Which explanation should the nurse give to a male client on why benign prostatic hyperplasia (BPH) often causes urinary retention

Polycystic kidney disease (PKD) is a genetic disorder characterized by the formation of multiple fluid-filled cysts in the kidneys. One of the complications associated with PKD is hypertension, which often occurs due to activation of the renin-angiotensin-aldosterone system (RAAS). Here's how the pathophysiological process of the RAAS contributes to the client's elevated blood pressure:

A) Intravascular fluid deficit:

In polycystic kidney disease, the development of multiple cysts in the kidneys can impair renal function and lead to decreased filtration and reabsorption capacity. However, this impairment typically leads to fluid retention rather than intravascular fluid deficit, contributing to hypertension rather than hypotension.

B) Renin angiotensin mechanism:

Correct. In PKD, the cysts disrupt normal kidney architecture and function, leading to activation of the renin-angiotensin-aldosterone system (RAAS). Reduced renal blood flow and glomerular filtration rate (GFR) stimulate the release of renin from the juxtaglomerular cells of the kidneys. Renin acts on angiotensinogen to convert it into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that increases peripheral vascular resistance, leading to elevated blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which promotes sodium and water retention, further contributing to hypertension.

C) Inflammatory process of bladder mucosa:

This option is not directly related to the pathophysiological process of hypertension in polycystic kidney disease. Flank pain and hematuria in PKD are often associated with cyst rupture or hemorrhage within the cysts rather than an inflammatory process of the bladder mucosa.

D) Mineral precipitation in urine:

Mineral precipitation in urine, such as the formation of kidney stones, can occur in polycystic kidney disease but is not directly associated with hypertension. Kidney stones may contribute to flank pain and hematuria but do not typically cause systemic hypertension.

Pressure injuries, also known as pressure ulcers or bedsores, result from prolonged pressure on the skin, leading to tissue ischemia and damage. Early recognition of the pathophysiological processes involved in pressure injury development is crucial for prevention and timely intervention. Here's why option D is the correct choice:

A) Epidermal fragility and skin excoriation with serous drainage:

This description more closely aligns with the characteristics of a superficial wound or abrasion rather than the early stages of a pressure injury. In pressure injuries, epidermal breakdown may occur later in the process, after prolonged pressure and tissue ischemia.

B) Hypodermal fluid accumulation and blister formation:

While fluid accumulation and blister formation can occur in some types of wounds, such as friction blisters or burns, they are not typically characteristic of the early stages of pressure injury development. Pressure injuries primarily involve tissue ischemia and damage due to pressure and shear forces.

C) Necrotic tissue, purulent exudate, and eschar formation:

This description is more indicative of advanced or severe pressure injuries rather than the early stages. Necrotic tissue, purulent exudate, and eschar formation typically occur in pressure injuries that have progressed to deeper tissue involvement and infection.

D) Ischemic inflammatory response marked by erythemic skin:

Correct. In the early stages of pressure injury development, the affected area may exhibit signs of tissue ischemia and inflammation, which can manifest as erythema (redness) of the skin. This erythema is a result of the body's inflammatory response to tissue damage caused by pressure and may indicate the need for intervention to relieve pressure and prevent further injury.