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PATH 2542 Lecture Notes - Midterm Exam Review 3

PATH 2542 Lecture Notes - Midterm Exam Review 3 - kidney...

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Unformatted text preview: kidney kidney functions: • excretion of waste products of metabolism • regulation of body concentration of water and salt • maintenance of appropriate acid balance of plasma 7.2-7.4 • secretion of some hormones: renin, erythropoietin-cause production of rbc’s, prostaglandins functional unit: nephron 4 compartments of kidney glomeruli(diseases mostly immunological mediated diseases) tubules( vulnerable to infection and toxins) interstitium(vulnerable to toxins and infection) renal blood vessels kidney areas cortex pyramids- collecting area papillae minor/major calus kidney pelvis capsule with nociceptors sensitive to distention structure of glomeruli afferent arteriole- blood in juxtaglomerular cells- control of BP in afferent arteriole endothelial cells-holes are psuedofenestrations glomerular basement membrane epithelial cells-cover basement membrane, aka podocytes , aka 3 rd layer filtration slit-between foot processes of podocytes, nephrin between as well- controls selection of things to be filtered, h2o usually very permeable, not permeable to proteins parietal cells- cover inner lining of glomeruli or bowman’s capsule mesangial cells- fill space between arterioles of glomeruli, help repair damaged tissue glomerulopathy- diseases of glomeruli glomerulonephritis (GMN)- inflammation of glomeruli of kidney pathological mechanisms: 1. C irculating immune complex deposition glomerulonephritis –(type III hypersensitivity) accumulating antigens in blood, leading to vasculitis 2. Anti-GBM glomerulonephritis- type II hypersensitivity in glomerulus against kidney tissue, in-situ Heymann glomerulonephritis- formation of antibodies against antigens of podocytes and antigens against which can be implanted there, in-situ, not a specific hypersensitivity Syndromes of GMN: NEPHRITIC SYNDROME Destruction of arteriole wall change in glomeruli, cannot filter blood effectively • not permeable to h20 oliguria azotemia • permeable to rbc’s into urine (hematuria) • biochemical abnormality: decreased filtration rate of blood high concentration of urea and creatinine in blood(azotemia) when at toxic levels is uremia and get symptom/signs • hypertension - low BP renin angiotensin II vasoconstriction increase resistance increase BP Diseases associated with nephritic syndrome: • Acute proliferative (poststreptococcal) glomerulonephritis- from B hemolytic streptococcus infection A, found in SLE, childhood disease-mild, in adults-severe, 15-50% don’t recover die in 15-20yrs, cured with corticosteriods • Rapidly progressive (crescent) glomerulonephritis – proliferation of parietal cells of glomerulus compression of glomerulus hyperplasia, associated with severe oliguria, attraction of monocytes, pyuria, death within weeks-months, biopsy kidney Types of rapidly progressive GMN: 1. I – Anti-GBM, type II hypersensitivity, idiopathic Goodpasture’s Syndrome- Ab’s against alveolar and glomerular...
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PATH 2542 Lecture Notes - Midterm Exam Review 3 - kidney...

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