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Renal II, Exam 3 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

definition of hypertension

A

normal = below 120/80
preHTN: 120-139, 80-89
Stage 1 HTN = 140-159, 90-99
Stage 2 HTN = >160, >100

MAP = CO x TPR: so reduce CO or reduce TPR to reduce BP

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2
Q

4 ways to block the production of Ang?

A
  1. Ang receptors on vessels
  2. B-Receptors of JG cells that release renin
  3. blocking Renin
  4. Blocking ACE
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3
Q

sympathoplegic agents

A

those that alter symp. function

  1. vasomotor center
  2. Beta-receptors of heart
  3. alpha receptors of vessels
  4. Beta receptors of cells that release renin
  5. vasomotor center in brain
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4
Q

patients with CKD? what are renal protective?

A

ACE inhibitors

ARBs (Angiotensin receptor blocker)

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5
Q

Patients without CKD that are black?

A

thiazide diuretic

CCB

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6
Q

nonblack patients without CKD?

A

thiazide
ACE inhibitors
ARB
CCB

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7
Q

proximal tubule

A

= Carbonic anhydrase inhibitors

CT and straight

Actively reabsorbed
85% sodium bicarbonate (NaHCO3)
65% sodium chloride (NaCl)
65% potassium (K+) reabsorbed via paracellular pathway
100% glucose and amino acids

Passively reabsorbed
60% Water

Na+/K+ ATPase maintains low intracellular Na+ concentrations

Carbonic anhydrase – enzyme that catalyzes the formation/dehydration of carbonic acid

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8
Q

NHE3

A
  • Na+/H+ exchanger located in luminal membrane of PT

- initiates reabsorption of NAHCO3 into the cell

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9
Q

Loop of Henle

A

Loop Diuretics

TDL = water reabsorption
TAL: Na,K, Cl, Mg, Ca2+ reabsorption

25% sodium reabsorption

Na+/K+/2Cl- cotransporter (NKCC2) establishes the ion concentration gradient in the interstitium (selectively blocked by loop diuretics)

Increase in K+ concentration in the cells causes back diffusion of K+ into the tubular lumen, allowing a lumen-positive electrical potential to drive reabsorption of cations (Mg2+, Ca2+) via the paracellular pathway

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10
Q

DCT

A

10% NaCl reabsorbed

Thiazides

Relatively impermeable to water

Na+/Cl- cotransporter (NCC) actively transports NaCl out of lumen (blocked by thiazides)

Ca2+ is reabsorbed by calcium channels (regulated by PTH)

RESULT: tubular fluid is diluted

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11
Q

collecting tubule and ALDO

A

The most important site of K+ secretion by the kidney

Site at which all diuretic-induced changes in K+ balance occur – more Na+ delivered to collecting tubule leads to more K+ secretion

  • Proton pumps increase urine acidity (–> alkalosis w/ diuretics)

Epithelial sodium channel (ENaC)
- Responsible for 2-5% of Na+ reabsorption
- Creates electrical gradient that facilitates K+ secretion down the concentration gradient
(–> hypokalemia w/ diuretics)

Aldosterone – increases the expression of ENaC and basolateral Na+/K+ ATPase → increases Na+ reabsorption and K+ secretion → water retention and increase in blood volume and BP

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12
Q

CT and ADH

A

Antidiuretic hormone (ADH, vasopressin)

Controls permeability of the collecting tubule to water by regulating the expression levels of aquaporin-2 (AQP2) water channels

ADH levels are controlled by serum osmolality and volume status

No ADH → collecting tubule is impermeable to water and urine is dilute

ADH → water reabsorped and small volume of concentrated urine is produced

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13
Q

where do potassium sparing diuretics act?

A

cortical collecting tubules

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14
Q

acetazolamide

A

carbonic anhydrase inhibitor = prototype

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15
Q

brinzolamide

A

CA inhibitor

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16
Q

-amide

A

CA inhibitor

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17
Q

Dorzalamide

A

CA inhibitor

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18
Q

Methazolamide

A

CA inhibitor

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19
Q

Bumetanide

A

Loop Diuretic

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20
Q

Ethacrynic acid

A

Loop Diuretic

= prototype

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21
Q

Furosemide

A

= Lasix (*prototype)

Loop Diuretic

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22
Q

Torsemide

A

Loop Diuretic

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23
Q

-iazide

A

Thiazide diuretic
+ chlorothalidone
+ Metolazone

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24
Q

Bendroflumethiazide

A

Thiazide Diuretic

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25
Q

Chlorothiazide

A

Thiazide Diuretic

ii) Chlorothiazide is not very lipid-soluble and must be given in relatively large doses (only thiazide available for parenteral administration)
iii) Chlorthalidone is the longest acting thiazide with a half-life of approximately 47 hours

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26
Q

Chlothalidone

A

Thiazide Diuretic

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27
Q

Hydrochlorothiazide

A

Thiazide Diuretic = prototype

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28
Q

hydroflumethiazide

A

Thiazide Diuretic

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29
Q

Indapamide

A

Thiazide Diuretic

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30
Q

Methyclothiazide

A

Thiazide Diuretic

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31
Q

Metolazone

A

Thiazide Diuretic

popular choice for combo w/ loop agents

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32
Q

Polythiazide

A

Thiazide Diuretic

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33
Q

Trichlormethiazide

A

Thiazide Diuretic

34
Q
  • one
A

Aldo Antagonists

35
Q

K+ sparing diuretics?

A

Aldo Antagonist: eplernon, spironolactone*

ENaC inhibitors: Amiloride*, Triamterene

36
Q

Eplerenone

A

Aldo Antagonist

Eplerenone is a spironolactone analog with greater selectivity for the MR

37
Q

Spironolactone

A

Aldo Antagonist**

38
Q

Amiloride

A

ENaC inhibitor **

39
Q

Triamterene

A

ENaC inhibitor **

Triamterene is metabolized extensively in the liver and has a shorter half-life than amiloride (must be given more frequently than amiloride, which is not metabolized)

Triamterene may precipitate in the urine and cause kidney stones and, when combined with indomethacin, can cause acute renal failure

40
Q

mannitol

A

osmotic diuretic: aquaretic

41
Q

Isosorbide

A

osmotic diuretic: aquaretic

42
Q

Conivaptan

A

ADH antagonist: aquaretic

43
Q

Tolvaptan

A

ADH antagonist: aquaretic

44
Q

CA inhibitors

A

prototype: acetazolamide

all end in - amide

MOA: inhibits the membrane-
bound and cytoplasmic forms
of carbonic anhydrase

Results in:
↓ H+ formation inside PCT cell
↓ Na+/H+ antiport
↑ Na+ and HCO3- in lumen
↑ diuresis

Urine pH is increased and body pH is decreased (opposite!) and alkalosis

sodium and bicarb are stuck outside of lumen – where sodium goes, water goes, results in increased diuresis

because h+ is trapped in cells the urine pH is increased and body pH is decreased

45
Q

PK of acetazolamide

A

i) Well absorbed following oral administration
ii) Excretion of the drug is by secretion in the proximal tubule segment (dosing must be reduced in renal insufficiency)
iii) Excreted drug is unchanged (no hepatic metabolism)

46
Q

PD of acetazolamide

A

i) MOA: inhibition of the membrane-bound and cytoplasmic forms of carbonic anhydrase, resulting in nearly complete abolition of NaHCO3 reabsorption in the proximal tubule (primary site of action)
ii) Carbonic anhydrase inhibition results in decreased H+ formation inside PCT cells, decreased NHE3 activity, increased Na+ and HCO3- in the lumen, and increased diuresis
iii) Up to 45% of whole kidney HCO3- reabsorption is inhibited
iv) Urine pH is increased and body pH is decreased (An increase in urine pH from HCO3- diuresis is apparent within 30 minutes)
v) Diuretic efficacy decreases significantly with use over several days (HCO3- depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, defeating the purpose of diuretic action)
vi) As a result of systemic toxicity and eventual NaCl reabsorption, major clinical applications involve targeting carbonic anhydrase at sites other than the kidney

47
Q

adverse effects of CA inhibitors?

A

acidosis, hypokalemia, renal stones, drowsiness, paresthesias (with high doses), sulfonamide hypersensitivity

48
Q

clinical indications of acetazolamide?

A

Rarely used as antihypertensives due to low efficacy as single agents and development of metabolic acidosis
Used for glaucoma, acute mountain sickness, and metabolic alkalosis

49
Q

contraindications of CA acetazolamide?

A
  1. patients w/ cirrhosis: increase of urine pH decreases urinary excretion of ammonia and may contribute to development of hyperammonemia and hepatic encephalopathy
  2. patients with hyperchloremic acidosis or severe COPD: cause worsening of acidosis
50
Q

Loop Diuretics

A

Prototypes: furosemide and ethacrynic acid

MOA: inhibit the luminal
Na+/K+/2Cl-cotransporter (NKCC2)
in the TAL of the loop of Henle

Results in:
↓ intracellular Na+, K+, Cl- in TAL
↓ back diffusion of K+ and positive potential
↓ reabsorption of Ca2+ and Mg2+
↑ diuresis

Ion transport is virtually nonexistent

Among the most efficacious diuretics available

** use for patients with CHF and LOTS of edema

51
Q

PK of Furosemide?

A

Diuretic activity tied to secretion rates (act at luminal side of tubule)
Half-life correlated to kidney function
0.5 - 2 hours (healthy) vs. 9 hrs (end stage renal disease) for furosemide

iv) Coadministration of loop diuretics with other weak acids (NSAIDs, probenecid) may result in a reduction in loop diuretic secretion due to competition for weak acid secretion

52
Q

PD of furosemide?

A

i) MOA: cause inhibition of the luminal Na+/K+/2Cl- cotransporter (NKCC2) in the thick ascending limb of the loop of Henle, bringing ion transport in this section of the nephron to a virtual standstill (Na+, K+, Cl- by blocking cotransporter; Mg2+ and Ca2+ by abolishing the lumen-positive electrical potential)
ii) Loop diuretics increase the excretion of K+ and titratable acid due to the delivery of Na+ and H+ to the DCT and CCT (total body pH increases)
iii) Induce the synthesis of renal prostaglandins (note: NSAIDs interfere with the actions of loop diuretics by reducing prostaglandin synthesis, which may be significant in patients with nephritic syndrome or hepatic cirrhosis)
iv) Cause increases in renal blood flow in vascular beds
v) Some are weak inhibitors of carbonic anhydrase

53
Q

adverse effects of loop diuretics?

A

hypokalemia, alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia (gout!), ototoxicity (hearing loss), sulfonamide hypersensitivity (not all)

54
Q

clinical indications for loop diuretics?

A

** one of most effacacious diuretics **

acute pulmonary edema, heart failure, HTN, ARF, anion overdose, hypercalcemic states

55
Q

contraindications for loop diuretics?

A

i) Furosemide, bumetanide, and torsemide are sulfonamides and may cause allergic reactions in patients with sulfonamide sensitivity
ii) May be deleterious in patients with hepatic cirrhosis, borderline renal failure, or heart failure
iii) Avoid in postmenopausal osteopenic (with reduced bone volume) women due to hypocalcemic effects
iv) Drug interactions with aminoglycosides (enhanced ototoxicity), lithium (may increase or decrease serum concentrations of lithium), and digoxin (increased toxicity due to electrolyte disturbances)

56
Q

thiazide diuretics

A

Prototype: hydrochlorothiazide (HCTZ)
MOA: cause inhibition of the Na+/Cl- cotransporter (NCC) and block NaCl reabsorption in the DCT
Results in:
↑ luminal Na+ and Cl- in DCT
↑ diuresis
Enhance the reabsorption of Ca2+ in PCT due to volume contraction
Largest class of diuretic agents- SO MANY!

57
Q

clinical uses for HCTZ?

A

hypertension, mild heart failure, nephrolithiasis (calcium stones), nephrogenic diabetes insipidus

(1) Mechanism for hydrochlorothiazide (HCTZ) use in nephrogenic diabetes insipidus: HCTZ acts by inhibiting the Na/Cl transporter in the distal convoluted tubule. Administration of HCTZ to any individual will increase diuresis and subsequently reduce extracellular fluid volume. The reduction in volume will result in less volume filtered at the glomerulus and a decrease in GFR. A decrease in GFR will cause an increase in proximal tubule sodium and water reabsorption (tubuloglomerular feedback). This will lead to less sodium and water delivery to the collecting duct and will decrease urine output.

58
Q

adverse effects of HCTZ?

A

Adverse effects include hypokalemia, alkalosis, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, sulfonamide hypersensitivity

More hyponatremic effects than loop diuretics

Use with caution in patients with diabetes mellitus

ii) Impaired carbohydrate tolerance: thiazides decrease glucose tolerance, causing hyperglycemia, and may unmask latent diabetes during treatment. This effect may be due to impaired pancreatic release of insulin and diminished tissue utilization of glucose. Hyperglycemia may be partially reversible with correction of hypokalemia.
iii) Hyperlipidemia: thiazides cause a 5-15% increase in total serum cholesterol and low-density lipoproteins (LDL) except for indapamide; levels may equilibrate toward baseline after prolonged use
iv) Hyponatremia: deficiency of Na+ in the blood due to a combination of hypovolemia-induced elevation of ADH (which increases AQP2 levels and subsequently increases blood volume), reduction in the diluting capacity of the kidney (because of the thiazide), and increased thirst
v) Weakness, fatigability, paresthesias, and impotence may occur
vi) Sulfonamide hypersensitivity

59
Q

PK of HCTZ?

A
  • all can be given orally
    iv) Secreted in the PCT by the organic acid secretory system (competes with the secretion of uric acid, which may elevate serum uric acid levels)
60
Q

PD of HCTZ?

A

i) MOA: inhibits the Na+/Cl- cotransporter (NCC) and inhibits NaCl reabsorption from the luminal side of epithelial cells in the DCT
ii) Enhance the reabsorption of Ca2+ (in the PCT due to volume contraction and in the DCT due to enhanced Na+/Ca2+ exchange in the basolateral membrane); rarely causes de novo hypercalcemia, but can unmask hypercalcemia due to other causes (e.g., hyperparathyroidism, carcinoma, sarcoidosis)
iii) Some are weak inhibitors of carbonic anhydrase

61
Q

contraindications of HCTZ?

A
  • use w/ caution in diabetes
    ii) Thiazide efficacy may be reduced in combination with NSAIDs and COX-2 inhibitors due to inhibition of prostaglandin synthesis (similar to loop diuretics)
    iii) Excessive use is dangerous in hepatic cirrhosis, borderline renal failure, or heart failure
62
Q

Mineralocorticoid receptor antagonists

A

K+ sparing diuretics

**Spironolactone and eplerenone

  • blocks the receptor which downregulates and REDUCES the expression of the channel

Uses include hyperaldosteronism, adjunct to K+-wasting diuretics, antiandrogenic uses (female hirsutism), reduces mortality of heart failure

Adverse effects include hyperkalemia, acidosis, and antiandrogenic effects

Do not require access to the tubular lumen to induce diuresis

63
Q

ENaC inhibitors

A

K+ Sparing diuretics

Na+ channel (ENaC) inhibitors

Amiloride and triamterene

Uses include adjunct to K+-wasting diuretics and lithium-induced nephrogenic diabetes insipidus (amiloride)

Adverse effects include hyperkalemia and acidosis

64
Q

look at changes chart

A

do it now!

65
Q

PK of potassium sparing?

A

Spironolactone and eplerenone

(1) Both agents are given orally
(2) Inactivation occurs in the liver and several days are needed before benefits are observed
(3) Eplerenone is a spironolactone analog with greater selectivity for the MR

Amiloride and triamterene

(1) Oral preparations
(2) Triamterene is metabolized extensively in the liver and has a shorter half-life than amiloride (must be given more frequently than amiloride, which is not metabolized)

66
Q

PD of MR antagonists?

A

i) Spironolactone and eplerenone
(1) MOA: MR antagonists are synthetic steroids that act as competitive inhibitors of aldosterone binding to the MR
(2) The MR is a nuclear hormone receptor responsible for regulating the expression of multiple gene products, such as Na+ (ENaC) and Na+/K+ ATPase pumps in the epithelial cells in the late distal tubule and CCT (as well as other cell types)
(3) As a result, MR antagonists reduce Na+ reabsorption to the interstitium in the CCT and therefore, reduce K+ (as well as H+, Ca2+, Mg2+) secretion (remember, K+ secretion is coupled with Na+ entry in this segment)
(4) MR antagonists are the only diuretics that do not require access to the tubular lumen to induce diuresis

67
Q

PD of ENac inhibitors?

A

ii) Amiloride and triamterene
(1) MOA: directly inhibit Na+ entry by blocking epithelial Na+ channels (ENaC) in the apical membrane of the CCT
(2) Reduce Na+ reabsorption to the interstitium in the CCT and therefore, reduce K+ (as well as H+, Ca2+, Mg2+) secretion (same as MR antagonists)

68
Q

toxicity of potassium sparing diuretics?

A

i) Mild, moderate, or even life-threatening hyperkalemia
(1) Risk is increased by renal disease or by the use of agents that reduce renin (β-blockers, NSAIDs) or angiotensin II activity (angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs))
(2) Can combine K+-sparing diuretics with other diuretics that increase K+ secretion
ii) Metabolic acidosis due to reduced H+ secretion
iii) MR antagonists are steroids that can also act on other hormone receptors, causing gynecomastia, impotence, and benign prostatic hyperplasia (eplerenone has less antiandrogenic effects)

69
Q

contraindications of potassium sparing?

A

i) Patients with chronic renal insufficiency are vulnerable to severe or fatal hyperkalemia
ii) Concomitant use of K+-sparing diuretics with β-blockers, NSAIDs, ACEIs, or ARBs is discouraged
iii) Patients with liver disease may have impaired metabolism of spironolactone and triamterene
iv) Strong inhibitors of CYP3A4 can increase blood levels of eplerenone, but not spironolactone

70
Q

clinical indications of potassium sparing diuretics?

A

i) Most useful in states of mineralocorticoid excess or hyperaldosteronism, due either to primary hypersecretion (Conn’s syndrome, ectopic adrenocorticotropic hormone production) or to secondary hyperaldosteronism (evoked by heart failure, hepatic cirrhosis, nephritic syndrome, or other conditions associated with diminished effective intravascular volume)
ii) Thiazides and loop diuretics can cause secondary hyperaldosteronism, which can increase renal wasting of K+; K+-sparing diuretics can be used to blunt the K+ secretory response
iii) The MR antagonists are used to treat heart failure

71
Q

mannitol

A

osmotic agent that alters water excretion

(2) MOA: Increases the osmotic pressure of glomerular filtrate, which inhibits tubular reabsorption of water and electrolytes and increases urinary output
(3) Oppose ADH effects in the CCT
(4) The increase in water diuresis increases urine flow rate and decreases the contact time between fluid and the tubular epithelium, which also reduces Na+ reabsorption
(5) Resulting natriuresis is of lesser magnitude than the water diuresis, eventually leading to excessive water loss and hypernatremia

risks: Dehydration, hyperkalemia, and hypernatremia (can be avoided by monitoring serum ion composition and fluid balance)

Contraindications
(1) Severe renal disease (anuria); severe dehydration; severe pulmonary edema or congestion

Clinical indications

(1) Promoting urinary excretion of toxic substances
(2) Reduction of intracranial and intraocular pressure
(3) Although FDA-labeled indications, use for prevention of acute renal failure and/or promotion of diuresis is not routinely recommended

72
Q

loop agents and thiazide diuretics?

A

i) Can be combined if patients fail or become refractory to the usual dose of loop diuretics
ii) Loop agents and thiazides in combination will often produce diuresis when either agent acting alone is minimally effective (2 reasons)
(1) Salt and water reabsorption in either the thick ascending loop (blocked by loop diuretics) or DCT (blocked by thiazides) can increase when the other is blocked; inhibition of both can produce more than an additive diuretic response
(2) Thiazides often produce mild natriuresis (sodium excretion) in the PCT that is usually masked by increased absorption in the thick ascending loop; this combination can therefore block Na+ reabsorption from all three segments (PCT, ascending loop, and DCT)
(3) Metolazone (thiazide) is a popular choice for combination with loop agents
iii) Combination can cause profuse diuresis and therefore, routine outpatient use is not recommended (K+ wasting is extremely common)

73
Q

K+ sparing diuretics + loop/thiazides

A

i) Hypokalemia is a common side effect of loop agents and thiazide diuretics, which can initially be managed with dietary NaCl restriction or KCl supplementation
ii) When hypokalemia is unmanageable in this way, the addition of K+-sparing diuretics can lower K+ secretion
iii) This combination is generally safe but should be avoided in patients with renal insufficiency and in those receiving angiotensin antagonists

74
Q

heart failure

A

(1) Heart failure reduces cardiac output, which results in a decrease in blood pressure and blood flow to the kidney
(2) Decreases in BP and blood flow is sensed as hypovolemia and leads to renal retention of salt and water
(3) Pulmonary or interstitial edema occur when the plasma volume increases and the kidney continues to retain salt and water, which then leaks from the vasculature

75
Q

kidney disease

A

(1) Most kidney diseases cause retention of salt and water
(2) When loss of renal function is severe, there is insufficient glomerular filtration to sustain a natriuretic response and diuretic agents are of little benefit
(3) Patients with mild cases of renal disease can be effectively treated with diuretics when they retain sodium
(4) Diuretics are beneficial in glomerular diseases, such as systemic lupus erythematosus or diabetes mellitus, that exhibit renal retention of salt and water
(5) Loop and thiazide diuretics are beneficial in individuals that develop hyperkalemia associated with early stage renal failure

76
Q

hepatic cirrhosis

A

(1) Diuretics are useful when edema and ascites (accumulation of fluid in the abdominal cavity) become severe due to liver disease
(2) Aggressive use of diuretics can be disastrous in patients with liver disease (more so than heart failure)

77
Q

HTN

A

(1) Thiazides are often used because of their diuretic and mild vasodilator activities
(2) Loop diuretics are often reserved for patients with mild renal insufficiency or heart failure
(3) Diuretics are often used in combination with vasodilators (hydralazine, minoxidil) because vasodilators cause significant salt and water retention

78
Q

nephrolithiasis

A

(1) 2/3 of kidney stones contain calcium phosphate or calcium oxalate
(2) Thiazide diuretics enhance Ca2+ reabsorption in the DCT and reduce urinary Ca2+ concentration, making them appropriate agents in the treatment of kidney stones

79
Q

hypercalcemia

A

(1) Loop diuretics reduce Ca2+ reabsorption and promote Ca2+ diuresis, but can also cause marked volume contraction when used alone (counterproductive)
(2) Saline can be administered simultaneously with loop diuretics to maintain effective Ca2+ diuresis

80
Q

DI

A

iv) Diabetes insipidus
(1) Can be due to either deficient production of ADH (neurogenic or central diabetes insipidus) or inadequate responsiveness to ADH (nephrogenic diabetes insipidus)
(2) Supplementary ADH or one of its analogs is only effective in central diabetes insipidus
(3) Thiazide diuretics can reduce polyuria and polydipsia in both types of diabetes insipidus

Renal II, Exam 3 (9 decks)

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