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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Why do we generally use diuretics for and what is their effect shortly

A

Diuretics are among the most commonly prescribed drugs, and play an important role in the treatment of heart failure and hypertension. They exert most of their therapeutic effects through inhibiting the reabsorption of sodium at different sites along the nephron of the kidney. Diminished reabsorption of sodium results in increased urinary loss of both sodium and water, leading to a reduction in plasma volume, and a reduction of blood pressure. Thiazide diuretics also exert an additional vasodilator effect on arterial smooth muscle by a still poorly understood mechanism.

[they increase diuresis]

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2
Q

what are the five main types of diuretics?

A

carbonic anhydrase inhibitors
thiazides
loop diuretics
potassium sparing diuretics
osmotic diuretics

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3
Q

What are some of the key areas that carbonic anhydrase is found in the body?

Where do you find CA to be in the highest concentration?

A

CA is abundant in the nephron
(luminal membrane, basolateral membrane, cytoplasm of tubular epithelial cells) and is also present
the eye, CNS, pancreas and red blood cells.

The highest concentration of carbonic anhydrase is found
at the luminal membrane in the proximal tubule.

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4
Q

What is the net effect of the carbonic anhydrase inhibitor?

A

Less transport of NaHCO3 from the lumen to the
interstitium (reducing the total bicarbonate in the body), followed by less movement of H20 into the
interstitium. This leads to systemic acidosis with long term use and to a more alkaline urine. The
diuretic efficiency clearly decreases after a few days.

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5
Q

Explain the mechanism of CA inhibitors. And also CA action

A
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6
Q

Where do CA mechanism work in?

A

In the proximal tubule cells

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7
Q

Effect of CA inhibitors

A

Increased urinary loss of bicarbonates and interferes with reabsorption of NA and Cl

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8
Q

What is hypokalemia?

A

Increased delivery of Na to the collecting duct results in reabsorption of Na (through epithelial Na channels) in exchange for increased K efflux, which can cause hypokalemia.

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9
Q

What is the basolateral Na/K ATPase responsible from?

A

It maintains a low intracellular Na concentration, which is necessary for reabsorption of Na it also facilitates the efflux of H+ by the Na/H exchanger on the luminal side

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10
Q

what is at the joining point of lumen of the proximal tubule and the epithelial cell?

A

on the apical membrane there is Na+ - H+ exchanger.

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11
Q

highly lipophilic substances such as carbondioxide can effectively move from lumen into the epithelial cell. Is this true or false

A

True

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12
Q

What do we call increased excretion of potassium ions?

A

hypokalemia

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13
Q

Diuretic action of acetazolamide is mild because …

A

Most of the sodium is reabsorbed in later portion of the tubule (in the collecting duct)

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14
Q

Acetazolamide has a self limiting action and tolerance develops after 2-3 days. Is that true, and why?

A

True. Since blood bicarbonate levels drop and the glomerular filtrate levels of bicarbonate drops, after some point the low levels of CO2 and H2O is enough for the reuptake process.

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15
Q

The loss of bicarbonate produces a metabolic acidosis. Why?

A

Because the loss of bicarbonate with urine causes blood to be more acidic.

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16
Q

Most of the fluid loss resulting from inhibition of carbonic anhydrase is reclaimed in more distal segments of the nephron, especially the loop of Henle. True or false?

A

True

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17
Q

Indications of acetazolamide

A

+Glaucoma = topical -eye drops- to minimize renal side effects
+Mountain Sickness -lowers production and ph of cerebrospinal flued-
+Introducing decongestion in heart failure
+Metabolic alkalosis in severe heart failure : contraction of ECV due to loss of bicarbonate free fluid. Salt cannot be administered to correct alkalosis so we use acetazolamide
+Metabolic alkalosis
+Urine alkalisation: Acids dissolve better in alkalinik urine - aspirin

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18
Q

Where does thiazides mechanism of action belong?

A

Distal convoluted tubule.

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19
Q

Under normal conditions, 100 percent of aminoacids and glucose, 90 percent of bicarbonate and 65 percent of Sodium, potassium and water gets reabsorbed in the proximal convoluted tubule

A

True

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20
Q

Usually wherever sodium ions go, chloride and water tend to follow.

A

True

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21
Q

Why is filtrate more concentrated at the descending loop of henle?

A

As H2O can escape there but sodium cannot.

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22
Q

Thick ascending limb is permeable to sodium but impermeable to water

A

True. about 25 percent of sodium gets reabsorbed passively there.

23
Q

Explain the pharmacokinetics of acetazolamide?

A

Good absorption after oral intake, urinary PH increases after 30 minutes, maximal effect after 2 hours. The effect lasts for 12 hours. Renal excretion

24
Q

Toxicity of acetazolamide?(5 or them)

A

+Worsening of metabolic or respiratory acidosis
+Kidney stones since calcium salts are less soluble in alkalinic urine
+renal loss of potassium
+More ammonia in systemic circulation - liver cirrhosis
+at high doses: drowsiness and paraesthesia (numbing of hands and feet)

25
Q

what is edema?

A

Abnormal fluid retention

26
Q

Where is na+ cl- symporter located?

A

in the apical membrane of distal convoluted tubule
This symporter moves sodium and cloride from lumen into the epithelial cell. From there, NA+K+ atpase pump pumps sodium out of the cell and cl- channel moves cl out of the cell into the interstitium. and there they are reabsorbed into the blood

27
Q

What is the mechanism of action of thiazides?

A

They block thiazide sensiive Na+ Cl- symporter on the luminal side of epithelial cells. (co-transporter)

28
Q

Thiazides are only moderately efficacious. Is that True, if so, why?

A

Yes its true because 90 percent of Na+ and Cl- was already reabsorbed before it reaches to the distal tubule.

29
Q

Side effects - explain dehydration

A

Since it causes a sodium, chloride and H2O loss it leads o dehydration and subsequently acute kidney injury.

30
Q

Which levels are lowered in the body/blood upon thiazides?

A

Low sodium, (hyponatreame) chloride and potassium levels.

31
Q

Which levels are increased in the body/blood upon thiazides?

A

Glucose (due to loss of blood volume)
Calcium
Uric acid

32
Q

What should we consider when giving patients thiazides?

A

Diabetes(since it increases glucose)
Hypercalcaemia (since it increases calcium levels)
Gout (Since it increases uric acid levels)

33
Q

Loss of blood volume due to thiazides can cause postural hypotention.What is this?

A

When the patent stands up the blood pression goes down.

34
Q

Pharmacokinetics of thiazides

A

Oral intake, thiazides are secreted by secretion mechanism for organic acids in renal tubule. They compete with uric acid.

35
Q

Side effects on transient hyperlipidemia upon thiazides results in:

A

Cholesterol and LDL levels to rise up but it is often transient

36
Q

Paresthesias and erectile dysfunction is another side effects of thiazides

A

TRUE

37
Q

GFR has to be minimum …. for thiazides to be used in first line treatment.

A
  1. normal GFR is 120.
38
Q

When are thiazides more effective and result in less K loss?

A

when oral salt restriction is introduced.

39
Q

Thiazides are weak vasodilators. Morbidity and mortality drops in the treatment of hypertension but it only allows us to maintain the treatment of congestive heart failure.

A

True, but GFR has to be min 30ml/min if we want to use it for congestive heart failure.

40
Q

Thiazides have been found to be the best drugs for prevention of heart failure in patients with hypertension (superior to ACE inhibitors, alpha blockers & calcium channel blockers)

A

TRUE

41
Q

Side effects of thiazides

A

Hypokalemic Metabolic Alkalosis
-same mechanism of loop diuretics-
Hyperuricemia - potentially leading to the development of gout
Hyperglycemia -There is evidence that the hyperglycemia may be related to loss of body potassium, which may affect the ability of pancreatic beta cells to regulate the release of insulin via ATP-sensitive K channels. Appropriate correction of hypokalemia can typically reverse thiazide-induced hyperglycemia
Hyperlipidemia

42
Q

Why is removing the water in the body useful? 5 indications

A

-Congestive cardiac failure
-pulmonary oedema
-peripheral oedema
-renal failure
-hypertension

43
Q

thiazide + lithium. What kind of effect can it have?

A

The natriuresis induced by thiazides will result in increased reabsorbtion of sodium. Since sodium and lithium are similar and structure and characteristics, we can say that thiazides can increase lithium reabsorbtion and may lead to lithium toxicity.
IMPORTANT: it is also already known that Thiazide diuretics can increase the risk of lithium toxicity by reducing the kidney’s ability to eliminate lithium in the urine.
We know that lithium interacts with diuretics, NSAIDS antibiotics, verapamil, ACE inhibitors and theophylline.

44
Q

thiazide+ digoxin

A

Thiazide is a distal tubule diuretic that inhibits sodium reuptake. Increased sodium load in the tubule leads to potassium secretion and possible hypokalemia
Digoxin is a myocyte NA/K/ATPase inhibitor and hypokalemia can potentiate digoxin effect. Heart failure risk.
They both reduce potassium levels i the blood. therefore they increase risk of hypokalemia and hypokalemia can potentiate the effects of digoxin since it competes with potassium for its binding site.
Low levels of potassium can also cause abnormal heart rhythms.

45
Q

thiazide + ibuprofen

A

Drugs known as nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin), naproxen (Naprosyn), and nabumetone (Relafen) can reduce the effectiveness of thiazide diuretics in lowering blood pressure because they may reduce the ability of the kidneys to make urine, particularly in patients who have reduced kidney function. NSAIDs are antidiuretic.

46
Q

Thiazide ibuprofen and capropril

A

Triple whammy (TW) is a potentially dangerous drug combination that can lead to acute kidney injury (AKI). This drug interaction (DI) occurs when angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) are used together with diuretics and non-steroidal anti-inflammatory drugs (NSAIDs).
ACE inhibitors or ARBs generally preserve renal function. However, these medicines can also decrease glomerular filtration by causing vasodilation of the efferent renal arteriole.1 Diuretics can also contribute to AKI by causing hypovolaemia.1

NSAIDs are associated with an increased risk of AKI, due to blockade of the COX-2 enzyme preventing prostacyclin synthesis, which causes afferent arteriolar vasoconstriction.

47
Q

Where do loop diuretics work?

A

They work in thick ascending limb of henle’s loop

48
Q

what do loop diuretics do?

A

Selectively inhibit reabsorption of NaCl

49
Q

Why are loop diuretics are the most powerful diuretics?

A

Due to the high potency of this segment for NaCl reabsorption and due to the fact that diuresis is not limited by development of acidosis.

50
Q

Development of acidosis limits carbonic anhydrase inhibitors

A

TRUE

51
Q

Loop diuretics produce a more potent diuresis & less vasodilation than thiazide diuretics. Therefore they are less effective in lowering BP than thiazide diuretics. They are primarily used in the treatment of edema

A

TRUE

52
Q

The cells lining the thick ascending limb of the loop of Henle express…

A

Na/K/2Cl cotransporter that has a high sensitivity to inhibition by loop diuretics such as furosemide.

53
Q
A

Pharmacology (11 decks)

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