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104-theme 3-the excretory system and renal function > drugs which affect the kidney: diuretic agents > Flashcards

drugs which affect the kidney: diuretic agents Flashcards

1
Q

what types of drugs can affect the kidney? 9

A
  • ACE inhibitors
  • Anticancer drugs
  • Antiviral agents
  • Aminoglycosides
  • Beta blockers
  • Lithium
  • NSAIDs
  • Radiocontrast media
  • Vasodilators
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2
Q

what are diuretic agents? 4

A
  • Any compound that causes the excretion of an increased volume of urine from the body
  • A drug which increases the excretion of both fluids and solutes
  • Natriuretic= increases Na+ excretion
  • Kaliuretic= increase K+ excretion
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3
Q

what do diuretics do to the kidney? 3

A
  • Increase excretion of Na+ and water by the kidneys:
  • They reduce reabsorption of Na+ from the filtrate
  • They increase water loss secondary to Na+ excretion
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4
Q

what do aquatic agents do?

A
  • increase urine excretion without increasing Na+ excretion
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5
Q

what are the modes of action of diuretics? 2

A
  • Direct action on the cells at the nephron (more common)

- Modification of content of the filtrate

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6
Q

why do we use diuretics? 12

A
  • Reduce circulating fluid volume
  • Removal of excess body fluid (oedema)
  • Hypertension
  • Chronic heart failure
  • Liver cirrhosis
  • Renal disease
  • Premenstrual oedema
  • Toxic oedema
  • Increase elimination of drugs
  • Rapid weight loss. (abuse)
  • Glaucoma (reduces intra-ocular pressure)
  • Epilepsy (reduces pressure of CSF
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7
Q

describe the reabsorption of water and Na+? 2

A
  1. 5% of water is reabsorbed

99. 4% of Na+ is reabsorbed

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8
Q

what are the different classes of diuretic agents? 5

A
  • Carbonic anhydrase inhibitors= proximal tubule
  • Osmotic diuretics= proximal tubule, descending loop of Henle
  • Loop diuretics= ascending loop of Henle
  • Thiazides and thiazide like diuretics= early distal tubule
  • Potassium- sparing diuretics (aldosterone antagonists, non-aldosterone antagonists) = late distal tubule, early collecting tubule
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9
Q

describe loop diuretics? 4

A
  • Most effective diuretics available
  • Often called high-ceiling diuretics: lead to torrential urine flow
  • Inhibit the Na+/K+?2Cl- transporters (NKCC2) in the thick ascending limb of the loop of Henle: this reduces reabsorption of Na+, K+ and Cl-
  • Reduced Na+ reabsorption leads to rapid and profound diuresis: a single dose can increase urine volume from 200 to 1,2000 ml over 3 hours
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10
Q

what are the clinical uses of loop diuretics? 6

A
  • Acute pulmonary oedema
  • Chronic heart failure
  • Cirrhosis of the liver
  • Resistant hypertension
  • Nephrotic syndrome
  • Acute kidney injury
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11
Q

what are the unwanted effects of loop diuretics? 5

A
  • Dehydration
  • K+ loss leading to low plasma K+ (hypokalaemia)
  • Metabolic alkalosis (due to H+ loss in the urine)
  • Hypokalaemia can potentiate effects of cardiac glycosides
  • Deafness (when used with aminoglycoside antibiotics)
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12
Q

describe the sodium-potassium exchange in the DT? 3

A
  • Loop diuretics cause increased Na+ delivery to the distal tubule
  • This is exchanged for K+ in the DT which is excreted in the urine
  • This K+ loss contributes to the hypokalaemia associated with loop diuretics
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13
Q

describe thiazide diuretics? 5

A
  • Act in the distal tubule to inhibit the apical Na+/Cl- co-transporter
  • Cause moderate but sustained Na+ excretion with increased water excretion
  • Moderately powerful diuresis: but maximum diuresis produced is considerably lower than that produced by loop diuretics
  • Well absorbed from the GI tract and long duration of action: up to 24 hours
  • Main thiazide is Bendroflumethiazide= useful for moderate/mild heart failure
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14
Q

describe thiazide- like diuretics? 2

A
  • Similar but different molecular structures

- Indapamide- preferred for resistant hypertension due to lower incidence of unwanted effects

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15
Q

what are the clinical uses of thiazide and thiazide like diuretics? 3

A
  • Hypertension
  • Oedema
  • Mild heart failure
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16
Q

what are the unwanted effects of thiazide and thiazide like diuretics? 6

A
  • Plasma K+ depletion (due to urinary K+ loss)
  • Metabolic alkalosis (due to urinary H+ loss)
  • Increased plasma uric acid- gout
  • Hyperglycaemia (increased blood glucose)
  • Increased plasma cholesterol (with long term use)
  • Male impotence (reversible)
17
Q

describe why hypokalaemia can be a problem? 3

A
  • Due to increased loss of K+ in the urine, loop diuretics and thiazides can cause hypokalaemia
  • Mild= fatigue, drowsiness, dizziness, muscle weakness
  • Severe= abnormal heart rhythm, muscle paralysis, death
18
Q

describe potassium sparing diuretics? 3

A
  • Potassium sparring diuretics can avoid this problem by acting on distal tubules to inhibit Na+ reabsorption however K+ is not secreted into the distal tubule
  • Two subcategories:
  • Aldosterone antagonists (eplerenone, spironolactone)
  • Non-aldosterone antagonists (amiloride, triamterene)
19
Q

describe spironolactone and eplerenone? 5

A
  • Spironolactone is metabolised to canrenone (its active metabolite)
  • A competitive antagonist of aldosterone (mineralocorticoid) receptor
  • Reduces Na+ channel formation and its absorption from the distal tubule
  • Limited diuretic action (not as potent as loop diuretics or thiazides)
  • As mechanisms depends on reduction of protein expression in distal tubular cells, effects normally take several days to develop
20
Q

what are the clinical uses of spironolactone and eplerenone? 4

A
  • Heart failure
  • Oedema
  • Short term use
  • Can also be used for resistant hypertension but some concerns over long- term use due to possible incidence of cancer
21
Q

what are the unwanted effects of spironolactone and eplerenone? 5

A
  • Hyperkalaemia (increased plasma K+ levels)- needs to be monitored regularly)
  • Metabolic acidosis (due to increased plasma H+)
  • GI upsets (peptic ulceration reported)
  • Gynaecomastia, menstrual disorders, testicular atrophy
  • Eplerenone produces less unwanted effects than spironolactone
22
Q

describe triamterene and amiloride? 3

A
  • Weak diuretics act on distal tubule to inhibit Na+ reabsorption and decrease K+ excretion
  • Blocks luminal Na+ channel by which aldosterone produces its main effects
  • Of little therapeutic use alone but are useful in combination with potassium depleting diuretics as they limit hypokalaemia
23
Q

describe the unwanted effects of triamterene and amiloride? 4

A
  • Hyperkalaemia
  • Metabolic acidosis
  • GI disturbances
  • Skin rashes
24
Q

why do we use diuretics in combination? 6

A
  • To increase diuretic effect:
  • Some patients do not respond well to just one type of diuretic for unknown reasons
  • Combinations of diuretics with different sites of action can sometimes provide synergistic action which can become complicated
  • .
  • To avoid the unwanted effects of hypokalaemia (reduces plasma K+ levels):
  • Combinations of loop diuretics or thiazides with potassium sparing diuretics
  • Diuretic preparations containing K+
25
Q

what are the different diuretic combinations to avoid hypokalaemia? 4

A
  • Loop diuretics and spironolactone
  • Loop diuretics with amiloride or triamterene
  • Thiazides with spironolactone
  • Thiazides with amiloride or triamterene
26
Q

describe carbonic anhydrase inhibitors? 4

A
  • Acetazolamide
  • Block’s sodium bicarbonate reabsorption in the PT
  • These were the earliest diuretics developed
  • Causes only weak diuresis so not now used commonly
27
Q

describe the use of carbonic anhydrase inhibitors?

A
  • Glaucoma

- Epilepsy

28
Q

describe the unwanted effects of carbonic anhydrase inhibitors? 2

A
  • Metabolic acidosis (due to excretion of HCO3-)

- Enhances renal stone formation (due to alkaline urine)

29
Q

describe osmotic diuretics? 4

A
  • Mannitol
  • Non-resorbable solute which undergoes glomerular filtration
  • Excreted within 30-60 minutes
  • Diuresis begins in 30-60 minutes and persists for 6-8 hours
30
Q

what are the clinical uses of osmotic diuretics? 4

A
  • Treatment of raised intercranial pressure (cerebral oedema)
  • Treatment of intraocular pressure
  • If given orally can cause osmotic diarrhoea which eliminates toxins
  • May be useful for treatment of acute renal failure
31
Q

what are the unwanted effects of osmotic diuretics?

A
  • Presence in blood also exerts osmotic pressure leading to increased plasma volume so can’t be used in patients with hypertension
32
Q

describe water as a diuretic? 3

A
  • Under normal conditions, increased water intake leads to an increase in the volume of urine excreted
  • Process is controlled by ADH which is the most important hormone in regulating water balance
  • Normally some ADH is present in the circulation maintaining urine volume at around 1.5L/day
33
Q

describe ADH antagonists? 7

A
  • Potential ADH antagonists:
  • Investigational drugs which inhibit the effects of ADH at the collecting tubule
  • Two non-selective agents (orally active) = lithium and demeclocycline
  • Toxicity is a problem:
  • Can cause diabetes insipidus
  • Renal failure reported for both Li+ and demeclocycline
  • Li+ can cause tremors, mental confusion, cardiotoxicity, thyroid dysfunction and leucocytosis
  • Demeclocycline shouldn’t be used in patients with liver disease
34
Q

describe an agent which inhibits ADH release?

A
  • Alcohol (although tolerance develops rapidly so diuresis is not sustained)
35
Q

describe an agent which increases ADH release? 4

A
  • Nicotine
  • Ether
  • Morphine
  • Barbiturates
36
Q

describe Xanthine’s? 5

A
  • Commonly found in tea of coffee
  • Produce their weak diuretic effect by increasing cardiac output
  • Possibly also some vasodilation of the glomerular afferent arteriole
  • Results in increased renal and glomerular blood flow which increases glomerular filtration rate and urine output
  • Rarely used clinically due to gastric irritant effects (but theophylline used clinically as a bronchodilator for asthma)

104-theme 3-the excretory system and renal function (14 decks)

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