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30 Cards in this Set
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Innate immunity -1st line of defense |
Born With Known as natural or native including barriers (physical, biochemical,mechanical, inflammation) Activates inflammation (humoral response) "Non-specific" |
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Inflammation- 2nd line of defense |
First response to injury. activates when surface barriers breached. Protects from further injury to cell; prevents infection, promote healing; RAPID. "Non-specific" |
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Adaptive (acquired) immunity -3rd line of defense |
Immune response. inducible (must recognize pathogen as foreign or non-self. SLOWER than inflammatory response. Memory. "Specific" to one pathogen. Get this type of immunity after infection or vaccination |
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Inflammatory Response: first response to injury |
1. Occurs in tissues with blood supply (vascularized). 2. Rapid, within seconds after damage occurs. 3. depends on activity of cellular and chemical components 4. non-specific |
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Changes occurring in Micro-circulation- (arterioles, venules, capillaries) during inflammation. |
1.Vasodilation- ( widening of blood vessel ) 2.Increased vascular permeability 3.WBC adhere to "blood vessel wall" & migrate into surrounding tissue |
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Clinical Manifestations of Chronic Inflammation Long-term response (months or years) |
Can cause: Artherosclerosis, Rheumatoid arthritis, Hay fever, Cancer, Periodontitis Diseases with chronic inflammation: asthma, peptic ulcer, Tuberculosis, Hepatitis, Crohns-disease |
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Clinical Manifestations of Acute inflammation |
Diseases that can result in Acute inflammation: Bronchitis, Intense exercise, Scratch-cut on skin, A blow, Tonsillitis, Ingrown toe-nail, Sore throat, Flu |
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Acute Inflammation starts rapidly; becomes severe
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Self-limiting-continues only until threat is eliminated takes 8 to 10 days or inadequate response can persist for weeks/months...GRANULOMATOUS response-contains infection. Local Manifestation: Redness (erythema); heat, swelling (edema); pain; loss of function. Exudate (pus) Systemic Manifestation: Fever induced by cytokines released from neutrophils and macrophages |
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FEVER (pyrogen) induced by Cytokines |
Beneficial: syphillis, gonococcal urethritis sensitive to temp increase. Harmful: hospitable environment for endotoxins (gram (-) bacteria |
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Types of Exudate (pus) |
Serous- watery (fluid in a blister) Fibrinous- lungs (pneumonia) Purulent- walled-off lesions Hemorrhagic- bleeding |
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Physical barrier |
Skin- (epithelial cells) drying out, peeling, acidity. Cilia-in nose and respiratory tract, genitourinary Mucous- lining of GI tract |
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Mechanical Barrier |
Sloughed off with dead skin cells; coughing; sneezing; vomiting; flushed through urine |
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Biochemical barrier |
Mucous; Sweat; Saliva; Tears; Earwax Sweat, tears, saliva contain lysozyme (enzyme) attacks cell walls of gram(+) bacteria. pH 3-5 makes environment inhospitable. Epithelial derived chemicals: Antimicrobial Peptides (small) - Cathelicidins & Definsins-Kill/inhibit growth of disease causing bacteria, fungi, virus e.g. Adenovirus- common cold; HIV |
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Sebaceous gland secrete |
Biochemicals: Fatty acids & Lactic acid ( kills bacteria & fungi) |
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Lungs secrete (Collectins) |
React with carbohydrates on surface of bacteria to help (macrophages) recognize and kill microorganisms.
Has surfactant proteins A-D and Mannose Binding Lectin (MBL)-activates plasma protein systems (complement). |
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Plasma Protein System (essential to effective inflammatory response) |
Complement, Clotting, Kinin system. |
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COMPLEMENT SYSTEM (Large proteins) Function: Opsonization, anaphlaxis, chemotaxis, cell lysis. |
consist of 10% of circulating serum protein. destroy pathogens; sequential activation-cascade; Most important function of cascade -C3 and C5; C3a- potent anaphylatoxin- degranulation of mast cells C3b- serve as opsonin for phagocytosis or activ. next component C5a- anaphylatoxin, chemotactic for neutrophils C5b- membrane attack complex (C5-9) - creates pores for water to enter; cell burst and die. Major Pathways: 1. Classical- activated by antibodies 2. Alternative- activ. by subst. on surface of pathogen; e.g., Lipopolysaccharides (endotoxin) 3.Lectin- independent of antibody, activ by MBL. |
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Clotting System |
Blood clot (Fibrin)-stabalizes platelet plug, traps pathogens, plugs-damaged vessels, stops bleeding. Framework for repair and healing. 2 pathways: 1. Extrinsic path (Tissue Factor) reacts with VII- tissue injury 2. Intrinsic path- (contact activation) - abnormal vessel wall; activ.Hageman Factor XII. Both pathways converge with X (activ. of fibrin) Fibrin releas. fibrinopeptides-chemotactic for neutrophils, increas. permeability, enhance effects of bradykinin. |
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Kinin System |
Activ. by Hageman Factor (XII) to XIIa called Prekalikrein.- first component of kinin sys. Final product: Bradykinin-dilation of blood vessels, smooth muscle contraction, increased vascular permeability. Acts with prostaglandins to induce pain. |
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Their Action in the Inflammatory Response Mast Cells Neutrophils Eosinophils Monocytes Leukotrienes Histamine |
Mast Cells: most import. activ of inflam. response. near blood vessels. degranulation- release of histamine, and synthesis of mediators-Leukotrienes- slow-later stages, (sulfur-containing lipids) Like histamine- smooth muscle contraction; Prostaglandins- longchain unsatur. fatty acids) neutrophil chemotaxis, pain; Platelet activ. factor. smooth muscle retraction, leukocyte adhesion, platelet activation. HALLMARKS of inflammation. Neutrophils: granulocyte wbc, predominant, Kill bacteria, Remove debris, arrive within 6 to 12 hrs to inflam site. No divide, Acidic sensitivity-short-lived becomes purulent exudate. Eosinophils: Regulate inflamm. resp. mediators, defend against parasites. Monocytes: immature macrophage, largest normal blood cell; prod. in bone marrow; Tissue Macrophages (mature): Kuppffers-liver; Alveolar-lungs; Microglia-brain. Enter after 24 hrs. replace neutrophils. Wound healing (phagocytosis), angiogenesis, rel. cytokines, growth factors, fibroblasts, extracellular matrix and collagen formation. Resistant bacteria: tuberculosis, salmonella, leprosy, listeria Histamine-dilation-widen/slows circulation; H1 - chemotaxis, prostaglandin,contraction/retraction at endoth. junc. occurs H2- secrete gastric acid; decreases chemotaxis, degranulation, lymphocytes, eosinophils. |
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Types of Cytokines (cellular product of inflammation) Interferons- Effects: Protects against viral infections Interleukins (IL) 30 identified Effects; chemotaxis, alter adhesion (cellular respiration), proliferation of leukocytes in bone marrow, enhance or suppress inflammation. |
Interferon: Macrophage secretes alpha/beta INF's to induce cells to produce antiviral proteins. IL 1- Prod. by macrophage. Action: Enhance innate/acquired immunity by activ. macrophages, lymphocytes, monocytes. synthesis of Acute phase reactants; Fever-causing cytokine. IL 6- PBM, lymphocytes, fibroblasts. Action: Induce liver cells (hepatocytes) for proteins needed in inflammation. IL 10- "down regulation" of inflammatory and acquired immune response. Suppress growth of lymphocytes, pro-inflammatory cytokines. |
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Tumor Necrosis Factor ( cellular product of Inflammation) Secreted by Mast Cells and Macrophages |
Induce pro-inflammatory effects: fever, increased serum proteins by liver, cachexia - muscle wasting, thrombosis (blood clot). High levels result in Fatalities from Shock; caused by gram (-) bacterial infections. |
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Diapedisis |
emigration of the cells through the inter-endothelial junctions that have loosened in response to inflammatory mediators; to tissues. Once wbc inside tissues they undergo chemotaxis...... |
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Chemotaxis |
Directed migration whereas there is attraction to the inflammatory site by chemotatic factors Primary chemotatic factors: Neutrophils prod by mast cells, Complement fragments- C3a and C5a, clotting , kinin system and bacterial products. |
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Endocytosis |
process of engulfment of a living cell to produce a vacuole-(protects self from microorganisms and own enzymes). A step involved in phagocytosis. |
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Acute-Phase reactants ( synthesized by IL -1) Pro-inflammatory or Anti-inflammatory |
The synthesis of plasma proteins by liver during inflammation. Reach max circulating levels in 10 to 40 hours after the start of inflammation. |
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Lab test measures Acute phase reactants |
Erythrocyte Sedimentation Rate measures rate of RBC sediment in a tube (1 hour). Increased RBC sedimentation indicates an acute inflammatory response. |
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Stages of Wound Healing |
Stage I- Acute inflammation- lasts 1-2 days. Platelets form clot, neutrophils clear debri, macrophage phagocytize, rel. mediators, and growth factors. Stage II-Proliferation and new tissue formation- begins 3-4 days after the injury continues as long as 2 weeks. Wound sealed, Fibrin clot replaced by normal tissue or scar. TGF-Forms collagen; Angiogen Factors-forms decrease pH; MMP'S-degrade, remodel EC matrix. Stage III- Remodeling and maturation-several weeks after injury completes within 2 years. Fibroblasts (secrete collagen)- major cell of tissue remodel. Tissue generation, and wound contraction continue. Scars become avascular (lack of blood vessels), capillaries disappear, gains 2/3 strength back within 2-3 weeks. |
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Collagen |
Most abundant protein in the body with high concentration of proteins. |
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1. Absence of Iron, ascorbic acid (vitamin C), Oxygen results in. 2. Wound contraction is necessary for... 3. Myofibroblasts |
1. Impaired wound healing. 2. Closure of all wounds including those that heal by secondary intention. 3. Responsible for wound contraction |
