Diuretics pt. 2 (Exam III) Flashcards
What does H₂O movement look like in the DCT?
How much Na⁺ absorption occurs in the DCT?
- ↓H₂O movement
- very little Na⁺ absorption
What ion gets reabsorbed in the DCT?
How does this occur?
Ca⁺⁺ is reabsorbed by PTH (Parathyroid hormone)
How do Thiazide diuretics elicit their effects?
Do they affect any other things?
Inhibition of NCC transporter (causing NaCl loss)
CA (Carbonic Anhydrase) inhibited slightly.
Combination of which two diuretic classes would cause a massive H₂O loss and require hospitalized monitoring?
Loop Diuretics + Thiazides
Which Thiazide diuretic is prototypical?
HCTZ (Hydrochlorothiazide)
Where is the final site of Na⁺ reabsorption?
Which site is the most important for K⁺ secretion?
Collecting Tubule
Collecting Tubule
Where do mineralcorticoids (like Aldosterone) elicit their effects?
Cortex portion of Collecting Tubule
Which channel is responsible for reabsorbing Na⁺ from the collecting tubule back into the blood?
ENaC (Epithelial Na⁺ Channel)
What potentiates the ENaC channel to increase Na⁺ retention?
Aldosterone
Where is Cl⁻ reabsorbed into the blood?
How is Cl⁻ reabsorbed into the blood?
- Collecting Tubule
1. ENaC retains Na⁺
2. Less K⁺ driven out makes urinary lumen (-)
3. (-) charge drives Cl⁻ through paracellular route into blood.
Which two diuretic classes are K⁺-wasting?
Which wastes more K⁺?
Loop Diuretics and CA Inhibitors (Acetazolamide)
Acetazolamide
Name two K⁺-sparing diuretics and their mechanism of action.
Spironolactone - blocks aldosterone receptors
Amiloride - Inhibits ENaC, blocking Na⁺ movement and thus K⁺ movement.
Rate of _____ secretion is positively correlated with aldosterone levels.
K⁺
What are the primary uses for K⁺-sparing diuretics?
States of excessive mineralcorticoids
- Conn’s Syndrome (excessive edema)
- Ectopic ACTH Production.
What are secondary uses for K-sparing diuretics?
- CHF
- Nephrotic Syndrome
What are 3 contraindications to K⁺-sparing diuretics?
- Patient takes K⁺ supplement
- Patient on drugs affecting K⁺ levels
- Liver Disease
What is the most common result of K⁺-sparing diuretic toxicity?
What exacerbates this?
How can this be avoided?
- Hyperkalemia
- Renal Disease
- Toxicity avoided by administering K⁺-sparing drug with a loop diuretic, balancing K⁺ levels.
How does ADH increase H₂O reabsorption?
- ADH binds to receptor
- Aquaporin carrying vesicle merges with urinary cell membrane.
- H₂O has more aquaporins to move through
What would osmolality be at the very apex of the thick ascending limb?
100 mOsm/L
What drug directly inhibits ADH?
Conivaptan
What is the primary use of mannitol?
What is a secondary use of mannitol?
- Reduction of ICP
- Removal of renal toxins (acute hemolysis or after radiocontrast)
How does Mannitol elicit its effect?
Mannitol is essentially artificial osmolality, increasing urine volume by pulling H₂O towards it.
What would the effects of mannitol toxicity be on serum Na⁺ specifically?
- Initial ↓ serum Na⁺
- Secondary ↑↑↑ serum Na⁺
What would mannitol toxicity encompass?
Would this differ if the patient had renal failure?
- Dehydration
- ↑Na⁺
- ↑K⁺
If the patient had renal failure then ↓Na⁺
What diuretic can crystallize when given parenterally and must be given with an in-line filter?
Mannitol
What is the most common reason for diuretic use?
Edema (peripheral or pulmonary)
What syndrome is characterized by insufficient endogenous ADH?
What would the s/s be?
Diabetes Insipidous
Polydipsia & polyuria
What is the treatment for Nephrogenic Diabetes Insipidous?
Thiazide Diuretics
- ↓ plasma volume, ↓ GFR, H₂O & NaCl reabsorption.
Where does ADH elicit its effects?
Medulla portion of Collecting Duct
