B - 22. Potassium excreting (wasting) diuretics

Question 1

Loop diuretics - location of action

Answer 1

Loop of Henle - thick ascending limb

Question 2

Loop diuretics names

Answer 2

Sulfonamide derivative - Furosemide

Phenoxyacetic acid derivate - Ethacrynic acid

Question 3

Loop diuretics mode of action

Answer 3

Binds to Cl- side of the Na+/K+/2Cl- cotransporters on the apical side of cells of the thick ascending limb, blocking it -> the ions does not get reabsorbed, and water follows

Question 4

Loop diuretics indications

Answer 4

• Hypertension
• Edema
• Hyperkalemia
• Hypercalemia (Calcium and magnesium passively follows the Na+ gradient)
• Acute bromide/iodide/fluoride intoxication (also reabsorbed in thicc ascending limb)

Question 5

Loop diuretics contraindications

Answer 5

• Dehydration

Probably more lol

Question 6

Loop diuretics SE

Answer 6

GO PANDA:
Gout
Ototoxicity
(low) Potassium
Allergies
Nephritis 
Dehydration
Alkalosis

Question 7

Thiazides - location of action

Answer 7

Absorbed into proximal convoluted tubule

Travels to distal convoluted tubule

Question 8

Thiazides names

Answer 8

Hydrochlorothiazide - (thiazide)

Indapamide - (thiazide-like)

Question 9

Thiazides mode of action

Answer 9

Competes with uric acid upon absorption into proximal convoluted tubule, increasing uric acid levels

Blocks Na+ reabsorption in distal convoluted tubule (on Na+/Cl- cotransporter I think)

Ca++/Na+ exchanger (Na+ -> cell, Ca++ -> blood) will work overtime to compensate and cause increased Ca++ reuptake

Question 10

Thiazides indications

Answer 10

• 1st line antihypertensive agents
• 2nd line therapy for edamatous states
• calciuria/hypocalcemia
• osteoporosis (calcium reab)
• nephrogenic diabetes insipidus (kidneys do not respond to ADH)

Question 11

Thiazides SE

Answer 11

HyperGLUC: hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia

• Messes with sugar and fat metabolism -> hyperglycemia, increased serum cholesterol and LDL
• Hypercalcemia
• Hyperuricemia -> gout
• Short term -> hyponatremia
• Hypokalemic metabolic acidosis

Hyponatremia feedback loop - Urine output increased -> hypovolemia -> ADH released to counter, binds to V2 receptors of collecting duct -> more water reabsorption -> dilution of blood -> hyponatremia

Question 12

Diabetes insipidus - thiazide logic

Answer 12

Thiazides cause mild hypovolemia -> kidneys increase Na+ and water reabsorption in the PROXIMAL convoluted tubule -> less fluid reaches DISTAL C.T. -> fluid balance is maintained

Question 13

Carbonic anhydrase inhibitors - location of action

Answer 13

Kidney: tubular cells of proximal CT
Eyes: ciliary bodies
Brain: choroid plexus

Question 14

Carbonic anhydrase inhibitors - names

Answer 14

Acetazolamide

Question 15

Carbonic anhydrase inhibitors - action

Answer 15

Decreased bicarbonte reabsorption in proximal CT -> decreased Na+ reabsorption -> increased urine output

Question 16

Carbonic anhydrase inhibitors - indication

Answer 16

Much weaker than other diuretics, so only used in cases edema with alkalosis

Used against kidney stones and gout, as it alkalizes urine and prevents precepitation of cystine

Question 17

Carbonic anhydrase inhibitors - SE

Answer 17

• Metabolic acidosis (due to bicarbonate loss)
• Renal stones (due to phosphate and calcium excretion -> precipitation -> stones)
• Renal potassium wasting (potassium follows sodium)
• Neurological side effects
• Contraindicated in cirrhosis (decreases ammonia clereance -> liver cant deal with ammonia levels -> hepatic encephalopathy)