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Proximal Convoluted Tubule (PCT): Pathophysiology

by Carlo Raj, MD
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    Up until now we have looked at overview of the nephron and we have introduced the different parts of the nephron and I have gone through an overview. And at some point if you got a little confused or perhaps even tripped up with some of the information that I have given you, not to worry, reinforcement. So here we will walk into and dive into further detail of each segment of the nephron and go through all the relevant information so that you can get your questions on any aspect of medicine on the nephron absolutely correct. So let us take a look at the PCT in that respect. Once again, to review, take a look at this. Obviously, I am not going to spend time going through each one in details, but I will go through the details of what I referred to. For example, the carbonic anhydrase and its inhibition and what that means to you? Stop here for one second and what does that mean to you if you inhibit that enzyme? You are getting rid of your bicarb. Why might you want to do that? Do you remember our discussion on high altitude? How fast are you breathing? Very quickly. Blowing off the carbon dioxide so maybe perhaps you might want to on purpose, help your patient by inhibiting the carbonic anhydrase so that patient can then compensate by getting rid of that bicarb in the kidney. At this point, you should be able to figure out what the figure looks like in its organization pattern? I have established that over and over again in previous discussions. For example, on the left is your urine, in the middle is your cell and on the right is your interstitium, moving towards your blood. We have also...

    About the Lecture

    The lecture Proximal Convoluted Tubule (PCT): Pathophysiology by Carlo Raj, MD is from the course Diseases of the Nephron. It contains the following chapters:

    • Proximal Nephron
    • Proximal Convoluted Tubular Mechanics
    • Correlations

    Included Quiz Questions

    1. It is reabsorbed at around 300 mOsm/kg with water in the PCT.
    2. 90% of Na reabsorption occurs in the PCT.
    3. It is responsible for paracellular transport of other cations
    4. Reabsorption is inhibited in the PCT by parathyroid hormone.
    5. It is exchanged for K+ in response to aldosterone stimulation.
    1. Flapping tremors
    2. Gynecomastia
    3. Easy bruising
    4. Jaundice
    5. Caput medusa
    1. All are correct.
    2. It is an alkaline substance.
    3. It is metabolized in the liver.
    4. It converts to ammonium in the distal convoluted tubule.
    5. It is generated in the proximal convoluted tubule.
    1. Hypercalciuria
    2. Hypophosphaturia
    3. Hyperphosphatemia
    4. Hypocalcemia
    5. Dysfunction of PTH receptors
    1. Decreased urine pH.
    2. Preferential vasoconstriction of the afferent arteriole.
    3. Increase urine sodium concentration.
    4. Decreased glomerular filtration rate
    5. Increase in sodium filtered load.
    1. Increased oncotic pressure in the peritubular capillaries.
    2. Increased hydrostatic pressure in the peritubular capillaries.
    3. Decreased hydrostatic pressure in the peritubular capillaries.
    4. Increased oncotic pressure in the tubular lumen.
    5. Increased hydrostatic pressure in the tubular lumen.
    1. It is secreted.
    2. Filtered load of inulin = excretion rate of inulin.
    3. It is freely filtered.
    4. It is not reabsorbed.
    5. Inulin concentration increases along the tubule.
    1. Afferent arteriole
    2. Efferent arteriole
    3. Distal convoluted tubule
    4. Proximal convoluted tubule
    5. Bowmans space
    1. Creatinine is slightly secreted.
    2. Inulin concentration is proportional to skeletal muscle mass.
    3. Inulin is completely secreted.
    4. Creatinine is completely reabsorbed.
    5. Inulin is freely filtered.
    1. Albumin is not freely filtered.
    2. Reabsorption of albumin.
    3. Reabsorption of water.
    4. Protein binding of albumin.
    5. Secretion of albumin.
    1. Increased hydrostatic pressure in the afferent arteriole
    2. Decreased oncotic pressure in the afferent arteriole
    3. Increased oncotic pressure in the afferent arteriole
    4. Increased hydrostatic pressure in Bowman’s space
    5. Decreased oncotic pressure in Bowmans’ space
    1. Plasma
    2. Extracellular fluid (plasma and interstitial fluid)
    3. Interstitial fluid
    4. Total body water
    5. Intracellular fluid
    1. Conn’s syndrome
    2. Cirrhosis
    3. Dehydration
    4. Internal hemorrhaging
    5. Congestive heart failure
    1. Increase filtration fraction
    2. Increased glomerular filtration rate
    3. Increased renal plasma flow
    4. Decreased oncotic pressure in the peritubular capillaries
    5. Increased hydrostatic pressure in the glomerular capillaries
    1. Overall increased reabsorption from the tubular lumen.
    2. Increased hydrostatic pressure in the peritubular capillaries.
    3. All are expected changes.
    4. Decreased filtration fraction.
    5. Increased hydrostatic pressure in the glomerular capillaries.
    1. Luminal bicarbonate transporter
    2. Carbonic anhydrase type 1 on luminal membrane
    3. Carbonic anhydrase type 2 in epithelial cell
    4. Na-K-ATPase
    5. Na-H antiporter
    1. Reabsorption involves conversion to carbon dioxide then it is converted back to bicarbonate in the epithelial cell.
    2. 80% is reabsorbed in the proximal convoluted tubule.
    3. Bicarbonate is produced de novo in the distal convoluted tubule.
    4. Reabsoprtion in the proximal convoluted tubule occurs without the use of transporters.
    5. Each bicarbonate molecule reabsorbed requires excretion of one hydrogen ion.

    Author of lecture Proximal Convoluted Tubule (PCT): Pathophysiology

     Carlo Raj, MD

    Carlo Raj, MD


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