Diuretics and Renal Diseases Flashcards
Diuretics
-increases urine output
-they work by interfering with reabsorption of Na, with reduced water reabsorption being a secondary effect (Na inside the tubule increases osmolarity of the filtrate). Since Na reabsorption is associated with excretion of other ions (K, Cl, Mg, Ca), diuretics will affect their excretion as well
Clinical relevance of diuretics
-they are given to reduce the volume of extracellular fluid (eg. Edema, and hypertension)
Diuretics speed
-work within minutes to hours
>increase urine volume up to 20-fold
-after a few days, kidneys use compensatory mechanisms to overcome the effects of diuretics (eg. through enhanced renin-angiotensin II system)
Types of diuretics
1.Osmotic diuretics
2. loop diuretics
3. Thiazide diuretics
4. Carbonic anhydrases inhibitors
5.Competitive inhibitors of aldosterone
6. Na channel blockers
Osmotic diuretics
-they enhance osmotic pressure within tubules (keep water inside the tubule)
-ex. urea, mannitol, sucrose
Loop diuretics
-they reduce Na/Cl/K reabsorption by blocking Na/2Cl/K transporters at the thick ascending segment of the loop of Henle
-very potent drugs, which can cause excretion of up to 30% GFR
Loop diuretics effects
1.increased solutes in the tubule interferes with water reabsorption
2. interferes with countercurrent multiplier system and this reduces the osmolarity of renal medullary interstitium, so the capacity for concentrating urine is reduced
Thiazide diuretics
-they reduce Na/Cl reabsorption at the distal tubule
-can lead to excretion of up to 10% GFR
Carbonic anhydrase inhibitors
-Reduce the Na/HCO3- reabsorption at the proximal tubule
-the reduced HCO3- reabsorption reduces the Na reabsorption via the Na/H counter transporter
Competitive inhibitors of aldosterone
-Reduce Na reabsorption and K secretion at the cortical collecting tubules
>antagonists of mineralocorticoid receptors
>K+ sparing diuretics
Na channel blockers
-Block Na channels at the cortical collecting tubules
>K+ sparing diuretics
-Reduced Na within the cell leads to a decreased activity of Na/K pumps at basolateral membrane so less K enter the cell and less K+ is secreted
Acute renal failure
-a major sudden interruption in renal failure which can be reversed
>affects K+ and H+ secretion and may lead to K+ retention and metabolic acidosis
Categories of Renal failure
1.Prerenal acute renal failure- main problem is outside the kidneys
2. Intrarenal acute renal failure- main problem is within the kidneys
3. Postrenal acute renal failure- main problem is in the urinary collecting system
Prerenal acute renal failure cause
-main cause is reduced blood flow to the kidney which leads to reduced GFR and reduced urine output
Eg. heart failure, reduced blood pressure/volume, hemorrhage
**normal renal blood flow rate is ~20% cardiac output
-can lead to intrarenal failure due to damage to kidney
Oliguria
-reduced urine output below intake of water and solutes
Prerenal acute renal failure problems
1.Results in reduced GFR which effects the kidneys ability to remove waste products and adjust electrolytes, acid-base
2. Results in reduced blood flow to kidney which when prolonged can result in renal blood flow damaging the renal cells due to a lack of oxygen and nutrients
Intrarenal acute renal failure areas of damage
1.Glomerular capillaries
2.Tubules (epithelial cells)
3. Renal interstitium