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MS2 Renal > 9/11- Pharmacology and the Kidney I: Diuretics > Flashcards

9/11- Pharmacology and the Kidney I: Diuretics Flashcards

1
Q

What hormone primarily regulates the serum sodium level?

A. ADH (anti-diuretic hormone)

B. ALdosterone

C. Renin

D. WCH (water controlling hormone)

A

What hormone primarily regulates the serum sodium level?

A. ADH (anti-diuretic hormone)

B. ALdosterone

C. Renin

D. WCH (water controlling hormone)

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2
Q

Clinical manifestations of excess salt (volume overload) in the body include:

A. Increased thirst

B. Peripheral edema

C. ?

D. ?

A

Clinical manifestations of excess salt (volume overload) in the body include:

A. Increased thirst

B. Peripheral edema

C. ?

D. ?

  • Increased thirst is more for hypernatremia
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3
Q

Define:

  • Natriueresis:
  • Aquaresis:
  • Diuresis:
  • Diuretic:
A
  • Natriueresis: increased renal excretion of sodium
  • Aquaresis: excretion of water without electrolyte loss
  • Diuresis: increased urine excretion
  • Diuretic: substance that increases the excretion of urine (caffeine, alcohol, cranberry juice)
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4
Q

Body volume disturbances reflect what? Dysnatremias reflect what?

A

Body volume disturbances reflect sodium content changes

  • Volume depletion: loss of Na and water
  • Volume overload: retention of Na and water

Dysnatremias reflect water balance

  • Hyponatremia- too much ADH
  • Hypernatremia- in access to water, DI
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5
Q

What are the proximal tubule transport mechanisms?

A

NaHCO3 reabsorption is most relevant to diuretic action in the PCT

  • Na-H exchanger in luminal membrane (Na in; H out)
  • H couples with HCO3- in lumen before CA converts it to H2O and CO2
  • CO2 is taken up over apical membrane to reverse reaction, creating HCO3 and H inside cell

—- H can then be pumped out by Na-H exchanger

—- HCO3 pumped over basal membrane

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6
Q

What is the mechanism of Acetazolamide? Effects?

A

Carbonic anhydrase inhibitor in the proximal tubule

Effects:

  • Na bicarbonate diuresis
  • Hyperchloremic metabolic acidosis
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7
Q

Clinical uses of Acetazolamide?

A
  • Glaucoma: Decreases the rate of aqueous humor formation with decrease in intraocular pressure
  • Urinary alkalinization: uric acid and cysteine are more soluble in alkaline urine
  • Metabolic alkalosis: diuretic induced
  • Acute mountain sickness: acidosis leads to increased ventilation.
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8
Q

Toxicity of Acetazolamide?

A

(Recall: CA inhibitor)

  • Hyperchloremic metabolic acidosis
  • Hypokalemia (renal K wasting)
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9
Q

How do diuretics induce renal K wasting?

A

Increased distal Na delivery drives K secretion

  • High aldosterone
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10
Q

What is the mechanism of Mannitol? Effects?

A

Osmotic diuretic

  • Prevents water reabsorption in the proximal tubule and tDLH (freely water permeable)
  • Opposes ADH action in the collecting tubule

Effect = increased urine volume

  • Reduced Na reabosrption (Increase in urine flow rate decreases the contact time between fluid and tubular epithelium)
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11
Q

What are the clinical uses of osmotic diuretics?

A

- Cerebral edema: decreased ICP - alter Starling forces so that water leaves cells and reduce intracellular volume

- Acute congestive glaucoma: reduction of intraocular pressure

- Increase urine volume to prevent an oliguric phage of an AKI in setting of Hemolysis or Rhabdomyolysis.

(Not typically liked/used by nephrologists)

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12
Q

Toxicity of osmotic diuretics?

A

- Extracellular volume expansion along with hyponatremia: extracts water from cells

(This effect can complicate CHF and may produce florid pulmonary edema)

- Dehydration and hypernatremia: can ultimately lead to excessive free water losses

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13
Q

What diuretics work in the proximal tubule?

A
  • Acetazolamide
  • Osmotic diuretics (mannitol)
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14
Q

What are the transport mechanisms in the loop of Henle?

A

Apical:

  • Na-K-2Cl cotransporter
  • K channel

Basal:

  • Na-K exchanger
  • K-Cl cotransporter
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15
Q

What are the main diuretics that work in the LoH?

What channel/process do they block?

A

Loop diuretics: Furosemide

  • Inhibits Na-K-2Cl co-transporter in TALH (thick)
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16
Q

What are the effects of loop diuretics?

A
  • Very potent diuretic
  • Induce NaCl diuresis
  • Decrease positve lumen, the driving force for Mg2+ and Ca2+ absorption, cause an increase in Mg2+ and Ca2+ excretion
  • Cause K+ wasting
  • Induce renal prostaglandin synthesis that increases renal blood flow and vasodilation
17
Q

Clinical Uses of loop diuretics?

A
  • Acute pulmonary edema
  • Edematous conditions: heart failure, cirrhosis, nephrotic syndrome
  • Hypercalcemia and Hyperkalemia
  • SIADH

Hypertension:

  • Refractory cases
  • Associated with renal insufficiency or heart failure
  • Hypertensive emergencies
18
Q

How do loop diuretics help with SIADH?

A
  • In LoH, Na reabsorption without water concentrates the medulla (hypeosmolar medulla provides urine concentrating ability)
  • Loop diuretics block Na reabsorption in LoH, getting rid of hyperosmolar medulla and blocks responses to ADH
19
Q

Toxicity of loop diuretics?

A
  • Hypokalemic metabolic alkalosis
  • Hypomagnesemia
  • Hyperuricemia (hypovolemia-associated enhancement of uric acid reabsorption in the proximal tubule)
  • Ototoxicity (hearing loss; dose-related)
20
Q

What are the transport mechanisms in the distal convoluted tubule?

A

Apical:

  • Na-Cl cotransporter
  • Ca transporter

Basal:

  • Na-K- ATPase
  • Na-Ca exchanger
  • Cl channel
21
Q

What is hydrochlorothiazide (HCTZ) (broad class)?

A

Thiazide diuretic

22
Q

What channel do thiazide diuretics block?

A

Inhibits Na-Cl cotransporter in the DCT

23
Q

What are the effects of thiazide diuretics?

A

(Blocks Na-Cl contransport)

  • Induce NaCl diuresis
  • Icrease Ca reabsorption:

— In the PCT, thiazide-induced volume depletion -> enhanced Na and passive Ca reabsorption

—- In the DCT, lowering IC Na by thiazide -> more Na/Ca exchange in teh basolateral membrane

  • Renal K wasting
24
Q

What are some clinical uses of thiazide diuretics?

A
  • HTN
  • Heart failure
  • Renal stones due to idiopathic hypercalcuria
  • Nephrogenic diabetes insipidus
25
Q

How do thiazide diuretics help in diabetes insipidus?

A
  • The absence of ADH (central DI) or resistance to ADH actions in the kidney (nephrogenic DI)

—- Causes rapid loss of water and an increase in osmolality

  • Thiazide-induced Na losses -> more Na reabsorption in the proximal tubule and decreases urine formation
26
Q

Toxicity of thiazide diuretics?

A

Hypokalemic metabolic alkalosis

Hyperuricemia

Hyponatremia

  • Hypovolemia-induced elevation of ADH
  • Reduction in the diluting capacity of the kidney
  • Increased thirst

Hyperglycemia

  • Impaired insulin release
  • Diminished tissue utilization of glucose

Hyperlipidemia

27
Q

What are the ion transporters at play in the collecting duct?

A

Apical:

  • Na channel (into cell)
  • K channel (into lumen)
  • H2O (into cell)

Basal:

  • ALD action (Mineralocorticoid receptor, MR)
  • ADH receptor
  • Na-K-ATPase

INTERCALATED CELLS

Apical:

  • H-ATPase (pumping H into lumen)

Basal:

  • HCO3-Cl exchanger (HCO3 out, Cl into cell)
28
Q

____ diuretics inhibit the effects of aldosterone at the late distal and cortical collecting tubules

A

K-sparing diuretics inhibit the effects of aldosterone at the late distal and cortical collecting tubules

29
Q

What are the mechanisms of action/blocked transporters of K-sparing diuretics?

A

1. Direct antagonism of mineralocorticoid receptors (aldosterone)

  • Spironolactone
  • Eplerenone

2. Inhibition of Na entry thru ion channels in the luminal membrane

  • Amiloride
  • Triamterene
30
Q

What are the effects of K-sparing diuretics?

A
  • Increase urine NaCl excretion
  • Hyperkalemia
  • Metabolic acidosis
31
Q

What are clinical uses of K-sparing diuretics?

A
  • Primary and secondary hyperaldosteronism
  • Heart failure
  • Cirrhosis
32
Q

What is toxicity of K-sparing diuretics?

A

- Hyperkalemia

- Hyperchloremic metabolic acidosis: like type IV renal tubular acidosis (similar to type IV RTA)

- Gynecomastia: spironolactone-adrogen receptor (dihydrotestosterone) (painful breasts)

33
Q

How can you measure diuretic effectiveness?

A
  • Depletion of extracellular volume to treat hypertension or edematous states is easily measured as a decrease in body weight
  • Check Daily Weights
  • “I’s & O’s” are usually inaccurate and net changes over time are rarely available
  • Plasma electrolytes are limited in value
34
Q

Describe diuretic resistance- what could cause it?

A
  • Normal Response: Compensation
  • Inadequate Dose
  • Inadequate control of salt intake
  • Drug interactions (e.g., NSAIDs)
  • Reduced bioavailability: (CHF, CKD, Hypoalbuminemia)
35
Q

How do you deal with diuretic resistance?

A
  • Assess Compliance with Salt restriction and medicine intake. If necessary, measure the amount of salt and diuretic in the urine
  • Discontinue NSAIDs
  • Adjust the dose of the diuretic in patients with renal impairment
  • Switch to intravenous administration to overcome problems associated with impaired absorption
  • Switch to a continuous intravenous infusion of a loop diuretic to avoid postdiuretic salt retention
  • Combine loop diuretics with other diuretics, preferably a thiazide diuretic
36
Q

What diuretics work at the:

  • Proximal tubule
  • LoH
  • DCT
  • Collecting tubule
A

Proximal tubule

  • Carbonic anhydrase inhibitors
  • (Osmotic agents)

LoH

  • Furosemide
  • Bumetanide
  • Ethyacrinic acid

DCT

  • Thiazides

Collecting tubule

  • Aldosterone receptor antagonists (spironolactone)
  • Epithelial sodium channel inhibitors (amiloride)

MS2 Renal (25 decks)

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