Term
| are K and Na levels in the plasma similar? are they found in the same compartment? |
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Definition
| yes, but Na is found mainly in the extracellular fluid, at a conc of 145 mEq/L and K is found mainly in the intracellular space, at a conc of 3-4 mEq/L. |
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Term
| do changes to the plasma Na or K conc have similar effect? |
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Definition
| no, Na plasma changes can be sustained easily by the body, but K plasma changes can only occur within a narrow range (a change of 1-2 mEq/L can lead to cardiac problems) |
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Term
| how does the kidney manage K? |
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Definition
| the kidney secretes K (up to a 10x safety factor), which covers hyperkalemia but does not have a method of addressing hypokalemia |
|
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Term
| what is obligatory K loss? does stress affect this? |
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Definition
| the kidney attempts to reabsorb K, but there is always some K excreted due to the Na/K pump action necessary for maintenance of blood volume. stress (esp sx) can affect this, and require K+ supplementation to counter the loss |
|
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Term
| where is the main point of reabsorption for K+ in the nephron? how much is usually reabsorbed? how are K levels controlled? |
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Definition
| in the PCT, where 80-90% of the filtered K+ load is reabsorbed, however there is little control over the PCT's role in K levels. in the DCT and collecting ducts, K is secreted, and *this mechanism is how circulating plasma is controlled |
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Term
| since K+ is freely filtered at the glomerulus, what is its concentration in the filtrate? |
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Definition
| the same as plasma, 3-4mEq/L |
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Term
| what forces factor into K's movement into and out of cells? how does this inform K's movement through the PCT and back into systemic circulation? |
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Definition
| there is a large electrical gradient driving K into cells, but a large chemical gradient driving it out. K passes back through the PCT via solvent drag |
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Term
| how does the solvent drag mechanism of K moving into the PCT work? |
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Definition
| Na is pumped into the lateral sacs, H2O follows, creates hydrostatic pressure which K can follow through the tight junctions (luminal membrane is impermeable to K), then through the lateral sacs and peritubular interstitium via the K/Cl cotransporter. the system is designed for K to be reabsorbed principally due to permeability differences between luminal and basolateral membranes |
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Term
| what part does the Na/K pump play in K transport into the interstitium? |
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Definition
| the Na/K pump is not the primary means of Na movement, that role is carried by the Na/H pump. the Na/K pump mainly keeps the K levels in the interstitium low, so that K will move across the basolateral membrane from the lateral sac |
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Term
| how is the membrane in the DCT different than in the PCT? |
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Definition
| the luminal/basolateral membranes of the DCT are equally permeable to K |
|
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Term
| how does K move across the DCT? why is it drawn into the lumen? |
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Definition
| Na/K ATPases pull K from the interstitium into the DCT cells, and K then simply diffuses out into the lumen of the DCT due to 1) a lower conc gradient (4 in the interstitium, .5 in the lumen) and 2) a lower electrical gradient 70 mV in the interstitium, 20 in the lumen |
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Term
| how does aldosterone affect K levels in the DCT? |
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Definition
| aldosterone increases Na absorbtion, which increases the activity of the Na/K pump on the basolateral membrane, which brings K intracellularly to the DCT lining cells, causing K to diffuse out into the lumen at a higher rate (K loss). increased plasma K will also stimulate this pump. |
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Term
| when does K secretion become dangerous? |
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Definition
| when K levels drops below the level that is obligated to be secreted |
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Term
| what role does HCO3- play in the body, and what concentration is it found in? |
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Definition
| HCO3- is a critical buffer in the body and is present at concentrations of 24 mEq/L |
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Term
| what is critically involved in the reabsorption of HCO3-? where in the nephron is it seen? |
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Definition
| carbonic anhydrase, which catalyzes the breakdown of HCO3- to CO2 and H2O. carbonic anhydrase is mainly found in the PCT |
|
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Term
| what is HCO3-'s path through the nephron? |
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Definition
| HCO3- is freely filtered by the glomerulus as NaHCO3, then Na+ dissociates into the tublar lumen cells via Na+/H+ antiporters. H+ exits the cell and binds to HCO3-, forming carbonic acid (H2CO3). carbonic anhydrase then hydrolyzes the H2CO3 into H2O and CO2, which can both diffuse back into the cell. once H20 and CO2 diffuse into the cell, they are recombined via carbonic anhydrase to form carbonic acid, which then dissociates back into H+ and HCO3- (which is then transported to the interstitium). there is no net change of H+, only *net reabsorption of Na+* |
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Term
| what is the interplay between H+, HCO3- and Na- reabsorption? |
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Definition
| when the Na+ is reabsorbed, an H+ is secreted. this H+ is then used to make the carbonic acid which carbonic anhydrase acts upon. this is important enough that if H+ secretion were inhibited, there would be a 50% reduction in the rate of Na+ reabsorption. there are also electrogenic (called such since no negative charge is involved) proton pumps whose sole purpose is to actively pump H+ into the lumen, which then can also be used for making carbonic acid in the lumen |
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Term
| what are the 2 mechanisms that HCO3- has to get across the basolateral membrane? |
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Definition
| a Na+/HCO3- cotransporter and a Cl-/HCO3- antiporter |
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|
Term
| what characterizes the reabsorption of HCO3- in the DCT? |
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Definition
| there is very little carbonic anhydrase in the lumen DCT (plenty intracellularly), so the process described in the PCT occurs in the same way, except much slower. *also KHCO3 forms with secreted K+, which does not dissociate and is lost in the urine. thus, if there is higher K secretion due to diet, aldosterone, etc, more HCO3- will be lost in the DCT |
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Term
| what are the titratable and non-titratable acids when referring to renal physiology? |
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Definition
| titratable: phosphoric and sulfuric acid, nontitratable: ammonia |
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Term
| how is titratable phosphoric acid excreted in the kidneys? |
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Definition
| the Na/H antiporter is presented with Na2HPO4, from which one Na is extracted and replaced with an H to make NaH2PO4, which is excreted in urine |
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Term
| where do the protons in the cell come from that are used in this equation: Na2HPO4 + H+ -> H2PO4 + Na+? where does this happen in the nephron? |
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Definition
| from PCO2, which crosses the basolateral membrane, and when it meets with a CO2 and and H20, creates H2CO3, which provides the protons (no pumps on basolateral side), and the resulting HCO3- is transported back across the basolateral membrane to the interstitium. this happens largely in the cortical collecting ducts, which have the luminal membrane electrogenic H+ pumps as well as the Na-HCO3 cotransporters on the basolateral membrane |
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Term
| why does the kidney produce ammonia? |
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Definition
| ammonia is a nontitratable acid, which is necessary if the urinary ph has has gone lower than 4.4, which is the point where the H+ pumps are functioning maximally and titratable acids can no longer be secreted |
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Term
| how are nontitratable acids excreted? |
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Definition
| the kidney deaminates amino acids such as glutamine to form free NH3, lipid soluble gas that freely diffuses into the tubular lumen which *is protonated* and then breaks up Na2SO4 to form (NH4)2SO4 and 2Na+. the H+'s on (NH4)2SO4 cannot ionize and thus do not contribute to the pH of the urine. (there is also a Na+/NH4+ cotransporter on the tubular lumen side that pumps out NH4+) |
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Term
| what is the mechanism of ammonium formation in the kidneys? |
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Definition
| if plasma pH is low enough (under 4.4) it stimulates the deamination of amino acids in the *PCT and subsequent formation of NH3 and eventual formation of NH4+. this travels down descending limb to ascending limb. in ascending limb there is a Cl-/Na+/NH4+ transport system. this pumps ammonium ions into the interstitium of renal medulla where it is deprotonated to form NH3 where it then enters the collecting ducts and forms NH4+ one last time and is excreted |
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Term
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Definition
| the process of expelling the final tubular fluid from the body |
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|
Term
| do any further changes occur to the tubular fluid once it leaves the collecting ducts? |
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Definition
|
|
Term
| what is the path of tubular fluid as it leaves the kidney? |
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Definition
| through the minor, then major calyces, to the renal pelvis, to the ureter, to the bladder |
|
|
Term
| what is the flow rate through each ureter? |
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Definition
| .6-.7 mL/min (GFR = 130 ml/min; 99% of GFR is reabsorbed…so 1.3 ml/min ends up in bladder, and 1.3/2 (each kidney) is 0.6-0.7 ml/min) |
|
|
Term
| what happens as fluid enters the ureters? |
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Definition
| the ureters stretch and stimulate peristaltic movement which propels urine to the bladder (why you can pee in space) |
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Term
| what characterizes the bladder's muscular composition? |
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Definition
| the bladder is a hollow organ which is composed of 3 smooth muscle layers that are oriented at various angles to each other (detrusor muscle) |
|
|
Term
| what does the bladder do when empty? |
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Definition
| fold up thanks to a continous layer of transitional epithelial cells |
|
|
Term
| what does the bladder do when maximally filled? |
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Definition
| the folds stretch out and the transitional epithelial cell form a continous, monocellular sheet lining the lumen |
|
|
Term
| what kind of sphincters does the urethra have? |
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Definition
| internal (involuntary) external (voluntary) |
|
|
Term
| what does parasympathetic innervation result in? |
|
Definition
| bladder contraction and involuntary sphincter (internal) relaxation |
|
|
Term
| what does somatic control of the bladder result in? |
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Definition
| relaxation of the voluntary (external) sphincter |
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|
Term
| do sympathetic nerves play a role in micturition? |
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Definition
|
|
Term
| what is the max capacity of the bladder before micturition contractions start? |
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Definition
| 3-400 mL, beyond which the pressure begins to increase rapidly along with superimposed smooth muscle contractions |
|
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Term
| what happens if a person feels the need to pee, but it is inconvenient? |
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Definition
| voluntary motor activity in the muscles of the pelvic floor can reinforce constriction of the urethral sphincters |
|
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Term
| what happens when someone pees? |
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Definition
| cortical inhibition is released and the spinal micturition reflexes activate parasympathetic fibers in the pelvic nerves, producing a contraction of the detrusor muscle and dilation of the internal sphincter muscle - allowing urine to enter the urethra. urine in the urethra activates receptors which send afferent information (via the pudendal nerves) to reinforce the parasympathetic-mediated contraction of the detrusor muscle (positive feedback loop). fluid in the urethra also causes a reflex relaxation of the external urethral sphincter. |
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Term
| what is the complete cycle of the micturition reflex? |
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Definition
| 1) progressive and rapid increase of pressure 2) period of sustained pressure (similar to tetanus, not peristalsis) 3)a return of basal tone to the bladder |
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Term
| how does the kidney regular GFR in response to arterial pressure? |
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Definition
| the system is designed to keep GFR from changing in response to changing arterial pressures. with increased arterial pressure comes increased hydrostatic pressure in the glomerular capillaries, which increases GFR, increasing the rate through the PCT/loop of henle, increasing flow through the macula densa - detected there as an increase in NaCl delivery, the macula densa signals arteriole cells to constrict, decreasing hydrostatic pressure in the glomerular capillary |
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Term
| how is water balance in the body regulated in situations of decreased plasma water volume? |
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Definition
| BP is down, which is detected by baroreceptors which increase ADH secretion, causing water reabsorption to increase, increasing total body water |
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Term
| how is water balance in the body regulated in situations of increased water ingestion? |
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Definition
| fluid osmolarity decreases, which is detected by osmoreceptors which decrease ADH secretion, which decreases water reabsorption, which decreases total body water |
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Term
| how is plasma aldosterone regulated? |
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Definition
| low Na+ conc is sensed by the body as low BP, which if this is the case, renin secretion is increased, increasing angiotensin II conversion, increasing aldosterone secretion, increasing plasma aldosterone, increasing tubular reabsorption of Na+ and secretion of K+ *in the collecting ducts* |
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Term
| what should increase during severe sweating? |
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Definition
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|
Term
| what does the body do with increased K+ secretion? |
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Definition
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