Which of the following bones is part of the axial skeleton?

Correct Answer: C

Rationale: The sternum, or breastbone, is part of the axial skeleton, anchoring ribs to protect thoracic organs. Humerus and femur are appendicular (limbs). Scapula is pectoral girdle, appendicular. Sternum's axial role, per skeletal framework, makes 'c' correct.

Correct Answer: C

Rationale: The skull is axial, not appendicular, which includes limbs and girdles (humerus , clavicle , femur ). Skull's midline role contrasts with appendicular's limb focus, per skeletal division, making 'c' correct.

Correct Answer: A

Rationale: Cancer cells lack differentiation, remaining unspecialized and 'generic,' unlike normal cells (e.g., liver cells) with specific roles, driving uncontrolled growth. They retain reproduction , often excessively, and responsiveness to some signals, not both . Loss of differentiation, a hallmark of cancer per pathology, makes 'a' correct.

Correct Answer: B

Rationale: The heart lies in the mediastinum, a central thoracic cavity subdivision between the lungs, housing heart and vessels. Cranial cavity holds the brain, posterior/dorsal includes spinal/brain cavities not heart. Not all only mediastinum fits. Its thoracic centrality, per anatomy, makes 'b' correct.

Correct Answer: C

Rationale: Myasthenia gravis causes muscle weakness by reducing acetylcholine receptors at the neuromuscular junction. Autoantibodies attack these receptors, impairing signal transmission from motor neurons to skeletal muscle, leading to fatigue, especially in facial and limb muscles. Muscle dystrophy involves progressive fiber degeneration, not receptor loss. Intermittent claudication stems from vascular insufficiency, weakening muscles via oxygen deprivation, not neurotransmission. Tetanus, from bacterial toxin, causes rigid contractions, not weakness, by overstimulating neurons. Fibromyositis (likely fibromyalgia) involves pain and stiffness, not receptor deficits. In myasthenia gravis, the postsynaptic membrane's receptor scarcity confirmed by immunological and electromyographic studies disrupts voluntary movement, often relieved by acetylcholinesterase inhibitors boosting acetylcholine. This autoimmune mechanism contrasts with structural or infectious muscle disorders, highlighting a specific synaptic failure. Clinical data show receptor density dropping 70-90% in affected junctions, underscoring its unique pathophysiology among neuromuscular diseases.