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8 Cards in this Set
- Front
- Back
GI Defense |
Flow of liquid, lysozyme, normal flora- oral cavity Peristalsis and flow- esophagus Low pH- Stomach persistalsis, peyer patches, IgA, mucus- SI normal flora, shedding of epi- Colon |
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Specific Defenses |
Antibodies M Cells- Sample and present to peyers patches Commensural Bacteria- compete for nutrients Glycocalyx- in mucin traps bacteria into binding and then excretes in the feces |
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Infectious Onest |
Anatomic Alterations- blind loops lead to lack of flow and foothold establishment Stomach Acid- use of antacids can increase pH and allow bacterial growth Normal Flora Change- broad antibiotics can wipe commensurate flora out allowing other more harmful bacteria in Specific Agents- can be especially virulent and attack the patient |
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Damage |
Enterotoxins- alter normal function and provoke diarrhea and systemic response Local Inflammation- inflitration of the area by bacteria Deep Tissue Invasion- leads to bacteremia Perforation- rupture of lining and peritonitis |
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Mouth Infections |
Often introduced via Fecal-Oral Route Nonpathogenic Flora- combat the ability of new more harmful pathogens Mechanical actions of Tongue and Saliva Antimicrobial Parts of Saliva- Lysozyme and IgA selectively combat recognized antigens. |
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Candidiasis |
Candida Albicans- yeast found in the environment forms pseudo membranes within the oral cavity that can be easily peeled off. Typically in immunocompromised and young children. Treat with Anti-fungal agens like nystatin |
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Stomach Infections |
Typically acid-resistant Gram + organisms: Lactobacillus, Peptostreptococci, Staph, and Strep H. Pylori- assctd. with gastritis and peptic ulcers- produces urease which increases surrounding pH by turning acid into ammonia. Also has flagella |
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H. Pylori |
Gram - helical shaped Infects 1/2 global population, thrives in acid via urease neutralization. Colonizes mucus layer and epithelial surface via VacA toxin (stops T cell) Causes a persistant chronic gastritis---> PUD, cancer, and MALT |