A 28-year-old African American woman presents to her primary care physician with two weeks of nausea, abdominal pain, and increased urination. She states she has had kidney stones in the past and is concerned because her current pain is different in character from what she had experienced then. In addition she reports increasing weakness and fatigue over the past several months as well as mild shortness of breath. Chest radiography shows bilateral hilar adenopathy. Which of the following processes is most likely responsible for her current symptoms?

Increased intestinal absorption of calcium

Osteoclast-driven bone resorption

Ectopic parathyroid hormone release

Increased production of parathyroid hormone

Increased renal calcium reabsorption

A 72-year-old man who was involved in a traffic collision is brought to the emergency room by the ambulance service. He was in shock and comatose at the time of presentation. On examination, the heart rate is 60/min, and the blood pressure is 70/40 mm Hg. The patient dies, despite resuscitative efforts. Autopsy reveals multiple internal hemorrhages and other evidence of ischemic damage affecting the lungs, kidneys, and brain. The patient’s heart shows evidence of gross anomaly similar to the picture. While acute hypovolemia is the likely cause of the ischemic changes seen in the lungs, kidneys, and brain, which of the following best explains the gross anomaly of his heart?

Senile calcific aortic stenosis

Accumulation of amyloid in the myocardium

A 65-year-old man comes to the physician for evaluation of a neck mass and weight loss. He first noticed the growing mass 2 months ago. The mass is not painful. He also has decreased appetite and intermittent abdominal pain. He has lost 10 kg (22 lb) of weight over the past 3 months. Sometimes, he wakes up in the morning drenched in sweat. He takes daily over-the-counter multivitamins. He appears pale. His pulse is 65/min, blood pressure is 110/70 mm Hg, and temperature is 38.1°C (100.6°F). Physical exam shows a painless, golf ball-sized mass in the anterior triangle of the neck. A biopsy shows large cells with a bilobed nucleus that are CD15-positive and CD30-positive. Laboratory analysis of serum shows a calcium level of 14.5 mg/dL and a parathyroid hormone level of 40 pg/mL. Which of the following is the most likely explanation of this patient's laboratory findings?

Ectopic PTH-related protein production

Pathologic calcification for USMLE Step 2 CK: High-Yield Pathology Lessons

Pathologic Calcification - Stone-Cold Facts

Dystrophic Calcification: Deposition in damaged or necrotic tissue despite normal serum Ca2+ levels.
- Examples: Atherosclerosis, aging/damaged heart valves, caseous necrosis in TB.
Metastatic Calcification: Deposition in normal tissue due to hypercalcemia (↑ serum Ca2+).
- Examples: Hyperparathyroidism, sarcoidosis, vitamin D toxicity. Affects kidneys, lungs, gastric mucosa.

⭐ Psammoma bodies are lamellated calcifications seen in Papillary thyroid carcinoma, Serous cystadenocarcinoma of ovary, Meningioma, and Mesothelioma (PSaMMoma).

Dystrophic Calcification - Damage Deposits

Pathogenesis: Calcium deposition in damaged, dying, or necrotic tissue, occurring despite normal serum calcium and phosphate levels. It is a common indicator of previous cell injury.
Mechanism:
- Initiation: Begins in the mitochondria of dying cells that accumulate calcium due to membrane damage and loss of calcium regulation.
- Propagation: Phosphatases in vesicle membranes bind calcium, creating a nidus for further calcium phosphate crystal formation and deposition.
Morphology:
- Grossly: Fine, white, gritty granules or clumps.
- Microscopically: Basophilic, amorphous, granular clumps. Can form lamellated psammoma bodies.
Clinical Examples:
- Atherosclerosis plaques
- Aging or damaged heart valves
- Caseous necrosis in tuberculosis

Pathogenesis of dystrophic calcification in aortic valve

⭐ Key Distinctor: Dystrophic calcification occurs with normal serum calcium levels, differentiating it from metastatic calcification, which is driven by hypercalcemia.

Metastatic Calcification - Systemic Stones

Pathogenesis: Deposition of calcium salts in previously normal tissue, driven by a systemic mineral imbalance.
Core Defect: Always secondary to hypercalcemia (↑ serum Ca²⁺). Normal serum calcium is 8.5-10.2 mg/dL.
Mechanism: ↑ serum Ca²⁺ leads to an elevated calcium-phosphate product, causing precipitation in tissues with alkaline environments.
Major Causes of Hypercalcemia:
- Hyperparathyroidism: Primary (adenoma) or secondary (renal failure).
- Bone Resorption: Malignancy (myeloma, PTHrP), Paget disease, immobilization.
- Vitamin D Disorders: Intoxication, sarcoidosis (macrophage activation of Vit D).
Favored Tissues (lose acid → alkaline pH):
- Kidneys (nephrocalcinosis)
- Lungs (alveolar septa)
- Stomach (gastric mucosa)

Metastatic calcification in lung, kidney, and stomach

⭐ In contrast to dystrophic calcification, which is often incidental, metastatic calcification can cause significant organ dysfunction, such as renal failure from extensive nephrocalcinosis.

High‑Yield Points - ⚡ Biggest Takeaways

Dystrophic calcification deposits in damaged or necrotic tissue with normal serum calcium.

Metastatic calcification deposits in normal, living tissue due to hypercalcemia.

Dystrophic sites include atherosclerotic plaques, aging heart valves, and caseous necrosis.

Metastatic sites include kidneys (nephrocalcinosis), lungs, and gastric mucosa.

Psammoma bodies are lamellated calcifications seen in papillary thyroid carcinoma, meningioma, and serous ovarian tumors.

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Pathologic calcification