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162 Cards in this Set
- Front
- Back
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what percent of body weight is TBW?
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60%
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how much of TBW is ICF?
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two thirds
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what are the major cations of ICF?
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K+ and Mg2+
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what are the major anions of ICF?
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protein and organic phosphates
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how much of TBW is ECF?
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one third
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what is the major cation of ECF?
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Na+
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what are the major anions of ECF?
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Cl- and HCO3-
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how much of ECF is plasma?
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plasma volume is one fourth of ECF volume
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how much of ECF is interstitial fluid?
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interstitial fluid is three-fourths of ECF volume
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what fraction of TBW is plasma?
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plasma is 1/12 of TBW
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what fraction of TBW is interstitial fluid?
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interstitial fluid is 1/4 of TBW
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what is the 60-40-20 rule?
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60% of body weight = TBW
40% of body weight = ICF 20% of body weight = ECF |
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what formula is used with the dilution method to determine volumes of fluid compartments?
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Volume = Amount/Concentration
Volume = vol. of body fluid compartment Amount = amount of substance present Concentration = concentration in plasma |
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what markers are used to calculate TBW?
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* Tritiated water
* D2O * Antipyrene |
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what markers are used to calculate ECF volume?
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* Sulfate
* Inulin * Mannitol |
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what markers are used to calculate plasma volume?
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* Radioiodinated serum albumin (RISA)
* Evans blue |
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how is interstitial fluid volume measured?
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indirectly as ECF - Plasma Volume
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how is ICF volume measured?
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indirectly as TBW - ECF
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what is the clearance equation?
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C=UV/P
C = clearance (mL/min or mL/24hr) U = Urine concentration (mg/mL) V = urine volume/ time (mL/min) P = [plasma] (mg/mL) |
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what percent of cardiac output is renal blood flow?
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RBF is 25% of the cardiac output
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what produces vasoconstriction of the renal arterioles?
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sympathetic nervous system and angiotensin II
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what renal arterioles are preferentially constricted by low concentrations of Ang II?
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efferent arterioles
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how do low concentrations of Ang II impact GFR and why?
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low concentrations of Ang II increase GFR by preferentially constricting efferent arterioles
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what produces vasodilation of renal arterioles?
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(1) Prostaglandins
(2) Bradykinin (3) Nitric oxide (4) Dopamine |
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what is the autoregulatory range in the renal vasculature?
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80-200 mmHg
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describe the two mechanisms for autoregulation of RBF?
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(1) Myogenic mechanism: renal afferent arterioles contract in response to stretch
(2) Tubuloglomerular feedback: increased renal arterial pressure leads to increased delivery of fluid to the macula densa, which then causes constriction of the nearby afferent arteriole (increasing resistance) |
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what substance is used to measure renal plasma flow (RPF) and why?
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Para-aminohippuric acid (PAH) is filtered and secreted
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what equation uses measured RPF to calculate RBF?
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RBF = RPF/(1-Hct)
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what substance is used to measure GFR and why?
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Inulin is filtered, but is not reabsorbed or secreted
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how does serum [creatinine] change when GFR decreases?
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when GFR decreases, serum [creatinine] increases
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what is the formula for filtration fraction?
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filtration fraction = GFR/RPF
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how do changes in filtration fraction impact protein concentrations in peritubular capillary blood, and how does it impact reabsorption in the proximal tubule)
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Increased filtration fraction results in increased protein concentration of peritubular capillary blood (leading to increased reabsorption in proximal tubule)
Decreased filtration fraction does the opposite |
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what is the driving force for glomerular filtration?
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net ultrafiltration pressure
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how does constriction of the afferent arteriole impact GFR, RPF, and filtration fraction?
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decreases GFR, decreases RPF, does not change filtration fraction
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how does constriction of the efferent arteriole impact GFR, RPF, and filtration fraction?
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increases GFR, decreases RPF, and increases filtration fraction
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how does increased plasma [protein] impact GFR, RPF, and filtration fraction?
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decreased GFR, no change to RPF, decreases filtration fraction
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how does ureteral stone impact GFR, RPF, and filtration fraction?
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decreased GFR, no change to RPF, decreased filtration fraction
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what is the equation for Filtered Load?
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filtered load = GFR x [plasma]
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what is the formula for excretion rate?
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excretion rate = V x [urine]
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what is the formula for reabsorption rate?
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reabsorption rate = filtered load - excretion rate
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what is the formula for secretion rate?
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secretion rate = excretion rate - filtered load
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where is glucose reabsorbed?
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proximal tubule
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how is glucose reabsorbed?
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Na+-glucose cotransport in the PCT
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where is most of the filtered Na+ reabsorbed?
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in the PCT
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how is Na reabsorbed in the early PCT?
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* Via cotransport with glucose, amino acids, phosphate, and lactate
* Via Na+-H+ exchange that is linked directly to reabsorption of filtered HCO3- |
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where and how do carbonic anhydrase inhibitors act?
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early proximal tubule, by inhibiting the reabsorption of filtered HCO3-.
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how is Na+ reabsorbed in the late PCT?
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Na+ is reabsorbed in the late PCT along with Cl-
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how do ECF volume changes impact PCT reabsorption?
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ECF volume contraction increases reabsorption
ECF volume expansion decreases reabsorption |
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where is 25% of the filtered Na+ reabsorbed?
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thick ascending limb of the LoH
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how is Na+ reabsorbed in the thick ascending limb of the LoH?
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via a Na+-K+-2Cl- cotransporter in the luminal membrane
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what is the site of action of loop diuretics?
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inhibition of the Na-K-2Cl cotransporter in the thick ascending limb of the LoH
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where is 8% of the filtered Na+ reabsorbed?
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DCT and collecting duct
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how is NaCl reabsorbed in the DCT?
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via a Na+-Cl- cotransporter
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what is the site of action of thiazide diuretics?
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Na+-Cl- cotransporter in the DCT and collecting duct
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what are the two cell types of the late DCT and collecting duct?
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(1) Principal cells
(2) alpha-intercalated cells |
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describe principal cells of the DCT?
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* Reabsorb Na+ and water
* Secrete K+ * Aldosterone increases Na+ reabsorption and increases K+ secretion (via increased synthesis of ENaC) * ADH increases H2O premeability * K+-sparing diuretics decrease K+ secretion |
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how does aldosterone impact principal cells?
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aldosterone stimulates synthesis of ENaC channels in principal cells to increase Na+ reabsorption and increase K+ secretion
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what part of the nephron does ADH act on?
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principal cells of the DCT and collecting duct
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where do K+-sparing diuretics act?
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they act on principal cells of the DCT and collecting ducts
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what is spironolactone
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K+ sparing diuretic
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what is triamterene?
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K+ sparing diuretics
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what is amiloride?
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K+ sparing diuretics
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what is furosamide?
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loop diuretic
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what is ethacrynic acid?
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loop diuretic
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what is bumetanide?
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loop diuretic
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where do thiazide diuretics act?
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Na+-Cl- cotranspoters of the early distal tubule
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what cells of the DCT secrete H+?
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alpha-intercalated cells
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what stimulates H+-ATPase of the alpha-intercalated cell of the late DCT?
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aldosterone
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how is H+ secreted by the late DCT?
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via H+-ATPase in alpha-intercalated cells, under influence of aldosterone
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how is K+ reabsorbed by in the late DCT?
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via H+,K+-ATPase
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where does most of the K+ reabsorption take place?
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in the PCT
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where is 20% of the filtered K+ reabsorbed?
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thick ascending limb of LoH
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how is K+ reabsorbed in the thick ascending limb of the LoH?
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via the Na-K-2Cl cotransporter
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where is the Na-K-2Cl cotransporter located?
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thick ascending limb of the LoH
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under what conditions does reabsorption of K+ take place in the DCT?
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low-K+ diets (K+ depletion)
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what cells of the DCT reabsorb potassium?
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alpha-intercalated cells
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what cells of the DCT secrete K+?
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principal cells
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what is the mechanism of K+ secretion from principal cells?
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(1) K+ is actively transported into cells via the Na-K ATPase on the basolateral membrane of the principal cells
(2) At the luminal membrane, K+ is passively secreted into the lumen through K+ channels * the magnitude of K+ passive secretion into the lumen is determined by chemical and electrical driving forces across the luminal membrane |
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how does aldosterone impact K+ secretion (with mechanism)
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* Aldosterone increases K+ secretion by increasing Na+ reabsorption into principal cells, which then stimulates the Na-K exchanger to simultaneously increase K+ uptake into the principal cells.
* The increased intracellular K+ in the principal cells is an increased driving force for K+ passive secretion * Aldosterone also increases the number of luminal membrane K+ channels |
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how does hyperaldosteronism impact K+ secretion?
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Hyperaldosteronism increases K+ secretion and causes hypokalemia
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how does hypoaldosteronism impact K+ secretion?
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hypoaldosteronism decreases K+ secretion and causes hyperkalemia
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how and why does acid-base balance impact K+ secretion?
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* H+ is effectively exchanged for K+ across the basolateral cell membrane.
* Acidosis decreases K+ secretion because the high blood [H+] leads to increased exchange of H+ and K+ across the basolateral membrane. This lowers the intracellular K+ and therefore decreases K+ driving force for secretion * Alkalosis increases K+ secretion |
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what is the impact of acidosis and alkalosis on K+ secretion?
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Acidosis decreases K+ secretion
Alkalosis increases K+ secretion |
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what type of diuretics increase K+ secretion?
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Loop diuretics and thiazide diuretics BOTH increase K+ secretion and can cause hypokalemia
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what type of potassium disorder can be caused by loop diuretics?
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hypokalemia due to increased K+ secretion
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what mechanism causes loop diuretics and thiazide diuretics to cause hypokalemia?
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These diuretics increase flow through the DCT and therefore cause dilution of luminal K+ concentration, increaseing the driving force for K+ secretion
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what potassium disorder can be caused by K+-sparing diuretics, if used alone?
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hyperkalemia
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what is the mechanism of action of spironolactone?
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aldosterone antagonist, K+ sparing diuretic
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what is the mechanism of amiloride?
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K+ sparing diuretic that acts directly on principal cells
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what is the most important use of K+-sparing diuretics?
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in combination with thiazide or loop diuretics to reduce urinary loss of K+
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how would increased luminal anion concentration (ie increased HCO3- in the lumen) impact K+ secretion, and why?
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increased luminal anion concentration would cause increased K+ secretion by increasing the negativity of the lumen, which favors K+ secretion
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how, and how much urea is reabsorbed in the PCT?
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50% of the filtered urea is passively reabsorbed in the PCT
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how does urea excretion change with urine flow rate?
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as urine flow rate increases, so does urea excretion
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where and how is the majority of phosphate reabsorbed?
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85% of the filtered phosphate is reabsorbed in the PCT by Na+-phosphate cotransport
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how much of filtered phosphate is excreted in urine?
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15%
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what is the impact of parathyroid hormone on phosphate reabsorption and why?
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PTH inhibits phosphate reabsorption in the PCT by generating increased cAMP, which inhibits Na+-phosphate cotransporter
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how is the majority of filtered calcium reabsorbed?
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more than 90% of the filtered calcium is reabsorbed by the PCT and thick ascending limb via passive processes that are coupled to Na+ reabsorption
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what is the impact of loop diuretics on calcium reabsorption and why?
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loop diuretics decrease calcium reabsorption (and therefore increase urinary calcium excretion) by inhibiting the sodium reabsorption to which calcium reabsorption is linked
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how can loop diuretics be used to treat calcium disorders?
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if volume is replaced, loop diuretics can be used to treat hypercalcemia because they increase calcium excretion in the urine
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how is calcium reabsorbed in the distal tubule and collecting duct?
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8% of filtered calcium is reabsorbed in the DCT and collecting duct, via active processes
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how does PTH impact calcium movement in the kidney?
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PTH increases Ca reabsorption in the kidney by activating adenylate cyclase in the distal tubule
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how do thiazide diuretics impact calcium movement in the kidneys?
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thiazide diuretics increase calcium reabsorption in the distal tubule
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compare the impacts thiazide diuretics and loop diuretics have on calcium movement in the kidney
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thiazide diuretics increase calcium reabsorption in the distal tubule
loop diuretics increase calcium excretion by inhibiting reabsorption in the distal tubule |
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where is magnesium reabsorbed?
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PCT, thick ascending limb of LOH, and DCT
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how is magnesium reabsorption linked to calcium reabsorption?
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in the thick ascending limb of the LOH, Mg and Ca compete for reabsorption and therefore hypercalcemia causes an increase in magnesium excretion (by inhibiting magnesium reabsorption).
Likewise, hypermagnesemia causes an increase in calcium excretion by inhibiting calcium reabsorption |
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how is plasma osmolarity regulated by the kidneys?
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by varying the amount of water excreted relative to the amount of solute excreted
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what acids are considered fixed acids?
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sulfuric, phosphoric, ketoacids, lactic acid, and salicylic acid
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in what ph range are buffers the most effective?
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within 1.0 pH units of the pK of the buffer
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what is the major extracellular buffer and what is its pK?
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CO2/HCO3- buffer, with a pK = 6.1
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what is the minor extracellular buffer and its pK?
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H2PO4/HPO4 buffer, with a pK = 6.8
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what is the most important role of phosphate buffer?
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as urinary buffer (titratable acid)
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what are the most important intracellular buffers?
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organic phosphates and proteins
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what are the protein buffers intracellularly?
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* Imidazole and alpha amino groups
* Hemoglobin (deoxy is more effective than oxy form) |
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what is the henderson-hasselbalch equation?
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pH=pK+log([A-]/[HA])
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when is the pH of the solution equal to the pK of the buffer?
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pH = pK when the concentrations of HA and A- are equal
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where in the kidney is does bicarb reabsorption primarily take place?
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PCT
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describe renal compensation for respiratory acidosis
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increases in PCO2 result in increased rates of HCO3- reabsorption because the supply of intracellular H+ for secretion is increased
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describe renal compensation for respiratory alkalosis
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decreases in pCO2 result in decreased rates of HCO3- reabsorption becaues the supply of intracellular H+ for secretion is decreased
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how does ECF volume expansion impact HCO3- reabsorption?
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increased ECF volume results in decreased HCO3- reabsorption
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what is the impact of Ang II on HCO3- reabsorption, and why?
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Stimulates Na-H exchange and thus increases HCO3- reabsorption
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why does ECF volume contraction lead to contraction alkalosis?
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* ECF volume expansion results in increased HCO3- reabsorption
* Decreased ECF volume stimulates Ang II production, which stimulates Na-H exchanger that increases HCO3- reabsorption |
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how does NH3 excretion change during acidosis and why?
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in acidosis, an adaptive increase in NH3 synthesis occurs and aids in the excretion of excess H+
This occurs because NH3 excretion increases as urinary pH decreases. The NH3 is secreted and combines with the H+ in the urine to form NH4+. This frees up the HCO3- to be reabsorbed. |
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with respect to NH3, how does hyperkalemia impact H+ excretion?
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Hyperkalemia inhibits NH3 synthesis which produces a decrease in H+ excretion
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what causes metabolic acidosis?
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overproduction or ingestion of fixed acid or loss of base produces an increase in arterial H+ (acidemia)
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in metabolic acidosis, why does serum [HCO3-] decrease?
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HCO3- is used to buffer the extra fixed acid, resulting in decreased HCO3-
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what is the primary disturbance in metabolic acidosis?
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decreased serum bicarb that results when serum bicarb is used to buffer the increased acid
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what is the respiratory compensation for metabolic acidosis?
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Kissmaul breathing (hyperventilation)
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what is the correction of metabolic acidosis?
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* Increased excretion of the excess fixed acid as titratable acid and NH4+
* Increased reabsorption of "new" HCO3-, which replenishes the bicarb used to buffer the added fixed acid * In chronic metabolic acidosis, there is an adaptive increase in NH3 synthesis that aids in the excretion of excess H+ |
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what is the serum anion gap formula?
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serum anion gap = [Na+] - ([Cl-]+[HCO3-])
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what is represented by the serum anion gap?
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unmeasured anions in the serum including phosphate, citrate, sulfate, and protein
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what is the normal value of the serum anion gap?
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12mEq/L
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how are H+ and HCO3- levels altered in metabolic acidosis?
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H+ is increased
HCO3- is decreased (primary disturbance) |
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how are H+ and HCO3- levels altered in metabolic alkalosis?
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H+ is decreased
HCO3- is increased (primary disturbance) |
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how are H+ and HCO3- levels altered in respiratory acidosis?
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H+ and HCO3- are BOTH increased
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how are H+ and HCO3- levels altered in respiratory alkalosis?
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H+ and HCO3- are BOTH decreased
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in metabolic acidosis, what ions should increase in concentration to maintain electroneutrality when HCO3- is depleted?
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Cl- or an unmeasured anion
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what would increase the serum anion gap?
|
during metabolic acidosis, the serum anion gap is increased if the concentration of an unmeasured anion is increased to replace HCO3-
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what causes hyperchloremic metabolic acidosis?
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increased concentration of Cl- that occurs to compensate for decreased HCO3- during metabolic acidosis
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what is the primary disturbance in metabolic alkalosis?
|
increased arterial [HCO3-]
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how does serum [HCO3-] change when a patient is vomiting?
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HCO3- increases
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what is the respiratory compensation for alkalemia?
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hypoventilation
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what is the correction for metabolic alkalosis?
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* Increased excretion of HCO3-
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what causes respiratory acidosis?
|
decrease in respiratory rate and retention of CO2
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what is the primary disturbance in respiratory acidosis?
|
increased arterial pCO2
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what is the respiratory compensation for respiratory acisosis?
|
there is none
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name 7 causes of metabolic acidosis
|
(1) Ketoacidosis
(2) Lactic acidosis (3) Chronic renal failure (4) Salicylate intoxication (5) Methanol/formaldehyde intoxication (6) Ethylene glycol intoxication (7) Diarrhea |
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what acid/base disturbance is caused by diarrhea?
|
metabolic acidosis
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what acid/base disturbance is caused by vomiting?
|
metabolic alkalosis
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name 3 causes of metabolic alkalosis
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(1) Vomiting
(2) Hyperaldosteronism (3) Loop or thiazide diuretics |
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name some causes of respiratory acidosis
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(1) Drugs: Opiates; sedatives; anesthetics
(2) Guillian-Barre syndrome; polio; ALS; MS (3) Airway obstruction (4) Adult respiratory distress syndrome; COPD |
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name 4 causes of respiratory alkalosis
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(1) Pneumonia; pulmonary embolus
(2) High altitude (3) Psychogenic (4) Salicylate intoxication |
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mechanism of action of acetazolamide
|
carbonic anhydrase inhibitor that acts on PCT to increase HCO3- excretion
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mechanism of action of loop diuretics?
|
* Act on thick ascending limb of LOH to inhibit Na-K-2Cl cotransport
* Increased NaCl excretion, increased K+ excretion (via increase DCT flow rate), increased Ca excretion * Also result in decreased ability to concentrate urine, and decreased ability to dilute urine |
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why do loop diuretics decrease ability to concentrate urine?
|
they decrease corticopapillary gradient
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why do loop diuretics decrease ability to dilute urine?
|
the inhibit the diluting segment (the thick ascending limb of the LOH)
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what is the mechanism of action of thiazide diuretics?
|
Act on early DCT to inhibit Na-Cl cotransporter
* Increase NaCL excretion, increase K+ excretion, decrease calcium excretion * Also decrease ability to dilute the urine |
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what is the mechanism of action of K+-sparing diuretics?
|
* Act on late DCT to inhibit Na+ reabsorption, inhibit K+ secretion, and inhibit H+ secretion
* Increase Na+ excretion (small effect), decrease K+ excretion, and decrease H+ excretion |
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|
what are the 3 direct effects of aldosterone on the kidney?
|
(1) Increase Na+ reabsorption
(2) Increased K+ secretion (3) Increased H+ secretion |
|
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why would hypoaldosteronism cause volume contraction?
|
low aldosterone levels result in decreased sodium reabsorption and therefore increased water excretion
|
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why does hypoaldosteronism lead to hyponatremia?
|
low aldosterone causes decreased sodium reabsorption which leads to volume contraction, which then also stimulates ADH secretion from posterior pituitary (resulting in a further decrease in sodium concentration)
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does diarrhea cause acidosis or alkalosis?
|
diarrhea causes metabolic acidosis
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does vomiting cause acidosis or alkalosis?
|
vomiting causes metabolic alkalosis
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