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CRRAB II Week 2 > Diuretics & ADH - Full PPT > Flashcards

Diuretics & ADH - Full PPT Flashcards

1
Q

Where do Carbonic Anhydrase Inhibitors act?

A

Proximal tubule

ex. Acetazolamide

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2
Q

Is acetazolamide used as a kidney diuretic?

A

No, not a clinical use

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3
Q

Where do loop diuretics act?

A

Ascending loop of Henle

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4
Q

How useful are loop diuretics?

A

Extremely!

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5
Q

What do Loop diuretics do (mech.)?

A

Inhibit Na, K, 2 Cl transporter

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6
Q

Where do Thiazide diuretics act?

A

DCT (distal convoluted tubule)

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7
Q

What are Thiazide diuretics extremely useful for?

A

Hypertension

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8
Q

What do thiazide diuretics do?

A

Inhibit NaCl symporter

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9
Q

Where do Potassium sparing diuretics work?

A

In Cortical collecting tubule

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10
Q

What are K+ sparing diuretics useful for? What are their mechanisms?

A

-Useful for prevention of K+ loss
-Either:
1. Inhibit aldosterone receptors
OR
2. Block Na exchange for K and H

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11
Q

Where does AHD work? What does it do?

A

Works in medullary collecting duct.

Acts to recruit aquaporin channels.

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12
Q

Where do osmotic diuretics work?

A

Proximal tubule and/or descending limb of the loop of Henle

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13
Q

What two Loop Diuretics must you know?!

A

Furosemide (Lasix)

Bumetanide

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14
Q

What is the mechanisms of Loop Diuretics?

A

Inhibit Na, K, 2 Cl transporter in the ascending loop of Henle

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15
Q

Normally the ascending loop of Henle accounts for how much of the Na+ reabsorption?

A

25%

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16
Q

How do loop diuretics influence ions?

A

-Tubular fluid becomes hypo-osmolar as Na, K and Cl are pumped out but water remains inside (no aquaporins here!)

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17
Q

What od loop diuretics prevent?

A

Decrease in osmolarity –> results in greater retention of ions and water in later segments of nephron

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18
Q

What effect do loop diuretics have on urine composition?

A
  • Inc. NaCl excretion
  • Inc. K excretion
  • -> Some increased nephron Na is exchanged for K in the collection tubule
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19
Q

What side effect can loop diuretics cause by altering K+ concentration?

A

They decrease K+ concentration in body (inc. in urine) which can cause K+ to be too low in the cochlea and inhibit hearing.

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20
Q

What are the therapeutic uses of Loop Diuretics?

A
  • Pulmonary edema
  • Other edematous conditions
  • Hyperkalemia
  • Acute renal failure
  • Anion overdose (Bromide, Fluoride, and Iodide)
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21
Q

How do loop diuretics compare in terms of effect to thiazides?

A

Loop diuretics work earlier in the tubule than thiazide diuretics so more Na+ and Cl- gets absorbed here and these drugs have larger effect!

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22
Q

What are the three thiazide diuretics?

A

Chlorathalidone
Hydrochlorothiazide
Metalazone

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23
Q

What is the mechanism of thiazide diuretics and where do they work?

A

Block NaCl transporter in the DCT

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24
Q

What does blocking the NaCl transporter cause?

A
  • NaCl transporter normally accounts for 8% of NaCl reabsorption
  • Block of this transport mechanism results in excretion of water, Na, Cl and K in urine
  • K gets excreted because some of the increased Na is exchanged for K in the cortical collecting tubule
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25
Q

What are thiazide diuretics used for therapeutically?

A
  • HTN
  • Heart failure
  • Nephrolithiasis caused by hypercalcemia
  • Nephrogenic diabetes insipidus
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26
Q

What are major side effects of thiazide diuretics?

A
  • Hyperglycemia
  • Hyperuricemia –> kidney stones!
  • Hypokalemia
  • Hyperlipidemia
  • Hyponatremia
  • Allergic reactions
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27
Q

How are thiazide diuretics like Type 1 diabetes?

A

Thiazides are sulfonylureas

  • They bind to SUR (sulfonyl urea receptor) on K+ channel controlling insulin release, opening the channel and hyper polarizing the beta cell
  • Thus, they suppress insulin release!
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28
Q

What happens after thiazide diuretics bind to SUR on beta cells?

A
  • SUR is on the K+ channel and controls insulin release, opening the channel
  • Opening the K+ channel causes hyper polarization
  • This suppress Ca2+ channels from allowing Ca2+ to flow in
  • Thus, supressing insulin release from secretory granules
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29
Q

What part of the blood pressure equation do thiazides affect?

A

Major effect on resistance (R) –> hyper polarizes smooth muscle –> vasodilators

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30
Q

Why are thiazides used in HTN?

A
  • They hyper polarize smooth muscle –> vasodilation

- They also dec. blood volume –> dec. BP

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31
Q

What do thiazides do to uric acid levels?

A

They raise uric acid levels/ prevent secretion/ precipitate gout

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32
Q

What are the three main potassium sparing diuretics?

A
  • Spironolactone
  • Triamterene
  • Amiloride
33
Q

What is the mechanism of action fro Spironolactone?

A

Inhibits aldosterone receptors

34
Q

What is the mechanism for Triamterene and Amiloride?

A

Inhibit Na+ exchange for K+ and H+ in the cortical collecting duct.
-Inhibit Enac channels!!

35
Q

What does blocking the exchange of intraluminal Na+ for extraluminal K+ cause?

A
  • Less K+ to be excreted

- this exchange occurs on the abluminal (away from lumen) side - Na+/K+ exchange

36
Q

What is the major use of K+ sparing diuretics?

A
  • Hyperaldosteronism

- Prevent K+ wasting caused by other diuretics

37
Q

What is special about Eplerenone and the heart?

A

Prevents fibrotic changes in kidneys and hearts caused by aldosterone, and has been shown to improve survival in heart failure

38
Q

What is special about Eplerenone and the kidney & heart?

A

Prevents fibrotic changes in kidneys and hearts caused by aldosterone, and has been shown to improve survival in heart failure

39
Q

What are side effects of K+ sparing diuretics?

A
  • Hyperkalemia
  • Hyperchloremic metabolic acidosis (normal anion gap, dec. plasma bicarbonate, inc. plasma chloride)
  • Gynecomastia (spironolactone)
  • Acute renal failure (specific to triamterene and indomethacin)
  • Kidney stones
40
Q

Where is aldosterone synthesized?

A

Adrenal cortex in the adrenal gland

41
Q

What does aldosterone do?

A

Increases resorption of ions and water in the kidney (stimulated by angiotensin II)

42
Q

Where does aldosterone act?

A

On nuclear mineralcorticoid receptors (MR)

43
Q

What are the ADH-like diuretics?

A

ADH = Vasopressin

Desmopressin (synthetic congener)

44
Q

What are Vasopressin and Desmopressin used to treat?

A
  • Diabetes insipidus

- Bedwetting

45
Q

What is the MOA for Vasopressin (ADH) and Desmopressin?

A

Stimulation of G-protein coupled receptors in the collecting duct to recruit aquaporin channels
–> Water moves by osmosis through the aquaporin channels to the hyperosmolar medullary region of the kidney

46
Q

How can Vasopressin or Desmopressin be administered?

A

Parenterally (intravenously), Intranasally or orally

47
Q

What is Demecocycline?

A

An antibiotic with some activity as an ADH antagonist

48
Q

What is the major osmotic diuretic?

A

Mannitol

49
Q

How does mannitol work?

A

It is not reabsorbed in the nephron!

-Thus, it exerts an osmotic effect to retain water

50
Q

What is mannitol used for?

A

It’s used to reduce body water or to reduce intracranial or intraocular pressure

51
Q

What are some toxicities of mannitol?

A
  • Extracellular volume expansion
  • Dehydration, hyperkalemia, hypernatremia
  • Hyponatremia when renal function is impaired
52
Q

What are SGLT-2 (sodium glucose transporters)?

A
  • Symporters for sodium and glucose into the cells.
  • Typically reabsorb 90% of filtered glucose
  • Transport maximum of about 240 mg/dL (above this glucose spills in urine)
  • Present in PROXIMAL TUBULE
53
Q

What is the mechanism of SGLT-2 inhibitors?

A

Reduce reabsorption of glucose

-Cause loss of glucose in urine

54
Q

What are SGLT-2 inhibitors used for?

A

Helps reduce blood sugar levels in diabetes mellitus

-Causes weight loss (loss of energy)

55
Q

What types of side effects are SGLT-2 inhibitors associated with?

A

MANY side effects:

-Ketoacidosis, UTI, yeast infections, hypoglycemia

56
Q

What are three examples of sodium-glucose transport inhibitors?

A
  1. Canigliflozin
  2. Dapagliflozin
  3. Gliflozin
57
Q

What is the ending of SGLT-2 inhibitors?

A

-Flozin’

Inhibiting flo of glucose

58
Q

What is the major carbonic anhydrase inhibitor?

A

Acetazolamide

59
Q

Why aren’t carbonic anhydrase inhibitors useful as diuretics?

A

Carbonic anhydrase is too important of an enzyme.

-When you block it, there are an incredible number of side effects

60
Q

What are carbonic anhydrase inhibitors used for?

A
  • Treat glaucoma
  • Produce urinary alkalinization
  • Treat metabolic alkalosis (usually treated with restoration of volume and chloride)
  • Treat acute mountain sickness
61
Q

What side effects are associated with carbonic anhydrase inhibitors?

A
  • Hyperchloremic metabolic acidosis
  • Renal stones
  • Renal K+ wasting
62
Q

What proximal tubule process is carbonic anhydrase directly related to?

A

Conversion of H2O + CO2 to H2CO3

63
Q

What is the function of Organic Anion Transporters?

A

Transport small hydrophilic organic molecules into (secretion) or out of (reabsorption) the nephron lumen

64
Q

What drives the transport of small hydrophilic organic molecules in OATs?

A

Driven by decarboxylate simport or antiport

–> Dicarboxylate is typically alpha keto glutarate

65
Q

What is the important of OATs?

A

They have a role in gout!

66
Q

What does OAT1, OAT3 and OAT4 do?

A

Tranport Uric acid from the proximal tubule lumen (ureter) into the epithelial cell and then to the circulation (blood)

67
Q

What are three ways to treat gout?

A
  1. Reduce inflammation
  2. Reduce uric acid
  3. Inhibit renal OATs
68
Q

How do you reduce inflammation in gout?

A

NSAIDs

-> don’t use salicylates!

69
Q

How do you reduce uric acid in gout?

A

Allopurinol!

70
Q

How does Allopurinol reduce uric acid?

A

It blocks the formation of gout by blocking xanthine oxidase and inhibiting the formation of uric acid

71
Q

What can be used to inhibit renal OATs?

A

Probenicid or Sulfinpyrazone

72
Q

What is the mechanism of Probenicid/Sulfinpyrazone?

A

Inhibits renal organic acid transporters of urate to facilitate excretion (normally 90% of urate is reabsorbed in proximal tubule)

73
Q

How do Thiazide diuretics relate to OATs?

A

Thiazide diuretics are substrates for OATs

  • They inhibit secretion of uric acid by OAT1 on the basolateral (blood) side of the nephron
  • They also serve as substrates for the URAT antiporter to increase urate reabsorption on the luminal side of the nephron
  • –> Net effect is that they increase blood uric acid
74
Q

Where does Aldosterone bind/act?

A

Nuclear mineralcorticoid receptors (MR) within the principle cells of the distal convoluted table and collecting duct.

75
Q

What does Aldosterone do in the principle cells?

A
  • Activates Na+/K+ pumps

- Upregulates Enac channels!

76
Q

What is Convaptan?

A

An ADH antagonist that can be used to treat syndromes involving inappropriate ADH secretion

77
Q

Where is ADH created?

A

Hypothalamus

78
Q

Where is ADH stored?

A

Posterior pituitary

79
Q

How does ADH lead to the insertion of aquaporin channels?

A
  1. ADH binds V2 receptors - G protein coupled receptors on basolateral plasma membrane of the epithelial cells
  2. This G protein receptor couples to the heterotrimetic G protein Gs
  3. This activates adenylyl cyclases III and VI to convert ATP to cAMP + 2Pi
  4. Rise in cAMP triggers insertion of Aquaporin-2 water channels by exocytosis of intracellular vesicles containing the channels

CRRAB II Week 2 (8 decks)

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