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29 Cards in this Set
- Front
- Back
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What is the ion that is not at least 99% reabsorbed?
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K+
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How does GFR change renal sodium excretion?
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Increased GFR -> increased sodium excretion
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How does Mineralcorticoids change renal sodium excretion?
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Increased aldosteron -> increased Na+ reabsorption -> decreased Na+ excretion.
However, ALDOSTERONE ESCAPE OCCURS to re-increase aldosterone concentrations |
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How does Intrarenal physical forces change renal sodium excretion?
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Increased saline loading -> buildup of interstitial fluid in PCT due to Starling forces -> forces open tight junctions -> increased Na+ excretion.
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How does ANP, BNP, urodilatin, guanylin, uroguanylin, prostaglandins, and bradykinin change renal sodium excretion?
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All increase Na+ excretion.
ANP -> released in heart atria BNp -> brain Urodilatin -> renal nattriuretic hormone Guanylin, uroguanylin -> produced by small intestine Prostaglandins, bradykinin inhibits sodium reabsorption. |
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How does renal sympathetic nerves change renal sodium excretion?
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Decreased Na+ excretion, due to reduced GFR, NE effect on tubules, and renin release.
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How does changes in intrarenal distribution of blood flow change renal sodium excretion?
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Disputed.
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How does estrogens change renal sodium excretion?
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Increased Na+ reabsorption in tubues -> decreased Na+ excretion
Think swelling |
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How does osmotic diuretics change renal sodium excretion?
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Increased Na+ and H2O excretion.
20% Mannitol forces more higher Na+ to be reabsorbed in the proximal tubule, such that the tubule Na+ concentration falls along the length of the PCT. Na+ diffuses back into the PCT, such that less sodium is reabsorbed. More sodium and water enters the loop of Henle, to overwhelm the distal nephron and lead to increased sodium and water excretion. |
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How does poorly reabsorbable anions change renal sodium excretion?
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Increased reabsorbed anions -> increased Na+ in urine for electroneutrality
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How does diuretic drugs change renal sodium excretion?
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They directly inhibit Na+ reabsorption -> thus as a result lead to less water reabsorption and more water excretion.
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How can you control ECF in your body?
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Control dietary Na+ intake
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How does the regulation of ECF, with regards to Na+ excretion, occur?
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Increased ECF -> increased sensors (cardiovascular stretch receptors, kidneys) -> increased effectors in kidneys (GFR, aldosterone, Intrarenal physical forces, natriuretic horones and factors, sympathetic nerve activity -> increased Na+ excretion -> decreased extracelluar fluid volume
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What is the main extracellular ion? What is the main intracellular ion?
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Main EC ion -> K+.
Main IC ion -> Na+. |
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What does hypernatremia lead to? What does hyponatremia lead to?
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Hyponatremia -> decreased plasma volume, circulaory collapse, death.
Hypernatremia -> |
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What does hyperkatremia lead to? What does hypokatremia lead to?
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Hyperkatremia -> Cardiac arrhythmias.
Hypokatremia -> Muscle Weakness |
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What are the 6 factors that lead to hyperkatremia, in terms o Na/K-ATPase, acid-base, insulin, epinephrine, osmolality, cells?
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Digitalis overdose, or inadequate oxygen supply
Low pH: decrease in pH by 0.1 increases K+ by 0.6mEq/L Insulin: favors uptake of K+ in liver and muscle Epinephrine: cell uptake of K+ Hyperosmolality - raises plasma K+ by pullling out water Cell breakdown - tissue trauma -> raisesplasma K+ |
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What is the major site of K+ excretion in the nephron?
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Cortical Collecting Duct
Due to -50 - 0 - -70mV mechanism Too little excretion - Addison's disease, acute renal failure, chronic renal failure when GFR is <20mL/mn Too much excretion - hyperaldosteronism, most diuretic drugs |
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How does potassium excretion change with potassium intake?
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Increase K+ intake -> increase K+ in plasma -> increase aldosterone -> increase K+ secretion
Increased K+ in plasma also increases uptake of K+ by principal cells. |
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How does potassium excretion change with aldosterone?
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Increase.
Aldosterone increases number and activity of ENAC, Na+/K+ ATPase, permeability of cell membrane to K+ |
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How does potassium excretion change with alkalosis? How about acute or chronic acidosis?
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Increased K+ secretions, due to H+ moving out of cells in exchange for K+.
Acute acidosis -> hyperkatremia and decreased renal potassium excretion Chronic acidosis -> increased K+ excretion (think of it in terms of diabetes mellitus) |
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How does potassium excretion change with increased excretion of poorly reabsorbed anions?
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increased anions -> increased excretion, to maintain electroneutrality
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How does potassium excretion change with sodium deprivation (2 reasons)? How about increased sodium excretion in the PCT?
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Increased sodium deprivation -> increases aldosterone secretion -> increased K+ secretion.
HOWEVER, Decreased Na+ -> Decreased GFR and proximal Na+ reabsorption -> decreased fluid delivery to cortical collecting ducts -> decreased K+ secretion. However, if you increase Na+ excretion, you increase K+ excretion 1) Increased Na+ excretion -> increase fluid flow (due to less water reabsorption) -> maintains gradient for passive diffusion of K+ into cortical collecting duct. 2) Na+ reabsorption dpolarizes the membrane to favor K+ secretion Therefore, diuretic drugs -> increased Na+ excretion -> inreased K+ excretion |
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Where is the majority of phosphate reabsorbed in kidneys?
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Majority is reabsorbed in PCT
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How does Tm of phosphate reabsorption compare to phosphate load? What does PTH do to Tm?
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Phosphate load is usually higher than Tm.
PTH decreases the Tm of phosphate, by endocytosis of sodium-phosphate transporter With chronic renal failure -> loss of phosphate excretion -> hyperphosphatemia. |
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What does hyperphosphatemia lead to?
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Bone disease, due to inhibited 1-alpha hydroxylase activity -> decreased Vitamin D3 -> decrease Ca2+ -> increase PTH -> bone resorpion
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Where is Calcium reabsorbed?
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majority is in PCT (60%) with half in the DCT (30%)
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What does PTH do to Calcium reabsorption
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Increases calcium reabsorptino by the THICK ASCENDING LIMB, DISTAL CONVOLUTED TUBUE, and CONNECTING TUBULE
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Where is the major site of Mg reabsorption?
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Loop of Henle
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