| Term | Definition |
|---|
| Resistance | ability to ward off disease |
| Susceptibility | lack of resistance |
| Innate Resistance | certain things you can't get, because you are human |
| Nonspecific | protection from any invader |
| Specific | protection from particular invader |
| Hosts Mechanical 1st line of defense | intact skin, mucus membranes, lacrimal apparatus, saliva, ciliary escalator, nasal hairs, urine and vaginal discharge, ear wax |
| Intact Skin | dermis, epidermis |
| Dermis | connective tissue/ thick/ collage/ elastin |
| Epidermis | layers of epithelial cells/ keratin/ tightly packed |
| Opportunistic Invaders | typical only when epidermis is damaged (subcutaneous) - staphylococcus sp. |
| Mucus Membranes | line GI tract, urogenital tract, respiratory tract, epithelial layer - secretes mucus, connective tissue below |
| Lacriaml Apparatus | makes and drain tears in eyes, lacrimal glands (upper and outer eye) dilution |
| Saliva | decrease number of invaders by dilution wash from mouth |
| Ciliary Escalator | lower respiratory tract, move mucus and invader up and out (1-3 cm/hr) |
| Nasal Hairs | vibriassiae, mucus coatin, traps airbourne invaders |
| Chemical Factors | sebum, perspiration, gastric juice |
| Sebum | oil produced by sebaceous glands of skin protective film on skin (unsaturated fatty acids) that do not allow growth of many pathogenic invaders, pH 3-5, some bacteria eat sebum and produce products that cause inflammation of acne |
| Sweat | sweat glands can wash invaders from skin, contains lysozyme (G+ peptidoglycan destruction), also in tears, saliva, nasal mucus, tissue fluids |
| Stomach Juice | HCl, enzymes and mucus, pH 1.2-3, kills most invaders and toxins, clostridium botulinum/ staphylococcus surive, pathogens can survive sithin food particles, helicobacter pylori neutralizes stomach acid cause of ulcers |
| Host's 2nd line of defenses | phagocytosis, Inflammation, Fever, Antimicrobial substances |
| Phagocytosis | WBC/leukocytes, infection->leukocytosis up eg. meningitis, mono, infection->leukopenia down eg. salmonellos, brucellosis, both above conditions detected by differential WBC count % of each type of WBC per 100 WBC |
| Granulocytes | neutrophils, basophils, eosinophils |
| Neutrophils | (stain red/blue with acid and base dyes), 2-5 nuclei lobes, highly phagocytic 60-70%, motile, initial infection, can leave blood system into tissues |
| Basophils | (stain blue with base dye methylene blue), release histamine (inflammation allergic response), .5-1%, release heparin (anticoagulant) |
| Eosinophils | (stain red with acid dye eosin), slightly phagocytic and can leave blood, release helminth toxins (peroxide ions) 2-4% |
| Monocytes/ Agranulocytes | grow into macrophages, when maturing during infection slightly responsible for swollen lymph nodes, 3-8% |
| Lymphocytes | not phagocytic, part of specific defenses, (B&T lymphocytes), 20-25%, Tonsils, lymph noes, spleen, etc, circulate in blood |
| Infection -> | neutrophils and monocytes migrate to the area -> monocytes mature into macrophages/ mostly neutrophils-> infection drops and mostly macrophages "wondering macrophages" |
| "Fixed Macrophages" | kupffer cells (liver) alveolar macrophages (lungs) microglial cells (brain) |
| Steps of Phagocytosis | 1. chemotaxis and adherence of invader to phagocyte (neutrophils and macrophages) - capsules/M.protein 2. Ingestion of invader by phagocyte 3. form phagosome/ vescicle 4. fusion of phagosome with a lysosome 5. digestion of ingested invader 10-30 min 6. form residual body with indigestable stuff 7. discharge waste |
| Inflammation | redness, pain, heat, swelling and loss of function |
| Inflammation Function | destroy invader, limit effects by walling off invader and by products, repair/ replace damaged tissues |
| Inflammation Process | damage to tissue |
| Damage to Tissue | cell release histamine, kinins, prostaglandins, and leukotrienes, vasodilation and increase in permeability of blood vessels, increases blood flow into area (redness/heat), blood clot walls microorganisms from spreading, after an hour phagocytes appear and stick to inner lining of blood vessels, phagocytes move into damaged area with pseudopods, phagocytosis, pus forms |
| Inflammation | damage to the body's tissues triggers a local defensive response |
| Complement | Proteins that can lyse invading cells 20 different protein found in serum C3 |
| Vasodilation | permeability allows leukocytes to enter area, platlets can enter damgaged area to encourage clots |
| Blood clot walls microorganisms from spreading | absess forms (pus collections caused by breakdown of body tissues) |
| Margination | after an hour, phagocytes appear (neutrophils and monocytes) and stick to inner lining of blood vessels |
| Phagocytes move into damaged area with speudopods | diapedesis |
| Phagocytosis | neutrophils arrive 1st but dies quickly macrophages take over |
| Pus Forms | dead cells and body fluids |
| Fever | temp. contorl in hypothalamus, G- bacteria |
| Fever Starts | blood vessel constrictriction, increase metabolism rate and shivering (skin is still cold.... chill) when body reaches new temp. chill disappears, stay high until Interleukin 1 is eliminated |
| Endivasodilation and sweating | initial fever intensifies effect of interferon (binds iron needed by invaders) and helps injured tissues to repair themselves |
| Antimicrobial Substances | Complement, Interferons |
| C3 | detect foreing antigen, breaks in 2 pieces, 1/2 in inflammation, 1/2 opsonization, increases infinity of phagocytosis, end up with cytolusis, cell memebrane, osmosis |
| Interferons | antiviral protein that interfere with viral multiplication, host- all specific, human interferon will only help human cells, alpha, beta, gamma, made by lympocytes and other leukocytes infected host cells can make interferon to neighboring cells to uninfected cells produce antiviral proteins to prevent viral multiplication if the are infected, only effective for short time, acute, short term infections, no effect on infected cells |
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