ACSM-EP Pathophysiology 5

Question 1

Which pathophysiological mechanism explains why fibromyalgia patients experience widespread pain hypersensitivity?

Accepted Answer

Central sensitization with amplified pain signaling in the spinal cord and brain

Answer

Fibromyalgia involves central sensitization where the central nervous system amplifies nociceptive signals, causing widespread pain disproportionate to peripheral stimuli.

Question 2

In a patient with stroke resulting in hemiplegia, which secondary musculoskeletal pathology is most likely to develop without proper exercise intervention?

Accepted Answer

Disuse atrophy and spastic contracture in the affected limbs

Answer

Upper motor neuron lesions from stroke cause spasticity and paresis; without movement, muscles atrophy and spastic muscles shorten into contractures limiting joint range of motion.

Question 3

Which physiological abnormality is the primary driver of exercise intolerance in patients with systolic heart failure?

Accepted Answer

Severely reduced cardiac output reserve due to depressed left ventricular contractility

Answer

Depressed left ventricular systolic function limits the heart's ability to increase stroke volume and cardiac output during exercise, creating the primary ceiling on aerobic capacity.

Question 4

A 45-year-old woman with polycystic ovary syndrome (PCOS) presents for exercise programming. The EP should be aware that PCOS most commonly involves which pathophysiological process?

Accepted Answer

Insulin resistance and hyperandrogenism affecting metabolic and reproductive function

Answer

PCOS is characterized by insulin resistance, compensatory hyperinsulinemia, and excess androgen production, predisposing women to metabolic syndrome and type 2 diabetes.

Question 5

Which pathological change in atherosclerosis is most responsible for acute myocardial infarction rather than stable angina?

Accepted Answer

Fibrous cap rupture triggering complete thrombotic occlusion of the coronary artery

Answer

Acute MI occurs when a vulnerable plaque's thin fibrous cap ruptures, exposing thrombogenic lipid core contents that trigger rapid platelet aggregation and complete vessel occlusion.

ACSM Practice Test

ACSM Practice Test

ACSM-EP Pathophysiology 5