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(UNI) Clinical (2nd Year) > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What is a diuretic?

A

An agent that causes increased urine flow.

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2
Q

What is a natriuretic?

A

An agent that produces an increase in sodium output/excretion. All useful diuretics are natriuretic.

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3
Q

Continued administration of a diuretic agent leads to a point of dynamic compensation when physiological mechanisms balance diuresis. Outline this process.

A
  • Activation of sympathetic nervous system due to decreased BP.
  • Activation of renin-angiotensin-aldosterone axis.
  • Decreased renal BP and loss of renal fluid output.
  • Changes in natriuretic factors (kinins, atrial natriuretic factor).
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4
Q

Describe loop diuretics.

A

These are chemically related agents containing sulphonamide. They are powerful diuretics with rapid onset of action (1 hour) and short duration (6 hours).

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5
Q

Describe the mechanism of action of loop diuretics.

A

Binds to and closes the Na/K/2Cl contransporter in the ascending thick limb of the loop of Henle, preventing reabsorption. Have a direct vasodilatory action. High concentrations inhibit carbonic anhydrase.

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6
Q

Give some examples of loop diuretics.

A

Furosemide, bumetanide, torasemide.

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7
Q

What unwanted effects are associated with loop diuretics?

A

Hyperuricaemia. Electrolyte disturbances.
Metabolic alkalosis.
Rare blood disorders.
Hyperglycaemia.
Skin rashes and photosensitivity reactions.

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8
Q

What electrolyte disturbances are associated with loop diuretics?

A

Hypokalaemia, hypocalcaemia, hypomagnesaemia.

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9
Q

What rare blood disorders are associated with loop diuretics?

A

Thrombocytopenia.
Lecuopenia.
Aplastic anaemia.

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10
Q

Describe the thiazide diuretics.

A

They are diuretics that cause moderate natriuresis with marked loss of potassium ions. They act within 1 or 2 hours with a duration of action of 12 to 24 hours.

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11
Q

Where is the site of action of the thiazide diuretics?

A

The tubular surface of the early distal convoluted tubule.

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12
Q

What are the uses of thiazide diuretics?

A

Long term control of hypertension. Chronic therapy of congestive heart failure as an add on to loop.

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13
Q

Do thiazide diuretics cause metabolic acidosis?

A

No.

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14
Q

What are thiazide-like diuretics?

A

Term originally used to describe agents with a ‘thiazide’ ring system. Now also used to describe agents with similar pharmacological action. Are all weak acids, substrates for proximal convoluted tubule secretion.

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15
Q

Give some examples of thazide-like diuretics?

A

Chlorothiazide, bendroflumethiazide, hydrochlorothiazide.

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16
Q

What is the mechanism of action of the thiazide/thiazide-like diuretics?

A

They inhibit the Na/Cl symporter in the early distal convoluted tubule. This prevents the reabsorption of water into the blood.

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17
Q

What are some problems with the use of the thiazide/thiazide-like diuretics?

A

Hypokalaemia, hyponatraemia, hypercalcaemia, uricosuric action (reduced PCT secretion of uric acid),
Glucose intolerance,
Hyperlipoproteinaemia.

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18
Q

Describe the glucose intolerance seen with the use of thiazide/thiazide-like diuretics.

A

This is secondary to hypokalaemia and is caused by the hyperpolarisation of the islet cell membrane, reducing insulin release.

19
Q

What drugs may show an interaction with the thiazide/thiazide-like diuretics?

A

Sulphonylureas, uricosuric agents, NSAIDs, agents that may predispose the patient to torsade des pointes (quinidine, terfinadine).

20
Q

What classes of diuretics are classed as potassium sparing?

A

Aldosterone antagonists, sodium ion channel blockers.

21
Q

Give some examples of aldosterone antagonist diouretics?

A

Spironolactone, eplerenone.

22
Q

Describe the mode of action of the aldosterone antagonist diuretics.

A

They bind to the mineralocorticoid receptor in the intercalated cells, thus blocking the binding of aldosterone to its receptor. This inhibits the expression of the Na/K pump, thus inhibiting sodium ion reabsorption and preventing potassium ion secretion.

23
Q

What are the side effects of aldosterone antagonist diuretics?

A

Low sodium, high potassium, gynecomastia, vaginal bleeding.

24
Q

What is the oral absorption of spironolactone?

A

60-70%.

25
Q

What is the half life of spironolactone?

A

1.4 hours.

26
Q

What conditions is spironolactone used for?

A

Heart failure, hypertension, ascites.

27
Q

How do sodium ion channel blocking diuretics work?

A

The main site of action for these agents is luminal sodium ion channels. They reduce sodium ion movement which maintains high luminal membrane potential gradient (-85mV), which opposes potassium ion secretion. These agents have some weak inhibitory action on luminal sodium-potassium ATPase. At very high concentrations, agents inhibit the sodium/potassium/chlorine co-transporter.

28
Q

Give some examples of sodium ion channel blockers.

A

Amiloride, triamterene.

29
Q

What are sodium ion channel blockers used for?

A

These agents are used in combination with more potent diuretics to reduce overall potassium ion loss.

30
Q

With what drugs/compounds should caution be taken when using potassium sparing diuretics?

A

Potassium supplements, ACE inhibitors/ARBs.

31
Q

Why should caution be taken with potassium sparing diuretics and potassium supplement?

A

Possible hyperkalaemia.

32
Q

Why should caution be taken with potassium sparing diuretics and ACE inhibitors/ARBs?

A

o Increase monitoring of potassium levels as both ACE inhibitors/ARBs and potassium sparing diuretics will increase levels.
o Lots if patients are successfully on ACEI and aldosterone antagonists together. If necessary, reduce the dose of spironolactone or increase dosing intervals to alternate days.
o Important to keep aldosterone antagonist in HF patients as it will reduce mortality.

33
Q

Describe osmotic diuretics.

A
  • Pharmacologically inert.
  • Freely filterable at glomerulus and enter tubule.
  • Limited or no tubular reabsorption.
  • Generally, are non-electrolytes (e.g. mannitol).
34
Q

What effects to osmotic diuretics exert on the body?

A
  • Primarily diuretics.
  • Increase solutes (e.g. sodium and potassium ions) concentration in the tubule lumen.
  • Decreased osmotic gradient between blood and tubular fluid, and so impair water reabsorption.
  • Expand ECFV (extracellular fluid volume) and (BV (blood volume)) and so increase GFR.
35
Q

What are osmotic diuretics used for?

A

Mainly reduction in cerebral oedema and IOP (intraocular pressure).

36
Q

What problems can be seen with use of osmotic diuretics?

A

Volume expansion with chronic use.

37
Q

Give an example of a carbonic anhydrase inhibitor diuretic.

A

Acetazolamide.

38
Q

Describe carbonic anhydrase inhibitor diuretics.

A
  • Competitive inhibitor of carbonic anhydrase.
  • Causes rapid natriuresis.
  • Increased renal loss of HCO3- (max dose about 50% overall inhibition).
39
Q

What is the main side effect seen with the carbonic anhydrase inhibitor diuretics?

A

Marked tachyphylaxis.

40
Q

What is the main use of carbonic anhydrase inhibitor diuretics?

A

Main use is for the treatment of acute glaucoma to reduce IOP.

41
Q

What supplement should be given when a patient is on carbonic anhydrase inhibitor diuretics?

A

Dietary potassium.

42
Q

How do carbonic anhydrase inhibitor diuretics work?

A

A carbonic anhydrase inhibitor that reduces the formation of hydrogen and bicarbonate ions from carbon dioxide and water by inhibiting, in proximal renal tubule, the enzyme carbonic anhydrase, thereby promoting renal excretion of sodium, potassium, bicarbonate, and water.

43
Q

In what clinical conditions may diuretics be used?

A

Hypertension, congestive heart failure, ascites, renal failure, increased intracranial pressure and IOP.

44
Q

Describe the monitoring of U&Es in patients on diuretic treatment.

A
  • Mainly for a possible renal decline and electrolyte imbalances.
  • If potassium is low, check magnesium also.

(UNI) Clinical (2nd Year) (19 decks)

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