Will need more information regarding this UW question. AMBOSS says “Inflammation (e.g., COPD) → ↑ inflammatory cell infiltration of intima → thickened endothelial wall → intimal fibrosis” under 1 of the pathophysiology of pulmonary hypertension. https://next.amboss.com/us/article/w50hmg#T0X629 The term “hyperplasia” is not found on the AMBOSS page for pulmonary hypertension. FA24 p. 698 calls it “intimal fibrosis of pulmonary arteries”
This is enough to reject @DillingerMed
The rationale does not explain with evidence that UWorld says hyperplasia and not fibrosis
Without direct quotation from the UWorld question then we can’t make a change
In limited cutaneous systemic sclerosis (SSc), pulmonary hypertension is most often caused by hyperplasia of the intimal smooth muscle layer of the pulmonary arterioles and consequent increased pulmonary vascular resistance (ie, pulmonary arterial hypertension). The lung parenchyma is generally unaffected, evidenced in this patient by the absence of infiltrates on chest x-ray and normal FEV1 and FEV1/FVC ratio on pulmonary function testing (PFT).
This is the line of explanation given by UWorld
Althought I think It might simply refer to the PHTN caused by SSc and not PHTN in general so I get the rationale for rejection