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Flashcards in Cardio: RAAS Drugs Deck (25)
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1

  • Drugs that:
    • Prevent the formation of Angiontensin II
    • Prevent degredation of bradykinin

ACE Inhibitors: ("-PRIL")

Lisinopril

Captopril

Enalapril

2

Clinical use of ACE inhibitors:

  • HTN
  • CHF
  • HCM
  • MI
  • Renal failure and fibrosis
  • Diabetes

3

Contraindications for ACE inhibitors and ARBs:

  • Renal artery stenosis → Renal Failure
  • Elevated serum K+ (>5.5 mEq/L)
  • Symptomatic hypotension
  • Pregnancy (chronic mgmt of Hypertension)
    • Methyldopa
    • Hydralazine

4

Side effects of ACE inhibitors and ARBs:

  • Severe hypotension
  • Chronic nonproductive dry cough (ACEs)
  • Dysgeusia (altered taste)
  • Renal hemodynamic dysfunction
    • Renal Artery Stenosis (contraindicated)
      → Renal Failure
  • Hyperkalemia (Lack of Aldosterone)
  • Angioedema (rare)

5

  • Drugs that:
    • Nonpeptide AT1 receptor antagonism that interferes w/ binding of Angiotensin II to its receptor
    • DOES NOT effect the breakdown of bradykinin

ARBs (AT1 receptor blockers) ("-SARTAN")

Losartan

Vaisartan

6

Clinical use of ARBs:

  • HTN
  • CHF

7

Aldosterone receptor antagonist drugs:

  • Spironolactone
    • Aldosterone receptor antagonist
  • Eplerenone (Inspa)
    • Selective aldosterone receptor blocker

8

Mechanism of action for Aldosterone antagonists:

  • Aldosterone (a mineralocorticoid hormone) produced in the adrenal cortex and in extra-adrenal sites) whose synthesis and secretion are affected by Angiotensin II, plasma potassium levels, ACTH, and other stimuli
  • Angiotensin II is the most potent stimulus
  • Kidney: stimulates sodium retention by distal nephrons, potassium excretion, blood volume expansion, elevation of blood pressure
  • Other sites: increases blood pressure by a CNS mechanism, stimulates myocardial fibrosis, reduces arterial elasticity and increases inflammation

9

Clinical use of Aldosterone receptor antagonists:

  • Hypertension
  • CHF

10

Contraindications of Aldosterone antagonists:

  • Hyperkalemia
  • Cirrhosis

11

Side effects of Aldosterone antagonists:

  • Hyperkalemia (both drugs)
  • Progestational and antiandrogenic side effects (Spironolactone only):
    • Gynecomastia
    • Impotence
    • Menstrual irregularities

12

  • Increases kidney tubular fluid osmolarity - pulls water from the interstial space into the tubules via osmosis - more water is excreted into the urine and less water reabsorbed into the ciruclation
  • Acts on the Proximal tubule
  • Tx: Intracranial Pressure, Increased Ocular Pressure
  • Can pull fluid into the blood and lead to Hypervolemia --> which can lead to peripheral and pulmonary edema

Mannitol

13

Drug acts on the Proximal Convoluted Tubule

Acetazolamide and Osmotic Agents (Mannitol)

14

Drug acts on the Descending Limb

Osmotic agents (Mannitol)

15

Drug acts on the Thick Ascending Limb

Loop Diuretic Agents (Furosemide)

Ethacrynic acid

16

Drug acts on the Distal Convoluted Tubule

Loop Agents (Furosemide)

Thiazides

Aldoesterone antagonists

17

Drug acts on the Collecting Duct

ADH antagonists

Osmotic agents (Mannitol)

18

  • Prevents the conversion of HCO3- into CO2 by carbonic anhydrase primarily at the brush border of the proximal tubule cells, necessary for the reabsorption of HCO3-
  • Proximal convouted tubule
  • Tx: Metabolic alkalosis, Altitude sickness, Glaucoma, or Intracranial HTN (Pseudotumor cerebri)
  • SEx: Metabolic acidosis due to HCO3-, urine pH goes up, blood pH goes down, also allergic rxns to sulfa group

Acetazolamide

19

  • Inhibits Na+ K+ 2Cl- channel in the thick ascending limb of the loop of Henle - Loop diuretics - OH DANG!
  • Na+ and K+ abolish the Hypertonicity of the Medulla (urine cannot be collected in the collecting ducts)
  • Marked diuresis --> Ca2+ excretion
  • Tx: Edema (CHF, Cirrhosis, Nephrotic syndrome, PE), moderate to severe HTN, Acute ion overdose, and Hypercalcemia
  • SEx: Azotemia, Ototoxicity, Hyponatremia, Hypokalemia, Hypercalciuria, Hypocalcemia, Dehydration, Allergy to sulfa (furosemide, not ethacrynic acid), Nephritis, Gout

Furosemide (Lasix)

Ethacrynic acid (Edecrin)

Bumetanide (Bumex)

OH DANG!

  • Ototoxicity
  • Hypokalemia, Hypercalcuria
  • Dehydration
  • Allergy to sulfa (Furosemide)
  • Nephritis
  • Gout

20

  • Thiazide diuretics
  • Inhibit Na+, Cl- co-transporter, which blocks the reabsorption of Na+ and Cl- in the Distal Convoluted Tubule - competing for the Cl- site
  • NaCl is excreted along with water into the urine --> increases Ca2+ reabsorption
  • Action is addivitve to Ethacrynic acid and Furosemide
  • Tx: Mild to moderate HTN, mild CHF, Nephrogenic diabetes insipidus, Idiopathic Hypercalcuria
  • SEx: Hyperglycemia, Hyperlipidemia, Hyperuricemia, Hypercalcemia, Sulfa allergy - HyperGLUC

Hydrochlorothiazide

Chlorothiazide

Metolazone

  • HyperGLUC
    • HyperGlycemia
    • HyperLipidemia
    • HyperUricemia
    • HyperCalcemia

21

  • Competitive antagonist at the Aldosterone receptor in the Collecting tubule (indirectly inhibits Na+) reabsorption (1st)
  • Directly blocks Na+ channels in the Collecting tubule (2&3)
  • K+ sparing properties:
    • Less K+ secretion occurs due to inhibiton of Na+ reabsorption in the Distal Tubule (Na+ reabsorption and K+ secretion are coupled in this segment of the nephron) --> they do not greatly increase flow
  • Tx: Prevents K+ waisting w/ other diuretics, CHF
  • SEx: Hyperkalemia, Spironolactone causes Gynecomastia

Spironolactone

Triamterene

Amiloride

22

  • Centrally acting sympatholytics
  • Selective α2-agonist - Brain stem - reduces cental sympathetic outflow - decreased CO and SVR
    • BP = CO x SVR
  • Drug of choice for Hypertension in Pregnant patients
  • SEx:
    • M: Sedation, Positive Coombs test in 10% of patients (reversible upon discontinuation of drug)
    • C: Sedation, Dry mouth, Severe rebound Hypertension with abrubt discontinuation

Methyldopa

Clonidine

23

  • Selective α1-receptor antagonist; α1-blockade decreases SVR by preventing arteriolar vasoconstriction - decreased BP
  • Primarily α1-receptors on arterioles, Bladder sphincter
  • Tx: Mild to Mod HTN, and BPH - α1-blockers to treat urinary hesitancy for pts. w/ benign prostatic Hypertrophy (preventing bladder sphincter contraction)
  • SEx: First-dose syncope orthostatic hypotension, Reflex tachycardia, Secondary Na+ retention in Kidney (use w/ diuretic), Urinary incontinence

Prazosin

α1-receptor blocker - ends in 'osin

Doxazosin

Terazosin

24

  • β-receptor blockers (ANS, decrease Renin release))
  • Reduce HR, Contractility, Inhibit Renin
  • β1-receptors on heart and kidney, β2-receptors on arterioles
  • Tx: HTN, Angina, Pts. w/ previous MI, CHF
  • SEx: Asthma (Bronchoconstriction (β2)), Vasospastic,  Bradycardia, Blunted response to hypoglycemia - dangerous in Diabetics (masks Hypoglycemic events) on insulin therapy, Sexual dysfunction, small increase in LDLs and TGs

Propranolol

Carvedilol

Metoprolol

Esmolol

Atenolol

Tinolol

25

Drug that blocks the production of Renin:

Aliskiren

Prevents the conversion of:
Angiotensinogen → Angiotensin I