Diuretics Flashcards

1
Q

What does the glomerulus do

A

filtration

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2
Q

What does the proximal tubule do

A

reabsorption (mostly NaCL)
- also secretes hydrogen, foreign substances, organic anions and cations
- isotonic

Carbonic Anhydrase Inhibitors and osmotic diuretics work here

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3
Q

What does the loop of Henle do

A

concentrates urine
-isotonic, hypertonic, hypotonic

Descending Loop: NaCl diffuses in, water reabsorbed
Ascending Loop: NaCl actively reabsorbed, water stays in

Loop diuretics work here

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4
Q

What does the distal tubule do

A

Reabsorption of Nacl, water (ADH required), bicarb

  • isotonic or hypotonic

Thiazides work here

This is where blood pressure changes are made - thiazides work here and they work on decreasing pressure…WHERE THE RAAS system begins

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5
Q

What does the collecting duct do

A

final concentration
- reabsorbs water (ADH required), NaCL

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6
Q

What is the GFR for CKD diagnosis

A

less than 60 for over 3 months with/without kidney damage

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7
Q

Are longer intervals between HD and surgery associated with a higher risk of post-op mortality?

A

YES

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8
Q

What BUN/SCR is dehydration?

A

BUN/SCR > 20

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9
Q

Where does each group of diuretic work?

A

Proximal tubule - Carbonic anhydrase inhibitors AND osmotic diuretics
Loop of Henle - Loop diuretics
Distal Tubule - Thiazides
Distal tubule / collecting duct - potassium sparing

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10
Q

Are carbonic anhydrase inhibitors used as diuretics these days?

A

Not really - Acetazolamide (Diamox) is used off label for metabolic alkalosis (commonly happens when “over-diuresing” CHF patients)

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11
Q

What is an interesting use for Acetazolamide?

A

Altitude sickness

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12
Q

What do carbonic anhydrase inhibitors do?

A

Inhibit CA which inhibits H+ secretion in the proximal tubule. Bicarb and sodium are blocked from reabsorption

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13
Q

Do carbonic anhydrase inhibitors cross the BBB?

A

YES

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14
Q

What do osmotic diuretics do (mannitol and urea)

A

Uncouples Na and H2O reabsorption by increasing the osmotic gradient in the proximal tubule. Na reabsorption initially, but H2O is not, leading to decreased Na reabsorption distally.

They “pull water” and increase intravascular volume.

Osmotic diuretics primarily inhibit water reabsorption in the proximal convoluted tubule and the thin descending loop of Henle and collecting duct, regions of the kidney that are highly permeable to water.

Osmotic diuretics also extract water from intracellular compartments, increasing extracellular fluid volume. Overall, urine flow increases with a relatively small loss of Na+. In fact, urine osmolarity actually decreases.

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15
Q

What are Mannitol’s different uses?

A

Prophylaxis against acute renal failure (ARF)…loop diuretics are too

Differential diagnosis of acute oliguria (if the patient responds to mannitol, they are just dehydrated…if not, they have actual renal damage)

Treatment of increased intracranial pressure (ICP)

Decreasing intraocular pressure (IOP)

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16
Q

Is mannitol REALLY nephroprotective? What does current research say about it?

A

NOPE.

No better than plain saline pre-radiocontrast dye
EXCEPT: renal transplant surgery

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17
Q

Do you need an intact BBB when using mannitol?

A

YES

If not, it will pull water into the brain and increase ICP, which is the opposite of what we want

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18
Q

What are dangerous side effects of mannitol?

A

Pulmonary edema, hypovolemia, hypernatremia

electrolyte disturbances, plasma hyperosmolarity d/t water and NaCl secretion (hypernatremia)

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19
Q

What electrolyte abnormality can mannitol create?

A

Hypernatremia from excess water loss

20
Q

What negative side-effect is urea associated with?

A

Venous thrombosis and tissue necrosis after extravasation (not seen with mannitol)

21
Q

What is loop diuretics MOA?

A

Inhibits Na and Cl reabsorption in the ascending loop and to a lesser extent in the proximal tubule

22
Q

Which two diuretics are nephroprotective?

A

mannitol (osmotic) and loop diuretics (furosemide)

23
Q

What are loop diuretics clinical uses?

A

Mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction

Treatment of increased ICP

Treatment of hypercalcemia

Differential diagnosis of acute oliguria

24
Q

What happens when you take NSAIDS while on a loop diuretic?

A

Furosemide-induced increases in renal blood flow are inhibited by NSAIDs resulting in an attenuated diuretic effect

25
Q

What is braking phenomenom?

A

Acute Tolerance (Braking Phenomenon) – ceiling effect with diuretic where giving more doesn’t increase outcome but can increase side effects.

Associated with loop diuretics

26
Q

Loop diuretics electrolyte side-effects

A

All low basically

Hypokalemia
Hypochloremia
Hyponatremia
Hypomagnesemia

Hypokalemic Metabolic alkalosis (thiazides also cause this)

27
Q

Which diuretic can cause deafness?

A

Loop diuretics

28
Q

Which type of medication are loop diuretics cross-sensitive to?

A

Sulfa antibiotics, sulfonylureas, thiazide diuretics

29
Q

Do antibiotics increase the chance of nephrotoxicity when using loop diuretics?

A

YES, for aminoglycosides and cephalosporins
- penicillins and furosemide together are associated with allergic interstitial nephritis

30
Q

What is thiazides (chlorothiazide, hydrochlorothiazide) MOA?

A

Compete for the Na-Cl cotransporter in the distal tubule to inhibit reabsorption. Inhibit only urinary diluting capacity, not concentrating capacity.

31
Q

Which electrolyte do thiazide diuretics INCREASE?

A

calcium (increased calcium reabsorption)

32
Q

What are thiazides clinical uses?

A

hypertension and mobilization of edema

33
Q

Thiazides electrolyte side-effects

A

Hyperglycemia
Hyperuricemia
Hypercalcemia

Decreased renal or hepatic function
Decreased intravascular volume
metabolic alkalosis with chronic administration

34
Q

Are thiazides associated with hyper or hypo blood sugar and uric acid?

A

HYPERglycemia and HYPERuricemia

35
Q

Do potassium-sparing diuretics cause hyperglycemia and hyperuricemia like thiazides?

A

NOPE

36
Q

What are the MOA of potassium-sparing diuretics?

A

Amiloride and Triamterene: inhibit Na reabsoprtion induced by aldosterone. Inhibit active counter transport of Na and K in the collecting duct. MESS UP THE the Na-K-ATPase pump

Spironolactone and Eplerenone: competes for aldosterone receptor sites in the distal tubule to block Na reabsorption and K secretion. Competitive inhibitors of aldosterone

37
Q

What is the main side-effect of potassium-sparing diuretics and what makes this issue worse?

A

HYPERKALEMIA

Made worse when also taking NSAIDs, Ace inhibitors (i.e. lisinopril), Beta-blockers

38
Q

Which two diuretics cause hypokalemic, hyperchloremic metabolic alkolosis?

A

Thiazides and loop diuretics

39
Q

EKG changes with hyperkalemia

A

Tall peaked T wave
Loss of P wave
Widened QRS with tall T wave

40
Q

Why do we give calcium when correcting hyperkalemia?

A

Stabilizes the heart and lowers the threshold potential of the myocardium.

Caution in patients who are on digoxin – calcium has been reported to worsen the myocardial effects of digoxin toxicity..could use Mg as an alternative to stabilize the myocardium

41
Q

Treatment for hyperkalemia

A

C = Calcium (cardiac stabilizer)
B = inhaled beta2 agonists (intracellular shift)
I = Insulin (followed by..)
G = Glucose (given with insulin)
K = Kayexalate (mainly chronic RF)
D = Diuretics (renal elimination)
ROP = Renal unit for dialysis Of Patient

42
Q

What are some causes of hyponatremia?

A

Loss of body fluid, thiazides, loops, CHF, SSRIs, Carbamazepine, Lithium, Liver disease

43
Q

Hyponatremia correction rates

A

Severe symptomatic hyponatremia: 6-12 mEq/L in the first 24 hrs and 18 mEq/L or less in 48 hrs

Chronic hyponatremia: 0.5 mEq/L/hr with max change of 8-10 mEq/L in a 24 hr period

44
Q

What is calcium dependent on?

A

Albumin

45
Q

What are some causes of hypercalcemia?

A

Hyperparathyroidism

Chronic renal failure or vitamin D deficiency

Vitamin D intoxication

Malignancy

Diuretics (usually mild)

46
Q

What antibiotics can cause nephrotoxicity when using with loop diuretics?

A

Aminoglycosides and cephalosporins