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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are mannitol, glucose and carbonic anhydrase?

A

Osmotics

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2
Q

What does acetazolamide do?

A

It’s an inhibitor

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3
Q

What is hydrochlorothiazide?

A

Thiazide

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4
Q

What is metolazone?

A

Thiazide

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5
Q

What is furosemide?

A

A loop diuretic

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6
Q

What is bumetanide?

A

A loop diuretic

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7
Q

What is ethacrynic acid?

A

A loop diuretic

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8
Q

What is spironolactone?

A

A potassium sparing diuretic

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9
Q

What is eplerenone?

A

A potassium sparing diuretic

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10
Q

What is conivaptan?

A

ADH antagonist

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11
Q

What is dapaglifozin?

A

A sodium glucose transport inhibitor

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12
Q

What is the definition of a diuretic?

A

Agents which increase urine flow

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13
Q

Why are we clinically interested in diuretics?

A

Interest is in renal solute excretion (sodium and water)

It blocks sodium absorption and water will follow

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14
Q

What is the aim of therapy of diuretics?

A

We only need to increase the urine flow by a few %
A change of 5% has a great effect - the body reabsorbs 99.6% of Na every day, so a decrease to 95% would represent 9 L of extracellular fluid loss

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15
Q

What happens in the proximal tubule?

A

It is critical for bicarbonate reabsorption (85%)
It is important for glucose reabsorption (there should be no glucose in the urine - glucose in the urine happens when the transporters are saturated in diabetics)
55-75% of filtrate water and electrolytes are reabsorbed

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16
Q

What happens in the loop of Henle

A

It is important for sodium, potassium and chloride co-transporter, and calcium and magnesium follow
Water is not reabsorbed here

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17
Q

What happens in the distal tubule

A

Sodium/chloride reabsorption and calcium excretion

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18
Q

What happens in the collecting ducts?

A

It is impermeable to sodium and water unless the proper hormones are available (aldosterone release enhances reabsorption at the expense of potassium)
ADH aka vasopression will work here to open channels and water will be reabsorbed but electrolytes won’t follow (urine concentration)

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19
Q

How does the nephron filtrate compare to the plasma?

A

It is the same but it is protein free

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20
Q

What drugs alter processes in the proximal tubule?

A

Mannitol and unreabsorbed glucose affect the reabsorbtion of water and electrolytes
Dapaglifozin affects glucose reabsorption
Acetazolamide affects bicarbonate reabsorption

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21
Q

What drugs alter processes in the loop of Henle?

A

Furosemide affects sodium, potassium and chloride are co-transportation (as well as calcium and magnesium)

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22
Q

What drugs alter processes in the distal tubule?

A

Metolazone affects sodium and chloride reabsorption

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23
Q

What drugs alter processes in the collecting ducts?

A

Eplerenone affects aldosterone’s affect on sodium reabsorption and potassium and hydrogen excretion
Conivaptain affects ADH’s affect on increasing water permeability (and water reabsorption)

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24
Q

What are classes of diuretics? What are diuretics within those classes

A 
Minor diuretics (osmotic, carbonic anhydrase inhibitors)
Major diuretics (thiazide, loop diuretics, potassium sparing diuretics)
Other diuretics (vasopressin receptor antagonists, glycosuric agents)
25
Q

What are osmotic diuretics? How do osmotic diuretics work? What properties make a perfect osmotic diuretic?

A

Osmotically active compounds in the plasma
They ‘hold’ onto water (high urine volume, little sodium)
A perfect osmotic diuretic needs to be filtered, not reabsorbed, pharmacologically inert and resistant to alteration

26
Q

What are osmotic diuretics used for?

A

They have few uses (IV mannitol and oral glycerol)
Vascular surgery
Renal transplant
Ophthalmological procedures

27
Q

Is glucose an osmotic diuretics?

A

100% of glucose should be reabsorbed, but in diabetic patients, the transporters become saturated, leading to glucose in the urine. Glucose is osmotically active, so water follows, leading to lots of sweet urine

28
Q

What are carbonic anhydrase inhibitors?

A

Acetazolamide (brand name: Diamox)
They are very weak diuretics
It inhibits carbonic anhydrase, which decreases absorption of bicarbonate in the proximal tubular cells and increases bicarbonate excretion (with some sodium)

29
Q

When do we use carbonic anhydrase inhibitors? What are the main uses?

A

In severe alkalosis (increases renal excretion of bicarbonate)
Alkalization of filtrate ionizes acidic drugs and ionization increases renal excretion (e.g., aspirin)
The main uses are for acute mountain sickness, increasing excretion of weak acids, and glaucoma (decreases aqueous humour formation)

30
Q

What is chlorthalidone?

A

It’s a thiazide, but it’s not on most formularies

31
Q

What do thiazides do in the distal tubule?

A

They in the distal tubule (primary site of action) to increase NaCl excretion (decreases reabsorption) and decreases Ca excretion (increases reabsorption)
Loop diuretics do the opposite

32
Q

What do thiazides do in the proximal tubule?

A

Normally not important (compensation in the loop of Henle)

Important when combined with loop diuretics

33
Q

What do thiazides do? What are they used for?

A

They may decrease blood pressure without a perceivable volume loss (a low dose may be effective and also have a decreased toxicity)
They are used for oedema and hypertension

34
Q

How does a thiazide work to lower blood pressure?

A

A low dose of a thiazide will increase NaCl excretion. This will lower the blood volume, which lowers cardiac output. This lowers the blood pressure. After a period of time, there will seem to be a tolerance; blood volume and cardiac output return to normal, but blood pressure will still be lowered (and may even continue to decrease), meaning that the thiazide has decreased total peripheral resistance

35
Q

What are the problems with thiazides?

A

They increase the incidence of other risk factors for cardiovascular disease by causing hyperglycemia (decreases insulin and tissue utilization) and increasing LDL levels. So these levels must be monitored
They can also increase erectile dysfunction
They can cause plasma volume contraction due to increased urine loss, which increases proximal tubule reabsorption (response to fluid loss) and increase lithium and urea reabsorption

36
Q

What are the advantages of thiazides?

A

They are orally active, they have low toxicity, there is no postural hypertension (becoming dizzy from standing up quickly)
They potentiate other antihypertensive drugs

37
Q

What is ethacrynic acid?

A

A loop diuretic (non sulfonamide)

38
Q

Are loop diuretics good?

A

They are very potent and efficacious (high ceiling diuretics)
Up to 20% of filtered load is excreted (can be dangerous)

39
Q

How are loop diuretics administered?

A

Oral and IV (very rapid) application

40
Q

What do loop diuretics do?

A

They increase prostaglandin production (causing vasodilation, which is useful in acute pulmonary oedema because it vasodilates veins.
They increase Na, Cl and K excretion and Mg and Ca follow
Inhibits renal diluting ability and abolishes the renal concentrating ability (urine becomes more isotonic or slightly dilute)

41
Q

How do NSAIDs affect loop diuretics?

A

They can decrease the function of loop and thiazide diuretics

42
Q

What are the problems with loop diuretics?

A

In addition to electrolyte imbalances, they can cause deafness (never combine with an amino glycoside antibiotics)
They cause chronic dilutional hyponatremia (due to excretion of an isotonic urine)

43
Q

What are the uses of loop diuretics?

A

Good in renal insufficiency (GFR

44
Q

What should be done if someone is not responding to a loop diuretic?

A

If the patient is refractory (not responding) to loop diuretics, add a thiazide diuretic, such as metolazone (proximal effect is important here

45
Q

Why does adding a thiazide to a loop diuretic help a refractory patient?

A

If the proximal tubule is reabsorbing lots of the sodium, then by the time it gets to the loop, there’s nothing to inhibit. A thiazide helps helps by inhibiting reabsorption of sodium and chloride reabsorption

46
Q

What is electrolyte disturbances (with regards to thiazide and loop diuretic use)?

A

Potassium depletion due to thiazide and/or loop diuretics
It’s not a problem with “healthy individuals”
It’s more of a problem if low potassium is already a problem for long (e.g., heart failure, cirrhosis, etc.)

47
Q

What are the two major causes of electrolyte imbalance?

A
  1. Secondary hyperaldosteronism due to plasma volume depletion (increase in renin, AG-II increases, aldosterone increases causing the reabsorption of sodium at the expense of potassium and protons)
  2. Increased distal delivery (increased distal delivery is due to the inhibition of Na reabsorption in loop and distal tubule. The collecting tubules therefore increases Na reabsorption to conserve sodium)
48
Q

Describe the treatment for potassium depletion

A

Dietary intake (apricots, bananas, etc.)
Potassium chloride tablets, chloride salts, dilute solution
Slow potassium tablets (can cause ulceration)
In emergencies, IV KCl 40 mEq (repeat cautiously until potassium rises)
Potassium sparing diuretics (weak diuretics that we give with other diuretics to decrease potassium loss. This may cause hyperkalemia so never combine with potassium supplements. Examples: spironolactone, eplerenone, triamterene)

49
Q

What is ADH? What conditions cause it to increase?

A

Anti-diuretic hormone (ADH aka vasopressin) increases water reabsorption (no effect on electrolytes).
Vasopressin increases in heart failure and syndrome of inappropriate ADH (SIADH) secretion. The chronic increased water reabsorption may produce hyponatremia (diluted sodium)

50
Q

What are ADH antagonists?

A

ADH antagonist, such as conivaptan, blocks ADH receptor in the collecting tubes, which increases water excretion (without electrolytes)
ADH antagonists have been used in SIADH when water restriction alone is not effective

51
Q

What risk is involved with the use of ADH antagonists?

A

It may produce nephrogenic diabetes insidious (increased urine flow due to the lack of renal effects of ADH)

52
Q

What are the main uses of ADH antagonists?

A

Treatment of SIADH (relatively new)

53
Q

What are sodium glucose co-transproter 2 (SGLT-2) inhibitors?

A

A major site of glucose reabsorption is in the proximal tubule (90%)
The blockade of this transport increases urinary excretion of glucose (associated with a small decrease in plasma glucose)
This may be useful as a third line drug (e.g., for diabetes)
It is associated with a decrease in blood pressure and weight
Long term safety is not clear

54
Q

How can furosemide cause hyponatremia?

A

Furosemide causes the kidney to be unable to concentrate or dilute the urine. The body is constantly excreting isotonic urine (loss of sodium ions)

55
Q

What should be done in the case of an inability to concentrate the urine (save water)?

A

Simply drink more water to excrete the solutes

56
Q

What should be done in the case of an inability to dilute urine (excrete excess water)?

A

Ingest hypotonic solution and excrete isotonic urine
There is a net loss of electrolytes including plasma sodium
Chronic dilution hyponatremia

57
Q

How can diuretics affect calcium?

A

Thiazides can decrease calcium excretion (good for hypoclaciuria)
Furosemide can increase calcium excretion (good for hypercalcemia)

58
Q

What are the clinical uses of diuretics?

A

Primarily for oedema forming conditions and arterial hypertension
If oedema is present, fluid shift into into the extracellular space has exceeded 3 to 4 L
This is due to salt and water retention
It is observed in congestive heart failure, hepatic cirrhosis at ascites, nephrotic syndrome, acute or chronic renal failure

Pharmacology (15 decks)

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