lecture 5.docx

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Department
Biochem. and Medical Genetics
Course
BGEN 3020
Professor
Jason Leboe- Mcgowan
Semester
Fall

Description
Lecture 5 Adaptations to environmental stress: Growth alterations Atrophy: Diagnosis: the decrease in tissue mass and the cell decreases in size. The cell has just enough organelles to survive, ie less mitochondria then normal cells, therefore, just trying to ‘eek’ it out until whatever it needs to stimulate can come back. 1. Example: hydronephrosis, the compression atrophy is causing thinning of cortex and medulla, MCC hydronephrosis is stone in the ureter (the pelvis is dilated). Question can be asked what kind of growth alteration can occur here. Answer is atrophy b/c of the increased pressure on the cortex and the medulla and produces to ischemia, blood flow decreases and can produce atrophy of renal tubules. 2. Example: Atrophied brain due to atherosclerosis (MC) or degeneration of neurons (alzheimers, related to beta amyloid protein, which is toxic to neurons). 3. Example: In muscle, many causes of atrophy – ie Lou Gehrig’s Dz (amylateral sclerosis) knock off neurons to the muscle, so it is not stimulated, leading to atrophy. 4. Example: Endocrine related: a) Hypopituitarism will lead to atrophy of adrenal cortex: the zona fasiculata and retiucularis layers of the adrenal cortex; NOT the glomerulosa b/c ACTH has nothing to with stimulating aldosterone release. The fasiculata is where glucocorticoids (cortisol) are made, while reticularis is where sex hormones are made (17 ketosteroids and testosterone). ACTH is responsible for stimulating these, therefore zona fasiculata and zona reticularis are atrophied. b) Taking thyroid hormone will lead to atrophy of thyroid gland. This is due to a decrease of TSH and therefore nothing is stimulating the thyroid gland which leads to atrophy. 5. Example: Slide showing a biopsy of a pancreas in a patient with cystic fibrosis. What is growth alteration? Atrophy, b/c the CFTR regulator on c’some 7 is defective and has problems with secretions. The secretions become thicker and as a result, it blocks the ducts and so that means that the glands that were making the fluids (the exocrine part of the gland) cannot make fluids b/c of the back pressure blocking the lumen of the duct, which leads to atrophy of the glands, which then leads to malabsorption in all children with cystic fibrosis. 6. Example: Slide of an aorta, with atherosclerotic plaque, which leads to atrophy of the kidney and secondary HTN (renovasuclar HP, leading to high renin level coming out of the kidney). In the other kidney, it is overworked, therefore there is hypertrophy (renin level coming out of this vein is decreased and suppressed). Hypertrophy increase of the SIZE of cell, not number Scenario: A cell biology question: what is the N of this? Hypertrophy of a cardiac muscle (permanent muscle), suppose there is a block just before the G2 phase. What is the number of chromosomes? Answer: # of c’somes is 4N, b/c it already underwent synthesis: already doubled. 1 N = sperm (23 c’somes) 2 N = normal (diploid cell) 3 N = trisomy 4 N = double the number Hyperplasia – increase in the # of cells In normal proliferative gland, there are thousands of mitoses, therefore see more glands with hyperplasia. 1. Example leading to cancer: With unopposed estrogen, you may end up with cancer, b/c if you didn’t have progesterone (undoes what estrogen did-counteracts the estrogen), you will get cancer. The cells will go from hyperplasia, to atypical hyperplasia to endometrial cancer. Therefore hyperplasia left unchecked there is an increased risk of cancer. One exception: benign prostatic hyperplasia; hyperplasia of the prostate does NOT lead to cancer; just urinary incontinence. 2. Example: gravid uterus (woman’s uterus after delivery). This is an example of 50:50: 50% hypertrophy of the smooth muscle cells in the wall of the uterus, and 50% related to hyperplasia. 3. Example: Bone marrow: normally should have 3X as many WBC’s as RBC’s. Slide shows few WBC’s, and increased RBC’s. Therefore, have RBC hyperplasia. This is not expected to be seen in Iron def anemia nor in thalassemias b/c in those, there a defect in Hb production. It is expected to be seen in chronic obstructive pulmonary dz (COPD) b/c the hypoxemia causes the release of hormone EPO (erythropoietin); which is made in the endothelial cells of the peritubular capillaries. So in the slide this is an example of EPO stimulated marrow. 4. Example: psoriasis on elbow –an exampl
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