearing, sinus inflam.)
Inhibiting Inflammation w/ Pharma Corticosteroids Prednisolone inhibits phospholipase A NSAIDs Non-steroidal anti-inflammatory drugs like aspirin or ibuprofen Inhibit action of cyclo-oxygenase Leukotriene inhibitors (ie, Singulair) inhibit lipooxygenase Anti-histamines Decrease mast cell histamine release Reduces inflammation response
Complete resolution of Acute Inflammation Regeneration and restoration of normal tissue Deactivation of chemical mediators, cleaning debris, normal vascular restoration, apoptosis of WBCs
Healing by connective tissue acute inflammation outcome: scar tissue replaces normal tissue if exudates and debris remain
Chronic, persistent inflammation which does not recede Acute inflammation cannot resolve due to comorbidities or other interference
Chronic macrophages ROS, proteases, cytokines, angiogenesis growth factors, and fibroblast activators Tissue repeatedly damaged, healing delayed, cell death (necrosis)
Granuloma (chronic inflammation) Aggregated macrophages transformed into GIANT CELLS inside granuloma Ex: Tuberculosis of lungs; WBCs wall off infection as tubercles
Inflammation protective, coordinated response of the body to an injurious agent increases vascular permeability and blood flow (helps WBCs) First stage in healing process - promotes tissue regeneration after injury signal to 'turn on' defense system 'to set afire' + itis bronchitis, tonsillitis, appendicitis, cellulitis, conjunctivitis, meningitis, gastritis, cholecystitis, pyelonephritis, colitis
Acute inflammation Short, reactive period of attack and resolution (hours to days) Can be triggered by infections, toxins, physical injury, surgery, cancer, chemical agents (chemo, burns, medicines), necrosis, foreign bodies, and immune reactions 3 main stages of acute inflammation Vascular permeability Cellular chemotaxis Systemic responses
Chronic inflammation When inflammatory disorders permanently damage the body (months to years) Tissue damage long term due to continued presence of inflammatory agents: monocytes, lymphocytes, and macrophages
5 features of inflammation Redness (erythema) - rubor Swelling (edema) – tumor Pain (algesia) – dolor Heat – (febrile/thermo) – calor Loss of function – functio laesa
Created by: meagangraf



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