Pharmacology Flashcards

1
Q

What is the #1 drug that cause hyponatremia?

A

Thiazide diuretics

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2
Q

What are the types of diuretics?

A
  1. Loop diuretics
  2. Thiazides
  3. Potassium-sparing diuretics
  4. Carbonic anhydrase inhibitors
  5. Osmotic diuretics
  6. ADH antagonist
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3
Q

How do Loop diuretics work ?

A

Na+K+-2Cl receptor in proximal glomerulus tubule MOST POWEFULL - ACUTE STATES

  1. Used in the acute management of pulmonary oedema and in the treatment of chronic HF or peripheral oedema (orally) NOT BP, resistance can develop because of kidney function (nehron remodelling, low renal blood flow…)
  2. Most commonly used loop diuretic is furosemide
  3. Adverse effects include vasodilation, hypokalemic metabolic alkalosis, ototoxcity (hearing loss, can be prevented by giving the drug slowly), gout
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4
Q

How do Thiazides work?

A

Na+Cl receptor in distal glomerulus tubule BLOOD PRESSURE

  1. Indapamide, Chlorothiazide, Metolazone
  2. Also have an effect on calcium reabsorption (can be used to decrease kidney stones)
  3. Adverse effects: hypokalemia, metabolic alkalosis, hyponatremia, hyperuricemia, hyperglycemia, weakness, fatigability, and paresthesias
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5
Q

How do Potassium-sparing diuretics work?

A

Receptor in most distal part of glomerulus - BLOOD PRESSURE

  1. Potassium-sparing diuretics prevent K+ secretion by antagonizing the effects of aldosterone in collecting tubules
  2. 3 important: Triamterine, Amiloride (block ENac )and Spironolactone (competes with aldo at the receptor which leads to fewer ENac)
  3. Called K sparing because they do not cause hypokalemia
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6
Q

All diuretics act in the tubular lumen except?

A

Spironolactone

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7
Q

If the GFR is low, what will happend to the action of diuretics?

A

Decrease, so will have to give a higher dose

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8
Q

How do Carbonic anhydrase inhibitors work?

A

Inhibition of carbonic anhydrase activity decreases HCO3 reabsorption in the proximal tubule, so Na leaves with it, used for glaucoma

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9
Q

How do Osmotic diuretics work?

A

Used to reduce intracranial pressure

Side effects include extracellular volume expansion, dehydration, hyperkalemia, hypernatremia and hyponatremia

Manitol

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10
Q

How do we treat SIADH?

A

Demeclocycline and conivaptan OR tolvaptan.

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11
Q

In general, how do diuretics work?

A

Reduce intravascular volume by promoting the elimination of sodium and water through the kidney (ß venous return to the heart and preload). With the exception of osmotic diuretics, all target transporters (or enzyme) in the kidney.

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12
Q

What are the 2 diuretics used for hypertension?

A
  1. ACE inhibitors
  2. Angiotensin receptor blockers
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13
Q

Common nephrotoxins?

A

NSAIDs

  • 1% to 5% of patients who ingest NSAIDs will develop nephrotoxicity
  • Patients with a history of heart failure and hypertension, as well as those treated with diuretics are at greatest risk of NSAID-induced renal failure
  • NSAIDs block prostaglandin synthesus, causing loss of afferent arteriole dilation. This results in afferent arteriole constriction, and a drop in glomerular pressure therefore a lower GFR
  • Aspirin (ASA) and Tylenol (acetaminophen) DO NOT cause this effect so are safe for patients with AKI, CKD or on ACEI/ARBs

Aminoglycosides

  • Aminoglycosides have important antibacterial properties for the treatment of gram-negative infections in clinically unstable patients.

Intravenous contrast dyes

  • Radiocontrast media can lead to a reversible form of acute renal failure that begins soon after the contrast dye administration and generally is benign.

Chemotherapy

  • Cisplatin and carboplatin are among the most widely used antineoplastic agents.
  • Nephrotoxicity is the primary dose-limiting toxicity of cisplatin.
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14
Q

Medication to preent kidney injury?

A
  • NAC may be of benefit in preventing kidney damage due to contrast agents by acting as a antioxidant. Not used as much due to limited evidence
  • Hydration
  • Limiting dose e.g. of radiocontrast especially in those at risk due to chronic kidney disease and decreased GFR
  • Holding ACEi and ARB, diuretic drugs the morning of contrast administration
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15
Q

Hyperkalemia treatment?

A
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16
Q

Treatment for Hyperparathyroidism?

A
  1. ¯ GFR ® ­PO4 ® Ca2+ because calcium is bound to phosphate ® ­ PTH
    * Phosphate diet restriction + phosphate binders
  2. ¯ Mass ® ¯ enzyme that converts vitamin D into active vitamin D ® ­ PTH +® ¯ Ca2+ absorption
  • Active vitamin D (125)
  • Cinacalcet (inhibits PTH)
17
Q

Treatment for hyperphosphotemia?

A
  • Restriction of dietary phosphate
  • Phosphate-binding meds such as CaCO3 and sevelamer