diuretics

Question 1

Front

Answer 1

Back

Question 2

Where do carbonic anhydrase inhibitors act?

Answer 2

Proximal convoluted tubule (PCT)

Question 3

Mechanism of carbonic anhydrase inhibitors

Answer 3

Block carbonic anhydrase → ↓ HCO₃⁻ reabsorption → ↑ NaHCO₃ excretion → metabolic acidosis

Question 4

Major electrolyte effect of CA inhibitors

Answer 4

Severe K⁺ wasting (negative lumen drives K⁺ loss)

Question 5

Key CA inhibitor drug

Answer 5

Acetazolamide

Question 6

CA inhibitor clinical uses

Answer 6

Altitude sickness; metabolic alkalosis; glaucoma; weak diuretic

Question 7

Where do loop diuretics work?

Answer 7

Thick ascending loop of Henle

Question 8

Loop diuretic mechanism

Answer 8

Block NKCC2 → ↓ Na⁺/K⁺/Cl⁻ reabsorption → powerful diuresis

Question 9

Loop diuretic electrolyte effects

Answer 9

↑ Ca²⁺ & Mg²⁺ loss; moderate K⁺ wasting; metabolic alkalosis

Question 10

Loop diuretic prototypes

Answer 10

Furosemide; ethacrynic acid (no sulfa)

Question 11

Loop diuretic clinical use

Answer 11

Rapid volume removal (pulmonary edema; CHF exacerbation; hypercalcemia)

Question 12

Where do thiazides act?

Answer 12

Distal convoluted tubule (DCT)

Question 13

Thiazide mechanism

Answer 13

Block NCC (Na⁺/Cl⁻ cotransporter)

Question 14

Key thiazide electrolyte effect

Answer 14

↑ Ca²⁺ reabsorption; moderate K⁺ wasting; metabolic alkalosis

Question 15

Thiazide prototype

Answer 15

Hydrochlorothiazide (HCTZ)

Question 16

Thiazide clinical use

Answer 16

Hypertension; mild edema; nephrolithiasis prevention

Question 17

Where do potassium-sparing diuretics act?

Answer 17

Collecting tubule/duct

Question 18

K-sparing mechanisms

Answer 18

Aldosterone antagonists (spironolactone/eplerenone) AND ENaC blockers (amiloride/triamterene)

Question 19

K-sparing electrolyte effect

Answer 19

Hyperkalemia risk

Question 20

K-sparing uses

Answer 20

Heart failure; hyperaldosteronism; prevents K⁺ loss with other diuretics

Question 21

Where do osmotic diuretics act?

Answer 21

PCT and descending loop (water-permeable segments)

Question 22

Osmotic mechanism

Answer 22

Increase tubular osmotic pressure → inhibit water reabsorption

Question 23

Osmotic prototype

Answer 23

Mannitol

Question 24

Osmotic uses

Answer 24

↓ intracranial pressure; ↓ intraocular pressure; flush nephrotoxins (rhabdo)

Question 25

Osmotic caution

Answer 25

Early volume expansion → later dehydration; hypernatremia; filter to avoid crystals

Question 26

Primary function of the kidney

Answer 26

Maintain fluid, electrolyte, and acid-base balance + excrete wastes + endocrine functions

Question 27

Nephron functional unit components

Answer 27

Glomerulus + Bowman's capsule + tubules (PCT, Loop, DCT, Collecting duct)

Question 28

Percentage of cardiac output to kidneys

Answer 28

~20% (because life depends on filtration more than biceps)

Question 29

GFR definition

Answer 29

Volume of plasma filtered per minute by glomeruli

Question 30

Primary determinant of GFR

Answer 30

Glomerular capillary pressure (driven by renal blood flow)

Question 31

Effect of afferent arteriole constriction

Answer 31

↓ RBF, ↓ GFR

Question 32

Effect of efferent arteriole constriction

Answer 32

↓ RBF, ↑ GFR (until severe → ↓ GFR)

Question 33

Driving force of filtration

Answer 33

Starling forces (hydrostatic pressure vs oncotic pressure)

Question 34

Filtration barrier layers

Answer 34

Endothelium + basement membrane + podocytes (slit diaphragm)

Question 35

Molecule blocked by filtration barrier

Answer 35

Albumin (size + charge exclusion)

Question 36

Proximal tubule primary job

Answer 36

Bulk reabsorption of Na⁺, water, HCO₃⁻, glucose, amino acids

Question 37

Percentage of Na⁺ reabsorbed in PCT

Answer 37

~65%

Question 38

Unique PCT feature

Answer 38

Carbonic anhydrase drives H⁺/HCO₃⁻ cycling

Question 39

Loop of Henle purpose

Answer 39

Create medullary osmotic gradient for water reabsorption

Question 40

Descending limb permeability

Answer 40

Water only (passive)

Question 41

Ascending limb permeability

Answer 41

Solutes only (NKCC2 active transport) — no water

Question 42

DCT primary role

Answer 42

Fine-tune Na⁺ and Ca²⁺ (PTH-dependent Ca²⁺ reabsorption)

Question 43

Collecting duct key hormones

Answer 43

Aldosterone (Na⁺/K⁺) & ADH (water)

Question 44

Aldosterone effect

Answer 44

↑ ENaC + Na/K-ATPase → ↑ Na⁺ reabsorption, ↑ K⁺ secretion

Question 45

ADH effect

Answer 45

Inserts aquaporin-2 channels → ↑ water reabsorption

Question 46

Renin release triggers

Answer 46

↓ renal perfusion, ↓ NaCl at macula densa, ↑ sympathetic activity (β1-receptors)

Question 47

Angiotensin II effects

Answer 47

Vasoconstriction, ↑ aldosterone, ↑ Na/H exchange in PCT, thirst

Question 48

ANP/BNP effect on kidney

Answer 48

↓ Na⁺ reabsorption, ↑ GFR via afferent dilation/efferent constriction

Question 49

Tubuloglomerular feedback

Answer 49

Macula densa senses NaCl → adjusts GFR via renin & arterioles

Question 50

Macula densa response to high NaCl

Answer 50

Constrict afferent arteriole → ↓ GFR

Question 51

Macula densa response to low NaCl

Answer 51

Renin release → ↑ GFR, ↑ Na⁺ retention

Question 52

Transport maximum (Tm) concept

Answer 52

Max rate a transporter can reabsorb (e.g., glucose)

Question 53

Reason for glucosuria in diabetes

Answer 53

Exceeds Tm → glucose spills into urine

Question 54

Acid handling: kidney role

Answer 54

Reabsorb HCO₃⁻ and excrete H⁺ (NH₄⁺ + titratable acids)

Question 55

Ammonium (NH₄⁺) purpose

Answer 55

H⁺ buffer and secretory pathway for acid removal

Question 56

Why kidneys correct chronic acidosis

Answer 56

Generate new HCO₃⁻ (lungs only blow off CO₂)

Question 57

Role of urea in kidney

Answer 57

Maintains medullary osmotic gradient (reabsorbed in collecting duct)

Question 58

Effect of high protein diet on urine concentration

Answer 58

Improves concentrating ability (more urea)

Question 59

Primary acid-base effect of carbonic anhydrase inhibitors

Answer 59

Metabolic acidosis (lose HCO₃⁻)

Question 60

Why acetazolamide causes paresthesias

Answer 60

CSF & neuronal pH changes from HCO₃⁻ loss

Question 61

Acetazolamide contraindication

Answer 61

Sulfonamide allergy, severe acidosis, cirrhosis (risk ↑ NH3)

Question 62

CA inhibitor effect on kidney stones

Answer 62

↑ risk of calcium phosphate stones (alkaline urine)

Question 63

Loop diuretics effect on prostaglandins

Answer 63

↑ Prostaglandins → renal vasodilation (blocked by NSAIDs)

Question 64

Loops + NSAIDs effect

Answer 64

↓ diuretic response (renal afferent constriction)

Question 65

Loop effect on uric acid

Answer 65

Hyperuricemia (competes for secretion → gout risk)

Question 66

Loop effect on glucose & lipids

Answer 66

Mild ↑ glucose, ↑ lipids

Question 67

Thiazide-induced hyponatremia mechanism

Answer 67

↑ ADH sensitivity + impaired dilution in DCT

Question 68

Thiazide effect on uric acid

Answer 68

Hyperuricemia (gout risk)

Question 69

Thiazides & glucose metabolism

Answer 69

May ↑ glucose (↓ insulin release + K⁺ depletion)

Question 70

Thiazide drug interaction concern

Answer 70

Lithium toxicity (↓ clearance)

Question 71

Difference in gynecomastia risk: spironolactone vs eplerenone

Answer 71

Spironolactone high, eplerenone low (more selective)

Question 72

Why spironolactone helps in heart failure

Answer 72

Blocks aldosterone → ↓ remodeling, ↓ mortality

Question 73

K-sparing diuretics + ACEI/ARB risk

Answer 73

Severe hyperkalemia

Question 74

Amiloride special indication

Answer 74

Lithium-induced nephrogenic DI

Question 75

Mannitol effect on sodium levels

Answer 75

Early hyponatremia → later hypernatremia

Question 76

Why mannitol contraindicated in CHF

Answer 76

Early plasma expansion → pulmonary edema

Question 77

Mannitol in renal failure caution

Answer 77

Can accumulate → worsen overload

Question 78

Best diuretic for cerebral edema

Answer 78

Mannitol

Question 79

Best diuretic combo for refractory CHF

Answer 79

Loop + thiazide (sequential nephron blockade)

Question 80

Definition of diuretic resistance

Answer 80

Inadequate diuresis despite optimal dosing

Question 81

Major cause of diuretic resistance

Answer 81

RAAS activation + distal nephron hypertrophy

Question 82

Management of diuretic resistance

Answer 82

Add thiazide, sodium restriction, improve renal perfusion

Question 83

Effect of RAAS activation on sodium handling

Answer 83

↑ Na⁺ reabsorption in proximal & distal nephron

Question 84

Site of aldosterone action

Answer 84

Collecting duct principal cells (↑ ENaC & Na/K-ATPase)

Question 85

ADH effect on collecting duct

Answer 85

↑ Aquaporin-2 → ↑ water reabsorption

Question 86

Which drug class blocks ADH?

Answer 86

Vaptans (tolvaptan) — not a diuretic class

Question 87

Best diuretic for hypercalcemia

Answer 87

Loop diuretics (with IV fluids)

Question 88

Best diuretic for calcium stone-former

Answer 88

Thiazides (↑ Ca²⁺ reabsorption)

Question 89

Best diuretic for hepatic ascites

Answer 89

Spironolactone first-line

Question 90

Why spironolactone is first in cirrhosis

Answer 90

Aldosterone excess drives ascites

Question 91

Diuretic class causing ototoxicity

Answer 91

Loops

Question 92

Diuretic class causing metabolic alkalosis

Answer 92

Loops & thiazides

Question 93

Diuretic class causing metabolic acidosis

Answer 93

CA inhibitors, K-sparing

Question 94

Diuretics safe in sulfa allergy

Answer 94

Ethacrynic acid, spironolactone, eplerenone, amiloride, triamterene, mannitol

Question 95

Definition of natriuresis

Answer 95

Sodium excretion in urine

Question 96

Definition of aquaresis

Answer 96

Electrolyte-free water excretion (vaptans)

Question 97

Clinical sign of overdiuresis

Answer 97

Orthostatic hypotension + prerenal azotemia (↑ BUN:Cr)