A patient presents with a wound that has reached the dermis. Which structure is most likely to be affected?

A. Enteric nervous system:The Enteric nervous system is a mesh-like system of neurons that governs the function of the gastrointestinal tract (the "brain of the gut"). It manages digestion, not the systemic stress response.

B. Central nervous system:While the brain (specifically the hypothalamus and amygdala) perceives the threat, the execution of the physiological "fight or flight" changes (racing heart, dilated pupils) is carried out by the autonomic nerves.

C. Peripheral nervous system:Similar to Question 45, this is a broad anatomical term. While the stress response nerves are located in the periphery, the specific functional system is the Autonomic Nervous System.

D. Autonomic nervous system:The Autonomic Nervous System has two main branches: the Sympatheticand the Parasympathetic. The Sympathetic division is directly responsible for the "fight or flight" response, mobilizing the body's energy during stress.

Question: 47 of 48

A middle-aged woman has been diagnosed with a vitamin D deficiency. How does this deficiency affect her musculoskeletal system?

1. Reduced calcium absorption leading to weak bones
2. Increased muscle mass
3. Enhanced collagen production
4. Hypercalcemia due to excess calcium

Correct answer: A

A. Reduced calcium absorption leading to weak bones:The primary physiological role of Vitamin D is to facilitate the absorption of calciumin the intestines. Without sufficient Vitamin D, the body cannot absorb enough calcium from the diet. To maintain blood calcium levels, the body will then leech calcium from the bones, leading to lower bone density (osteopenia/osteoporosis) and increased fracture risk.

B. Increased muscle mass:Vitamin D deficiency is actually associated with muscle weakness and pain (proximal myopathy), not an increase in muscle mass.

C. Enhanced collagen production:Vitamin D is not a primary driver of collagen synthesis; Vitamin C is the key nutrient for collagen production.

D. Hypercalcemia due to excess calcium:A deficiency in Vitamin D leads to hypocalcemia(low calcium levels) because the gut cannot absorb it efficiently. Hypercalcemia would be a sign of Vitamin D toxicity (overdose) or hyperparathyroidism.

A. Parathyroid hormone (PTH):PTH is the principal hormone that raises blood calcium. It increases bone resorption (releasing Ca²⁺), enhances renal calcium reabsorption, and stimulates activation of vitamin D (calcitriol) in the kidney, which increases intestinal calcium absorption.

B. Thyroxine:Thyroxine (T4) regulates metabolic rate and growth. It does not play a primary role in acute regulation of serum calcium, although chronic thyroid disease can influence bone turnover indirectly.

C. Cortisol:Cortisol (a glucocorticoid) can affect bone metabolism and calcium balance with long-term excess (promotes bone resorption and can reduce calcium absorption), but it is nota primary hormone for short-term physiologic regulation of serum calcium.

D. Insulin:Insulin primarily regulates glucose uptake and metabolism; it does not directly regulate serum calcium levels.

E. Calcitonin:Secreted by the thyroid C cells, calcitonin lowers blood calcium by inhibiting osteoclast activity and decreasing bone resorption. Its role in humans is less critical than PTH for everyday calcium homeostasis, but it is a classical calcium-lowering hormone.

F. Glucagon:Glucagon primarily raises blood glucose by stimulating glycogenolysis and gluconeogenesis. It does not have a primary role in calcium regulation.