3.A-Diuretics Flashcards

1
Q

True or false: hypertension is usually a multifactorial problem

A

true

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2
Q

How can the kidney play a role in hypertension?

A

fail to eliminate enough fluid–>fluid builds up in vessels–>blood pressure increase

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3
Q

If you were to explain to someone with zero knowledge about diuretics, how would you explain diuretics to them?

A

diuretics increase urine production to help reduce blood pressure
they block the reabsorption of sodium
more Na in the urine=more fluid excreted

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4
Q

Which parts of the nephron are responsible for Na+ reabsorption? (state the % of Na+ reabsorbed in each part)

A

proximal tubule (65%)
ascending loop of Henle (25%)
distal tubule (very little)

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5
Q

What is the major driver of fluid retention?

A

sodium reabsorption

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6
Q

True or false: the kidney filters 120ml/min, makes urine at 1ml/min, thus 99% of filtered fluid is reabsorbed

A

true

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7
Q

What structure connects the afferent arteriole and ascending loop of Henle? What does this structure do?

A

macula densa
it senses Na+ concentrations in the nephron

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8
Q

Describe tubuloglomerular feedback.

A

occurs at the macula densa cells
an increased concentration of Na at the macula densa cell causes vasoconstriction at the afferent arteriole
(high Na will decrease renal blood flow)

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9
Q

True or false: all diuretics have impact on blood pressure

A

false

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10
Q

List the classes of diuretics.

A

loop diuretics
thiazide diuretics
potassium-sparing diuretics
carbonic anhydrase diuretics
osmotic diuretics

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11
Q

Where do loop diuretics act?

A

ascending loop of Henle (Na-K-2Cl symport inhibitors)

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12
Q

True or false: loop diuretics block the reabsorption of Na only

A

false
they block the reabsorption of Na and Cl

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13
Q

What is the significance of blocking the reabsorption of Cl with loop diuretics?

A

less Cl in the interstitial space means less force to draw in Ca and Mg

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14
Q

What are some undesirable actions of loop diuretics?

A

Ca and Mg loss due to loss of electrical gradient that is normally causing by the reabsorption of Cl
K loss in urine due to RAAS
uric acid retention in blood

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15
Q

What are the loop diuretics listed in the Sask Formulary?

A

furosemide
bumetanide
ethacrynic acid

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16
Q

Why are loop diuretics not ideal for bp control?

A

short half life
potent stimulator of kidney activation
-RAAS activation
-single dose can result in over correction

17
Q

Normally loop diuretics are not ideal for bp control, what is the exception?

A

patients with poor kidney function
-half life is prolonged
-blood pressure effect is more stable

18
Q

Where do thiazide diuretics act?

A

distal tubule (Na-Cl symport inhibitors)

19
Q

True or false: thiazide diuretics are weaker than loop diuretics because there is less Na reabsorbed in the distal tubule

A

true
location of action matters!!!

20
Q

What are some differences that thiazides have compared to loops in regards to how they effect ions and blood pressure?

A

thiazides:
-Ca can increase with long term use
-Mg loss occurs but less likely than loops
-better for bp control

21
Q

What are the thiazide diuretics listed in the Sask Formulary?

A

chlorthalidone
hydrochlorothiazide
indapamide
metolazone

22
Q

At what GFR should thiazide diuretics not be used?

A

<30-40ml/min

23
Q

List off the common uses of TZD and loop diuretics.

A

high blood pressure: thiazides
high blood pressure in ppl with kidney disease: loops
heart failure: loop and thiazides

24
Q

What are the electrolyte problems with Na blocking diuretics?

A

hypokalemia (low K)
hyponatremia (low Na)
hypochloremia (low Cl)
hypomagnesemia (low Mg)
calcium (increases with TZDs, decreases with loops)

25
Q

What are the impacts on plasma metabolites and hemodynamics with Na blocking diuretics?

A

plasma metabolites:
-hyperuricemia (increased risk for gout)
-decreased glucose tolerance=increased blood glucose

hemodynamic effects:
-hypotension (cause of dizziness)
-reduced renal perfusion
-increased activity of RAAS

26
Q

Hypokalemia is known to be the most common electrolyte imbalance with Na blocking diuretics, what else can increase the risk for hypokalemia?

A

low K intake
receiving other K depleting drugs
accelerated loss (vomiting/diarrhea)

27
Q

Where do K-sparing diuretics act?

A

late distal tubule and collecting duct (inhibit ENaCs)
-decreased Na absorption exaggerates the polarization of the
epithelial membrane
-discourages K excretion

28
Q

How are K sparing diuretics mainly used in practice?

A

to prevent K decreased during diuretic therapy
commonly combined with a loop or TZD

29
Q

What are the K sparing diuretics listed in the Sask Formulary?

A

triamterine
amiloride

30
Q

Describe carbonic anhydrase inhibitors.

A

not effective diuretics
typically used for glaucoma
prevent the reabsorption of NaHCO3

31
Q

Describe osmotic diuretics.

A

freely filtered with little reabsorption
create an osmotic effect to keep water in urine
typically only used in hospital

32
Q

What are the agents used as osmotic diuretics?

A

glycerin
mannitol
urea

33
Q

What rate (ml/min) does the kidney filter at?

A

filters 120ml/min
makes urine at 1ml/min

34
Q

Which diuretic acts at the proximal tubule?

A

there are none that act at the proximal tubule

35
Q

Why are certain diuretics used to lower blood pressure?

A

high blood pressure often involves increased blood volume

36
Q

What is the most common electrolyte deficiency with Na blocking diuretics?

A

hypokalemia

37
Q

How strong is the diuretic effect of K sparing diuretics?

A

very weak (little Na is reabsorbed by the distal tubule)

38
Q

What is the main benefit of the carbonic anhydrase pathway?

A

enables re-absorption of HCO3- (critical buffer)