9. Diuretics used to treat hypertension Flashcards
What is the systolic pressure and diastolic pressure for stage 1, 2, and 3 of hypertension?
stage - 140-159/90-99
stage 2 - 160-179/100-109
stage 3 - >/= 180/ >/=110
List some risk factors for hypertension.
excessive salt intake, smoking, increased lipids, diabetes, family history
What % of hypertension has known causes vs. unknown causes?
Within the known cases, what are the 3 major causes?
known - 10 %
unknown - 90%
renal artery constriction, pheochromocytoma, hyperaldosteronism
BP is directly related to what? What does the RAA mechanism alter? How does this mechanism increase BP?
renal perfusion
plasma volume
vasoconstriction
Which receptors respond to lack of stretch in arterial walls? Once detected, where are the sensory impulses sent? Which centers respond? What is the response? Describe the effect of the 2 different impulses (motor vs. neural).
baroreceptors
CNS
Medullary cardiac and vasomotor
motor - sent to heart and veins: increase venous return & CO
neural - sent to resistance vessels: increase SVR
What is urgency of treatment related to? What are some examples of lifestyle modifications?
urgency (capillaries cannot tolerate chronically high BP)
dietary salt restriction, weight loss, exercise
BP control can be achieved through changes in 3 major things, what are they? What do diuretics influence?
CO, vasomotor tone, plasma volume
plasma volume
What are diuretics used primarily to treat?
How can they restore cardiopulmonary function?
HTN, CHF
decreased plasma volume, eliminating excess tissue fluid, influence acid-base balance
What is essential in treating HTN? Why?
multidrug therapy
compensatory mechanisms that assist with BP control
List some challenges to medication compliance.
asymptomatic disease, long-term therapy, benefits nit tangible, undesirable side effects
What % or CO do the nephrons receive? What does the nephron regulate?
20-25%
urine output/volume and physical and chemical characteristics
List and describe the 3 mechanisms of diuresis.
glomerular filtration - UF enters glomerular capsule
tubular reabsorption - water, glucose, and electrolytes removed from UF; returned to blood
tubular secretion - waste products removed from plasma, added to filtrate for elimination
Primary active transport:
How is Na reabsorbed?
How are the remaining ions reabsorbed?
sodium pump…reabsorbed by peritubular capillaries
passive diffusion
Secondary active transport:
How is Na, K, and Cl moved from UF?
What then happens to K?
Na/Cl symporters cause additional what?
by the peritubular capillaries by Na, K, Cl (NKCC2) symporter
leaks back into filtrate
reabsorption of electrolytes and water in distal nephron
What are the 5 groups of diruetics?
carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazide diuretics, K sparing diuretics
Which 2 classes of diuretics are not used as adjuncts to treat HTN or CHF?
carbonic anhydrase inhibitors and osmotic diuretics
Acetazolamine (Diamox):
Class? MOA? Indications?
carbonic anhydrase inhibitor
prevents water and CO2 from combining in the PCT, decreasing carbonic acid, inhibits Na/H antiporter mechanism, causes metabolic acidosis, alkaline urine
glaucoma, metabolic alkalosis
Mannitol (Osmitrol):
Class? MOA? Indications?
osmotic diuretic
increases UO without increased Na loss
acute renal failure prophylaxis during surgery, increased ICP and cerebral edema (neurosurgery)
Furosemide (Lasix):
Class? Drug of choice for what? MOA? What effects will you see with IV administration? Indications? Formulations? Precautions? Adverse effects?
loop diuretic
pulmonary edema caused by CHF
acts on ascending limb, inhibits NKCC2 symporter (increase excretion of Na, Cl, K, H, Ca, Mg, and HCO3)
acute hemodynamic effects: vasodilation secondary to renal release of prostaglandins (decreased PCWP/BP/SVR)
CHF, pulmonary edema, HTN, Ascites +/- liver cirrhosis, renal failure, SIADH, increased Ca or Mg
oral/parenteral preparations
hypokalemia, metabolic alkalosis, increased risk of digxon toxicity
volume depletion, dizziness, N & V, orthostatic hypotension, muscle weakness, arrhythmia
Chlorothiazide (Diuril):
Class? Formulations? Duration? MOA? Indications? Contraindications?
thiazide diuretic
oral/parenteral (act on distal tubule)
6-12hrs
inhibit Na/Cl symporter (natriuretic effect, chloruretic effect, diuretic effect), mild inhibition of carbonic anhydrase in PCT
edema, mild HTN
anuria, hypersensitivities
What are the 2 types of K+ sparing diuretics?
aldosterone antagonists and direct-acting
Spironolactone (Aldactone):
Class? MOA? General onset/DOA? Results in what? Indications? Precautions?
aldosterone antagonist
blocks hormone to prevent Na and water reabsorption from filtrate
slow onset, long DOA
increased Na and Cl excretion, decreased K excretion
HTN caused by increased aldosterone secretion
K retention (hyperkalemia)
Amiloride (Midamor):
Class? MOA? Useful in treatment of?
direct-acting
act on DCT to inhibit Na reabsorption and K secretion causing rapid diuresis
edema secondary to heart failure