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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are the classic diuretics?

A
  • hydrochlorothiazide (thiazide)
  • furosemide, ethacynic acid (loop)
  • spironolactone (potassium sparing)
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2
Q

What are the solute/ water excretion altering diuretics? (not clinically useful as diuretics)

A
  • mannitol (osmotic diuretic)
  • acetazolamide (carbonic anhydrase inhibitor)
  • tolvaptan (vasopressin receptor antagonist)
  • dapagliflozin (sodium/glucose co-transport 2 inhibitor)
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3
Q

The interest of diuretics is in what?

A
  • renal solute excretion (sodium and water)

- blocks sodium reabsorption - water will follow later

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4
Q

What is the aim of therapy with a diuretic?

A
  • only need to decrease sodium reabsorption a few percent
  • change of 5% has a great effect (1250 mol/day of Na is excreted and therefore this would represent a loss of 9 litres of extracellular fluid loss)
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5
Q

What drugs act on the proximal tubule of the kidney?

A
  • mannitol, unreabsorbed glucose, dapagliflozin, and acetazolamide
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6
Q

What drugs work on the ascending loop of henle?

A
  • furosemide
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7
Q

What drugs work on the distal tubule?

A
  • metolazone
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8
Q

What drugs work on the collecting duct?

A
  • spironolactone

- conivaptan

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9
Q

What are examples of thiazide diuretics?

A
  • hydrochlorthiazide, metolazone and chlorthalidone
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10
Q

Where is the primary site action of thiazide diuretics concentrated and what is their effect?

A
  • works in the distal tubule to: increase NaCl excretion (decreases reabsorption) and decreases Ca excretion (increases reabsorption) - loop diuretics do the opposite
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11
Q

What is the proximal tubular effect of thiazide diuretics?

A
  • there is some - normally not very important, compensation in the loop of henle
  • important when combined with loop of diuretic
  • may decrease blood pressure without a perceivable volume loss (low dose is usually effective - also decreased toxicity)
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12
Q

If we want to conserve calcium in a patient, we should put the patient on a ___ diuretic

A

thiazide

do not want to put on a loo diuretic because it will dump calcium and exacerbate a bone disorder

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13
Q

What is the process of action that thiazide diuretics have on blood pressure control?

A

thiazide diuretics -> increase NaCl excretion -> decrease blood volume and decrease cardiac output -> tolerances? -> blood volume and CO returns to normal -> blood pressure stays down and may decrease further -> (Cox decrease in TPR = decrease in BP)

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14
Q

What are the general problems associated with thiazide diuretics?

A
  • increased incidence of other risk factors for CV disease
  • hyperglycemia (decrease insulin resistance, decrease tissue utilization)
  • increased LDL levels
  • increased incidence of erectile dysfunction
  • plasma volume contraction due to increased urine loss
  • increased proximal tubule reabsorption, response to fluid loss —> increased lithium, urea reabsorption
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15
Q

What are the used of thiazide diuretics?

A

edema and hypertension

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16
Q

What are the advantages of the use of thiazide diuretics?

A
  • orally active, low toxicity and no postural hypotension

- potentiate other antihypertensive drugs

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17
Q

What are the three examples of loop diuretics?

A
  • furosemide
  • bumetanide
  • ethacrynic acid (non sulfonamide)
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18
Q

What are the two formulations that loop diuretics can be in?

A
  • oral and IV
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19
Q

Loop diuretics should increase the production of ______

A

prostaglandin

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20
Q

Loop diuretics are useful in acute ________ as they vasodilate veins.

A

pulmonary edema

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21
Q

____ may decrease function of loop and thiazide diuretics

A

NSAIDs

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22
Q

Loop diuretics increase the Na, Cl, and K excretion and what two minerals follow?

A
  • Mg and Ca
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23
Q

Loop diuretics inhibit the renal diluting ability and abolished the renal concentrating ability, so the urine becomes ____ or _____

A

isotonic or slightly dilute

24
Q

What are the main problems associated with loop diuretics?

A
  • deafness: never combine with amino glycoside antibiotics
  • chronic dilutional hyponatremia
  • due to excrete of an isotonic urine
25
Q

What are the uses of loop diuretics?

A
  • good in renal insufficiency (GFR <50 ml/mim)

- edema (pulmonary), hypertension (not as sole medication), hypercalcemia (opposite to thiazides), heart failure

26
Q

Is potassium depletion due to thiazide/loop diuretics a problem in healthy patients?

A
  • no, it is not — only a problem is low potassium is already a problem (heart failure, cirrhosis, etc)
27
Q

What is the two major causes of electrolyte disturbances?

A
  1. Secondary hyperaldosteronism (due to plasma volume depletion)
    - increase renin, increase A2, increase aldosterone
    - Na reabsorption at the expense of K (and H) loss
  2. Increased distal delivery
    - increased distal delivery- due to inhibition of Na reabsorption in loop and distal tubule
    - collecting tubules therefore increase Na reabsorption to conserve sodium
    * * see slide 16
28
Q

What are some treatments for potassium depletion?

A
  1. dietary intake (apricots, bananas)
  2. potassium chloride tablets - chloride salt - dilute solution
  3. slow potassium tablets - ulceration
  4. emergencies
    - iv KCl - repeat cautiously until potassium rinses
  5. potassium sparing diuretics
    - weak diuretics
    - give with other diuretics to decrease K loss
    - may cause hyperkalemia
    - never combine with K supplements
    - spironolactone (blocks aldosterone receptor, prevents cardiac remodelling- may delay progression of failure)
    - triamterene (decrease sodium permeability - have limited use)
29
Q

Wha other medications are known to increase plasma potassium concentrations?

A
  • Beta- adrenoreceptor antagonists, ACEI’s, ARB’s may also increase plasma potassium concentrations
  • beta- adrenoreceptor antagonists decrease potassium from entering the cells
30
Q

Amiloride and triamterene block ___ from entering into the collecting tubule/duct

A

Na

31
Q

Spironolactone blocks _____ from entering into the collecting tubule/duct

A

aldosterone

32
Q

Explain extracellular volume depletion as an electrolyte disturbance?

A
  • furosemide: kidney is unable to concentrate or dilute, so urine is excreted and is isotonic
  • inability to concentrate urine (can simply drink more water to excrete solutes)
  • inability to dilute urine (ingest a hypotonic solution, and excrete an isotonic urine. There is a net loss of electrolytes including plasma sodium. Chonic dilution hyponatremia)
33
Q

Thiazides ___ calcium excretion (good for hypocalciuria)

A

decrease

34
Q

Furosemide ___ calcium excretion and is good to hypercalcemia

A

increases

35
Q

Volume depletion and increased proximal tubule reabsorption causes an increase in uric acid ____. What can this lead to?

A

excretion

Can lead to gout

36
Q

When a person is taking both lithium as we’ll as diuretics, you can see a _____ in proximal tubular reabsorption

A

increase (we are concerned here about toxicity)

37
Q

What are the clinical uses for diuretics?

A
  • used for edema forming conditions and arterial hypertension
  • also for treating hepatic cirrhosis and cardiac failure
38
Q

Describe tissue edema?

A
  • fluid shift into the extracellular space that has exceeded 3-4 L - due to salt and water retention
  • loop diuretics are preferred for this - if there is no response, check for serum chloride concentration
39
Q

Fluid excreted in the urine is taken from the ______ - need to allow time for this to be replaced by the interstitial fluid (edematous)

A

vascular space

40
Q

What is the first line single therapy for treating hypertension?

A

thiazide diuretic

41
Q

What are the risks of using a thiazide diuretic in treating hypertension?

A
  • can increase LDL, can increase plasma glucose (not metabolically neutral)
  • good as second medication to treat sodium and water retention - common side effect go other anti-hypertensives
42
Q

How are diuretics useful to treat hepatic cirrhosis?

A
  • sodium/water accumulates in the abdomen and/or tissue
  • abdominal fluid movement into vascular space may be a concern
    • slower than fluid movement from interstitial to vascular space
    • aggressive treatment will remove fluid faster from the vascular space than can be replaced by the abdominal fluid
43
Q

What is the role of diuretics in cardiac failure?

A
  • fluid retention increases vascular volume
  • helps to increase preload and stimulate the heart
  • as failure continues so does fluid retention
    • preload increases to levels causing edema
    • diuretics decrease vascular volume
  • -successful tx of heart failure requires adequate control of vascular volume
44
Q

What are osmotic diuretics?

A
  • osmotically active components in the plasma
45
Q

What are the properties for a perfect osmotic diuretic?

A
  • filtered
  • not reabsorbed
  • pharmacologically inert
  • resistant to alteration
  • osmotically active compounds hold onto water (high urine volume- little sodium)
46
Q

What are the few uses for osmotic diuretics (mannitol and glycerol)

A
  • vascular surgery
  • renal transplant
  • ophthalmological procedures
47
Q

What is the example of carbonic anhydrase inhibitors?

A
  • acetazolamide
48
Q

Describe carbonic anhydrase inhibitors?

A
  • very weak diuretics
  • inhibits carbonic anhydrase (decreases reabsorption of bicarbonate in proximal tubular cells, increases bicarbonate excretion-with some sodium)
49
Q

What are the uses for carbonic anhydrase inhibitors?

A
  • in severe alkalosis (increases renal excretion of bicarbonate)
  • alkalization of filtrate ionizes acidic drugs - ionization increases renal excretion (salicylate)
  • acute motion sickness
  • increasing excretion of weak acids
  • glaucoma - decreases aqueous humor formation
50
Q

What does antidiuretic hormones do?

A
  • increases water reabsorption (no effect on electrolytes)
51
Q

What is an example of an antidiuretic hormone antagonist?

A
  • conivaptan
52
Q

What does conivaptan do?

A

blocks the ADH receptor in the collecting tubules - increases water excretion (without electrolytes)

53
Q

_____ is increased in heart failure and syndrome of inappropriate ADH secretion. The chronic increased water reabsorption may produce hyponatremia

A

vasopressin

54
Q

What is an example of a sodium glucose co-transport 2 inhibitor?

A

dapagliflozin

55
Q

Where is the major site of glucose reabsorption for the sodium glucose co-transport 2 inhibitor?

A

proximal tubule

56
Q

Blocking the sodium glucose co-transport increases what?

A
  • urinary excretion of glucose

associated with a small decrease in plasma glucose

57
Q

Sodium glucose co-transport 2 inhibitors are associated with what?

A
  • with a decrease in blood pressure and weight

Pharmacology (23 decks)

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