The infection control nurse is talking about the history of the H1N1 influenza. The nurse points out that the virus had genes from more than one source. What sources contributed to the H1N1 virus? (Select all that apply.)

Correct Answer: D

Rationale: The 2009 H1N1 influenza virus was a reassortant strain with genes from pig (swine flu viruses), bird (avian influenza), and human sources, reflecting its zoonotic origins. Pigs act as ‘mixing vessels,' allowing genetic exchange between flu strains from different species, which occurred here, creating a novel virus that jumped to humans. Bird genes contributed via prior avian flu strains, while human genes enabled efficient human-to-human transmission, fueling the pandemic. Cat-derived flu genes aren't documented in H1N1's makeup felines aren't typical influenza reservoirs. Pig genes alone don't tell the full story; it's the combination that matters. The nurse educates on this multi-species origin to highlight how influenza evolves, emphasizing vigilance for zoonotic threats, a key infection control lesson from H1N1's global spread, informing strategies like surveillance and vaccination.

Correct Answer: D

Rationale: ARDS lungs can be divided into infiltrated, consolidated, or collapsed areas (D), reflecting heterogeneous damage'. Choice A is false; abnormalities are not homogeneous some areas are spared, others severely affected. Choice B is incorrect; pneumonia often complicates fatal cases due to impaired clearance. Choice C is wrong; ARDS is typically unresponsive to O₂ therapy due to shunting (mortality ≈60%, not 20%). Choice E (60% mortality) is true but not listed. Page 716 notes ARDS's patchy nature ventilation-perfusion mismatch and fibrosis making D's regional division accurate, unlike A's uniformity or B's infection protection.

Correct Answer: B

Rationale: Nonatopic asthma has normal serum IgE levels (B), emphasizing bronchial hyperresponsiveness. Choice A is false; it's typically viral-triggered, not bacterial. Choice C is incorrect; skin tests are negative (no atopy). Choice D is wrong; occupational asthma is atopic (allergen-driven). Choice E (intrinsic label) is true but not listed. Page 726 details B's distinction lacking IgE elevation, it contrasts with atopic asthma's allergic basis, relying on mucosal inflammation lowering vagal receptor thresholds, unlike C's test results or D's category.

Correct Answer: B

Rationale: The most dangerous inhaled particles are 1-5 μm (B), reaching alveoli to cause fibrosis. Choice A is false; cases decline in the West due to regulation. Choice C is incorrect; larger particles (>10 μm) are filtered, causing less injury than 1-5 μm. Choice D is wrong; silica activates macrophages, releasing fibrogenic mediators (e.g., TNF), not inhibits. Choice E (not all exposed develop disease) is true. Page 733 confirms B's size range optimal for deep penetration and inflammation, unlike A's trend or D's mechanism.

Correct Answer: C

Rationale: Histologically, pulmonary alveolar proteinosis (PAP) shows acellular surfactant accumulation (C), not cellular exudate. Choice A is false; acquired PAP is most common. Choice B is true; acquired PAP is autoimmune (anti-GM-CSF). Choice D is incorrect; secondary PAP (e.g., silicosis) is rare. Choice E (congenital fatal) is true. Page 741 details C's morphology alveolar spaces fill with lipoproteinaceous material, contrasting with A's prevalence or D's frequency error.