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29 Cards in this Set
- Front
- Back
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What are the functions of the Proximal Tubule?
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Reabsorption of Na (Na+/K+ pump, co and counter transport) - 65 %
Reabsorption of numerous solutes (coupled to Na reabsorption): -Glucose = 100 % -AA = 100 % -HCO3 = 90 % -Cl = 50 % -K = 65 % -Phosphate, lactate, citrate, urea Iso-osmotic water reabsorption - 65 %: -reabsorption of osmotically active Na+ produces small osmotic gradient -water decreases volume of tubular fluid without changes in osmolarity Secretion: -Na+ - H countertransport provides bicarbonate reabsorption -organic acids and bases (urea, ammonia, creatine) |
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What is the Glomerular-Tubular Balance?
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the intrinsic ability of the tubules to change their reabsorption rate in response to changes in tubular load (GFR):
-constant fractional reabsorption of the filtered load (load increases, there is more reabsorption) importance: -prevention of overloading of distal tubular segments when GFR increases |
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What are properties of the Thin Descending/Ascending limb?
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Thin Descending Limb:
Impermeable to salts --> lack of solute reabsorption Permeable to water --> water reabsorption ( 15 % ) net result: -decrease in tubular fluid volume -hyperosmotic fluid Thin Ascending limb: -permeable to NaCl -impermeable to water Net result: -NO change in tubular volume -lowers fluid osmolarity but still remains hyperosmotic Thin Ascending Limb: - |
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What are properties of the Thick Ascending limb?
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Na+, K+, and Cl- are reabsorbed via Na/K/Cl tri-transporter located in apical membrane
reabsorption of Na by Na+ - H+ exchanger (secretion of H+) impermeable to water net result: -dilution of tubular fluid --> hypo-osmotic fluid (150 mosm/L) Loop diuretics: -attach to the Cl binding sites and stops reabsorption of Na+, Cl-, and K+ --> INCREASES solutes excretion |
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What are properties of the Early Distal Tubule?
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Reabsorption NaCl by Na/Cl cotransporter
minimal permeability to water reabsorption of Ca++ via tubular Ca++ channels Net result: -hypotonic tubular fluid Thiazide diuretics: -inhibit Na/Cl co-transporter |
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What do Principal cells do?
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Na reabsorption occurs primarily by epithelial Na channels, Cl- reabsorption via paracellular diffusion
Aldosterone: increase sodium reabsorption by increasing number of opened Na channels and activity of Na/K ATPase Secretion of K+ via K+ channels in apical membrane (by aldosterone) Minimal permeability to water (increased by ADH) K+ sparing diuretics: -prevent aldosterone induced Na+ reabsorption by blocking Na+ channels -inhibition of K+ secretion |
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What are Intercalated cells?
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Type A cells (also called alpha):
-outnumber B cells -Secretion of H+ via H+-K+ ATPase -Reabsorption of HCO3 Type B cells (also called beta): -secretion of bicarbonate in exchange for Cl- |
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What are properties of the Medullary Collecting Duct?
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permeability to water is controlled by ADH
reabsorption of Urea secretion of H+ |
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What are some factors increasing/decreasing Na Reabsorption?
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Increasing:
Aldosterone: -increase Na reabsorption in late distal tubule and collecting duct of cortical and medullary nephrons AT II: -Indirect: increase aldosterone secretion -direct: increase sodium reabsorption via Na-H exchanger in proximal tubule Sympathetic Activity: -indirect: lowers RPF and GFR, stimulates renin release -direct: stimulates proximal tubule reabsorption, stimulation of Na/H+ exchanger and Na-K ATPase ADH: -direct (weak): stimulation of Na/K/Cl tritransporter in Henle's loop, opening of Na channels in apical membrane of principal cells Decrease: Atrial and Brain Natriuretic Peptides (ANP, BNP): -decrease sodium reabsorption by collecting ducts -vasodilation of afferent arteriole and constriction of efferent --> increase GFR Prostaglandins: -vasodilatory effect on renal arterioles --> increase RPF and GFR -possible direct effect on renal epithelial cells |
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How is Potassium processed in the Tubules?
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Proximal tubule:
-iso-osmotic reabsorption of 2/3 of filtered K -passive diffusion driven by luminal electrical potential (caused by Cl) -paracellular solvent drag -MOST reabsorption occurs here Thick ascending limb: -Net reabsorption of constant K+ via Na-K-2Cl cotransporter (20-27 % of filtered K Distal Tubule and Collecting Duct: -net secretion of K (stimulated by aldosterone) in dietary K excess by principal cells (Luminal K channels AND basolateral Na-K ATPase) -net reabsorption in K+ deficiency by alpha intercalated cells (luminal H-K ATPase) |
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How is Potassium secretion regulated?
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depends on electrochemical gradient
2 types of determinant: luminal and cellular by Principal cells: Causes of Increase K+ secretion: -high K diet -Hyperaldosteronism -alkalosis -thiazide diuretics -loop diuretics -luminal anions Causes of Decreased K+ secretion: -low K+ diet -hypoaldosteronism -acidosis -K+ sparing diuretics |
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What are Aldosterone's effects on K and Na homeostasis?
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increase influx of Na via baso-lateral Na-K ATPase --> Increase Na reabsorption by the principal cells via luminal Na+ channels
increase influx of K+ into cells via baso-lateral Na-K ATPase transporter --> Increase K+ secretion by principal cells via luminal K+ channels |
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How is phosphate handled by the renal?
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reabsorption:
-Proximal convoluted tubule = 70 % -Proximal straight tubule = 15 % -Has Tm -Depends on PTH -Mechanism of reabosprtion = Na-Phosphate co-transport Excretion: -15 % of the filtered load -higher than that of other electrolytes -urinary phosphate serves as a buffer for H+ increase bone resorption (increase PTH) --> increase phosphate influx into ECF from bones inhibition of Na-Phosphate co-transport in proximal tubule (decreases Tm) --> higher proportion of phosphate lost in urine (phosphaturia) |
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How is calcium handled by the renal?
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free filtration of UNBOUND Ca++
Reabsorption: Proximal tubule - passive diffusion follows reabsorption of Na and water Thick ascending limb - passive diffusion through paracellular pathway driven by lumen positive potential generated by the Na-K-2Cl co-transport Late Distal tubule: -Ca reabsorption is NOT coupled with Na reabsorption -Ca reabsorption across luminal membrane via selective channels -cells have receptors that respond to extracellular Ca concentration, Vit D, and PTH -most important site for REGULATED reabsorption of Ca |
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How is Calcium Reabsorption regulated?
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PTH:
-increase calcium reabsorption in distal tubule -stimulates bone resorption -stimulates formation of Vit D3 Effects of Diuretics: -Loop diuretics inhibit Ca reabsorption in thick ascending tubule -Thiazide diuretics increase Ca reabsorption in distal tubule |
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How is Magnesium handled by the renal?
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Free filtration of UNBOUND Mg++
Reabsorption: Proximal tubule is much LESS permeable to Mg than other electrolytes - 30 % Thick ascending limb - 60 % -driving forces: lumen positive potential and high luminal Mg - passive diffusion -paracellular reabsorption collecting ducts - 5 % Excretion - 5 % of filtered load |
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How is Magnesium excretion regulated?
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mainly by regulation of tubular reabsorption
cause increase Mg excretion: -Increase ECF Mg -expansion of ECF volume -increase ECF Ca Loop diuretics will cause increase Mg excretion |
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What is the pathway for the response to water deprivation?
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1. increase in plasma osmolarity
2. Stimulates osmoreceptors in the hypothalamus 3. Increased ADH secretion from posterior pituitary 4. Increase H20 permeability in late distal tubule and collecting ducts 5. Increase water reabsorption 6. Increase urine osmolarity and decrease urine volume This restores the plasma osmolarity Hypothalamus can also stimulate increase in thirst leading to increase in water consumption |
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What is the Cortico-Papillary Osmotic Gradient?
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gradient from cortex (300 mOsm/L) to the papilla (1200 mOsm/L)
composed of NaCl and urea established by: -Countercurrent multiplication in loop of henle - deposition of NaCl in deep portions of renal medulla; countercurrent of ascending and descending tubules creates gradient -urea deposition: urea recycling in inner medullary collecting ducts maintained by: -countercurrent exchange in vasa recta |
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What are parts of the mechanism of the Countercurrent Multiplication mechanism?
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Proximal tubule - isoosmotic fluid
Thin descending limb: -reabsorption of water without solutes --> hyperosmotic (300 --> 1200-1400 mOsm/L) Ascending limb: -reabsorption of solutes without water (especially in thick ascending) --> dilution of fluid -development of a hyperosmotic gradient which drives water outside of descending limb -water is reabsorbed from the descending limb --> osmolarlity of the tubular fluid increases to level of adjacent ISF known as SINGLE EFFECT ADH: -increases single effect by increasing activity of Na-K-2Cl co-transporter |
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How does Urea play a role in the Cortico-Medullary Gradient?
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Cortical and outer medullary collecting ducts - concentration of urea:
-water reabsorption (stimulated by ADH) -Urea retention (ADH does NOT increase urea reabsorption) Inner Medullary Ducts - urea reabsorption: -high concentration gradient for urea -high permeability of the tubular wall for urea in the presence of ADH Urea recycling: -reabsorption from medullary collecting ducts --> peritubular interstitium --> loop of henle --> collecting ducts REABSORBED UREA INCREASES MEDULLARY OSMOLARITY |
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What does the Vasa Recta do?
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acts a countercurrent exchanger
"U" shape, slow blood flow, high permeability to water AND solutes Descending limb of vasa recta: -reabsorption of solute from hyperosmotic peritubular ISF -Osmosis of water into ISF -osmotic equilibrium between blood in vasa recta and ISF at bend of loop Ascending limb of vasa recta: -diffusion of solutes out of blood -osmosis of water into blood from ISF -dilution of blood Function of countercurrent exchanger: -maintenance of cortico-medullary osmotic gradient urea is maintained by vasa recta |
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What are the 3 effects of ADH on the nephron?
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-Increase Tm for Na+/K+/2Cl- transport in thick ascending limb
-increase urea permeability in inner medullary collecting duct -increase water permeability of principal cells in late distal tubule and collecting duct Insertion of vesicle-bound, preformed aquaporins into luminal membrane of principal cells |
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What happens in hyperosmotic urine?
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High ADH
Proximal tubule: -iso osmotic fluid reabsorption Thick ascending and early distal tubule: -impermeable to water but permeable to salt -dilution of fluid Late Distal Tuble and Collecting Duct: -Principal cells are permeable to water in presence of ADH -reabsorption of water down osmotic gradient --> concentration of tubular urine --> osmotic equilibrium between tubular fluid and high osmolarlity ISF --> Final urine osmolarity = osmolarity at the bend of the loop (1200) |
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What happens in hypoosmotic urine?
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Low ADH (increase water intake)
-smaller cortico-medullary osmotic gradient due to decreased countercurrent multiplication mechanism and urea recycling -decrease dilution of fluid in thick ascending segment due to inhibition of Na-K-2Cl cotransport in absence of ADH -late distal tubule and collecting ducts are impermeable to water --> lack of reabsorption of water --> lack of osmotic equilibrium between peritubular ISF and tubular fluid --> excretion of diluted urine |
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What is SIADH?
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SYndrome of Inappropriate ADH secretion
effects: -increase urine osmolarity, negative free water clearance -causes hyponatremia (suppression of aldosterone), edema |
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What are the two types of Diabetes Insipidus?
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Central:
-complete or partial failure of ADH secretion -results in polyuria, inability to produce concentrated urine, polydipsia Nephrogenic: -failure of renal response to ADH -defective receptors -Increase ADH plasma level |
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What is Inulin?
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synthetic polysaccharide
renal handling -free glomerular filtration -lack of tubular reabsorption -lack of tubular secretion -lack of renal metabolization flitration = excretion is a glomerular marker: clearance = GFR Creatine is the only substance that has a higher clearance |
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What is CH2O and iso, hyper, and hypo osmotic urine?
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CH2O = V (urine flow rate) - (UosmV)/Posm
Uosm = urine osmolarity Posm = plasma osmolarity isotonic: free water clearance = 0 hypertonic: CH20 = negative hypotonic: CH20 = positive |
