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Pharmacology > Module 3.1: DIURETICS > Flashcards

Module 3.1: DIURETICS Flashcards

1
Q

 Major effect is in the proximal tubule and descending Loop of Henle  Prevents normal absorption of water by interposing a countervailing osmotic force

A

OSMOTIC DIURETICS

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2
Q

[Thiazide Diuretic] only drug available in parenteral admin

A

CHLOROTHIAZIDE

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3
Q

[CARBONIC ANHYDRASE INHIBITORS] Indications: (what indication is this?) cystinuria – dissolves cysteine crystals by increasing urinary pH, leads to complete reabsorption of cysteine uric acid crystals – same effect ADR: formation of Ca salts

A

urine alkalinisation

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4
Q

Newer, more selective aldosterone blockers have fewer of the progestational and anti-androgenic effects than…

A

Spirinolactone

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5
Q
  • reduce pulmonary congestion and left ventricular filling pressures in heart failure before a measurable increase in urinary output occurs
A

FUROSEMIDE

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6
Q

[CARBONIC ANHYDRASE INHIBITORS] PROTOTYPE DRUG:

A

ACETAZOLAMIDE

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7
Q

ANTIDIURETIC HORMONE ANTAGONISTS in patients with CHF and and SIADH (x’ss ADH)

A

LITHIUM DEMECLOCYCLINE*

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8
Q

ADVERSE DRUG REACTIONS: ARF caused by …

A

combination of triamterene and indomethacin (NSAID)

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9
Q

[LOOP DIURETICS] ADVERSE DRUG REACTIONS

A
  • Hypotension - Dehydration losses excess volume [take note of patient’s fluid volume] - HYPOnatremia - HYPOkalemia o more effect than hyponatremia- monitor level] o if given with digoxin = arrhythmia [should be given simultaneously]
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10
Q

DIRECT Na CHANNEL BLOCKER

A

TRIAMTERENE AMILORIDE

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11
Q

[OSMOTIC DIURETICS] INDICATION

A

 to increase urine volume  reduce intracranial and intraocular pressure

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12
Q

[LOOP DIURETICS] ADVERSE DRUG REACTIONS

A
  • ototoxicity (ETHACRYNIC ACID) - hyperuricemia (hypovolemia-associated enhancement of uric acid reabsorption in the proximal tubule) - HYPOmagnesimia - allergic reactions (may be due to sulfur)
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13
Q

[ALDOSTERONE BLOCKERS/K-SPARING DIURETICS] ADVERSE DRUG REACTIONS

A

 HYPERkalemia  Hyperchloremic metabolic acidosis

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14
Q
A
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15
Q

[OSMOTIC DIURETICS] ADVERSE DRUG REACTIONS:

A

 extracellular volume expansion  dehydration, HYPERkalemia, and HYPOnatremia

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16
Q

[Thiazide Diuretic] slow absorption, longer duration

A

CHLORTHALIDONE

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17
Q
  • Ineffective in reducing BP in vast majority of individuals with HTN
A

LOOP DIURETICS

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18
Q

[ALDOSTERONE BLOCKERS/K-SPARING DIURETICS] INDICATIONS

A

Hyperaldosteronism treatment - due either to primary hypersecretion (Conn’s syndrome, ectopic adrenocorticotropic hormone production) or secondary hyperaldosteronism (evoked by heart failure, hepatic cirrhosis, nephrotic syndrome, or other conditions associated with diminished effective intravascular volume)

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19
Q

 decrease pH and increase luminal concentrations of Cl2 and Na  sometimes used in combination with high-ceiling diuretics to counteract alkalosis

A

ACIDIFYING SALTS [AMMONIUM CHLORIDE]

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20
Q

[CARBONIC ANHYDRASE INHIBITORS] ADVERSE DRUG REACTIONS:

A
  • Hyperchloremic Metabolic Acidosis - Renal stone (phosphaturia, hypercalcuria) - Renal K wasting - Drowsiness and paresthesias - CNS toxicities among renal failure patients - Hypersensitivity reactions
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21
Q

USED ONLY IN ACUTE PHASES not for chronic use; due to reduction of circulating volume

A

LOOP DIURETICS

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22
Q

MOA: Early renal (salt/water excretion) effects – act by inhibiting the Na/Cl reabsorption pump in the DCT; by blocking Na-Cl co-transporter (NCC)

A

THIAZIDE DIURETICS

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23
Q

[CARBONIC ANHYDRASE INHIBITORS] Indications: By decreasing cerebrospinal fluid formation and by decreasing the pH of the cerebrospinal fluid and brain leading to an increase in ventilation and diminish symptoms of ….

A

acute mountain sickness

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24
Q

 increasing cardiac output and promoting a higher glomerular filtration rate  seldom used as diuretics, but diuresis occurs under other clinical applications (e.g., for bronchodilatation)  MOA: antagonism of adenosine receptors

A

XANTHINE DIURETICS

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25
Q

[LOOP DIURETICS] INDICATIONS

A

 Mild HYPERkalemia - enhance urinary excretion of K +  Acute Renal Failure (ARF) – inc rate of urine outflow, inc excretion of K  Anion overdose

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26
Q

ANTIDIURETIC HORMONE AGONISTS in patients with CENTRAL DIABETES INSIPIDUS (low ADH)

A

VASOPRESSIN* DESMOPRESSIN

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27
Q

[CARBONIC ANHYDRASE INHIBITORS] Indications:

A
  • treatment of sleep apnea - adjuvant treatment of epilepsy and in some forms of hypokalemic periodic paralysis - treating patient with CSF leak(tumor or head trauma) - increasing urinary phosphate excretion during hyperphosphatemia
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28
Q
  • Prevent reabsorption of Cl and Na by blocking NaK2Cl transporter [leading to excretion of Na and Cl]
A

LOOP DIURETICS

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29
Q

[CARBONIC ANHYDRASE INHIBITORS] Indications: - Glaucoma by reducing aqueous humor production Topically active agents are…

A

DORZOLAMIDE BRINZOLAMIDE

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30
Q

[ALDOSTERONE BLOCKERS/K-SPARING DIURETICS] INDICATIONS

A
  • chronic liver disease leads to decreased possibility in development of ascites - chronic heart failure [CHF] - usually given with a thiazide diuretic [not as potent if alone]
31
Q

ADVERSE DRUG REACTIONS: Kidney stone/nephrolithiasis caused by…

A

triamterene

32
Q
  • Act on membrane ion transport mechanism in the thick ascending limb of the Loop of Henle
A

LOOP DIURETICS

33
Q

MOA of Loop Diuretics for patient with…..: - Loop diuretics effectively reduce ECF volume and BP - The renal and antinatriuretic mechanisms are blunted

A

Patient with renal dysfunction

34
Q
  • These are VENODILATORS and little arteriolar dilator effect
A

LOOP DIURETICS

35
Q

mild diuretic

A

CAFFEINE

36
Q

Should be given as IV, if given orally can cause osmotic diarrhea rather than diuresis

A

MANNITOL (non-reabsorbable solute)

37
Q

ALDOSTERONE ANTAGONISTS – competitive inhibitor of aldosterone

A

SPIRINOLACTONE EPLENERONE

38
Q

[OSMOTIC DIURETICS] INDICATION reduce cellular edema in case of hemorrhagic stroke to decrease ICP

A

MANNITOL (non-reabsorbable solute)

39
Q

[Thiazide Diuretic] ADVERSE EFFECTS

A

 HYPOkalemic metabolic alkalosis and hyperuricemia  impaired CHO tolerance  HYPERGLYCEMIA  Hyperlipidemia – inc in total cholesterol and LDL levels  HYPOnatremia  Allergy- photosensitivity, dermatitis; severe could lead to hemolytic anemia, thrombocytopenia, and acute necrotizing pancreatitis

40
Q

[CARBONIC ANHYDRASE INHIBITORS] CONTRAINDICATION

A

Liver cirrhosis, may contribute to development of hyperammonemia and hepatic encephalopathy

41
Q

MOA:  They provide effective Anti-HTN treatment especially in low-renin and salt sensitive forms of hypertension  Provide additional benefit in the treatment of heart failure (HF) when combined with ACE Inhibitors (ACE-I), digitalis, and loop diuretics

A

ALDOSTERONE BLOCKERS/K-SPARING DIURETICS

42
Q

[CARBONIC ANHYDRASE INHIBITORS] Indications: …..due to excessive use of diuretics among HF patients should only be treated with carbonic anhydrase inhibitors

A

metabolic alkalosis states

43
Q

ADVERSE DRUG REACTIONS: Gynecomastia, impotence, and benign prostatic hyperplasia caused by….

A

spironolactone and eplerenone due to steroid like structure

44
Q

MOA of Loop Diuretics for patient with…..: - Variety of mechanisms blunts the ability to persistently reduce ECF volume or BP - The initial diuresis is typically followed by longer period of Na retention (neutral or positive balance) *another reason why it’s not for chronic use

A

Normal GFR patient

45
Q

 Predominantly found in the luminal membrane of the PCT  Inhibitors that block NaHCO3 reabsorption

A

CARBONIC ANHYDRASE INHIBITORS {-ZOLAMIDE}

46
Q

[Thiazide Diuretic] use in combination with loop diuretics

A

METOLAZONE

47
Q
  • Induces production of COX-2 leading to production of prostaglandins like PGE2 which inhibits salt reabsorption in the TAL
A

FUROSEMIDE

48
Q

[OSMOTIC DIURETICS] PROTOTYPE DRUG:

A

MANNITOL (non-reabsorbable solute)

49
Q
  • If given IV, check BP before and after administration; if hypotensive from the start, given with this would lead to severe hypotension; if normal BP then administered, dramatic decrease in BP
A

FUROSEMIDE

50
Q

[Thiazide Diuretic] INDICATIONS

A

 Hypertension – mild; or as adjunct with other anti-HTN  Heart failure  Nephrolithiasis due to idiopathic hypercalciuria  Nephrogenic diabetes insipidus

51
Q

Topical for glaucoma

A

Brinzolamide, dorzolamide

52
Q

MOA:

Inhibition of the enzyme
prevents dehydration of
H2CO3 and hydration of
CO2 in the proximal convoluted
tubule

EFFECTS:

Reduces reabsorption of HCO3−, causing
self-limited diuresis • hyperchloremic
metabolic acidosis reduces body pH,
reduces intraocular pressure

CLINICAL APP:

Glaucoma, mountain sickness,
edema with alkalosis

A

Acetazolamide

53
Q

ROA: Oral and topical preparations available

• duration of action ∼
8–12 h

TOXICITY: Metabolic acidosis,
renal stones, hyperammonemia
in cirrhotics

A

Acetazolamide

54
Q

Sulfonamide loop agents like furosemide

A

Bumetanide, torsemide

55
Q

Not a sulfonamide but has typical loop activity and some uricosuric action

A

Ethacrynic acid

56
Q

MOA:

Inhibition of the Na/K/2Cl
transporter in the ascending
limb of Henle’s loop

EFFECTS:

Marked increase in NaCl excretion, some
K wasting, hypokalemic metabolic alkalosis,
increased urine Ca and Mg

A

Furosemide

57
Q

CLINICAL APP:

Pulmonary edema, peripheral
edema, hypertension,
acute hypercalcemia or
hyperkalemia, acute renal
failure, anion overdose

ROA: Oral and parenteral preparations
• duration of action 2–4 h

TOXICITY: Ototoxicity, hypovolemia,
K wasting, hyperuricemia,
hypomagnesemia

A

Furosemide

58
Q

Thiazide Popular for use with loop agents for synergistic effects

A

Metolazone

59
Q

Only parenteral thiazide available (IV)

A

Chlorothiazide

60
Q

Long half-life (50–60 h) due to binding to red blood cells

A

Chlorthalidone

61
Q

MOA:

Inhibition of the Na/Cl
transporter in the distal
convoluted tubule

A
62
Q

EFFECTS:

Modest increase in NaCl excretion • some
K wasting • hypokalemic metabolic
alkalosis • decreased urine Ca

A

Hydrochlorothiazide

63
Q

CLINICAL APP:

Hypertension, mild heart failure,
nephrolithiasis, nephrogenic
diabetes insipidus

ROA: Oral • duration 8–12 h

TOXICITY:
Hypokalemic metabolic alkalosis,
hyperuricemia, hyperglycemia,
hyponatremia

A

Hydrochlorothiazide

64
Q

Mechanism like amiloride, much less potent, more toxic

A

Triamterene

65
Q

Like spironolactone, more selective for aldosterone receptor

A

Eplerenone

66
Q

MOA:

Pharmacologic antagonist
of aldosterone • weak
antagonism of androgen
receptors

A

Spironolactone

67
Q

EFFECTS:

Reduces Na retention and
K wasting in kidney • poorly
understood antagonism
of aldosterone in heart and
vessels

A

Spironolactone

68
Q

CLINICAL APP:

Aldosteronism from any
cause • hypokalemia due to
other diuretics • postmyocardial
infarction

Slow onset and offset of effect
• duration 24–48 h

TOXICITY:
Hyperkalemia, gynecomastia
(spironolactone, not eplerenone)
• additive interaction with other
K-retaining drugs

A

Spironolactone

69
Q

MOA:

Blocks epithelial sodium
channels in collecting tubules

EFFECTS:

Reduces Na retention and
K wasting • increases lithium
clearance

A

Amiloride

70
Q

CLINICAL APP:

Hypokalemia from other
diuretics • reduces lithiuminduced
polyuria

ROA:

Orally active • duration 24 h

TOXICITY: Hyperkalemic metabolic
acidosis

A

Amiloride

71
Q

MOA:

Physical osmotic effect on
tissue water distribution
because it is retained in the
vascular compartment

EFFECTS:

Marked increase in urine
flow, reduced brain volume,
decreased intraocular
pressure, initial hyponatremia,
then hypernatremia

A

Mannitol

72
Q

CLINICAL APP:

Renal failure due to increased
solute load (rhabdomyolysis,
chemotherapy), increased
intracranial pressure, glaucoma

ROA: IV administration

TOXICITY:
Nausea, vomiting, headache

A

Mannitol

73
Q
A

Pharmacology (4 decks)

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