9. Diuretics used to treat hypertension Flashcards

1
Q

What is the systolic pressure and diastolic pressure for stage 1, 2, and 3 of hypertension?

A

stage - 140-159/90-99
stage 2 - 160-179/100-109
stage 3 - >/= 180/ >/=110

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2
Q

List some risk factors for hypertension.

A

excessive salt intake, smoking, increased lipids, diabetes, family history

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3
Q

What % of hypertension has known causes vs. unknown causes?

Within the known cases, what are the 3 major causes?

A

known - 10 %
unknown - 90%

renal artery constriction, pheochromocytoma, hyperaldosteronism

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4
Q

BP is directly related to what? What does the RAA mechanism alter? How does this mechanism increase BP?

A

renal perfusion
plasma volume
vasoconstriction

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5
Q

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).

A

baroreceptors
CNS
Medullary cardiac and vasomotor
motor - sent to heart and veins: increase venous return & CO
neural - sent to resistance vessels: increase SVR

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6
Q

What is urgency of treatment related to? What are some examples of lifestyle modifications?

A

urgency (capillaries cannot tolerate chronically high BP)

dietary salt restriction, weight loss, exercise

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7
Q

BP control can be achieved through changes in 3 major things, what are they? What do diuretics influence?

A

CO, vasomotor tone, plasma volume

plasma volume

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8
Q

What are diuretics used primarily to treat?

How can they restore cardiopulmonary function?

A

HTN, CHF

decreased plasma volume, eliminating excess tissue fluid, influence acid-base balance

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9
Q

What is essential in treating HTN? Why?

A

multidrug therapy

compensatory mechanisms that assist with BP control

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10
Q

List some challenges to medication compliance.

A

asymptomatic disease, long-term therapy, benefits nit tangible, undesirable side effects

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11
Q

What % or CO do the nephrons receive? What does the nephron regulate?

A

20-25%

urine output/volume and physical and chemical characteristics

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12
Q

List and describe the 3 mechanisms of diuresis.

A

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

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13
Q

Primary active transport:
How is Na reabsorbed?
How are the remaining ions reabsorbed?

A

sodium pump…reabsorbed by peritubular capillaries

passive diffusion

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14
Q

Secondary active transport:
How is Na, K, and Cl moved from UF?
What then happens to K?
Na/Cl symporters cause additional what?

A

by the peritubular capillaries by Na, K, Cl (NKCC2) symporter

leaks back into filtrate

reabsorption of electrolytes and water in distal nephron

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15
Q

What are the 5 groups of diruetics?

A

carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazide diuretics, K sparing diuretics

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16
Q

Which 2 classes of diuretics are not used as adjuncts to treat HTN or CHF?

A

carbonic anhydrase inhibitors and osmotic diuretics

17
Q

Acetazolamine (Diamox):

Class? MOA? Indications?

A

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

18
Q

Mannitol (Osmitrol):

Class? MOA? Indications?

A

osmotic diuretic

increases UO without increased Na loss

acute renal failure prophylaxis during surgery, increased ICP and cerebral edema (neurosurgery)

19
Q

Furosemide (Lasix):
Class? Drug of choice for what? MOA? What effects will you see with IV administration? Indications? Formulations? Precautions? Adverse effects?

A

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

20
Q

Chlorothiazide (Diuril):

Class? Formulations? Duration? MOA? Indications? Contraindications?

A

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

21
Q

What are the 2 types of K+ sparing diuretics?

A

aldosterone antagonists and direct-acting

22
Q

Spironolactone (Aldactone):

Class? MOA? General onset/DOA? Results in what? Indications? Precautions?

A

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)

23
Q

Amiloride (Midamor):

Class? MOA? Useful in treatment of?

A

direct-acting

act on DCT to inhibit Na reabsorption and K secretion causing rapid diuresis

edema secondary to heart failure