Diuretics Flashcards

Question

what are the **clinical indications** for Loop Diuretics?

Answer 1

**Acute Pulmonary Edema** → rapid removal of fluid from lungs **Heart failure** **Hypercalcemia** → because loops increase Ca²⁺ excretion **Hyperkalemia** → promotes K⁺ loss **Acute Renal Failure** → helps increase urine output (“kick-start” kidneys) **Anion Overdose** (Bromide, fluoride, iodide—reabsorbed by NKCC2) → blocking NKCC2 enhances elimination

Answer 2

**Hypokalemic Metabolic Alkalosis** * Increased Na⁺ delivery to collecting duct → increased Na⁺ reabsorption → K⁺ is exchanged for Na⁺ → increased K⁺ secretion (K⁺ loss) → H⁺ is also secreted → alkalosis **Ototoxicity** * NKCC2-like transporters exist in the inner ear → loop diuretics disrupt electrolyte balance → reversible hearing loss → higher risk with Renal failure and Aminoglycosides (also ototoxic) **Hyperuricemia** → Gout * Loops compete with uric acid for secretion in the PCT → less uric acid excreted → uric acid rises → can trigger gout attacks. **Hypomagnesemia** * NKCC2 block eliminates lumen positivity → Mg²⁺ cannot be reabsorbed **Allergic Reactions** * All except ethacrynic acid are sulfonamides → may cause sulfa allergy

Answer 3

**hypokalemic metabolic alkalosis** → K+ replacement **hyperuricemia** → lowering dose **hypomagnesmia** → oral magnesium preperations

Answer 4

block the **Na⁺/Cl⁻ (NCC) cotransporter** in the distal convoluted tubule * **prevents NaCl reabsorption** → Na⁺ stays in the urine → water follows → diuresis * Na⁺ inside the cell decreases → **Na⁺/Ca²⁺ exchanger becomes more active** → more Ca²⁺ is pulled from the lumen into the blood

Answer 5

**Hypertension** (first-line therapy) * Thiazides reduce blood volume and cause long-term ↓ peripheral resistance **Heart Failure** * Mild diuresis helps reduce fluid overload **Kidney Stones** from Hypercalciuria * Because thiazides increase Ca²⁺ reabsorption → less Ca²⁺ in urine **Nephrogenic Diabetes Insipidus** (Paradoxical Use) * They reduce polyuria by causing mild volume depletion → increases proximal tubular water reabsorption.

Answer 6

All derived from **sulfonamides**: * **Chlorthalidone** * **Indapamide** * **Metolazone** – very potent; works even in renal failure

Answer 7

**Hypokalemic Metabolic Alkalosis** * Na⁺ reabsorbed in exchange for K⁺ and H⁺ → K⁺ loss → H⁺ loss → metabolic alkalosis **Hyperuricemia** (↑ uric acid → gout) * Thiazides compete with uric acid for secretion in the PCT → Uric acid is retained → gout attacks **Impaired Glucose Tolerance** * Thiazides ↓ insulin release and ↓ glucose utilization → can cause hyperglycemia in diabetics or prediabetics **Hyperlipidemia** * ↑ LDL and cholesterol (usually mild and not clinically significant at low doses) **Hyponatremia** * Thiazides increase: ADH release (due to volume loss) and water retention → Leads to low sodium (dangerous)

Answer 8

drugs that act in the **late DCT** and **collecting tubule** to prevent K⁺ loss (potassium-sparing)

Answer 9

Aldosterone Antagonists ENaC Blockers

Answer 10

block the **mineralocorticoid receptor**, preventing **ENaC synthesis** and **Na⁺/K⁺ ATPase synthesis** * ↓ Na⁺ reabsorption * ↓ K⁺ secretion → K⁺ stays in the body * ↓ H⁺ secretion → metabolic acidosis

Answer 11

**Spironolactone** **Eplerenone** (more selective, fewer hormone side effects)

Answer 12

Directly **block ENaC** → Na⁺ cannot enter the principal cell → **no negative lumen** → K⁺ cannot be secreted * ↓ Na⁺ reabsorption * ↓ K⁺ secretion * Mild diuresis

Answer 13

Amiloride Triamterene

Answer 14

**Primary Hyperaldosteronism** (Conn’s syndrome) * Aldosterone antagonists treat this directly. **Secondary Hyperaldosteronism** due to Heart failure, Cirrhosis, Nephrotic syndrome, Volume depletion from thiazides or loops * These states cause ↑ renin → ↑ aldosterone * Blocking aldosterone helps reduce Na⁺ retention and K⁺ loss **Rescue therapy with loop or thiazide diuretics** * They protect against: Hypokalemia and Metabolic alkalosis

Answer 15

**Hyperkalemia** (most dangerous) * because the drugs stop K⁺ from being secreted, K⁺ can rise dangerously high **Hyperchloremic Metabolic Acidosis** * H⁺ secretion is reduced (especially with aldosterone antagonists) → H⁺ stays in the blood → Bicarbonate stays low → non-anion-gap acidosis **Gynecomastia (male breast tissue), Impotence, Benign prostatic hyperplasia** * Because spironolactone binds to other steroid receptors **Triamterene Toxicity** * Can cause **kidney stones** * Can cause **acute renal failure** when combined with indomethacin (NSAID) **Contraindicated in chronic renal insufficiency** * Because kidneys cannot excrete K⁺ well → severe hyperkalemia risk.

Answer 16

**Renal failure** Patients on **ACE inhibitors** Patients on **ARBs** Patients on **β-blockers** Patients on **NSAIDs**

Answer 17

Block **ADH from binding to V₂ receptors** * ADH cannot activate cAMP → ADH effect is turned OFF → AQP2 channels do NOT get inserted into the apical membrane → No water pores → Water stays in the urine instead of being reabsorbed *Water diuresis (“aquaresis”) occurs → this is not sodium loss → it is pure water loss* *Serum sodium increases because the body loses free water (not salt) → called “raising serum Na⁺ by removing water.”*

Answer 18

**Conivaptan** – IV **Tolvaptan** – PO

Answer 19

used when **ADH is inappropriately high** or **water is being retained excessively** → hyponatremia * Heart failure * Liver disease * SIADH (Syndrome of Inappropriate ADH) *These patients retain too much water → low serum sodium → Vaptans remove only water, fixing the Na⁺ level*

Answer 20

**Thirst** * because they cause water loss **Dehydration / Hypovolemia** * Due to excessive aquaresis **Rapid or excessive sodium correction** * If sodium rises too fast, it can cause → osmotic demyelination syndrome (central pontine myelinolysis) — a dangerous neurologic complication * This is why vaptans require strict monitoring in the hospital

Answer 21

**Expensive + monitoring needs** * Often not used as first-line therapy due to cost + risk of osmotic demyelination syndrome

Answer 22

**Diuretic Resistance** * some patients stop responding to loop diuretics Each diuretic **acts at a different segment** of the nephron * Blocking only one site can eventually become ineffective because the nephron adapts **Blocking multiple sodium reabsorption pathways** * This causes MUCH stronger sodium loss and MUCH stronger fluid loss

Answer 23

Severe heart failure Chronic kidney disease Cirrhosis Long-term loop diuretic use

Answer 24

**Loop diuretics block NKCC2 in the TAL and Thiazides block NCC in the DCT** → when you block BOTH: * MUCH more sodium is lost * MUCH more water is lost *This is why the combination works when each drug alone fails*

Answer 25

**Severe heart failure** with edema

Answer 26

**Furosemide + Metolazone**

Answer 27

Loop + Potassium-Sparing Diuretic * **Furosemide + Spironolactone** * **Furosemide + Amiloride**

Answer 28

**Aldactazide** → Spironolactone + HCTZ **Dyazide, Maxzide** → Triamterene + HCTZ **Moduretic** → Amiloride + HCTZ

Diuretics Flashcards

(52 cards)