BGEN 3020 Lecture Notes - Lecture 6: Ascending Limb Of Loop Of Henle, Ejection Fraction, Neuroma

• School: University of Manitoba
• Department: Biochem. and Medical Genetics
• Course: BGEN 3020
• Professor: Jason Leboe- Mcgowan

Document Summary

Acute inflammation: igm = main ig first, and then igg. Igm = main ig; need a lot of complement components in healing process; igm is the most potent activator, and have activation of complement pathway (all the way for 1-9); igm has. Igg can activate the classical system, but does not go passed c3 and stops and does not go onto c5-9. Difference in cell types: acute inflammtions = neutrophil, acute allergic reactions= eosinophils (mast cells are in tissues, viral infections = lymphocytes are the main inflammatory cells, chronic inflammations = monocytes/macrophages are imp. Another example: granuloma = chronic inflammation (never acute); ie caseious necrosis in someone with tb; roundish, pink, multinucleated giant cells = granulomas; pathogenesis = type. The main actors are cytoxic t cells; when they kill neoplastic, virally infected cells, these are also type iv hpy (no ab"s involved).