ATI NSG 533 ADVANCED PATHOPHYSIOLOGY EXAMS WITH 100% CERTIFIED
QUESTIONS AND DETAIL ANSWERS .
1. For what other health condition should the healthcare professional assess a patient with acute
respiratory distress syndrome (ARDS) as the priority?
A.Pneumonia
B.Heart failure
C.Pulmonary emboli
D.Acute pulmonary edema
A.Pneumonia
Pneumonia is a frequent cause of ARDS, triggering inflammation and fluid buildup in alveoli. Infection
damages alveolar-capillary barriers, reducing oxygen exchange. Assessing for pneumonia identifies the
underlying infection, guiding antibiotic therapy to halt progression, as it's a common precipitant in ARDS
cases requiring urgent intervention.
B.Heart failure
Heart failure can cause pulmonary edema, mimicking ARDS symptoms, but it's less likely the primary
trigger. ARDS stems from direct lung injury, not cardiac dysfunction. Assessing heart failure is secondary,
as it doesn't typically initiate the diffuse alveolar damage central to ARDS pathophysiology.
C.Pulmonary emboli
Pulmonary emboli obstruct blood flow, causing infarction, not diffuse alveolar damage typical of ARDS.
While emboli can worsen oxygenation, they're not a primary cause. Assessment is less urgent, as ARDS
more often follows inflammatory processes like infection rather than vascular occlusion.
D.Acute pulmonary edema
Acute pulmonary edema often results from heart failure, not ARDS. Though both involve lung fluid,
ARDS arises from non-cardiogenic injury. Assessing edema is relevant but not priority, as it's a symptom,
not the initiating condition, unlike pneumonia's direct link to ARDS onset.
,2.Around three weeks after razing an old chicken house, a 71-year-old retired farmer has developed
fever, nausea, and vomiting, diagnosed with histoplasmosis. Which physiological process is most likely
taking place?
A.Antibody production against the offending fungi is delayed by the patient's age and the virulence of
the organism
B.Macrophages are able to remove the offending fungi from the bloodstream but can't destroy them
C.Spore inhalation initiates an autoimmune response that produces the associated symptoms
D.Toxin production by Histoplasma capsulatum is triggering an immune response
A.Antibody production against the offending fungi is delayed by the patient's age and the virulence of
the organism
Delayed antibody production due to age or virulence may occur, but histoplasmosis primarily involves
cellular immunity. Macrophages engulf Histoplasma spores post-inhalation, yet in immunocompromised
states, like aging, they fail to kill the fungi, leading to dissemination and symptoms, not just a delayed
humoral response.
B.Macrophages are able to remove the offending fungi from the bloodstream but can't destroy them
In histoplasmosis, inhaled spores are phagocytized by macrophages, which clear them from blood but
can't eradicate them intracellularly. In this 71-year-old, reduced macrophage efficacy allows fungal
survival, causing systemic spread, fever, and nausea as the immune system struggles to contain the
persistent infection.
C.Spore inhalation initiates an autoimmune response that produces the associated symptoms
Spore inhalation doesn't typically trigger autoimmunity in histoplasmosis. Symptoms arise from direct
fungal infection, not an autoimmune reaction. The immune response targets Histoplasma, not self-
tissues, making this less likely than macrophage failure, which aligns with the disease's intracellular
pathogenesis.
D.Toxin production by Histoplasma capsulatum is triggering an immune response
Histoplasma capsulatum doesn't produce toxins as its primary mechanism. Symptoms result from fungal
proliferation within macrophages, not toxin-mediated immunity. While immune activation occurs, it's
driven by live fungi, not toxins, making macrophage containment failure a more accurate depiction of
the process.
, 3.What effect does atherosclerosis have on the development of an aneurysm?
A.Atherosclerosis causes ischemia of the intima
B.Atherosclerosis erodes the vessel wall
C.It increases nitric oxide
D.It obstructs the vessel
A.Atherosclerosis causes ischemia of the intima
Atherosclerosis doesn't primarily cause intimal ischemia; it involves lipid buildup and inflammation.
Ischemia affects downstream tissues, not the intima directly. While plaque narrows arteries, aneurysm
formation stems from wall weakening, not just ischemia, making this less relevant to the structural
defect.
B.Atherosclerosis erodes the vessel wall
Atherosclerosis erodes the vessel wall by degrading the media and adventitia via inflammation and
plaque growth. Lipid accumulation and macrophage activity weaken elastic fibers, increasing wall stress
and susceptibility to dilation, directly contributing to aneurysm development in arteries like the aorta.
C.It increases nitric oxide
Atherosclerosis reduces nitric oxide by damaging endothelium, impairing vasodilation. Increased nitric
oxide would protect vessels, not promote aneurysms. This contradicts the disease's effect, as
endothelial dysfunction exacerbates wall stress, not nitric oxide elevation, in aneurysm formation.
D.It obstructs the vessel
Vessel obstruction by atherosclerosis causes ischemia distally, not aneurysms. Aneurysms result from
wall weakening, not luminal blockage. While stenosis is a feature, it's the erosive, inflammatory process
within the wall that predisposes it to dilation, not mere obstruction.
QUESTIONS AND DETAIL ANSWERS .
1. For what other health condition should the healthcare professional assess a patient with acute
respiratory distress syndrome (ARDS) as the priority?
A.Pneumonia
B.Heart failure
C.Pulmonary emboli
D.Acute pulmonary edema
A.Pneumonia
Pneumonia is a frequent cause of ARDS, triggering inflammation and fluid buildup in alveoli. Infection
damages alveolar-capillary barriers, reducing oxygen exchange. Assessing for pneumonia identifies the
underlying infection, guiding antibiotic therapy to halt progression, as it's a common precipitant in ARDS
cases requiring urgent intervention.
B.Heart failure
Heart failure can cause pulmonary edema, mimicking ARDS symptoms, but it's less likely the primary
trigger. ARDS stems from direct lung injury, not cardiac dysfunction. Assessing heart failure is secondary,
as it doesn't typically initiate the diffuse alveolar damage central to ARDS pathophysiology.
C.Pulmonary emboli
Pulmonary emboli obstruct blood flow, causing infarction, not diffuse alveolar damage typical of ARDS.
While emboli can worsen oxygenation, they're not a primary cause. Assessment is less urgent, as ARDS
more often follows inflammatory processes like infection rather than vascular occlusion.
D.Acute pulmonary edema
Acute pulmonary edema often results from heart failure, not ARDS. Though both involve lung fluid,
ARDS arises from non-cardiogenic injury. Assessing edema is relevant but not priority, as it's a symptom,
not the initiating condition, unlike pneumonia's direct link to ARDS onset.
,2.Around three weeks after razing an old chicken house, a 71-year-old retired farmer has developed
fever, nausea, and vomiting, diagnosed with histoplasmosis. Which physiological process is most likely
taking place?
A.Antibody production against the offending fungi is delayed by the patient's age and the virulence of
the organism
B.Macrophages are able to remove the offending fungi from the bloodstream but can't destroy them
C.Spore inhalation initiates an autoimmune response that produces the associated symptoms
D.Toxin production by Histoplasma capsulatum is triggering an immune response
A.Antibody production against the offending fungi is delayed by the patient's age and the virulence of
the organism
Delayed antibody production due to age or virulence may occur, but histoplasmosis primarily involves
cellular immunity. Macrophages engulf Histoplasma spores post-inhalation, yet in immunocompromised
states, like aging, they fail to kill the fungi, leading to dissemination and symptoms, not just a delayed
humoral response.
B.Macrophages are able to remove the offending fungi from the bloodstream but can't destroy them
In histoplasmosis, inhaled spores are phagocytized by macrophages, which clear them from blood but
can't eradicate them intracellularly. In this 71-year-old, reduced macrophage efficacy allows fungal
survival, causing systemic spread, fever, and nausea as the immune system struggles to contain the
persistent infection.
C.Spore inhalation initiates an autoimmune response that produces the associated symptoms
Spore inhalation doesn't typically trigger autoimmunity in histoplasmosis. Symptoms arise from direct
fungal infection, not an autoimmune reaction. The immune response targets Histoplasma, not self-
tissues, making this less likely than macrophage failure, which aligns with the disease's intracellular
pathogenesis.
D.Toxin production by Histoplasma capsulatum is triggering an immune response
Histoplasma capsulatum doesn't produce toxins as its primary mechanism. Symptoms result from fungal
proliferation within macrophages, not toxin-mediated immunity. While immune activation occurs, it's
driven by live fungi, not toxins, making macrophage containment failure a more accurate depiction of
the process.
, 3.What effect does atherosclerosis have on the development of an aneurysm?
A.Atherosclerosis causes ischemia of the intima
B.Atherosclerosis erodes the vessel wall
C.It increases nitric oxide
D.It obstructs the vessel
A.Atherosclerosis causes ischemia of the intima
Atherosclerosis doesn't primarily cause intimal ischemia; it involves lipid buildup and inflammation.
Ischemia affects downstream tissues, not the intima directly. While plaque narrows arteries, aneurysm
formation stems from wall weakening, not just ischemia, making this less relevant to the structural
defect.
B.Atherosclerosis erodes the vessel wall
Atherosclerosis erodes the vessel wall by degrading the media and adventitia via inflammation and
plaque growth. Lipid accumulation and macrophage activity weaken elastic fibers, increasing wall stress
and susceptibility to dilation, directly contributing to aneurysm development in arteries like the aorta.
C.It increases nitric oxide
Atherosclerosis reduces nitric oxide by damaging endothelium, impairing vasodilation. Increased nitric
oxide would protect vessels, not promote aneurysms. This contradicts the disease's effect, as
endothelial dysfunction exacerbates wall stress, not nitric oxide elevation, in aneurysm formation.
D.It obstructs the vessel
Vessel obstruction by atherosclerosis causes ischemia distally, not aneurysms. Aneurysms result from
wall weakening, not luminal blockage. While stenosis is a feature, it's the erosive, inflammatory process
within the wall that predisposes it to dilation, not mere obstruction.
