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240 Cards in this Set
- Front
- Back
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What is the normal daily intake of Na+?
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about 150mEq
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Is sweat hypotonic, isotonic, or hypertonic?
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hypotonic
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What is the plasma Na+ concentration?
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about 140 mEq
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What does the urinary Na+ concentration depend on?
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Na+ intake, urine volume, and renal function
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Is Na+ freely filtered?
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yes
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How much Na+ is reabsorbed? Secreted?
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99.5%; 0.5%
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What % of Na+ is reabsorbed from the proximal tubule?
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70%
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What % of Na+ is reabsorbed from the thick ascending limb?
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20%
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What % of Na+ is reabsorbed from the distal tubule?
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5%
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What % of Na+ is reabsorbed from the collecting duct?
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3-5%
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What is the driving force on cells at the basolateral membrane?
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Na+/K+ ATPase
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What 2 ways is Na+ reabsorbed in the EARLY proximal tubule?
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symported with Tm substances; antiported with H+
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What 2 ways is Na+ reabsorbed in the late proximal tubule?
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antiported with H+; paracelluarly (NaCl)
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Where does H formate reabsorption take place?
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late proximal tubule
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What happens to water in the proximal tubule? What happens to the tubular fluid?
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it follows the solute; tubular fluid stays isosmotic
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What stimulates the Na+/H+ antiporter in the proximal tubule?
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angiotensin II
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What are the osmotic diuretics? Where do they act?
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urea, glucose, mannitol; proximal tubule
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What is the main mechanism for Na+ reabsorption in the thick ascending loop of Henle?
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"family sedan;" symported with K+ and 2Cl-
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Is the luminal membrane of the thick ascending limb permeable or impermeable to water?
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impermeable
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Where is the site of generation of the medullary osmotic gradient?
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thick ascending limb
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What is the site of action of the loop diuretics? What are the 3 loop diuretics?
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thick ascending limb; furosemide, bumetanide, ethacrynic acid
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In what part of the kidney does PTH act on Ca++ channels?
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distal convoluted tubule
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How is Na+ reabsorbed in the distal convoluted tubule?
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symported with Cl-
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Is the luminal membrane of the distal convoluted tubule permeable or impermeable to water?
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impermeable
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In the distal convoluted tubule does the tubular fluid become hypertonic or hypotonic?
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hypotonic
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What is the site of action for the thiazide-like diuretics? What are the thiazide-like diuretics?
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distal convoluted tubule; HCTZ and chlorthalidone
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How is Na+ reabsorbed in the collecting duct principal cell?
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through a Na+ channel
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Is the luminal membrane of the collecting duct principal cell permeable or impermeable to water?
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permeability depends on ADH concentration
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What stimulates Na+ reabsorption and K+ secretion in the collecting duct?
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aldosterone
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What is the site of action of the K+-sparing diuretics? What are the K+-sparing diuretic?
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collecting duct principal cell; spironolactone, amiloride, triamterene
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What two pathological conditions can cause diuresis?
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diabetes mellitus (due to increased proximal glucose concentrations) and renal failure (due to increased proximal urea concentrations)
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What are the two main functions of diuresis in pathological states?
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increased Na+ and water excretion
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What is the order of effectiveness of the diuretics?
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loop diuretics > thiazides > K+-sparing diuretics
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What diuretics block the Na+/2 Cl-/K+ transporter?
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loop diuretics
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What diuretics block the Na+/Cl- transporter?
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thiazide-like diuretics
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What diuretics decrease Na+ channel activity?
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K+-sparing diuretics
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What are the 2 main conditions that diuretics are used for?
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HTN and edema
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Do diuretics work in areas of the kidney that are permeable or impermeable to water?
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impermeable
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What is the primary action of diuretics?
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decrease the plasma osmolality
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What is the mechanism of action for the secondary action of diuretics?
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decreased plasma osmolality causes decreased ADH concentration; this decreases water reabsorption and increases water excretion
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What drugs won't work in patients with a problem pertaining to ADH?
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diuretics
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Na+ intake (in the absence of an acute condition) will equal?
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Na+ output
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If a patient is prescribed a diuretic, why must they keep taking the drug?
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for the first few days after taking the drug the pt will experience a large increase in their daily Na+ excretion; however the pt will stabilize and return to a plateau level of daily Na+ excretion; if the pt goes off the drug, they will have to start over at square one
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Does Na+ excretion depend on ECV or plasma Na+ concentration?
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ECV
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ECV relates to what?
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blood volume and CO
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ECV is?
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the pressure perfusing the arterial (high) pressure baroreceptors
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Where are the high pressure baroreceptors found?
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arteries (carotid sinus and aortic arch) and kidneys (JG cells)
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What do the renal peripheral baroreceptors control?
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renin, angiotensin, aldosterone
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Where are the low pressure baroreceptors found?
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atria, large veins, pulmonary artery
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What do the low pressure baroreceptors control?
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ANP
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What is the rate-limiting step in the renin-angiotensin-aldosterone system?
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renin
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What is the renin-angiotensin-aldosterone system?
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angiotensinogen
renin angiotensin I ACE angiotensin II aldosterone |
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What are the 4 ways to regulate Na+ excretion?
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1)increased renin, angiotensin, aldosterone
2)increased SNS 3)decreased ANP 4)decreased pressure natriuresis |
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What are the 4 things that stimulate renin release?
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1)decreased BP in afferent arteriole
2)decreased delivery of Na+ and Cl- to the macula densa 3)increased SNS activity 4)decreased ANP |
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What are the 5 things stimulated by angiotensin II?
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1)increased peripheral vasoconstriction
2)increased aldosterone release 3)increased renal arteriolar constriction (efferent > afferent) 4)increased activity of Na+/H+ countertransport in proximal tubule 5)increased thirst and increased ADH release |
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What mechanism does AII work through?
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Gq protein stimulates phospholipase C that splits PIP2 into IP3 and DAG
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What are the 2 main things that stimulate aldosterone release?
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increased AII plasma levels and increased K+ plasma levels
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What is secreted from the principal cell of the collecting duct?
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K+
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What is the effect of increased ANP on the secretion of aldosterone?
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decreases aldosterone release
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What hormone has a trophic effect on the adrenal cortex?
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ACTH
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What is the source of aldosterone? Is it a peptide or steroid hormone?
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zona glomerulosa of adrenal cortex; steroid
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What are the 4 direct actions of aldosterone?
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1)increased activity of the Na+ channels in the principal cells of collecting duct
2)increased activity of K+ channels in the principal cells of the collecting duct 3)increased activity of H+ ATPase of alpha intercalated cells of collecting duct (H+ secreted) 4)increased activity of Na+/K+ ATPase of principal cell |
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Do you have metabolic alkalosis or acidosis with increased aldosterone production?
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metabolic alkalosis
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What are the 4 acute effects of aldosterone?
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1)increased K+ excretion
2)decreased Na+ excretion 3)decreased Cl- excretion 4)increased H+ excretion |
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What part of the kidney has a difference in the osmolality of the tubular fluid and surrounding fluid?
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the collecting duct
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What is the stimulus for increased SNS activity?
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decreased blood volume
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What is the alpha-1 effect of increased SNS activity?
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decreased GFR
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What is the beta-1 effect of increased SNS activity?
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increased renin, angiotensin, aldosterone
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What is the effect of decreased GFR on Na+?
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decreased Na+ filtered
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Does increased SNS activity cause increased or decreased Na+ excretion?
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decreased Na+ excretion
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What is the source of ANP? Is it a steroid or peptide hormone?
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atrial and ventricular myocardial cells; polypeptide
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What stimulates the release of ANP?
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increased vascular volume
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What is the mechanism of action for ANP?
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increased cGMP
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What hormone level can be used to test for CHF? Does a high level or low level of this hormone indicate CHF?
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ANP; high level
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What are the 5 actions of ANP?
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1)general vasodilator
2)decreases Na+ reabsorption from deep medullary collecting duct 3)increases GFR (afferent dilation, efferent constriction) 4)decreases renin release 5)decreases aldosterone release |
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What is the source of aldosterone? Is it a peptide or steroid hormone?
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zona glomerulosa of adrenal cortex; steroid
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What are the 4 direct actions of aldosterone?
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1)increased activity of the Na+ channels in the principal cells of collecting duct
2)increased activity of K+ channels in the principal cells of the collecting duct 3)increased activity of H+ ATPase of alpha intercalated cells of collecting duct (H+ secreted) 4)increased activity of Na+/K+ ATPase of principal cell |
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Do you have metabolic alkalosis or acidosis with increased aldosterone production?
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metabolic alkalosis
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What are the 4 acute effects of aldosterone?
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1)increased K+ excretion
2)decreased Na+ excretion 3)decreased Cl- excretion 4)increased H+ excretion |
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What part of the kidney has a difference in the osmolality of the tubular fluid and surrounding fluid?
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the collecting duct
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The excretion of what two things is increased during pressure diuresis and natriuresis? Where in the kidney does this take place?
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water and Na+; proximal tubule
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What stimulates pressure diuresis and natriuresis?
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increased blood pressure
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What does high BP do to renin release?
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decreases
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What does high BP do to glomerular capillary pressure?
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increases
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What is the effect of increased glomerular capillary pressure on the peritubular pressure? The GFR?
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increases; increases
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What does the failing kidney excrete a large fraction of?
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filtered Na+
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What is an important index of kidney function?
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fractional excretion of Na+ (FE Na+)
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What does a low FE Na+ mean?
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normal kidney function; reabsorbing Na+
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What does a high FE Na+ mean?
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kidney failure; excreting Na+
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What is Conn's syndrome?
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primary aldosteronism
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What is the classic trilogy seen with primary aldosteronism?
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HTN, hypokalemia, metabolic alkalosis
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What is another name for adrenocortical insufficiency?
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Addison disease
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What is Addison disease?
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degeneration of the adrenal cortex resulting in deficient levels of ACTH
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What are the 5 effects seen in pts with Addison disease?
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1)hypotension
2)hyponatremia 3)hyperkalemia 4)metabolic acidosis 5)hypoglycemia |
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Why do pts with Addison disease have hypotension?
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decreased Na+ retention which leads to volume depletion
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Why do pts with Addison disease have hyponatremia?
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volume depletion leads to increased ADH secretion which causes water retention
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Why do pts with Addison disease have hyperkalemia?
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decreased activity of the principal cell K+ channels leads to decreased K+ secretion
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Why do pts with Addison disease have metabolic acidosis?
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decreased activity of the intercalated cell ATPase which increases bicarbonate excretion
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Why do pts with Addison disease have hypoglycemia?
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decreased levels of glucocorticoids
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What are some causes of renovascular HTN?
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congenital, atherosclerotic plaques,fibromuscular dysplasia
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What are the effects of renovascular HTN on the affected kidney?
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increased renin release leading to increased AII and aldosterone leading to HTN; will also see decreased RBF, GFR, salt, and water excretion
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What are the effects of renovascular HTN on the unaffected kidney?
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increased RBF, GFR, salt, and water excretion
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What happens to the afferent arteriole pressure in the kidney affected by renovascular HTN?
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decreases
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What happens to the afferent arteriole pressure in the kidney not affected by renovascular HTN?
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increases
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Will a pt with renovascular HTN be in Na+ balance?
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yes
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Where does our intake of water come from?
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liquids, water from oxidation, and water in food
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In what ways does the body output water?
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urine, sweat, feces
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What is the obligatory water loss of the body?
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water loss that is necessary for the excretion of normal solute content
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What is the facultative water loss of the body?
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the excretion of "extra" fluid intake
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What part of the kidney is permeable to water only in the presence of ADH?
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the collecting duct
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What parts of the kidney are completely non-permeable to water?
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thin and thick ascending loop of Henle and the distal tubule
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All water reabsorption is?
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passive secondary to solute reabsorption
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Is the thin descending limb of the loop of Henle permeable to water?
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yes, it has high water permeability
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In the thick ascending limb, what creates the Na+ gradient for lumenal transport?
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basolateral Na+/K+ ATPase
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What generates the gradient of 100mM NaCl between tubular fluid and interstitial fluid in the thick ascending limb?
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luminal Na+/K+/2Cl- transporter and the basolateral Na+/K+ ATPase
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Are the thin and thick ascending limb permeable to water?
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no
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Is the thin descending limb permeable to water?
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yes
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What happens in the countercurrent multiplier to maintain the NaCl gradient at 200 mOsm/kg?
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NaCl is pumped from the thick ascending limb into the interstitial fluid; then the fluid in the thin descending limb equilibrates with the interstitial fluid
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What is the osmolality of the tubular fluid in the proximal tubule?
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isotonic 300 mOsm
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Is the cortical and outer medullary collecting duct permeable to water? To urea?
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permeable to water; impermeable to urea
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What happens to the urea concentration in the cortical and outer medullary collecting duct?
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increases
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What happens to water in the cortical and outer medullary collecting duct?
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it is reabsorbed
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Is the inner medullary collecting duct permeable to water? To urea?
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permeable to water and urea
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What happens to urea in the inner medullary collecting duct?
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reabsorbed down gradient
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What is the action of ADH in the inner medullary collecting duct?
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increases urea permeability
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What generates the medullary osmotic gradient for NaCl and urea?
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countercurrent multiplier
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With the countercurrent multiplier, is urea accumulation passive?
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yes, it is secondary to the NaCl gradient
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What preserves the medullary osmotic gradient?
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countercurrent exchanger
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What is the countercurrent exchanger? Where does it take place?
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passive process of water and solute exchange by the vasa recta
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What happens to RBCs as they travel through the vasa recta? What pts can this cause a problem in?
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they shrink due to the increasing osmolality of the plasma; pts with Sickle Cell Anemia
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In the countercurrent exchanger, does NaCl travel from the afferent arteriole into the interstitium or vice versa? What about water?
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vice versa, from the interstitium into the afferent arteriole; water travels from the afferent arteriole into the interstitium
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In the countercurrent exchanger, does NaCl travel from the efferent arteriole into the interstitium or vice versa? What about water?
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yes, from the efferent arteriole into the interstitium; vice versa for water, from the interstitium into the efferent arteriole
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Is the cortical collecting duct permeable to water if ADH is absent?
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very small permeability to water
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What type of urine is produced when ADH is absent?
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high volume of dilute urine
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Is the collecting permeable to water if ADH is present?
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yes, very high permeability to water
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What type of urine is produced if ADH is present?
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small volume of concentrated urine
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What is the TF/P for creatinine in the proximal tubule?
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equal
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What is the TF/P for creatinine in the loop of Henle?
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3X plasma concentration
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What is the TF/P for creatinine in the medullary collecting duct with max ADH levels?
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100X plasma concentration
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What is the TF/P for creatinine in the medullary collecting duct with no ADH present?
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5X plasma concentration
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Is ADH a peptide or steroid hormome?
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peptide
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What is the source of ADH?
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SON and PVN nuclei of the hypothalamus
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What are 6 things that stimulate ADH release?
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1)high plasma osmolality
2)decreased blood volume 3)pain 4)fear and other stressors 5)pregnancy 6)many drugs |
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What are the 3 things that inhibit ADH release?
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1)decreased plasma osmolality
2)increased blood volume 3)ethanol |
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What happens to plasma osmolality as ADH levels increase?
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plasma osmolality decreases
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What is the effect of ADH on aquaporins?
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causes aquaporin channels to be deposited into the luminal membrane
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Are the aquaporin channels on the basolateral or luminal side unaffected by ADH?
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basolateral side; these aquaporins are always present
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Once ADH binds to the ADH receptor, what mechanism allows for the insertion of aquaporins into the luminal membrane?
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increased cAMP and protein kinase A
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What are the 4 mechanisms for the stimulation of thirst?
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1)increased plasma osmolality
2)decreased blood volume 3)increased AII 4)dry mouth |
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What gives you the sensation of water satiety?
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return to normal osmolality and blood volume
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Are the thirst receptors in the hypothalamus the same as the ADH receptors?
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no, but the stimuli are similar
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Urine osmolality depends on?
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molarity - the number of particles
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Specific gravity depends on?
|
mass - weight of particles
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What is the relationship between osmolality and specific gravity? What is the exception?
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linear; proteinuria
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What happens to specific gravity and osmolality of the urine in a pt with proteinuria?
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specific gravity increases, but the osmolality decreases
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What is neurogenic diabetes insipidus?
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not enough ADH being made
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What is nephrogenic diabetes insipidus?
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kidney insensitive to ADH
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What regulates urine Na+ concentration?
|
blood pressure
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With nephrogenic diabetes insipidus, what are the osmolalities of the serum and the urine?
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serum is hypertonic and urine is hypotonic
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In a pt with diabetes insipidus, what happens to water reabsorption? Na+ excretion?
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decreases water reabsorption; decreases Na+ excretion
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What are some causes of neurogenic (central) diabetes
insipidus? |
idiopathic, neurosurgery, trauma, primary or secondary malignancy
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What are some causes of nephrogenic diabetes insipidus?
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LITHIUM toxicity, hypercalcemia, osmotic diuresis, congenital
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If you give a pt with suspected diabetes insipidus ADH, and their urine osmolality increases, what type do they have?
|
neurogenic diabetes insipidus
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If you give a pt with suspected diabetes insipidus ADH, and their urine osmolality is unchanged, what type do they have?
|
nephrogenic diabetes insipidus
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What are some S/S of diabetes insipidus?
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hypertonic contraction, excessive urination and thirst, hypernatremia, inconsistency between high plasma osmolality and low urine osmolality
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What are some causes of SIADH?
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LUNG CA, pneumonia, many neurological conditions, many drugs
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What are the signs of SIADH?
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hypotonic expansion or normovolemia, inconsistency between low plasma osmolality and high urine osmolality
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Are pts with SIADH hypernatremic or hyponatremic?
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hyponatremic
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What is primary polydipsia?
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psychotic compulsion to drink excessive amounts of water
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What are the S/S of primary (psychogenic) polydipsia?
|
hypotonic expansion or normovolemia, consistency between low plasma osmolality and low urine osmolality, and often sluggish response to administered ADH
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Are pts with primary polydipsia hypernatremic or hyponatremic?
|
hyponatremic
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After a pt with primary polydipsia is given ADH, why does it take awhile to see an increase in their urine osmolality?
|
takes awhile for the pt to re-establish their medullary osmotic gradient
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The greatest amount of the body's K+ is intracellular or extracellular?
|
intracellular
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How does decreasing extracellular K+ affect cell membrane potential?
|
causes hyperpolarization
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How does increasing extracellular K+ affect cell membrane potential?
|
causes depolarization
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What is the effect of metabolic or respiratory acidosis on extracelluar K+ concentration?
|
increases
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What is the effect of metabolic or respiratory alkalosis on extracelluar K+ concentration?
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decreases
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What effect do insulin and aldosterone have on the extracellular K+ level?
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decrease
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What effect does exercise have on the extracellular K+ concentration?
|
increase
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What effect does hyperosmolality (for example hyperglycemia)have on extracellular K+ concentration?
|
increase
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K+ excretion depends on?
|
the rate of K+ secretion by the principal cells
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What % of K+ is reabsorbed in the proximal tubule and by what mechanism?
|
60%; passive secondary to Na+ and water
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What % of K+ is reabsorbed in the thick ascending loop of Henle and by what mechanism?
|
30%; active by Na+/K+/2Cl-
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What % of K+ is reabsorbed in the intercalated cell of the collecting duct and by what mechanism?
|
10%; active by H+/K+-ATPase
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What % of K+ is reabsorbed in the principal cell of the collecting duct?
|
variable secretion; passively through K+ channels
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K+ secretion in the principal cell depends on?
|
electrochemical gradient on K+ (greater intracellular level of K+ causes more to be secreted) and the activity of the K+ channel
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What 4 things stimulate the secretion and excretion of K+?
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1)increased dietary K+
2)increased aldosterone 3)alkalosis 4)loop and thiazide diuretics |
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What 2 things inhibit the secretion and excretion of K+?
|
1)acidosis
2)K+ sparing diuretics |
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What is the most common cause of hypokalemia?
|
loop or thiazide diuretics
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What are the 3 K+ sparing diuretics?
|
amiloride, triamterene, spironolactone
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What do amiloride and triamterene do?
|
block the principal cell Na+ channel
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What does spironolactone do?
|
blocks the aldosterone receptor
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What are fixed acids? How are they excreted?
|
all of the acids except for carbonic acid; by the kidney
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What are volatile acids? How are they excreted?
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carbonic acid; by the lung
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What is the purpose of buffering?
|
to get rid of free H+ ions
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How does the addition of inorganic fixed acid affect extracellular K+ concentration?
|
increases extracellular K+ concentration
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How does the addition of bicarbonate affect the extracellular K+ concentration?
|
decreases extracellular K+ concentration
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What does the kidney do to the destroyed bicarbonate?
|
resynthesizes it
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Is respiratory acidosis increased or decreased pCO2? What is the effect of this condition on the extracellular K+ concentration?
|
increased pCO2; increases extracellular K+ concentration
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Is respiratory alkalosis increased or decreased pCO2? What is the effect of this condition on the extracellular K+ concentration?
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decreased pCO2; decreases extracellular K+ concentration
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Does hypoventilation cause resp acidosis or alkalosis?
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acidosis
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Does hyperventilation cause resp acidosis or alkalosis?
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alkalosis
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The amount of H+ secreted is _____ than the amount of H+ excreted.
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greater
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For every H+ that is made, how many bicarbonate are made?
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1; 1:1 ratio
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In the alpha intercalated cell, what is the main mechansim for H+ secretion?
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H+ ATPase
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For every H+ secreted into the urine, one bicarbonate is returned?
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back to the body
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What happens to the H+ that is secreted into the urine?
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it combines with a filtered bicarbonate that is then broken down by carbonic anhydrase into CO2 and water
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How does the H+ that is secreted turn into the H+ that is excreted?
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1)one H+ combines with ammonia that is made in the kidney which is then excreted as urinary ammonium
2)one H+ combines with HPO4 2- and becomes H2PO4 which is then excreted as the "titratable aciditiy" |
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What mechanism prevents the body from developing acidiosis after the secretion of H+?
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For each 2 H+ that are excreted in the urine, 2 new bicarbonate are made; also for the H+ that is secreted, one bicarbonate is sent to the body and recycled
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What does plasma bicarbonate concentration depend on?
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the rate of renal H+ secretion
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Increased H+ secretion does what to the plasma bicarbonate concentration? What condition does this lead to?
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increases; metabolic alkalosis
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Decreased H+ secretion does what to the plasma bicarbonate concentration? What condition does this lead to?
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decreases; metabolic acidosis
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Does increased pCO2 stimulate or inhibit H+ secretion?
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stimulate
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Does decreased arterial pH stimulate or inhibit H+ secretion?
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stimulate
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Does increased plasma aldosterone stimulate or inhibit H+ secretion?
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stimulate
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Does increased plasma AII stimulate or inhibit H+ secretion?
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stimulate
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Does depletion of body K+ stimulate or inhibit H+ secretion?
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stimulate
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Does the administration of loop or thiazide-like diuretics stimulate or inhibit H+ secretion?
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stimulate
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Does decreased pCO2 stimulate or inhibit H+ secretion?
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inhibit
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Does increased pH stimulate or inhibit H+ secretion?
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inhibit
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Does decreased aldosterone stimulate or inhibit H+ secretion?
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inhibit
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Does decreased AII stimulate or inhibit H+ secretion?
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inhibit
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What is the metabolic compensation for respiratory acidosis?
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kidneys raise the plasma bicarbonate level
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Does the excessive use of loop or thiazide-like diuretics cause metabolic acidosis or alkalosis?
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alkalosis
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Do the K+ sparing diuretics cause metabolic acidosis or alkalosis?
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acidosis
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What is the goal of the body in buffering?
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to maintain a constant pH
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What is normal arterial pH?
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7.4
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What is the constant value of pK?
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6.1
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What should the normal ratio calculated by the Henderson-Hasselbalch equation be?
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20:1
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If the ratio is >20, is it acidosis or alkalosis?
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alkalosis
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If the ratio is <20, is it acidosis or alkalosis?
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acidosis
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What is the normal range for pH?
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7.35-7.45
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What is the normal range for PaCO2?
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33-44 mmHg
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What is the normal range for bicarbonate?
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22-28 mEq/L
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When interpreting acid base data, what is the first question that you ask?
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Is it acidosis or alkalosis?
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Can "overcompensation" occur?
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no
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When interpreting acid base data, what is the second question that you ask?
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Is it metabolic acidosis or metabolic alkalosis?
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When interpreting acid base data, what is the third question that you ask?
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Is it respiratory acidosis or alkalosis?
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When does respiratory compensation occur?
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with metabolic disorders
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When does metabolic compensation occur?
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with respiratory disorders
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