Medical Knowledge 6 Flashcards

A 58-year-old diabetic patient presents with a painless, punched-out ulcer on the plantar surface of the foot with surrounding callus formation. Peripheral pulses are intact. Which pathophysiological mechanism is primarily responsible for this presentation?

Answer: Peripheral neuropathy causing loss of protective sensation

The description — painless plantar ulcer with surrounding callus and intact pulses — is classic for a neuropathic (diabetic) foot ulcer. Diabetic peripheral neuropathy causes loss of protective sensation, allowing repetitive pressure trauma to go unnoticed, leading to callus buildup and eventual ulceration. Ischemic ulcers are typically painful, occur at distal tips or pressure points, and are associated with absent pulses.

Which of the following best describes the mechanism of action of metformin in type 2 diabetes mellitus?

Answer: Activates AMPK, primarily reducing hepatic glucose production

Metformin activates AMP-activated protein kinase (AMPK), which suppresses hepatic gluconeogenesis and glycogenolysis — its primary glucose-lowering mechanism. It also modestly improves peripheral insulin sensitivity. It does not stimulate insulin secretion (no hypoglycemia risk when used alone), unlike sulfonylureas. Alpha-glucosidase inhibitors (e.g., acarbose) and SGLT-2 inhibitors (e.g., empagliflozin) describe entirely different drug classes.

A 45-year-old woman presents with progressive dyspnea, bilateral leg edema, and elevated jugular venous pressure. Echocardiography shows a reduced ejection fraction of 30%. Which neurohormonal pathway is most inappropriately activated in this condition and is a primary target of therapy?

Answer: Renin-angiotensin-aldosterone system (RAAS)

In heart failure with reduced ejection fraction (HFrEF), the RAAS is pathologically activated: low cardiac output triggers renin release, generating angiotensin II (vasoconstriction, aldosterone release, sodium retention) and worsening the cardiac remodeling cycle. ACE inhibitors, ARBs, and ARNIs (sacubitril/valsartan) all target this axis and are cornerstone therapies. While the sympathetic nervous system is also activated (targeted by beta-blockers), the RAAS is the most 'inappropriately' activated classic neurohormonal axis in this context.

A neonate born at 28 weeks gestation develops increasing respiratory distress within 4 hours of birth, with grunting, nasal flaring, and intercostal retractions. Chest X-ray shows diffuse ground-glass opacities with an air bronchogram pattern. What is the underlying deficiency causing this condition?

Answer: Pulmonary surfactant

This is classic neonatal respiratory distress syndrome (RDS), caused by surfactant deficiency in premature infants. Surfactant (produced by type II pneumocytes from around 24–28 weeks gestation) reduces alveolar surface tension and prevents alveolar collapse. Without it, atelectasis and diffuse alveolar collapse cause the characteristic ground-glass appearance on X-ray. Treatment includes exogenous surfactant replacement and antenatal corticosteroids to accelerate lung maturation.

A 67-year-old man with a 40-pack-year smoking history presents with a 3-month history of hemoptysis, weight loss, and a right-sided Horner syndrome (ptosis, miosis, anhidrosis). Chest CT reveals an apical right lung mass. Which specific tumor type and location best explains this constellation of findings?

Answer: Pancoast (superior sulcus) tumor invading the cervical sympathetic chain

A Pancoast tumor (superior sulcus tumor) is a lung cancer arising at the apex of the lung. As it grows, it can invade the brachial plexus, subclavian vessels, and the cervical sympathetic chain (stellate ganglion), causing ipsilateral Horner syndrome. The triad of apical lung mass + shoulder/arm pain + Horner syndrome is called Pancoast syndrome. Squamous cell carcinoma is the most common histological type, though adenocarcinoma can also occur at this site.

Which of the following laboratory findings is most characteristic of disseminated intravascular coagulation (DIC) compared to liver failure alone?

Answer: Elevated D-dimer with low fibrinogen

Both DIC and liver failure can cause prolonged PT/aPTT and thrombocytopenia, making them difficult to distinguish. The key differentiating feature of DIC is markedly elevated D-dimer (reflecting active fibrinolysis of cross-linked fibrin clots) combined with low fibrinogen (consumed in widespread clotting). In liver failure, fibrinogen is typically low due to reduced synthesis, but D-dimer elevation is far more pronounced and consistent in DIC due to pathological systemic clot formation and degradation.