NR507 Pathophysiology midterm study guide

Pathophysiology classmates, lets all contribute to filling out the midterm study guide as a team! This not only helps us to fill out the whole study guide quickly but it also is a great way to see important information that maybe you didn’t understand or missed in your own reading!! Also please put page numbers if the information is from the textbook =) Chapters Chapter 1: Cellular Biology Chapter 2: Altered Cellular and Tissue Biology Chapter 6: Epigenetics and Disease Chapter 7: Innate Immunity: Inflammation Chapter 8: Adaptive Immunity Chapter 9: Alterations in Immunity and Inflammation Chapter 10: Infection Chapter 12: Cancer Biology Chapter 13: Cancer Epidemiology Chapter 14: Cancer in Children Chapter 30: Alterations in Hematologic Function in Children Chapter 34: Structure and Function of the Pulmonary System Chapter 35: Alterations in Pulmonary Functions Chapter 36: Alterations in Pulmonary Function in Children Chapter 37: Structure and Function of the Renal and Urologic Systems Chapter 38: Alterations of Renal and Urinary Tract Function Chapter 39: Alterations of Renal and Urinary Tract Function in Children Epigenetics (Note, Chapter 6 should be reviewed) Epigenetics and its role on human development Compare and contrast Prader-Willi syndrome and Angelman syndrome Cellular Proliferation the role of inactive MLH1 in the development of some forms of inherited colon cancer (p. 1468-1470) p.186 Inflammation403) MLH1 is a deoxyribonucleic acid (DNA) mismatch repair gene, essentially a tumor suppressor gene in this case. If MLH1 is inactive, repair is unable to be made to the DNA mismatches and the hereditary factor of colon cancer (see below) is able to proliferate. Progression from polyps to colon cancer (1) activation of proto-oncogenes (promote cell growth) (2) loss of tumor-suppressor gene activity (inhibit cell growth]); and (3) abnormalities in DNA mismatch repair (MMR) genes (fix errors in DNA replication and recombination Microsatellite instability = genetic hypermutability (predisposition to mutation) that results from DNA MMR. Usually right sided colon proximal to splenic flexure, associated with autosomal dominant hereditary polyposis colorectal cancer. as an etiology for cancer-note conditions in which this may occur (p. Chronic inflammation caused by infiltrating immune cells help to create a permissive tumor progressing environment. Also thought to precede and initiate malignant change in many cancers (colon, liver, lung) Numerous environmentally-linked reasons for inflammation (tobacco smoke, exhaust, asbestos, fine particles in air) and can be linked to many cancers (lung) Chronic inflammation and cancer development = continuous presence of cytokines (soluble factor that affects neighboring cell, can be pro- or anti- inflammatory, interleukins or interferons)(p203-205), chemokines (low- molecular weight peptide that induce leukocyte chemotaxis or directional movement of cells on a chemical gradient)(p203-205), reactive oxygen species (free radical that damages cell membrane)(p59-60), oncogenes (mutant genes that in their normal nonmutant state direct synthesis of protein that positively regulate or accelerate proliferation), amongst others