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64 Cards in this Set

  • Front
  • Back
3 hormones produced from the kidney:
-Active Vit D
What does the kidney do to vitamin d?
Hydroxylates it at the 1 position to produce 1,25 dihydroxyvitamin D3
What is another name for 1,25 Dihydroxy D3?
Where does Cholecalciferol come from?
In the skin via UV activation
Where does cholecalciferol get activated first?
In the liver
What is the product of liver action on inactive cholecalciferol?
-Powerful feedback inhibitor of anymore liver activation
-Goes on to kidney for 2nd hydroxylation
Where in the kidney is vit D activated?
Proximal tubule
What stimulates activation of Vit D3 in the kidney?
Decreased plasma calcium
Where is calcium reabsorbtion stimulated by Vit D3?
-Thick ascending limb
-Distal tubule
-Intestinal epithelium
Where is EPO produced in fetal stages?
Where is EPO made after birth?
In the kidney
Main stimulus for EPO production:
Tissue hypoxia
What is lack of EPO the main cause of?
Anemia associated with chronic renal failure.
What is the effect of increased EPO?
Increased red cell mass
5 factors that stimulate EPO:
-Pulmonary disease
-Decreased hemoglobin
-Decreased bloodflow
-Decreased blood volume
Where is Renin found?
In JG cells in the wall of the afferent arteriole.
3 Major stimuli for Renin release:
-Renal sympathetic nerve stimulation increase
-Decreased NaCl delivery to macula densa
-Decreased renal perfusion pressure
2 hormones stimulated by renin:
-Ang II (directly)
-Aldosterone (indirectly)
Where is aldosterone secreted?
In the zona glomerulosa of the adrenal cortex.
What important metabolic process is achieved by the kidney?
Renal gluconeogenesis
What does the kidney make glucose from? Where?
Amino acids + lactate in the proximal tubule cells.
When does renal gluconeogenesis become important?
During periods of prolonged fasting.
How much more glucose does the kidney produce relative to the liver during fasting?
What is the major amino acid substrate for the kidney's production of glucose?
What are the important byproducts of glutamine synthesis in the kidney?
What happens initially when a person takes a diuretic?
-Sodium/H2O Excretion rate rapidly goes up and exceeds intake
-Intake stays the same
-ECF volume goes down to 13 L
What happens in the 2-4 days after taking a diuretic?
Na/H2O excretion rates go DOWN to once again match intake
Why does excretion go down after taking a diuretic?
Bc hormones kick in to increase Na/H2O reabsorption to increase ECF vol up to 14L
How do osmotic diuretics work?
By altering the osmotic driving forces along the nephron.
How do osmotic diuretics alter the osmotic gradient?
By increasing the osmolarity in the tubular lumen so water will go where the solute is - down the tube.
Where do osmotic diuretics have their greatest effect?
-Proximal tubule
-Thin desc LOH
What is the maximal effect of osmotic diuretics?
Increased Na excretion to 10% of the filtered load.
So how do osmotic diuretics change the osmotic gradient?
They decrease it
What is an exogenous osmotic diuretic?
How does the kidney handle mannitol?
-Freely filtered
-Not reabsorbed
-Trapped in tubular lumen
What are 2 endogenous osmotic diuretics? When are they clinically important?
-Glucose - in uncontrolled diabetes mellitus
-Urea - in renal failure
What are the side effects of osmotic diuretics? (3)
-Increased K excretion
-Incresed Bicarb excretion
-Increased Ca excretion
How do the CA inhibitors work?
-Inhibit CA
-Limit activity of Na/H exchanger
-Decrease reabsorption of Na
Where is the major site of action of CA inhibitors? Why?
Proximal tubules - predominant site of CA.
What is the maximal effect of CA inhibitors?
Increased Na excretion to 5-10% of the filtered load.
What is a commonly used CA inhibitor?
Side effects of CA inhibitors:
-Increased K excretion
-Incresed Bicarb excretion
-Increased Ca excretion
What do loop diuretics target?
Na/K/2Cl transporters in the thick ascending limb of LOH
What is the effect of loop diuretics?
Decreased Na reabsorption
What is the major effect of inhibiting Na/K/2Cl transporter?
Impairs kidney's ability to concentrate OR dilute urine by: 1. Preventing Na/Cl reabsorption from the tubule cell to blood
2. Preventing Mg/Ca reabsorption from the lumen to the tubule cell
Side effects of Loop diuretics:
-Increased K excretion
-Increased Calcium excretion
-Impaired ability to concentrate and dilute urine
3 common loop diuretics:
-Ethacrynic acid
What is the maximum effect of loop diuretics?
They acutely increase Na excretion up to 20% of the filtered load.
Where do Thiazide diuretics work?
In the early distal tubule
What do Thiazide diuretics inhibit?
Inhibit the Na/Cl Symporter in the Apical membrane of the early distal tubule.
What is the maximum effect of the thiazide diuretics?
They acutely increase Na excretion to 5-10% of the filtered load.
What are 2 commonly used thiazide diuretics?
What are side effects of Thiazide diuretics?
-Increased K excretion
-Decreased urinary diluting ability
Are thiazide diuretics as strong as Loop? Why/not?
No because they're closer to the cortex and play less of a role in generating the medullary concentrating gradient.
What is affected by loop diuretics that isn't by Thiazides?
Ca excretion - this is coupled to the Na/K/2Cl transporter in TAL, but not in the distal tubule.
How does making the early distal tubule cells impermeable to NaCl work as a diuretic?
It decreases the kidney's ability to dilute urine
Why are K-sparing diuretics called that?
Bc they decrease sodium reabsorption AND K excretion.
What is the target site of K-sparing diuretics?
The principle cells of the late distal tubule and cortical collecting duct.
What is the maximum effect of K-sparing diuretics?
It increases sodium excretion to 3-5% of the filtered load.
2 classes of K-sparing diuretics:
-Aldosterone antagonists
-Na channel blockers
2 Aldosterone-antagonists:
2 Na-channel blockers in principle cells:
Side effects of K-sparing diuretics:
-Decreased K excretion
-Increased bicarb excretion