The nurse assesses the wound of a client who received sutures for a laceration of the hand two days ago. Which finding is a normal inflammatory response?

Leukotrienes are inflammatory mediators derived from arachidonic acid metabolism, primarily produced by leukocytes (white blood cells) such as mast cells, eosinophils, and basophils. In the context of asthma, leukotrienes play a significant role in the pathophysiology of the disease by contributing to airway inflammation and bronchoconstriction. Here's a breakdown of their immune response:

A) Produce the sensation of itching:

Leukotrienes are not directly involved in producing the sensation of itching. Itching is often associated with histamine release rather than leukotrienes.

B) Tighten airway and produce mucous:

Correct. Leukotrienes are potent bronchoconstrictors that cause smooth muscle contraction in the airways, leading to narrowing (constriction) of the bronchioles. Additionally, they stimulate the secretion of mucus from goblet cells in the airway epithelium, contributing to airway obstruction and mucus production, which are characteristic features of asthma exacerbations.

C) Causes formation of bradykinin:

Bradykinin is a peptide mediator that is generated from the plasma protein kininogen and is involved in vasodilation, pain sensation, and inflammation. Leukotrienes are not directly responsible for the formation of bradykinin.

D) Serves as a receptor for antigen:

Leukotrienes do not serve as receptors for antigens. Instead, they are lipid mediators released in response to various stimuli, including allergens, infections, and irritants, and they act on specific receptors (e.g., leukotriene receptors) to exert their effects, such as bronchoconstriction and inflammation

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.