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2013-02-04 20:38:49
Anti hypertensive diuretics

AntiHTN and Diuretics
Show Answers:

  1. Concerning hypertension, the majority of cases are considered primary. True or False?
  2. HTN is a multifactorial phenomenon: Name 4 of these factors.
    • physiology
    • genetics
    • stress
    • diet
  3. What percent is heredity estimated to account for essential HTN?
  4. What BP would be considered normal based on JNC 7 2003 guidelines?
    SBP <120 DBP <80
  5. What BP would be considered prehypertension based on JNC 7 2003 guidelines?
    SBP 120-139 DBP 80-89
  6. What BP would be considered stage I HTN based on JNC 7 2003 guidelines?
    SBP 140-159 DBP 90-99
  7. What BP would be considered stage II HTN based on JNC 7 2003 guidelines?
    SBP >160 DBP >100
  8. What is the main purpose for prescribing diuretics?
    to increase urine volume
  9. What is the difference between diuretic and natriuretic?
    • diuretic increases urine volume
    • natriuretic increases sodium excretion
  10. What is the MOA carbonic anhydrase inhibitors?
    blocks dehydrongenation of carbonic acid in the proximal convoluted tubule which increases sodium bicarbonate secretion leading to diuresis
  11. Name 4 indications for CAI use.
    • urinary alkalinization
    • glaucoma
    • acute mountain sickness
    • metabolic alkalosis
  12. Name 3 side effects of CAI use.
    • drowsiness
    • anorexia
    • paresthesias
  13. Name 4 contraindications for CAI use.
    • calcium stones
    • acidosis
    • renal potassium wasting
    • cirrhosis
  14. What is the MOA of loop diuretics?
    blocks reabsorption of NaCl in the thick ascending limb by interfering with Na/K/Cl transporter
  15. What percent of sodium reabsorption occurs in the thick ascending limb of the nephron?
  16. Loop diuretics interfere with potassium recycling. What affect does this have on Calcium and Magnesium?
    it increases the excretion for both Ca and Mg
  17. Name 4 clinical indications for loop diuretic use.
    • Edema
    • hypercalcemia
    • ARF
    • hyperkalemia
  18. The onset and clearance of loop diuretics depends on ____________ method and _____________ function.
    • delivery
    • kidney
  19. The absorption of loop diuretics is not affected by acidosis. True or False?
  20. Name 4 contraindications/cautions for loop diuretic use.
    • hypersensitivity due to SULFA allergy
    • hyperuricemia
    • ototoxicity
    • hypomag/hypokalemic metabolic alkalosis
  21. Name 3 side effects of loop diuretic use.
    • dizziness
    • hypotension
    • photosensitivity (lasix)
  22. What is the MOA for thiazides?
    • block reabsorption of NaCl in the Distal convoluted tubule
    • enhance Ca+ reabsorption
    • compete with uric acid secretion in the PCT
  23. Name 4 clinical indications for thiazides.
    • HTN
    • HF
    • Hypercalciuria
    • nephrogenic DI
  24. Name 3 side effects for thiazide use.
    • hypotension
    • electrolyte disturbance
    • photosensitivity
  25. Name 4 contraindications/cautions for thiazide use.
    • hypomag/hypokalemic metabolic alkalosis
    • SULFA allergy
    • hyperuricemia
    • hyperglycemia/hyperlipidemia
  26. What is the MOA for the potassium sparing diuretics?
    prevent K+ secretion by opposing aldosterone in DCT
  27. What are 4 clinical indications for potassium sparing diuretics?
    • HTN
    • primary or secondary hyperaldosteronism
    • Edema
  28. Name 3 side effects for the potassium sparing diuretics.
    • hyperkalemia
    • gynecomastia
    • sexual dysfunction
  29. Name 3 contraindications for the potassium sparing diuretics.
    • concomitant use of beta blockers, ACE inhibitors
    • liver impairment
    • potassium supplementation
  30. What diuretic might be appropriate for the CHF patient with metabolic alkalosis who still needs additional diuresis?
    CAI. because of the volume contraction alkalosis, CAI would be used to correct the pH and add additional diuresis
  31. How do CAI diuretics help with acute mtn sickness?
    with acute mtn sickness the s&s are weakness, dizziness, HA that can lead to pulmonary or cerebral edema. CAIs decrease CSF formation and pH, thus causing increase ventilation and reduction in symptoms
  32. Name 3 toxidromes caused by CAI diuretics.
    • hyperchloremic metabolic acidosis
    • renal stones
    • renal K+ wasting
  33. The hyperchloremic metabolic acidosis seen with CAI toxicity results from chronic loss of which anion?
  34. You have a patient with a toxic ingestion of halogenated substance such as bromide. Which diuretic is most appropriate?
    Loop diuretic due to anion overdose. Substances such as fluoride, iodide, and bromide are reabsorbed in the TAL and loop diuretics can help flush them out.
  35. Your patient is on gentamycin for the treatment of a nasty gram negative bacterial infection. He needs a diuretic to help mobilize extra fluid. Would a loop diuretic be appropriate?
    most likely not. there is a dose-related ototoxicity that is worsened with othe agents such as aminoglycosides that cause hearing loss
  36. All of the loop diuretics are sulfonamides. True or false?
    false. ethacrynic acid is not
  37. Name 3 toxidromes associated with thiazide diuretic use.
    • hypokalemic metabolic alkalosis & hyperuricemia
    • hyperlipidemia
    • hemolytic anemia (rare)
  38. Your patient reports that their blood sugars have been elevated for some unknown reason. The only new finding is the addition of HCTZ to their medication listing. Is this new medication a potential cause?
    yes, HCTZ is a thiazide and they can cause impaired pancreatic release of insulin and diminished tissue utilization of glucose leading to impaired CHO tolerance
  39. This type of diuretic is most useful in mineralcorticoid excess from conditions such as Conn's, CHF, or nephrotic syndrome.
    Potassium sparing
  40. Name 2 centrally acting sympathoplegic drugs.
    methyldopa & clonidine
  41. Name 3 side effects for centrally acting sympathoplegic drugs such as clonidine.
    • postural hypotension
    • mild sedation
    • dry mouth
  42. What is the purpose of centrally acting sympathoplegic medicatons such as clonidine?
    to block vasoconstriction
  43. Describe the MOA of clonidine.
    lower BP by reduction of CO due to decrease HR, relaxation of capacitance vessels and decreased PVR. This happens by direct stimulation of alpha 2 adrenoreceptors that reduces release of NE in the brain
  44. What is the most common undesirable effect of centrally acting sympathoplegics?
    pronounced sedation
  45. Name 3 negative side effects seen with long term use of either clonidine or methyldopa.
    • imparied concentration
    • lactation in men & women
    • + Coombs (makes cross-matching blood difficult)
  46. Name 2 ganglionic blocking agents and describe their MOA.
    • guanadrel & reserpine
    • block nicotinic Ach channels on sympathetic and parasympathetic ganglia to block vasoconstriction
  47. Name 3 side effects seen with ganglionic blockers.
    • profound orthostatic hypotension
    • sexual dysfunction
    • parkinsonian EPS effects
  48. List the 4 properties that characterize Guanethidine's mode of action on the presynaptic sympathetic terminal.
    • 1. enters the presynaptic nerve terminal via Uptake 1 receptor
    • 2. causes increased release of NE into the synaptic cleft
    • 3. it binds to the synaptic vesicles to cause the release of catecholamines that are then degraded by MAO
    • 4. causes adrenergic neuronal blockade by uncoupling the AP from NT release
  49. Does guanethidine cross the blood brain barrier?
  50. Which nervous system does guanethidine act exclusively on?
    the peripheral nervouse system, because it does not cross the BBB
  51. Name 2 sympathetic and 3 parasympathetic adverse effects of ganglionic blockers.
    • Sympathetic: orthostatic hypotension & sexual dysfunction
    • parasympathetic: urinary retention, blurred vision, dry mouth
  52. Describe the pharmacokinetics/dynamics of beta adrenoceptor antagonists. Specifically
    beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy (heart rate), inotropy (contractility), dromotropy (electrical conduction) and lusitropy (relaxation). Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate.
  53. Discuss the machanism of action or alpha blockers
    Alpha-blockers dilate both arteries and veins because both vessel types are innervated by sympathetic adrenergic nerves; however, the vasodilator effect is more pronounced in the arterial resistance vessels.
  54. Specifically describe the mechanism of action of prazosin
    • It works by selectively blocking alpha 1 receptors in arterioles and venules. Alpha-1 receptor selectivity allow NE to exert unopposed negative feedback (mediated by presynaptic alpha-2 receptors) on its own release.
    • How do hydralazine and Nipride differ in terms of their MOA?
    • hydralazine dilates arterioles only, whereas Nipride dilates both venous and arterial vessels to reduce PVR
  55. What medication activates guanylyl cyclase by nitric oxide release and direct enzymatic stimulation and increases cGMP which leads to relaxation of vascular smooth muscle?
    sodium nitroprusside
  56. What toxicty results from high doses or long treatment of Nipride?
  57. How are diltiazem and local anesthetic medications similar in terms of their MOA?
    • they both act from the inner side of the membrane and bind more effectively to open and inactivated channels
    • drug binding reduces the frequency of opening in response to depolarization
    • results in marked decrease transmembrane calcium current and long-lasting smooth muscle relaxation, decreased contractility, and SA & AV nodal conduction velocity
  58. What characteristic of ACE inhibitors makes them superior to other agents in patients needing blood pressure reduction and diagnosed coronary artery disease?
    they do not stimulate reflex tachycardia
  59. What is the MOA of ACE inhibitors?
    block conversion of angiotensin I to angiotensin II, this blocks vasoconstriction
  60. Describe the pharmacologic management of hypertensive emergencies.
    • reduce BP by 25%, NOT normalization
    • maintain DBP at no less than 100mmHG
    • continuous arterial BP
    • meticulous I/O and daily wgts
    • IV antihypertensives for rapid tx