The nurse admits a client with sepsis that has developed cool ecchymotic fingertips and toes. The healthcare provider (HCP) determines that the client has developed disseminated intravascular coagulation (DIC). Which findings support the pathophysiology of DIC?

Choice A reason: Pre-existing skin organisms, like Staphylococcus, colonize burn wounds and eschar, thriving in damaged tissue with impaired barriers. Burns disrupt skin integrity, allowing microbial invasion and biofilm formation, increasing infection risk. This is a primary reason for burn wound infections, supported by wound care microbiology.

Choice B reason: Burned epithelium loses its ability to produce antimicrobial peptides, which normally inhibit bacterial growth. This reduction weakens local defenses, allowing pathogens to proliferate in the wound. Compromised epithelial function is a key factor in burn infections, as it diminishes the skin’s innate immune response.

Choice C reason: Increased basal metabolic rate and heat radiation in burns elevate systemic stress but do not directly cause wound infections. While metabolism impacts healing, it is not a primary infection driver. Local factors like microbial colonization and loss of skin barriers are more directly responsible for burn wound infections.

Choice D reason: The skin’s acidic pH, which inhibits bacterial growth, is compromised in burns due to tissue destruction. This loss of the protective acid mantle allows pathogens to invade more easily, increasing infection risk. This is a critical pathophysiological reason for burn wound susceptibility, per dermatological infection models.

Choice E reason: Loss of serum proteins in burns, due to exudative leakage, impairs humoral immunity, including complement and antibody function. This weakens systemic defenses against wound pathogens, increasing infection risk. Protein loss is a recognized factor in burn-related immunosuppression, contributing to the high incidence of wound infections.

Choice A reason: Decreased red blood cell count indicates anemia, which may cause fatigue or exacerbate ischemia but is not a direct marker of atherosclerosis. Angina results from arterial plaque buildup, driven by elevated LDL cholesterol. Low RBCs do not contribute to plaque formation, making this inconsistent with the diagnosis.

Choice B reason: Elevated LDL cholesterol is a primary risk factor for atherosclerosis, as it deposits in arterial walls, forming plaques that narrow coronary arteries, causing angina. In overweight smokers with stress, high LDL is a key driver of cardiovascular disease, directly supporting the pathophysiology of angina, per evidence-based lipid guidelines.

Choice C reason: Decreased triglycerides are not associated with atherosclerosis, which is driven by high LDL and low HDL. Triglycerides contribute to cardiovascular risk when elevated, but low levels do not cause angina. Elevated LDL is the critical lipid abnormality in this client’s angina due to coronary artery narrowing.

Choice D reason: Increased HDL cholesterol is protective against atherosclerosis, as it removes cholesterol from arteries, reducing plaque formation. Angina is associated with low HDL and high LDL. High HDL would mitigate, not cause, the client’s condition, making this inconsistent with the diagnosis of atherosclerosis-induced angina.