34.1: Introduction to Diuretics
By the end of this section, you should be able to:
- 34.1.1 Discuss fluid volume excess and its impact on renal system disorders.
- 34.1.2 Explain the implications of diuretic use for fluid volume excess with renal system disorders.
Fluid Volume Excess and the Renal System
The renal system normally contributes to the homeostasis of extracellular fluid volume by regulating the glomerular filtration rate (GFR), which is the rate at which the kidneys filter blood, and the reabsorption of sodium and water. Successful maintenance of this balance depends on both intrinsic (internal) renal mechanisms and extrinsic (external) systemic mechanisms.
Intrinsic Renal Response to Fluid Volume Excess
Increased fluid volume triggers an intrinsic response from the kidneys, referred to as renal autoregulation. Autoregulation depends on two physiologic processes: the myogenic response and tubular glomerular feedback. When cardiovascular fluid volume increases, the smooth muscle of the renal blood vessels stretches, stimulating the myogenic response. This response causes afferent arterioles to contract in response to increased volume. In turn, this action decreases the GFR by reducing the blood flow to the renal vessels. The tubuloglomerular feedback process decreases the GFR through the macula densa by reducing sodium reabsorption and inhibiting renin production. These actions by the kidneys are effective only when the pressure in the arterioles is 80–180 mm Hg (Dalal et al., 2022).
Extrinsic Renal Response to Fluid Volume Excess
Outside of the kidneys when there is excess fluid volume, the circulating blood volume increases, stretching the walls of the right atrium and thereby triggering atrial natriuretic peptide (ANP) secretion and reducing secretion of antidiuretic hormone (ADH). The ANP activation dilates afferent arterioles and constricts efferent arterioles, which increases the GFR. The ANP also decreases sodium reabsorption in the collecting duct and inhibits the renin–angiotensin–aldosterone system (RAAS) response to promote vasodilation and sodium excretion. Each nephron segment has a specific sodium entry mechanism that dictates the effect of decreased ADH secretion. In the loop of Henle, the sodium transporting cells respond to decreased ADH levels by reducing the reabsorption of sodium, potassium, and chloride. Decreased ADH secretion also decreases sodium and water reabsorption in the proximal and distal tubules. Under normal circumstances, these actions increase urinary output and decrease fluid volume and blood pressure.
Diuretic Use and the Renal System
Diuretic therapy decreases circulating blood volume to reduce blood pressure and resolve interstitial edema. Diuretic drugs inhibit either the specific sodium reentry mechanism for the nephron segments that regulate sodium, potassium, and chloride or water reabsorption in the proximal and distal tubules. As noted in Figure 34.2, loop diuretics affect sodium, potassium, and chloride levels or reabsorption in the thick ascending loop of Henle. Osmotic diuretics inhibit water reabsorption in the proximal convoluted tubule and the collecting duct. Potassium-sparing diuretics inhibit sodium reabsorption in the collecting tubule, and thiazide and thiazide-like diuretics decrease sodium reabsorption in the distal convoluted tubule. Different diuretics are often used in combination to take advantage of the complementary effects of individual drugs.
Based on the information above, what diagnosis should the nurse anticipate from the health care provider?
- Answer
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Edema
Which diagnostic test would the nurse expect the health care provider to order for Gordon?
- Answer
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Chemistry panel