Structure and function of the kidney Flashcards

1
Q

What is a phosphate buffer system? How does it work and where? (Equilibrium equation)

A

An intracellular buffer and renal tubular buffer

Equation: H2PO4^–> H+ + HPO4^2-
- Hydrogen phosphate ions act in equilibrium with hydrogen ions

  • If you have Xs H+ ions, they bind to hydrogen phosphate and give you dihydrogen phosphate, making the environment more less acidic
  • If you have too little H+ ions, then dihydrogen phosphate dissociates to give H+ ions, making the environment more acidic
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2
Q

What are the 2 ways in which the kidneys maintain acid-base balance?

A
  1. Maintain the concentrations of HCO3- in the body by REABSORPTION of bicarbonate ions released through filtrate
  2. Regenerate new HCO3- from CO2, when CO2 is in excess in the blood
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3
Q

Explain the process of bicarbonate REABSORPTION in the kidneys

A
  • IN THE COLLECTING DUCTS by the intercalated cells
    1. H+ combines with HCO3- in the filtrate/lumen, forming H2CO3- (carbonic acid)
    2. Carbonic acid is broken down on the surface of the intercalated cell by carbonic anhydrase into CO2 and H20 so they can now get into the cell
    3. CO2 + H2O combine forming H2CO3- which quickly dissociates into HCO3- and H+ within the intercalated cell.
    4. HCO3- enters the peritubular capillary via the bicarbonate channel (chloride shift)
    5. H+ is excreted in the filtrate (Na/H ATP channel)
    6. Na+ is expelled into the ECF
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4
Q

What are the two cell types in the collecting ducts?

A
  1. Principal cells - main sodium/Na reabsorbing cells and site of action for aldosterone, K+ sparing diuretics, and spironolactone!
  2. Intercalated cells - reabsorb bicarbonate
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5
Q

2 processes in which the kidneys generate new bicarbonate?

A
  1. Ammonia buffer system AKA glutamine metabolism system

2. By phosphate

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6
Q

Explain the ammonia buffer system and bicarbonate is generated

A

Glutamine is part of the urine filtrate and so it is able to enter the cells = PCT, ascending loop of Henle and distal tubular cells. It can also come from inside the blood to the cells

  1. Glutamine is metabolised into NH4+ and HCO3- in the PCT, ascending loop of Henle and distal tubular cells.
  2. HCO3- enters the peritubular capillary
  3. NH4+ is secreted into the filtrate, down the loop of Henle, through the DCT and into the collecting ducts
  4. In the medullary and collecting tubules, NH4+ is reabsorbed and broken down into H+ and NH3
  5. NH3 is pushed out into the filtrate with H+, these two bind and are secreted as NH4+ + Cl- in the urine
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7
Q

Explain how the phosphate buffer system acts to generate new bicarbonate

A
  • Takes place within the intercalated cell
    1. CO2 combines with H20 forming H2CO3-
    2. Carbonic acid splits forming H+ and HCO3-
    3. H+ is secreted into the filtrate via the H+ ATPase pump, here they bind hydrogen phosphate and become dihydrogen phosphate which is excreted in the urine!
    4. HCO3- enters the peritubular capllary
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8
Q

What is metabolic acidosis? Include causes

A
  • Gain of acid or the loss of bicarbonate

Causes:

  1. Usually, generation of ketone bodies in uncontrolled diabetes mellitus
  2. Diarrhoea (loss of bicarbonate)
  3. Excess protein consumption (breakdown products are amino acids)
  4. Excess alcohol consumption
  5. Ingestion of acid (aspirin, ethanol, antifreeze)
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9
Q

What is metabolic alkalosis? Include causes

A
  • It is the gain of base or loss of acid. Primary abnormality being an increased HCO3-

Causes:

  • Increase in bicarbonate in the blood because of ingestion of excess bicarbonate in the form of antacid
  • Eating excess fruits
  • Loss of acid from vomiting
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10
Q

How do the lungs and kidneys compensate for deviation in pH?

A

Lungs: hyper or hypoventilation in order to remove/retain CO2

Kidneys:
1. low pH (Xs acid) = intercalated cells will secrete more acid into tubular lumen and make new bicarbonate and raise pH back to set point

  1. High pH (little acid / Xs base) = proximal convoluted cells will NOT reabsorb filtered bicarbonate and will eliminate it from the body to lower pH back toward normal
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11
Q

What makes infants and elderly people more at risk to acid-base imbalance?

A

Infants:

  • Low volume of lungs
  • Xs fluid shift (high rate of fluid intake and output)
  • High metabolic rate (x2 of adults)
  • Higher rate of water loss
  • Inefficiency of kidneys

Elderly:

  • Decrease in total body volume, leads to slow homeostasis
  • Unresponsive to thirst cues
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12
Q

Explain the formation of nephron capillary beds

A
  • The kidney has a portal system
  • We have the renal artery coming in which becomes an efferent arteriole, this goes to the bowman’s capsule and forms a capillary bed = glomerular capillaries
  • The glomerular capillaries branch out again (this how they differ to normal blood supply) rather than becoming venules –> veins.
  • Instead, they become efferent glomerular arterioles which branch out to become ANOTHER capillary bed
  • If this capillary bed is in the juxtamedullary nephron, it is called the vasa recta, if it is in the cortical nephron it is called the peritubular capillary
  • The 2nd capillary bed then branches out to form a vein, and the blood travels back to the renal vein
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13
Q

Explain the counter-current mechanism & the osmotic gradient setup within the medulla

A
  • Blood in the bowman’s capsule is being filtered, and it enters the PCT
  • As the filtrate descends down the loop of Henle, there is a difference in osmotic gradient between the filtrate and interstitial fluid, driving H2O out into the tissue
  • As water moves out, the osmolarity of the filtrate increases, up to 1200 at the arch of the loop of Henle
  • As the filtrate ascends up the loop of Henle, it is now travelling against the concentration gradient. So, Na and Cl are pumped out of the filtrate, into the interstitial fluid, causing the filtrate osmolarity of the filtrate to decrease and that of the interstitial fluid to increase
  • Travelling in tandem with the loop of Henle is the capillary bed.
  • The descending part of the arteriole is travelling against the ascending part of the loop of Henle, this is the counter-current mechanism
  • The descending part of the arteriole pushes out H2O which is picked up by the ascending loop of Henle, but at the same time is picking up the NaCl that the ascending loop is releasing
  • Vice versa, the descending loop releases H2O which is picked up by the ascending part of the arteriole.
  • THIS IS HOW URINE CONCENTRATION AND VOLUME IS REGULATED
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14
Q

How is water output regulated when we are dehydrated?

A
  • When dehydrated, BP decreases
  • The hypothalamus will stimulate release of ADH from the posterior pituitary gland
  • ADH goes back to the collecting ducts and stimulates reabsorption of water
  • > H2O reabsorption causes a decrease in ECF osmolarity and > plasma volume
  • This acts via a negative feedback loop to inhibit the osmoreceptors such that no more ADH is released.
  • We then get a small volume of concentrated urine
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15
Q

Anti-diuretic hormone. How is its release stimulated and where does it act and how

A

Hypothalamus stimulates the posterior pituitary gland to release ADH in response to increased osmolarity of extracellular fluids

  • It acts on the COLLECTING DUCTS
  • Increases the number of aquaporins (H2O channels) in the collecting duct
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16
Q

Describe the mechanism of action for aldosterone

A
  • Ang II activation stimulates ADRENAL CORTEX to release aldosterone
  • Works on the COLLECTING DUCTS to reabsorb water
  • It instructs the collecting ducts to REABSORB Na+ and SECRETE K+
  • This restores homeostatic plasma levels of Na+ and K+
17
Q

Influence of female sex hormones (oestrogen & progesterone) and glucocorticoids on kidney filtration

A
  1. Oestrogen: Acts similar to aldosterone. Enhance NaCl reabsorption by the renal tubules. Oestrogens are largely responsible for the oedema in pregnant women as water follows NaCl
  2. Progesterone: Decreases Na+ reabsorption by blocking the effect of aldosterone on the renal tubules by competing for receptors. So it has a DIURETIC-LIKE effect and promotes Na+ & H2O loss
  3. Glucocorticoids: Enhance tubular reabsorption of Na+, also promote increased GFR. At high plasma levels, glucocorticoids exhibit potent ALDOSTERONE-LIKE effects and promote oedema