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Diuretics Flashcards

1
Q

PCT

a) Major things reabsorbed here
b) main membrane transporter invovled
c) enzyme involved here

A
  1. responsible for 60-70% of total reabsorption of NA
  2. carries out isosmotic reabsorption of AA, glucose & many cations
  3. major site for reabsorption of Sodium Chloride& Bicarb

b) NHE3: apical membrane Na/H exchange via NHE3
Na/K ATPase is present in the basolateral membrane to maintain intracellular Na & K

c) Carbonic Anhydrase: bicarbonate is reabsorbed poorly through luminal membrane so it is converted to CO2 & H2O by Carbonic Anhydrase

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2
Q

TAL

a) Major things reabsorbed here
b) main membrane transporter invovled
c) enzyme involved here

A
  1. responsible for absorption of 20-30% of Na
  2. pumps out Na, K, Cl into interstitium
  3. major site for Mg & Ca reabsorption: positive potential in lumen allows Mg2+ and Ca2+ to be reabsorbed via paracellular pathway

b) NKCC2: reabsorption of Na, Cl & K via Na+/K+/2Cl- cotransporter

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3
Q

DCT

a) Major things reabsorbed here
b) main membrane transporter invovled
c) enzyme involved here

A
  1. reabsorption of 5-8% of Na
  2. actively pumps Na & Cl out of lumen via Na+/Cl- cotransporter NCC
  3. Ca also reabsorbed under control of PTH

b) NCC: actively pumps Na & Cl out of lumen (Na+/Cl- cotransporter)

c)

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4
Q

CD

a) Major things reabsorbed here
b) main membrane transporter invovled
c) enzyme involved here

A
  1. reabsorption of 2-5% of Na–last tubular site for Na reabsorption
  2. controlled by aldosterone, occurs via channels & is accompanied by equal loss of K or H ions
  3. primary site of acidification of union & K excretion
  4. Cl- reabsorbed via paracellular pathway because of negative lumen potential

b) ENaC: inward diffusion of Na via the epithelial sodium channel ENaC leaves lumen negative potential–> drives reabsorption of Cl- & efflux of K+

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5
Q

Carbonic Anhydrase Inhibitors

A
  1. acetazolamide

2. dorzolamide

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6
Q

Loop Diuretics

A
  1. Furosemide
  2. Bumetanide
  3. Torsemide
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7
Q

Thiazides

A
  1. Hydrochlorothiazide
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8
Q

Potassium Sparing Diuretics

A
  1. aldosterone antagonists: spironolactone & eplerenone
  2. Na channel Blockers: amiloride & triamterene
  3. ADH antagonists: Lithium & demeclocycline
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9
Q

Osmotic Diuretics

A

Mannitol

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10
Q

Acetazolamide

A

Carbonic Anhydrase inhibitor

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11
Q

Where do Carbonic Anhydrase Inhibitors Act

A

the PCT

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12
Q

Acetazolamide MOA & Effects & uses

A

inhibit CA both in the brush border & intracellular CA in PCT

Effects:

  1. Bicarbonate diuresis–>metabolic acidosis results
  2. Increased Na is presented to the CCD, where it is absorbed so more K is excreted–>causes significant K loss in urine–> HYPOKALEMIA
  3. CA inhibition in ciliary epithelium –>reduced secretion of aqueous humor

Uses:

  1. glaucoma
  2. urinary alkalinization for acidic drug toxicity
  3. tx acute mountain sickness
  4. significant metabolic alkalosis
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13
Q

drug used in high altitude sickness (mountain sickness)

A

acetazolamide (CA inhibitor)

acidosis of CSF results in hyperventilation

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14
Q

Uses of CA inhibitors

A
  1. glaucoma
  2. urinary alkalinization for acidic drug toxicity is salicylates
  3. tx acute mountain sickness
  4. significant metabolic alkalosis
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15
Q

Adverse Effects of Carbonic Anhydrase Inhibitors

A
  1. cross algernicity with other sulfonamides
  2. hyperchloremic metabolic acidosis
  3. renal stones: alkalization of urine by these drugs may cause Ca to precipitate –>renal stones
  4. Hypokalemia
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16
Q

How can CA inhibitors be used to treat glaucoma

A

CA inhibition in the ciliary epithelium –>reduced secretion of aqueous humor

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17
Q

Where do Loop Diuretics act?

A

Thick ascending limb

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18
Q

Furosemide

A

Loop Diuretic

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19
Q

Furosemide MOA & Effects & uses & ADR

A

Loop Diuretic, acts in TAL

  1. Inhibits NKCC2 (Na+/K+/2Cl- cotransporter)–>produce massive NaCl diuresis–>Edema fluid is rapidly excreted & blood volume is significantly reduced.

The Loop of Henle is the diluting segment, so blocking its function–>reduced ability to dilute urine

  1. also results in loss of lumen positive potential–>decreased reabsorption of ions like Ca & Mg–>Ca excretion is significantly increased
  2. More Na is presented to the CD–>it’s reabsorbed in exchange for K+ & H+–>hykalemic alkalosis

Uses:

  1. Tx of edematous states including HF & ascites
  2. *tx of acute pulmonary edema (LVF)
  3. mild to moderate CHF
  4. severe hypercalcemia
  5. seen commonly in malignancy (so we give large doses of furosemide with fluids & electrolytes)

ADR:

  1. *Hypokalemia–usually given with K sparing drugs
    - ——->Hypokalemic metabolic alkalosis
  2. Hypomagnesemia
  3. Hypocalcemia
  4. Hypovolemia
  5. *Ototoxicity–> don’t combine with other ototoxic drugs i.e. aminoglycosides
  6. cross hypersensitivity with sulfa drugs–> i.e. if allergic to sulfa drugs don’t use bc may also be allergic
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20
Q

Uses of Loop Diuretics

A
  1. Tx of edematous states including HF & ascites
  2. *tx of acute pulmonary edema (LVF)
  3. mild to moderate CHF
  4. severe hypercalcemia
  5. seen commonly in malignancy (so we give large doses of furosemide with fluids & electrolytes)
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21
Q

ADR of Loop Diuretics

A
  1. *Hypokalemia–usually given with K sparing drugs
    - ——->Hypokalemic metabolic alkalosis
  2. Hypomagnesemia
  3. Hypocalcemia
  4. Hypovolemia
  5. *Ototoxicity–> don’t combine with other ototoxic drugs i.e. aminoglycosides
  6. cross hypersensitivity with sulfa drugs–> i.e. if allergic to sulfa drugs don’t use bc may also be allergic
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22
Q

Site of action of Thiazides

A

Distal Convoluted Tubule

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23
Q

Hydrochlorothiazide

MOA

Uses

ADR

A

Thiazide, acts in Distal convoluted tubule

MOA: inhibits Na/Cl transporter (NCC) in early segment of distal convoluted tubule

Uses:

  1. HTN (Mild-moderate essential HTN)
  2. Chronic renal calcium stone (bc reduce urine Ca concentration)

ADR:
1. severe hyponatremia
2. hypokalemia
3. cross hypersensitivity w sulfonamides
4. hyperuricemia–>gout
(direct competition of thiazides for rate transport)
5. Hyperlipidemia–>increase serum CH & LDL 5-10%
6. Hyperglycemia due to diminished insulin secretion in patient with preexisting type 2 diabetes

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24
Q

Effects of Thiazides

A
  1. sustained Na & Cl Diuresis

reduction in transport of Na into tubular cell reduces intracellular Na –>promotes Na/Ca exchange
——->results in increased reabsorption of Ca from urine –>urine Ca content is decreased

  1. Reduces BP

initially decrease CO bc decrease blood volume, but later decrease TPR bc decrease Na concentration & Na is responsible for maintaining vessel stiffness.

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25
Q

Uses of Thiazides

A
  1. HTN (Mild-moderate essential HTN)

2. Chronic renal calcium stone (bc reduce urine Ca concentration)

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26
Q

Thiazides ADR

A
  1. severe hyponatremia
  2. hypokalemia
  3. cross hypersensitivity w sulfonamides
  4. hyperuricemia–>gout
    (direct competition of thiazides for rate transport)
  5. Hyperlipidemia–>increase serum CH & LDL 5-10%
  6. Hyperglycemia due to diminished insulin secretion in patient with preexisting type 2 diabetes
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27
Q

Potassium sparing Diuretics act in the

A

Collecting Duct

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28
Q

Downside of Potassium sparing diuretics & compensation

A

Weak therefore rarely used alone; Exception = hyperaldosteronism

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29
Q

Spironolactone

A

Aldosterone antagonist; K+ sparing diuretic

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30
Q

Amiloride & Triamterene

A

K+ Sparing Diuretics that directly block Na channels in CD

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31
Q

How do K+ Sparing Diuretics work

A

Inward diffusion of Na via epithelial sodium channel levels a lumen-negative potential which drives reabsorption of Cl- & efflux of K+

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32
Q

Spironolactone MOA, Effects, Uses, ADR

A

Antagonist of Aldosterone in Collecting Duct

MOA: by binding & blocking the aldosterone receptor–>reduce expression of genes controlling synthesis of epithelial Na ion channels & Na/K ATPase–>this increases sodium excretion bc less Na is being reabsorbed

Effects:

  1. increases Na excretion
  2. Decreases K+ & H+ ion excretion (bc whenever Na is reabsorbed K is exchanged & excreted
  3. may cause hyperkalemic metabolic acidosis

Uses:

  1. Hypokalemia causes by loop diuretics & thiazides
  2. Aldosteronism (occurs in cirrhosis; also seen in Conn’s syndrome & with late HF

ADR:

  1. Hyperkalemia–>can cause cardiac arrest
  2. Extreme caution needed when given with ACE-inhibitors bc both inhibit aldosterone
  3. gynecomastia (painful, enlargement of breast in males) hirsutism (excess body hair growth), loss of libido & impotence
    - –>all from anti-androgenic effects
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33
Q

gynecomastia (painful, enlargement of breast in males) hirsutism (excess body hair growth), loss of libido & impotence

A

all from anti-androgenic effects of spironolactone

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34
Q

Osmotic diuretics work where

A

PCT (where majority of isosmotic reabsorption occurs)

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35
Q

Mannitol

A

Osmotic diuretic; acts in PCT; given by IV
freely filtered in glomerulus but poorly reabsorbed, so it remains in the lumen

Holds water by virtue of its osmotic effect

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36
Q

Mannitol Effects & uses

A

Effects:

  1. urine volume is increased
  2. Can decrease intracranial pressure by osmotically extracting water fro tissue into blood
  3. similar effect in eye (reduces IOP)

Uses:

  1. Cerebral Edema
  2. Glaucoma
37
Q

Amiloride

A

K+ sparing diuretic used in lithium-induced diabetes insidious bc prevents lithium’s action on CD (Li acts like & replaces Na)

38
Q

Dorzolamide MOA

A

inhibition of CA in PCT

39
Q

Urinary Electrolytes in Acetazolamide

A

Increase Na
Increase K
VERY increased HCO3

40
Q

Urinary Electrolytes in Dorzolamide

A

Increase Na
Increase K
VERY increased HCO3

41
Q

Blood Chemistry & pH in Acetazolamide

A
  1. hypokalemia
  2. acidosis (low pH)
  3. Hyperchloremia
42
Q

Blood Chemistry & pH in Dorzolamide

A
  1. hypokalemia
  2. acidosis (low pH)
  3. Hyperchloremia
43
Q

Ethacrynic acid MOA

A

Inhibition of Na/K/2Cl cotransporter in TAL

44
Q

Furosemide MOA

A

Inhibition of Na/K/2Cl cotransporter in TAL

45
Q

Torsemide MOA

A

Inhibition of Na/K/2Cl cotransporter in TAL

46
Q

Urinary Electrolytes in Ethacrynic acid

A
  1. Very increased Na
  2. Increased K
  3. Increased Ca
  4. Increased Mg
  5. Increased Cl
  6. DECREASED HCO3
47
Q

Urinary Electrolytes in Furosemide

A
  1. Very increased Na
  2. Increased K
  3. Increased Ca
  4. Increased Mg
  5. Increased Cl
  6. DECREASED HCO3
48
Q

Urinary Electrolytes in Torsemide

A
  1. Very increased Na
  2. Increased K
  3. Increased Ca
  4. Increased Mg
  5. Increased Cl
  6. DECREASED HCO3
49
Q

Blood Chemistry & pH in Ethacrynic acid

A
  1. hypokalemia
  2. alkalosis (increased pH)
  3. hypocalcemia
  4. hypomagnesemia
50
Q

Blood Chemistry & pH in Furosemide

A
  1. hypokalemia
  2. alkalosis (increased pH)
  3. hypocalcemia
  4. hypomagnesemia
51
Q

Blood Chemistry & pH in Torsemide

A
  1. hypokalemia
  2. alkalosis (increased pH)
  3. hypocalcemia
  4. hypomagnesemia
52
Q

Hydrochlorthiazide MOA

A

Inhibition of Na/Cl cotransporter in DCT

53
Q

Indapamide MOA

A

Inhibition of Na/Cl cotransporter in DCT

54
Q

Metolazone MOA

A

Inhibition of Na/Cl cotransporter in DCT

55
Q

Thiazides

A
  1. Hydrochlorthiazide
  2. Indapamide
  3. metolazone
56
Q

Loop Diuretics

A
  1. Furosemide
  2. Torsemide
  3. Ethacrynic acid
57
Q

K+ sparing Diuretics

A
  1. Amiloride (blocks Na channels in CD)
  2. Triamterene (blocks Na channels in CD)
  3. Spironolactone (blocks aldosterone receptors in CD)
58
Q

Thiazides Urinary Electrolytes

A
  1. Increased Na, K, Cl

2. Decreased Ca

59
Q

Thiazides Blood Chemistry & pH

A
  1. hypokalemia
  2. alkalosis (increased pH)
  3. HYPERcalcemia
  4. Hyperuricemia
  5. Hyper glycemia
60
Q

Loop Diuretics Blood Chemistry & pH

A
  1. hypokalemia
  2. alkalosis (increased pH)
  3. hypocalcemia
  4. hypomagnesemia
61
Q

Loop Diuretics Urinary Electrolytes

A
  1. Very increased Na
  2. Increased K
  3. Increased Ca
  4. Increased Mg
  5. Increased Cl
  6. DECREASED HCO3
62
Q

K+ Sparing Diuretics Urinary Electrolytes

A
  1. Small amounts of Na

2. decreased K

63
Q

K+ Sparing Diuretics Blood Chemistry & pH

A
  1. Hyperkalemia

2. acidosis (decreased pH)

64
Q

Diuretics that result in acidosis (pH)

A
  1. CA inhibitors: acetazolamide & dorzolamide

2. K+ sparing diuretics

65
Q

Diuretics that result in alkalosis (pH)

A
  1. Loop Diuretics

2. Thiazides

66
Q

MOA of Spironolactone

A

Blocks Aldosterone receptors in CD

67
Q

MOA of triamterene

A

Blocks Na channels in CD

68
Q

MOA of Amiloride

A

Blocks Na channels in CD

69
Q

Best Diuretic for edema

A

Furosemide

70
Q

Best for HTN & as anti-diuretic

71
Q

Best to tx nephrolitiasis with hypocalcemia

72
Q

best to treat glaucoma

A

acetazolamide & mannitol

73
Q

best to treat cerebral edema

A

mannitol–NEVER USED IN CF

74
Q

Increases risk of HYPERkalemia seen with K sparing diuretics

A
  1. NSAIDS
  2. Beta blockers
  3. ACE-I
75
Q

Reduces Digoxin toxicity

A

K sparing diuretics

76
Q

Increases Digoxin toxicity

A

loop & thiazides

77
Q

reduces efficacy of diuretics by inhibiting secretion into renal tubule

A

Probenecid

78
Q

DOC in CCF

79
Q

DOC in Hepatic ascites

A

Thiazides with K+ supplements or

Thiazides with K+ sparing diuretics

80
Q

DOC in Pulmonary Edema of Cardiac origin (LVF)

A

Loop Diuretics

81
Q

DOC in increased intracranial pressure

A

osmotic diuretics

82
Q

DOC in renal edema–nephrotic syndrome

A

Thiazide & K-sparing or

loop & K-sparing

83
Q

DOC in Chronic Renal Failure

A

Loop Diuretics

84
Q

DOC in acute renal failure

A

osmotic diuretics

85
Q

Vasopressin & Desmopressin

What?
MOA
Effects
Used to Tx

A

Antidiuretic Hormone Agonists

MOA:

  1. facilitates H20 reabsorption from CD by activation of V2 receptors (Gs)
  2. increased cAMP–>insertion of additional aquaporin water channels into the luminal membrane of the tubule–> facilitates water reabsorption

Effects: reduce urine volume & increase it’s concentration

Used: in Neurogenic (pituitary) Diabetes Insipidus

86
Q

DOC in Neurogenic (pituitary) Diabetes Insipidus

A

Vasopressin or Desmopressin

87
Q

Demeclocycline

A

ADH Antagonist

MOA:

  1. oppose the actions of ADH & other peptides with act on V2 receptors
  2. such peptides are secreted by certain tumors (i.e. small cell carcinoma of the lung) and cause significant water retention & hyponatremia

This is syndrome of inappropriate ADH secretion (SIADH)

Remember: V2 receptors act through Gs–>increased cAMP–>insertion of additional aquaporin water channels into the luminal membrane of the tubule–> facilitates water reabsorption

88
Q

Conivaptan

A

ADH antagonist

MOA:

  1. oppose the actions of ADH & other peptides with act on V2 receptors
  2. such peptides are secreted by certain tumors (i.e. small cell carcinoma of the lung) and cause significant water retention & hyponatremia

This is syndrome of inappropriate ADH secretion (SIADH)

Remember: V2 receptors act through Gs–>increased cAMP–>insertion of additional aquaporin water channels into the luminal membrane of the tubule–> facilitates water reabsorption

89
Q

DOC for syndrome of inappropriate ADH secretion (SIADH)

A

Demeclocycline & conivaptan

Pharm (32 decks)

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