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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Edematous states caused by abnormal renal function

A

Heart failure
Hepatic ascites
Nephrotic syndrome
Premenstrual edema

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2
Q

Non-edematous states caused by abnormal renal function

A

Hypertension
Hypercalcemia
Diabetes insipidus

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3
Q

Loop diuretics MOA and actions

A

Furosemide

‘High-ceiling diuretic’ = has most dramatic effect on urine output. Highest efficacy in removing Na+ and Cl- from body

Acts on thick ascending limb of Loop of Henle –> blocks NKCC2 Na+/Cl-/K+ triple co-transporter –> normal K+ secretion from ROMK blocked too as there is no K+ reabsorption –> negative lumen potential causes paracellular secretion of Na+, Mg2+ and Ca2+

Actions:

  • Increased urinary excretion of Na+, K+, Ca2+ and Mg2+
  • Increased prostaglandin synthesis (induces COX2)
  • Decreased renal vascular resistance (due to PG)
  • Increased renal blood flow
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4
Q

Loop diuretics clinical applications and PK

A

Diuretics of choice for managing edema associated with heart failure, hepatic or renal disease

Hypertension (moderate-severe) - 2nd/3rd line

Oral and IV
Short half life = 2-4h

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5
Q

Loop diuretics AE

A

Ototoxicity
Hypokalemia - Increased Na+ delivery to distal tubule –> reabsorb Na+, increased secretion of K+
Hyperuricemia - competition of secretion system transporters in PCT
Acute hypovolemia
Hypomagnesemia
Hypocalcemia
Allergic reactions

Contraindication: sulfur allergy

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6
Q

Thiazides MOA and actions

A

Hydrocholothiazide
Chlorthalidone
Metolazone

Act on DCT –> block NCCT Na+/Cl- cotransporter –> decreased Na+ reabsorption so activity of Na+/Ca2+ exchanger on basolateral side is enhanced –> Pulls and reabsorbs Ca2+ from urine

Actions:

  • Increased urinary excretion of Na+, Cl-, K+, Mg2+
  • Decreased urinary excretion of Ca2+
  • Decreased peripheral vascular resistance –> initially due to decreased volume –> with chronic therapy, volume recovers –> decreased PVR not due to the increased urine output
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7
Q

Thiazides clinical applications and PK

A

Hypertension (1st line)
Heart failure (if mild edema)
Premenstrual edema
Hypercalciuria –> inhibit Ca2+ excretion therefore useful to treat kidney stones
Diabetes insipidus –> produces hyperosmolar urine which leads to decreased thirst –> only time where diuretics cause a decrease in urine volume

PK:
Oral
Long half life: 40h –> takes 1-3 weeks to produce a stable effect
Metalozone: more potent. Causes Na+ excretion in advanced kidney failure

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8
Q

Thiazides AE

A 
Hyperglycemia (secretion of insulin is K+ dependent)
Hyperlipidemia 
Sexual dysfunction
Hyperuricemia 
Hypercalcemia 
Hypokalemia 
Hyponatremia 
Allergic reactions

Contraindication: sulfur allergy

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9
Q

K+ sparing diuretics

A

Aldosterone antagonists:
Spironolactone
Eplerenone

Na+ channel inhibitors: Amiloride
Triamterene

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10
Q

Spironolactone and Eplerenone MOA

A

Act in collecting duct –> antagonize aldosterone at intracellular cytoplasmic receptor sites –> prevent translocation of receptor complex to nucleus –> inhibit affects of aldosterone on ROMK and ENaC channels –> decreased Na+ reabsorption and decreased K+ secretion

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11
Q

Spironolactone and Eplerenone clinical applications

A 
Heart failure - adjunct to prevent cardiac remodelling
Hypertension - 2nd line drugs
Used alone when there is excess aldosterone 
Primary hyperaldosteronism (diagnosis and treatment) 
Edema - associated with excess aldosterone excretion
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12
Q

Spironolactone and Eplerenone AE

A 
Gastric upset 
Peptic ulcers 
Hyperkalemia 
Nausea, lethargy, mental confusion 
Endocrine effects:
- Spironolactone can act as androgen receptor antagonist 
- Gynecomastia and reduced sperm count in men 
- Galactorrhea in women
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13
Q

Amiloride and Triamterene MOA and clinical applications

A

Act in collecting duct –> block ENac channels directly –> decreased Na+ reabsorption and decreased K+ secretion

Not very efficacious alone so used in combination to prevent K+ loss associated with thiazides and furosemide

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14
Q

Amiloride and Triamterene AE

A 
GI upset 
Leg cramps 
Hyperkalemia 
Hyponatremia 
Diziness, pruritus, headache, minor visual changes
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15
Q

Acetazolamide MOA

A

Carbonic Anhydrase inhibitor –> acts in PCT –> decreased HCO3- reabsorption and decreased intracellular H+ in PCT epithelial cells –> H+/Na+ exchanger will not work –> decreased Na+ reabsorption –> mild diuretic effect

Decreases activity of Na+/K+ ATPase (diuresis)
Increases urinary pH

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16
Q

Acetazolamide clinical applications and PK

A

Prophylaxis for mountain sickness (more bicarb entering urine –> metabolic acidosis –> will cause hyperventilation to blow off CO2 –> can create the acidosis to compensate for the drop in oxygen)

Glaucoma (HCO3- is an important component of aqueous humor in eye)

Epilepsy

Metabolic alkalosis

PK:
Oral and well-absorbed
IV for acute treatment of closed angle glaucoma
Half-life: 3-6h

17
Q

Acetazolamide AE

A 
Metabolic acidosis 
Hyponatremia 
Hypokalemia 
Crystalluria 
Malaise, fatigue, headache, depression, drowsiness 
GI upset 
Paresthesia
18
Q

Mannitol MOA

A

Osmotic diuretic - only drug that truly increases urine volume

Acts everywhere –> raises osmotic pressure of the plasma –> draws H20 out of body tissues –> does not affect Na+ excretion directly

19
Q

Osmotic diuretics clinical applications and PK

A

Increase urine flow in patients with acute renal failure

Reduce intracranial pressure and treatment of cerebral edema

Excretion of toxic substances

Can be used to reduce IOP in glaucoma

PK: Given IV only

20
Q

Osmotic diuretics AE and contraindications

A

Extracellular water expansion
Tissue dehydration

Contraindications:
Pulmonary edema
Congestive heart failure

21
Q

Conivaptan MOA

A

Acts at collecting ducts –> ADH antagonist –> antagonist at V1 and V2 receptors –> tubule is impermeable to water due to absence of ADH –> dilute urine

22
Q

Conivaptan clinical applications and PK

A

Hypervolemic or euvolemic hyponatremia
SIADH
Heart failure (only if benefits outweigh risks)

IV only
Metabolised by and potent inhibitor of CYP3A4

23
Q

Conivaptan AE and contraindications

A 
Infusion site reactions 
Thirst 
Atrial fibrillation 
GI and electrolyte disturbances 
Nephrogenic diabetes insipidus

Contraindications:
Hypovolemic hyponatremia
Renal failure

Pharmacology (20 decks)

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