Term
| What are the main functions of the kidney (3)? |
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Definition
| excrete metabolic waste, sythesis and release of renin and erythropoeitin, and regulation of extracellular fluid volume, electrolyte composition, and acid-base balance |
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Term
| What are the 3 parts of the nephron? |
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Definition
| vascular element, glomerulus, and tubular element |
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Term
| What are the vascular elements in the nephron? |
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Definition
| afferent arterioles (blood enters), efferent arterioles (blood leaves), vasa recta parallels the Loop of Henle |
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Term
| What is the glomerulus? What happens here? What can get through and what can't? |
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Definition
| a specialized capillary bed * fluid filtration * insulin and small molecules can get through but large moleculas like albumin can't |
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Term
| How much water is reabsorbed in the proximal tubules? The loop of Henle? |
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Definition
| 60-80% * in the loop of Henle 25% of filtered Na and K and 30% of filtered water are reabsorbed |
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Term
| What is the function of the distal tubule? |
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Definition
| has a regulatory mechanism that decreases GFR and prevents massive losses of fluid as a result of tubular reabsorption - the late distal tubule and collecting dut fine tune urinary volume and composition |
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Term
| What are the characteristics of acute renal failure? |
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Definition
| abrupt decline in GFR, which results in the buildup of nitrogenous wastes in the blood * adhesion of cells to the basement membrane in the tubular cells is disrupted which destroys tubular integrity |
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Term
| What are 2 major cellular adaptation mechanisms? |
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Definition
| metallothionine induction and stress protein induction |
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Term
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Definition
| a metal binding protein that binds metal and takes it into the cell in the kidney and liver - can be protective and damaging |
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Term
| What are stress proteins involved in? |
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Definition
| the maintenance of normal protein structure and the degradation of damaged proteins - they facilitate recovery and repair |
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Term
| When do you get a progressive deterioration of renal function? |
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Definition
| with long term exposure to chemicals - long term exposures overwhelm adaptive processes |
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Term
| Why is the kidney particularly susceptible to damage? |
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Definition
| it receives about 25% of the cardiac output so any drug in systemic circulation reaches the kidney in high amounts |
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Term
| Why do toxicants get concentrated in the kidney? |
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Definition
| the same process that forms concentrated urine also concentrates toxicants in tubular fluid - b/c of this, what is non-toxic in the plasma may be toxic in the kidney |
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Term
| What is the kidney particularly sensitive to? |
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Definition
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Term
| Where is the initial site of chemical exposure? What does this mean? |
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Definition
| the glomerulus * this means that nephrotoxicants can alter glomerular permeability to proteins |
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Term
| Other than nephrotoxicants, what else can cause glomerular damage? |
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Definition
| circulating immune complexes |
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Term
| What is the most common site of toxicant injury? Why? |
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Definition
| proximal tubules * cytochrome p450 is almost exclusively located here in the kidney, so if it bioactivates something that can contribute to lesions here |
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Term
| What happens if functional abnormalities occur at the loop of Henle,distal tubules, or collecting ducts? |
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Definition
| the ability to concentrate urine is impaired |
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Term
| What are 3 types of nephrotoxicity associated with NSAIDs? |
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Definition
| acute renal failure with a large dose (decreased GFR) - reversible after drug withdrawal * chronic consumption can lead to irreversible papillary necrosis * interstitial nephritis - slowly reversible |
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Term
| Why are metals toxic to the kidney? |
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Definition
| they can bind to sulfhydryl groups in critical proteins |
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Term
| What specifically does mercury do to the kidney? |
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Definition
| proximal tubule necrosis and acute renal failure 24-48 hours after exposure |
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Term
| What is the half life of Cd? How much can be found in the kidney? |
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Definition
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Term
| How is choloroform nehprotoxic? What does it target? |
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Definition
| the proximal tubules - p450 there converts it into trichloromethanol-->phosgene, which reacts with cellular macromolecules |
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Term
| How is choloroform nehprotoxic? What does it target? |
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Definition
| the proximal tubules - p450 there converts it into trichloromethanol-->phosgene, which reacts with cellular macromolecules |
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Term
| How are mycotoxins nephrotoxic? |
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Definition
| interfere with sphingolipid metabolism - increases urine volume, osmolality, and the MW of proteins that can get into the urine |
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Term
| What does acetaminophen do to the kidneys? |
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Definition
| proximal tubule necrosis, decreases GFR, increases excretion of water, Na, K, increases in urinary glucose |
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Term
| What are the main mechanisms of kidney toxicity? |
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Definition
| necrosis, dysfunction of cytoskeletal units (interferes with cell membranes), mitochondrial damage (no energy), and Ca depletion (essential for proper membrane fnc and cytoskeletal function) |
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Term
| Describe the renin-angiotensin-aldosterone pathway. What blocks this? |
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Definition
| Juxtaglomerular cells sense that BP is too low, rennin is released, acts on angiotensinogen – makes angiotensin I, where in the lung it gets converted to angiotensin II – stim aldosterone – increases blood volume, increases blood pressure |
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