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Renal M2 > Diuretics 01 30 2015 > Flashcards

Diuretics 01 30 2015 Flashcards

1
Q

Acetazolamide

  1. type of drug
  2. where does it work
  3. Effect
  4. side effect
  5. How does body react to drug?
  6. How is drug excreted?
A
  1. carbonic anhydrase inhibitor
    Proximal Tubule
  2. Blocks sodium bicarbonate reabsorption
  3. Decrease in Sodium Chloride reabosrption.
    Water is reabsorbed passively
  4. hyperchloremic metabolic acidosis ( due to bicarbonate loss).
  5. Effectiveness of acetazolamide decreases significantly over several days because of enhanced NaCl reabsorption at other sites due to bicarbonate depletion
  6. Excreted via tubular secretion in proximal tubule
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2
Q

What are other therapeutic uses for carbonic anhydrase inhibitors?

A
  1. Eye – glaucoma (decrease production of aqueous humor)
    - Dorzolamide and Brinzolamide ( topically both)
  2. Acute mountain sickness
  3. To correct acute mountain sickness: raise Co2 content of tissues – counteracts hyperventilation
  4. Can be used to alkalinize urine briefly ( for solubiliztion of uric acid)
  5. Anticonvulsants
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3
Q

Adverse Effects of Carbonic Anhydrase Inhibitors

Contraindications?

A
  • Paraesthesiasand somnolence
  • Allergic rxns to those sensitive to sulfonamides
  • Hyperchloremic metabolic acidosis from chronic use
  • renal K+ wasting ( Thiazide/ loop diuretics)

Contraindications: avoid in patients with hepatic cirrhosis. Decrease in NH4+ excretion may contribute to envelopment of hepatic encephalopathy and coma

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4
Q

Caffeine

  1. Mechanism
  2. location of action
A
  1. weak diuretic – nonspecifically blocked adenosine receptors involved in controlling proximal tubule Na+ reabsorption
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5
Q

What are the pharmacodynamics behind Osmotic diuretics:

  1. main role
  2. where do they act
  3. mechanism
A

increase urine volume and urine flow rates — reduces Na+ reabsorption.

Act in Proximal Tubule and descending limb of Henle’s Loop — cells are freely permeable to water.

Mechanism: expand the extracellular fluid volume, decrease blood viscosity and inhibit renin release.
– incresae renal blood flow

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6
Q

Clinical indications to use osmotic diuretics:

A
  1. increase Urine volume : increase H2O excretion in preference to sodium excretion.
  2. Reduction of intracranial and intraocular pressure : reduce total body water
    - can do this within 60-90 minutes
  3. promote prompt removal of renal toxins ( ex. radiocontrast agents)
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7
Q

Some toxicities associated with osmotic diuretics

A 
Water expansion (before diuresis) into extracellular compartment = hyponatremia
- complicate CHF, pulomary edmea, headache, nausea, vomitting

Dehydration and hypernatremia ( after diuresis)

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8
Q

Mannitol

  1. type of drug
  2. where does it act
  3. Metabolism?
  4. What happens when given orally/ it’s function for when to give orally
A

Osmotic diuretic
Acts in PCT and Descending limb of henle’s loop

  • is not metabolized and therefore has to be given parenterally.
  • handled by glomerular filtration without any important tubular reabsorption or secretion.

-If given orally = osmotic diarrhea = potentiate the effects of potassium-binding resins or eliminate toxic substances from the GI tract in conduction with activated Charcoal.

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9
Q

Furosemide

  1. type of drug
  2. Where does it act?
  3. What is it’s target
  4. main mechanism
  5. Consequences
  6. Specific use:
A
  1. Loop Diuretic
  2. Thick Ascending Limb
  3. NKCC2 co-transporter
  4. Selectively inhibit NaCl reabsorption = diminish normal lumen-positive potential that derives from K+ cycling
  5. Increase in Mg2+ and Ca2+ excretion;
    induce synthesis of PGE2 via increase in COX=2 = increase renal blood flow; inhibit salt transport
    - salt stays in lumen, and therefore,so does water.

POTASSIUM WASTING DIURETIC

  1. relieves pulmonary congestion and reduce left ventricular filling pressures in CHF before a measurable increase in urinary output occurs.
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10
Q

Name some loop diuretics

A

Furosemide
Bumetanide
Ethacrynic acid
Torsemide

Furosemide and ethacrynic acid = relieve pulmonary congestion in CHF patient. AND decrease left ventricular filling pressure

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11
Q

Loop diuretics pharmacokinetics:

A
  • rapidly absorbed
  • Eliminated by renal secretion
  • Rapid diuretic response.
  • Half-life is dependent on renal function
  • Act on luminal side, diuretic response correlates positively with their excretion in urine.
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12
Q

Therapeutic uses of loop diuretics

A
  1. Acute pulmonary edema
  2. edematous conditions
  3. Acute Hypercalcemia

Also:

  1. Hyperkalemia
  2. Acute renal failure
  3. Anion overdose ( Bromide, fluoride, and iodide)
  4. NOT used for HTN because of their short half-life
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13
Q

Toxicity of Loop Diuretics

A
  1. Hypokalemic Metabolic Acidosis
  2. Ototoxicity
  3. Hypomagnesmia
  4. Alltergic rxns
  5. Impaired carbohydrate tolerance: hyperglycemia
  6. dehydration
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14
Q

contradictions with Furosemide, bumetanide, and torsemide

A

Loop Diuretics

  • be careful with patients who are sensitive to sulfonamides. Overzealous use is dangerous in hepatic cirrhosis, borderline renal failure, or CHF
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15
Q

Hydrochlorothiazide

  1. type of drug
  2. where do they act?
  3. What is it’s target
A
  1. Thiazide
  2. Distal convoluted tubule
  3. NCC ( Na+/ Cl- symporter)

Decrease in intracellular sodium = enhanced calcium reabsorption.

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16
Q

Chlorothiazide

  1. Type of drug?
  2. Pharamcology?
A
  1. Thiazide

2. Less lipid soluble and must be given in relatively large doses.

17
Q

Indapamide

  1. Type of drug?
  2. Excreted how?
A
  1. Thiazide

2. Excreted primarily by the biliary system–

18
Q

How are thiazides excreted?

What is the overall mechanism of action?

What are the action of thiazides dependent on? Based on this, what drugs can decrease the effect of thiazides?

A

Organic acid secretory system and compete with the secretion of uric acid. ENHANCES Ca2+ reabsorption in the distal convoluted tubule (DCT).

Blocks NaCl reabsorption by the NCC in the distal convoluted tubule.

Renal prostoglandin production. Thus, thiazide can also be inhibited by non steroidal anti-inflammatory drugs (NSAIDs)

19
Q

Indications for using a thiazide?

A
  • Hypertension
  • Heart Failure
  • Nephrolithiasis due to idiopathic hypercalciuria
  • Nephrogenic diabetes insipidus (NDI) – wasopressin/ADH insensitivity
20
Q

Thiazide toxicities

A
  1. Hypokalemia Metabolic Alkalosis and Hyperuricemia.
  2. Hyperglycemia – in people with impaired carbohydrate tolerance. Impaired pancreatic release of insulin and diminished tissue utilization of glucose.
  3. Hyperlipidemia
  4. Hyponatremia: hypovolemia-induced elevation of ADH, reduction in diluting capacity of the kidney, and increased thirst
    - can be reduced with limiting water intake or reducing dose of drug
  5. Allergic rxn: sulfonamides - photosensitivity
  6. other: weakness, fatigue, paresthesias, impotence, HYPOMAGNESEMIA
21
Q

Aldosterone

  1. Where does it affect reabsorption and of what?
  2. does it have any other effects on other molecules?
A

Affects ENAC channel ( Na+ channel) on prinicpal cell – enchances Na+ reabsorption ( apical side)

On basolateral side of principal cell enchancs Na+ K+ ATPase – reabsorption of Na+ and secretion of K+
* SECRETION OF K+

In Intercalated cell, it has the effect of enhancing H+ secretion
* SECRETES H+

22
Q

Name the potassium sparing drugs?

Their mechanisms?
Elimination?

Are any drugs dependent on something for activation?

A

Spironolactone
Eplerenone
- these two bind to the cytoplasmic mineral corticoid receptors and prevent translocation of receptor complex to nucleus.
- Eplerenone has greater selectivity – approved for treatment of HTN.

Triamterene
Amiloride
- block ENAC (Na+ channel)
-Triamterene is metabolized in liver and excreted by kidneys
- Amiloride is excreted by kidney unchanged.

Triamterene and Spironolactone are dependent on renal prostaglandin production. Actions of these two may be inhibited by NSAIDS

23
Q

Indications for using a potassium-sparing diuretic

A
  • Cirrhosis with ascities
  • Renal vascular hypertension
  • Adrenal tumors
  • Cardiac or Nephrotic edema
  • Conn’s syndrome: aldosterone-producing adenoma.

Thiazide diuretics are generally ineffective when GFR falls below 30 ml/min – but may be combined with loop diuretic

24
Q

Toxicity of potassium sparing drugs

A
  • Hyperkalemia
  • Hyperchloremic Metabolic acidosis: inhibition of H+ secretion K+ secretion — causes acidosis.
  • Gynecomastia – use eplerenone vs. spironolactone because it is more specific
  • Acute Renal failure - combination of triamterene with indomethacin
  • Kidney stones mostly with triamterene (poorly soluable)
25
Q

Contradictions when using potassium sparing drugs?

A
  • Patients with chronic renal insufficiency
  • Patients with liver disease or impaired metabolism. (triamterene and spironolactone)
  • Cyp3A4 inhibitiors can increase levelsof eplerenone.
26
Q

Where does ADH have an effect and What are the effects?

A

Collecting Tubule
Principal cell

  • ADH - posterior pituitary due to hypovolemia or hypotension
  • serum osmolality and volume status (regulators)

Bind to V2 on basolateral side. Activates AQP2 (CAMP dependent mechanism)

Increases transport and synthesis of AQP2 = increase in water reabsorption.

27
Q

Vaptans

  1. mechanism of drug
  2. Name of FDA approved drug? How is it given?
  3. Contraindicated in which patients?
A

Tolvaptan; Conivaptan

  1. ADH receptor antagonists ( V2 - Tolvaptan; V1 and V2: Conivaptan)
  2. Conivaptan
    - intravenous infusion for the inhospital treatment of euvolemic hyponatremia
  3. hypovolemic hyponatremia ; pregnant women
28
Q

Li+ and Demeclocyline

  1. What are they?
  2. mechanism?
A
  • nonselective agents that affect aquaporins
  • reduce formation of cAMP in response to ADH
    = interefre with actions of CAMP in collecting tubule

Demeclocyline is no longer used as an ADH antagonist.

29
Q

Clinical indications of ADH anatgonists

A
  • Syndrome of inappropriate ADH secretion ( IADH)
    - use Tolvaptan: approved agent for euvolemic and hypovolemic hyponatremia

-other causes of ADH: deminished circulating volume ( CHF, liver disease)

30
Q

toxicity of ADH antagonists:

A
  • Nephrogenic Diabetes Insipidus: inadequate response to ADH
  • Renal failure
  • Other: cardio toxicity, thyroid dysfunction, mental obtundation, leukocytosis, tremulousness
31
Q

Diuretic combinations

A
  1. loop agents + thiazides
    - Metolazone is the usual choice of thiazide-like drug in patients refractory to loop agents alone.
  2. potassium sparing diuretics and Loop/ thiazides
    * avoid in patients with renal insufficiency
32
Q

What is the best treatment for edema associated with kidney failure?

A
  • loop diuretics

- loop diuretics + thiazide diuretic

33
Q

Diuretics and hepatic cirrhosis

  1. classic findings in someone with liver disease
  2. What are Cirrhotic patients resistant to? (what medication)
  3. Cirrhotic edema is highly responsive to who?
  4. what combination of drugs may be useful for some patients with edema due to hepatic cirrhosis?
A

Liver disease is associated with edema and ascites in conjunction with elevated portal hydrostatic pressures and reduced plasma oncotic pressures.

Cirrhotic patients are resistant to loop diuretics – high aldosterone leads to enhanced collecting duct salt reabsorption — decrease in secretion of drug into tubular fluid

Spironolactone

Loop diuretics with spironolactone

34
Q

What nonedematous states can diuretics be used in?

A
  1. Hypertension (thiazide): now a days we use ACEi.
  2. Nephrolithiasis = renal stones ( calcium phosphate or calcium oxalate)
  3. Hypercalcemia ( loop diuretic - furosemide + saline)
  4. Diabetes Insipidus (thiazide) - alleviate excessive thirst

Renal M2 (3 decks)

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