1. almost all the glucose, bicarbonate, AAs, organic solutes are reabsorbed.

2. 67% of the water is reabsorbed.

3. All the organic acids are secreted here (uric acid, diuretics, and some antibiotics. 

4. site for organic base secretion occurs here.

5. 99% of the glucose and amino acids are absorbed here.

Properties of descending loop of Henle

1. descends into medulla of kidney

2. impermeable to Na, Cl and permeable to water

3. The osmolarity increases down the loop due to counter current mechanism.

1. Cells impermeable to water

2. cells actively reabsorb Na, Cl and K

3. Major site for Na reabsorption in nephron

4. K back diffusion into lumen= Reason for Ca and Mg reabsorption.

1. Na is actively reabsorbed, Cl co-transported and water follows passively at terminal end.

2. Have Na/K exchange site. Fine tunning of K occurs here.

3. Na absorption and K secretion is stimulated by aldosterone.

1. Most diuretic agents are secreted in the renal tubule to act on transporters.

2. Increased delivery of Na in CD stimulate K secretion.

3. Most water and Na reabsorption occurs in PCT.

Mannitol, Urea, Glycerin and Isosorbide.

They are freely filtered by glomerulus, undergo renal tubular reabsorption, and usually inert.

They prevent re-absorption of water from the water permeable areas. Intra-luminal and extra-luminal mechanisms work for osmotic diuretics.

Uses

Extract water from eyes and brain. Used in reducing cerebral edema and intraocular pressure before opthalmic procedure.

Side effects:

Acute expansion of extracellular fluid, be careful with people in CHF or pulmonary edema. 

Headache, nausea, vomiting due to deacrease in Na. dehydration.

Acetazolamide, dichlorophenamide.

MOA:Block carbonic anhydrase, decrease H, decrease Na reabsorption. Decrease HCO₃ reabsorption, and increase excretion. Increase K secretion. Urine is alkaline pH, and causes metabolic acidosis.

Uses: Limited use as diuretic, but used for metabolic alkalosis in conjuct with other diuretics. Use for glaucoma (darzolamide, binzolamide).

Also, used for mountain sickness. (Dec. in HCO₃, causes metabolic acidosis, and causes hyperventilation.Dec CSF formation, pH and cerebral edema.

Side effects: CNS effects, parenthesias, drowsiness, metabolic acidosis, kidney stones, and contraindicated in patients with hepatic cirrhosis as increase in urine pH causes decreased NH₄ trapping in the urine and increases NH₃ and hepatic encephalopathy.

Furosemide, bumetanide, ethacrynic acid, torsemide.

They are known as high-ceiling diuretics and secreted by organic acid transport system in PCT.

They work in thick ascending Loop by inhibiting the Na/K/Cl symporter on the luminal membrane of the cells

Uses: pts those have poor renal function or other diuretics were unaffective.

People with edema related with CHF, hepatic or renal failure. Acute pulmonary edema by ↓volume, ↓VR, and ↓ right ventricular pressure and leads to ↓pulmonary capillary pressure.

Used in pts with hypercalcemia by ↓Na, and Cl reabsorption, ↓ k-back diffusion and ↓ calcium reabsorption. 

Mild hyperkalemia, by increasing K loss.

Side effects: Hypovolemia; can cause severe loss of blood volume leads to hypotension shock.

Hypokalemia/metabolic acidosis: ↑ Na and H in CD can cause ↑ K and H excretion.

Ototoxicity: Concurrent use with aminoglycoside antibiotic such as streptomycin. Can be reversed.

Thiazide diuretics and their MOA:

Names: HCTZ, indapamide, chlorthalidone, metolazone, and all the one with "thiazide" in word.

MOA: secreted by organic acid transport system in PCT. These block the Na and Cl symporter in the early segment of distal convulated tubule. Many actions depend on PG production. NSAIDs can blunt the effects.

Uses: First line of therapy for hypertension.

Acute edema.

Hypercalciuria by decreasing Na reabsorption, decreases intracellular Na, increases Ca/Na exchange, eventually decreases Ca in renal tubule, decreases kidney stones.

Side effects: Causes hypovolemia, triggers ADH and thirst.

Causes hypokalemia or metabolic alkalosis by ↓ Na reabsorption, causes ↑ K and H loss.

hyperuricemia can occur as it is secreted by organic acid system, can cause gout.

1: Aldosterone antagonists (spironolactone, eplerenone).Inhibits the aldosterone complex which ↑Na reabsorption, and ↓ K secretion.

2: K sparing, Na channel blockers (Triametrene and Amiloride). Blocks Na reabsorption, decreases K secretion. These are not aldosterone antagonists.

Uses: With other diuretics to decrease the K loss.

These are mild diuretics.

Side effects:

Hyperkalemia and metabolic acidosis due to H retention.

Stimulents: Hyperosmolarity, angiotensin II and volume depletion.

Inhibitors:Ethanol, glucocorticoid, and ANP.

List the metabolic and respiratory compensatory mechanisms?

Metabolic compensatory mechanism: HCO₃^- is controlled by carbonic anhydrase and brush borders of proximal tubules of kidney. Also, the H and K intracellular exchange.

Respiratory compensatory Mechanism: pCO₂ is controlled by lung function and respiratory control.

Mannitol, Uremia, Diabetic ketoacidosis, Protease inhibitors,

A                 A/C                    A                                  A/C

INH, Lactic acid, ethanol or ethylene glycol,  

 A/C      A                A

Salicylates or starvation.

    A                      C

Hyperailmentation, acid indigestion or addison's disease

a                          a                      c

Renal failure, diarrhea or diuretics,

c          a               c

uretosigmoidostomy, pancreatitis

C                 a/c