Nephron: Overview, Tubular Transport and Tubular Secretion

by Carlo Raj, MD

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    Our discussion earlier was dealing with bicarb. Talked about the physio of it all. Let us give some clinical correlations like you should be doing in every step of the way. Normally what this we are talking about lowering the renal threshold for bicarb. What does that even mean? That means that you actually not reabsorbing bicarb. Listen to what I just said. We are going to lower our standard terminology, the renal threshold for reclaiming bicarb, which means what? That means more the bicarb remains within the urine and you are going to get rid of it. So, therefore, your normal bicarb level, which is between 22 to 26 and we are using 24 has now dropped down to 15 where, please? In the plasma right. Now you tell me acid-base disturbances from physiology. If you want to drop your bicarb down to 15, what does that mean to you? Acidosis because you don't have as much bicarb. You have lost it. What kind of acidosis? Is this respiratory acidosis or would this be metabolic acidosis? Good. Metabolic acidosis. Are you clear? If you have metabolic acidosis let me take one step further just to make sure we are good here. If you have metabolic acidosis and how you are going to compensate, you are going to try to blow off your carbon dioxide very quickly so therefore within minutes, you are going to start hyperventilating so that you can blow off that carbon dioxide, aren't you? Continue. So now this results with what? Loss of more of the filtered bicarb than the normal renal threshold. Why might you want to do this as a method of compensation? As a method of compensation maybe perhaps you are doing this remember that high altitude patient that we talked about acutely...

    About the Lecture

    The lecture Nephron: Overview, Tubular Transport and Tubular Secretion by Carlo Raj, MD is from the course Diseases of the Nephron. It contains the following chapters:

    • Proximal vs. Distal Nephron
    • Tubular Transport by Nephron Segment
    • Tubular Secretion

    Included Quiz Questions

    1. 300-1200 mOsm/kg
    2. 0-300 mOsm/kg
    3. 1000-1200 mOsm/kg
    4. 300-800 mOsm/kg
    5. 800-1200 mOsm/kg
    1. Only juxtamedullary nephrons have proximal convoluted tubules.
    2. Juxtamedullary nephrons have longer loops of Henle compared to cortical nephrons.
    3. Peritubular capillaries surround the tubules of both classes of nephrons.
    4. Juxtamedullary nephrons are responsible for development of osmotic gradients in the renal medulla.
    5. Bowman’s space of both juxtamedullary and cortical nephrons are always located in the cortex.
    1. Na-K-ATPase
    2. Sodium-dependent glucose cotransporters
    3. All are apical membrane transporters.
    4. Phosphate-Na symporter
    5. Na-H+ antiporter
    1. Carbonic acid
    2. Sodium
    3. Phosphate
    4. Potassium
    5. Glucose
    1. Thin descending loop of Henle
    2. Proximal convoluted tubule
    3. Distal convoluted tubule
    4. Thick ascending limb
    5. Cortical collecting duct
    1. Furosemide
    2. Mannitol
    3. Amiloride
    4. Spironolactone
    5. Thiazides
    1. Apical K+ backleak channels
    2. Basolateral Na-K ATPase pump
    3. Apical K+/H+ antiporter
    4. Apical Na-K-2Cl symporter
    5. Basolateral K+ channels
    1. It is the primary dysfunction in Bartter’s syndrome.
    2. Excessive PTH action results in higher than normal levels of cyclic AMP in the urine.
    3. Stimulates calcium reabsorption in the distal convoluted tubule.
    4. Inhibits reabsorption of phosphate in the proximal convoluted tubule.
    5. Activates 1 alpha hydroxylase increasing calcitriol levels.
    1. Decreased levels of circulating PTH
    2. Short stature
    3. Low levels of urine cyclic AMP
    4. Hyperphosphatemic
    5. Hypocalcemica
    1. Basolateral membrane of collecting tubules.
    2. Apical membrane of collecting tubules.
    3. Basolateral membrane of distal convoluted tubule.
    4. Apical membrane of distal convoluted tubule.
    5. Basolateral membrane of proximal convoluted tubules.
    1. Na < 136 mEq/L, K > 5.5 mEq/L, pH < 7.35
    2. Na > 145 mEq/L, K < 3.5 mEq/L, pH > 7.45
    3. Na < 140 mEq/L, K > 4.0 mEq/L, pH < 7.4
    4. Na < 136 mEq/L, K < 3.5 mEq/L, pH < 7.35
    5. Na > 145 mEq/L, K > 5.5 mEq/L, pH < 7.35
    1. Apical K/H antiporter of intercalated cells.
    2. Apical K+ channel of the principal cells.
    3. Apical K+ channels of principal cells.
    4. Basolateral K+ channels of intercalated cells.
    5. Basolateral Na+/K+ ATPase of principal cells.
    1. Na-K-2Cl symporter
    2. Na/K+ antiporter
    3. Carbonic anhydrase
    4. Sodium dependent glucose transporters
    5. Na-K-ATPase
    1. Aldosterone
    2. Renin
    3. Anti-diuretic hormone
    4. Parathyroid hormone
    5. Angiotensin II
    1. …Peritubular capillaries.
    2. …Afferent arteriole.
    3. …Bowman’s space.
    4. …glomerulus.
    5. …Efferent arteriole.
    1. Hydrochlorothiazide
    2. Furosemide
    3. Spirinolactone
    4. Amiloride
    5. Mannitol
    1. Respiratory alkalosis
    2. Anion gap metabolic acidosis
    3. Metabolic alkalosis
    4. Respiratory acidosis
    5. Non-anion gap Metabolic acidosis
    1. To overcome transport competition with accumulated organic ions.
    2. Hyperfiltration causing excessive excretion.
    3. To overcome ionic bonding with organic ions.
    4. To stimulate production of membrane transporters.
    5. To overcome protein binding associated limitation of filtration.

    Author of lecture Nephron: Overview, Tubular Transport and Tubular Secretion

     Carlo Raj, MD

    Carlo Raj, MD

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