Regarding alveolar cells, which statement is INCORRECT?

Correct Answer: D

Rationale: Choice E is incorrect (assuming typo for D); Type II pneumocytes, not membranous, are cuboidal and produce surfactant, not Type I (flat, gas exchange). Choice A is false but not the focus; Type II repair epithelium post-injury, not Type I. Choice B is true; macrophages arise from monocytes. ' mast cells bind IgE via Fc receptors. Choice D is accurate; APUD cells (e.g., Kulchitsky) are endodermal. Type II cells' role in surfactant (e.g., DPPC) and repair distinguishes E's mischaracterization as the error.

Correct Answer: A

Rationale: To assess flu risk in a coughing, febrile deaf client, the nurse needs the vaccination history, symptom duration, and exposure details. Vaccination history reveals immunity status unvaccinated clients face higher risk, critical with current symptoms. Symptom duration indicates illness progression, helping gauge severity or complications. Known exposure pinpoints infection likelihood, especially in flu season. Deafness duration is irrelevant it's a communication factor, not a flu risk. Causative factors of deafness don't affect flu susceptibility. The nurse, via the interpreter, focuses on these questions to build a risk profile, tailoring care (e.g., antivirals) to the client's presentation and history, ensuring effective management despite communication barriers, aligning with comprehensive health assessment principles.

Correct Answer: A

Rationale: The nurse explains that influenza contagiousness spans 24 hours before symptoms to 5 days after onset, per CDC data, reflecting the virus's shedding pattern highest early but persisting as the body clears it. This informs the client to isolate effectively, protecting others, especially vulnerable contacts. Being contagious only with fever is false viral shedding occurs without fever, especially later. Ten days overestimates typical shedding (up to 7 days in some, not standard), risking unnecessary isolation. Until feeling better is vague contagiousness ties to virology, not subjective wellness. This precise timeline empowers the client to manage transmission, balancing recovery with public health, critical in flu's rapid spread scenarios.

Correct Answer: B

Rationale: Asthma (B) does not cause compressive atelectasis; it leads to resorption atelectasis via mucus plugs obstructing airways, trapping gas that's resorbed, collapsing alveoli. Compressive atelectasis results from external pressure on lung tissue. Pneumothorax (A) compresses lung via air in the pleural cavity. Congestive cardiac failure (C) causes fluid buildup (e.g., pleural effusion or pulmonary edema), compressing alveoli. Pleural effusion (D) collapses lung via fluid pressure. Peritonitis (original E) elevates the diaphragm, compressing lungs. Page 714 notes compression atelectasis shifts mediastinum away from the affected lung, unlike resorption's shift toward it. Asthma's mechanism bronchial obstruction differs from the external compression of A, C, D, relying on mucus rather than pleural or parenchymal pressure, making B the exception.

Correct Answer: D

Rationale: Increased mucosal gland depth (Reid index) (D) is a major morphological change in chronic bronchitis'. Choice A (lymphocyte infiltration) is true but less dominant. Choice B is false; goblet cells increase, especially in small airways. Choice C (smooth muscle hypertrophy) is asthma-related. Choice E (normal Reid index 0.4) is incorrect; it rises in disease. Page 722 emphasizes D's gland hyperplasia measured as gland-to-wall thickness ratio as the primary structural shift from chronic irritation, driving mucus production, unlike B's decrease or C's misplacement.