...BIO483 Exam #4 Review Comprehensive and/or early Weeks Know all conditions that cause splenomegaly All associated diseases with EBV Week 1 Mechanisms of Cellular Adaptation Types of necrosis and pathology where most likely found. Apply the definitions of Atrophy, hypertrophy, hyperplasia, hypoplasia, dysplasia, and metaplasia. Week 2 Pain Throughout Organ Systems General anatomy of kidneys, appendix, gallbladder, pancreas, spleen, male and female reproductive organs. Costochondritis vs Angina Pectoris vs Myocardial Infarctions. Rheumatoid arthritis Gout lab findings Week 3 Fluid Balance and Edema Electrolyte imbalances of sodium, potassium, calcium, and magnesium. Intra and Extra cellular concentrations of sodium and potassium as related to osmotic balance. Know the physical signs/symptoms of electrolyte imbalances including hyper and hypo natremia, kalemia, and calcemia. SIADH lab and imaging findings Diabetes insipidus lab and imaging findings Week 4 Topic 4 Acidosis and Alkalosis Know your acid-bases! Week 5 Topic 5 Cardiovascular Causes of Fatigue Cor-pulmonale, cardiomyopathies Week 6 Topic 6 Thyroid, Adrenal, Liver Fatigue Hashimoto’s thyroiditis vs. DeQuervain vs. nodular goiter vs. secondary hypothyroidism Cirrhosis, Addison disease lab tests and hormone responsible. Is it high or low? Week 7 Topic 7 Bleeding as Indicator of Disease Pathophysiology of Disseminated Intravascular Coagulation Pathophysiology of Hemophilia Ulcers ...
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...and encodes for a special chloride ion channel.4,5 The vast majority of mutations involve three or fewer nucleotides and result in primarily amino acid substitutions, frameshifts, splice site, or nonsense mutations.11 Of more than 800 identified CFTR mutations, the 3 base pair deletion of phenylalanine at position 508 is found worldwide in 70% of cystic fibrosis sufferers, therefore making F508 CFTR the most common deadly mutant in the Caucasian populations.6 Since cystic fibrosis has a genetic origin the opportunity to treat by replacing the defective gene with a normal healthy gene (gene therapy) offers a ‘novel therapeutic approach’ for sufferers.7 The estimated survival age of cystic fibrosis sufferers is 33.4 years (Fig 1). In this essay we will discuss the aetiology and symptoms of cystic fibrosis and the current available treatments, with particular emphasis on gene therapy and furanones, which prevent the build up of bacterial biofilms and thus reduce lung infection. Mutations in the CF gene can disrupt CFTR function within epithelial cells in different ways, ranging from complete loss of protein to surface expression with poor chloride conductance.12 The five major mechanisms by which CFTR function is altered are summarized in Figure 2. Class one mutations produce premature transcription termination signals resulting in unstable, truncated, or no protein expression. Class two mutations, including F508, cause the protein to fold incorrectly leading to premature...
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