Flashcards in HRM Week 10 Deck (75):
List some things reabsorbed by the PCT
Glucose, amino acids, protein, vitamins, lactate, urea, uric acid, Na,K,Ca, Mg,Cl, HC03, H2O
List some things reabsorbed by the DCT?
Na,Cl, HCO3, H2O( presence of ADH)
List some things secreted into the PCT?
Urea, uric acid, creatine, H+ , NH4+, some drugs
List some things reabsorbed by the descending limb?
List some things secreted into the descending limb?
List some things reabsorbed by the ascending limb?
Na, K, Cl
List some things secreted into the DCT?
List some things reabsorbed by the collecting duct?
Water ( presence of ADH) and urea
What are the ranges of osmolality of urine than can be excreted?
50-1200-1400 mosm/kg of H20
What volume of urine can be formed per day?
Osmolality of glomerular filtrate is the same as that of plasma, what is it?
Explain effect of increased ADH on urine volume and osmolality?
Small urine volume and high osmolality
What percent reduction in plasma volume is a potent stimuli for ADH release?
List some important actions of ADH on the renal tubules
Increase permeability of collecting duct to water, increases permeability of the medullary portion of the collecting duct to urea by inserting transporters UT-A1 and UT-A3, stimulates reabsorption of NaCl by the thick ascending limb of Henles loop, DCT and CD
What is free water?
Water that is free of solutes - generated in the diluting segments
When there is low ADH levels, what is the free water clearance?
Positive as there is dilute urine
What is obligatory urine volume?
Minimum urine volume in which the excreted solute can be dissolved and excreted - 500ml/day
What is central diabetes insipidus?
Failure to produce ADH
What is nephrogenic diabetes insipidus?
Failure to respond to ADH
Which segments of the tubule are diluting segments ?
Thick ascending and early distal tubule
Which cells become permeable to water in presence of adh
Principle cells of late distal tubule and cortical collecting duct
What does a high protein diet increase?
Increases kidneys ability to concentrate the urine as amount of urea formed is more
Which aquaporin channel is inserted onto the luminal membrane of principal cells?
Aquaporin 2 channels
Receptor type for ADH?
V2 receptor on basolateral membrane
Which aquaporin channels are inserted onto the basolateral membrane of principal cells?
Of the 1200mosm of the renal medulla, what are the two main contributors to the hyperosmolarity of it?
NaCl and Urea (600mosm each)
Why is the fact that medullary blood flow is low (5%) a good thing for maintaining hyperosmolarity?
Minimises loss of solute form medullary interstitium
What does the countercurrent mechanism work to create?
A Hyperosmotic renal medulla
What operates as a countercurrent exchanger?
What operates as a countercurrent multiplier?
Loops of Henle
List the four main factors contributing to medullary hyperosmolarity?
1.Active transport of Na+, K+and Cl-by thick ascending limb of the loop of Henleinto the medullaryinterstitium
2.Active transport of ions from the collecting ducts into the medullaryinterstitium
3.Facilitated diffusion of large amounts of urea from the medullarycollecting ducts
4.Diffusion of only small amounts of water from the medullarytubules into the medullaryinterstitium
How does the medullary interstitium get so concentrated?
Countercurrent exchanger by Vasa Recta -Passage of blood down & up the vessel
Countercurrent multiplier by loop of Henle -Passage of fluid down & up the vessel
Explain the countercurrent multiplier of the nephron Loop?
The counter current MULTIPLIER refers to the repetitive reabsorption of sodium chloride by the thick ascending limb of the loop of Henle and continued inflow of new NaCl by the PCT into the loop of Henle. Water moves out of the filtrate in the descending limb down the osmotic gradient. This concentrates the filtrate. The higher the osmolarity of the interstitium, the more water leaves the descending limb by osmosis. The more water that leaves the descending limb, the saltier the tubular fluid is in the tubule. The saltier the tubular fluid, the more salt the tubule pumps into the interstitium.
The sodium reabsorbed by the thick ascending limb keeps adding to the newly arrived NaCl, thus multiplying it's concentration in the medullary interstitium
Explain the countercurrent exchange of the vasa recta?
The Vasa recta runs parallel to the loop of Henle in the juxtamedullary nephrons. As blood flows down the descending limb of the vasa recta, solutes move into the vasa recta from the medullary interstitium and water leaves into the interstitium . As the vasa recta then ascends again back into the renal cortex (which is a less Hyperosmotic environment) the solutes leave the vasa recta again and are reabsorbed again in the descending limb and water is reabsorbed back in again. This constant exchange means much less solute is lost and the hyperosmolarity of the medulla is maintained.
How much of the filtered load of urea is reabsorbed in the PCT?
What is ADHs effect on urea ?
Increases urea permeability of medullary collecting tubule by activating Ut-1 transporter.
Explain the re circulation of urea?
Urea enters into the medullary collecting duct, diffuses out into the interstium (UTA1 and UTA3) and then enters again into the thin loop of Henle. It then goes back through the early DCT and CD and back again to the medullary CD where it repeats this process. Each time the urea recirculates, it contributes to a increased concentration excreted in the urine. This saves water . It also contributes to the hyperosmolarity of the medulla.
What is the major determinant of ECF osmolality?
What percent of sodium is lost be non renal routes?
What drives sodium reabsorption all along the renal tubule?
What percentage of filtered sodium is usually secreted?
Explain sodium reabsorption in the PCT?
Sodium reabsorption is coupled to the transport of several other solutes in the PCT including the absorption of nutrients and Cl-'and HCO3-. Glucose and amino acids are recovered from glomerular filtrate via sodium linked co transporters. Tight coupling between sodium and water reabsorption
Explain sodium reabsorption in the loop of Henle?
There is no active sodium transport in the thin limbs of the loop of Henle. Thick ascending limb is very metabolically active and sodium uptake occurs via co transport with Cl- and K+
Explain sodium reabsorption in the DCT and CD?
Early distal tubule -Na-Clcotransporters
•Aldosterone increases the activity of the Na+ transport proteins
•Sodium reabsorption and potassium secretion by the principal cells
•Na+/H+ exchange occurs all along the distal tubule and the cortical collecting duct and contributes to Na+ uptake
List factors controlling sodium excretion?
Renal Sympathetic Nerves (↑ in their activity: ↓ NaCl excretion)
•↓ GFR (constriction of afferent & efferent arteriole)
•↑ Na+reabsorptionalong the nephron
Angiotensin II stimulates aldosterone and ADH secretion; enhances Na+ reabsorption by the proximal tubule.
ADH acts in thick ascending limb of Loop of Henle to increase Na+ reabsorption
Aldosterone acts on the principal cells of the cortical collecting tubule -enhances reabsorption of Na+ by Principal cells.
ANP (atrial natriuretic peptide) decreases reabsorption from collecting duct (Principal cells)
Explain aldosterones action on maintaining sodium balance?
1. Aldosterone combines with a cytoplasmic receptor
2. Hormone receptor complex initiates transcription in the nucleus
3. New protein channels and pumps are made
4. Aldosterone induced proteins modify existing proteins
5. Result increase sodium reabsorption and potassium secretion
Where is ANP mostly secreted from?
Cardiac muscle cells in the atria
What stimulates ANP?
Increased serum sodium and increased ECF volume
What are some actions of ANP?
•act on the kidneys to increase Na+ excretion
•dilate afferent arterioles and relax mesangialcells in the kidney
•in the renal tubules -inhibit Na+ reabsorption
•increases capillary permeability -decrease blood pressure
What are some cell functions potassium is crucial for?
•regulation of cell volume
•regulation of intracellular pH
•resting membrane potential
•cardiac and neuromuscular activity
Where is most of the body potassium located in the body?
In the ICF
What constitutes hyperkalemia?
When potassium exceeds 5.0mEq/L
What constitutes hypokalemia?
When potassium is less than 3.5mEq/L
True or false- potassium is filtered freely and is not bound to any plasma proteins
How much of potassium is reabsorbed in the PCT?
How much of potassium is reabsorbed in the thick ascending limb?
How does potassium enter the cells and exit the cells when being reabsorbed?
K+ enters the cells via the Na+-K+-2Cl−cotransporter
•Leaves the cell along either of two possible routes: K+ may diffuse across the basolateralmembrane through K+channels, to be reabsorbed, and K+ may diffuse back into the lumen
Explain reabsorption of potassium in the DCT and Cd?
These segments either reabsorb or secrete K+
•A low K+ diet -there is reabsorption of K+ by the α-intercalated cells
•Normal or high K+diet -K+is secreted by the principal cells
Discuss potassium reabsorption by α-intercalated cells
Luminal membrane with H+-K+ATPase
•Pumps H+ from the cell to the lumen and simultaneously pumps K+ from the lumen into the cell
•K+ then diffuses from the cell into blood via K+ channels
Discuss potassium secretion by principal cells?
Net transfer of K+from blood into the lumen
•K+ diffuses across the luminal membrane through K+ channels
Explain aldosterones effect on potassium?
•Aldosterone induces the synthesis of more luminal membrane Na+ channels
•Increased Na+ entry into the cell
•Provides more Na+ to the Na+-K+ ATPase
•More Na+ is pumped out of the cell
•More K+ pumped into the cell
•Aldosterone increases Na+-K+ ATPase pumps
•Increases K+ pumped into the cell
•Raising the intracellular K+ concentration increases the driving force for K+ secretion from the cell into the lumen
•Aldosterone also increases the number of K+ channels in the luminal membrane
Explain acid base disturbances and alteration in potassium secretion in alkalosis?
There is a deficit of H+ in the ECF
•H+ leaves the cells to aid in buffering
•K+ enters the cells to maintain electroneutrality
•The increased intracellular K+ concentration increases to cause K+ secretion
Explain acid base disturbances and alteration in potassium secretion in acidosis?
There is an excess of H+ in the ECF
•H+ enters the cells for buffering
•K+ leaves the cells to maintain electroneutrality
•The intracellular K+ concentration decreases
•Decreases K+ secretion
How much of filtered calcium is reabsorbed?
How much of calcium is bound to plasma proteins and cannot be filtered across the glomerular capillaries?
40% and no it cannot be filtered
What is calcium reabsorption tightly coupled to in the PCT and loop of Henle?
Explain the movement of calcium in the PCT?
•67% of the filtered load is reabsorbed
•Two thirds is reabsorbed via a paracellularroute
•One third is reabsorbed via a transcellularroute -includes Ca2+ channels in the apical membrane and a primary Ca2+-ATPase or 3 Na+/1 Ca2+ exchanger in the basolateralmembrane
Explain the movement of calcium in the Thick ascending limb?
•25% is reabsorbed
•Ca2+ reabsorption occurs along a paracellularroute
•Due to Na+-K+-2Cl− cotransporterinduced lumen positive potential difference
•Loop diuretics [furosemide] will inhibit Na+-K+-2Cl− cotransporterhence inhibit calcium reabsorption [used in the treatment of hypercalcemia]
How much calcium is reabsorbed in the DCT?
What effects do thiazide diuretics have on the distal tubule?
increase Ca2+ reabsorption in this segment (prescribed in cases of hypercalciuria, osteoporosis and nephrolithiasis (kidney stone disease).Thiazides inhibit the luminal Na-Cl cotransporter in DCT leads to a fall in intracellular Na+ promotes Na+/Ca2+ exchange and increased basolateral extrusion of Ca2+
What is the role of PTH on calcium reabsorption?
(PTH) increases calcium reabsorption in the thick ascending loops of Henle, late distal tubules, and in early collecting ducts
How much of phosphate is filtered?
How much of phosphate is reabsorbed in the early PCT ?
How much of phosphate is reabsorbed in the late PCT?