Rapid Review·General Pathology
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NEOPLASIA
T1Must knowParaneoplastic Syndromes
P224
Focus on
Tumors that secrete hormones or provoke antibodies, causing disease in an organ the tumor never touched.
Key takeaways
Endocrine
- Hypercalcemia: PTHrP from squamous cell carcinoma of lung, head, or neck (also renal, bladder, breast, ovarian), or 1,25-(OH)₂ vitamin D (calcitriol) from lymphoma and granulomas.
- Cushing syndrome: ACTH from small cell lung cancer.
- SIADH with euvolemic hyponatremia: ADH from small cell lung cancer.
Hematologic
Hematologic syndromes
- Polycythemia: EPO from RCC, pheochromocytoma, HCC, hemangioblastoma, leiomyoma.
- Pure red cell aplasia: anemia with low reticulocytes, from thymoma.
- Good syndrome: hypogammaglobulinemia, also from thymoma.
- Trousseau syndrome: migratory superficial thrombophlebitis, from adenocarcinomas, especially pancreatic.
- Nonbacterial thrombotic (marantic) endocarditis: sterile platelet thrombi on heart valves, from adenocarcinomas.
Neuromuscular
- Lambert-Eaton myasthenic syndrome: antibodies against presynaptic P/Q-type Ca²⁺ channels, from small cell lung cancer. Weakness improves with use.
- Myasthenia gravis: antibodies against postsynaptic ACh receptors, from thymoma. Weakness worsens with use.
- Anti-NMDA receptor encephalitis: psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, from ovarian teratoma.
- Opsoclonus-myoclonus ataxia: "dancing eyes, dancing feet," from neuroblastoma in children and small cell lung cancer in adults.
- Paraneoplastic cerebellar degeneration: antibodies against Purkinje cells, namely anti-Hu (SCLC), anti-Yo (gynecologic and breast), anti-Tr (Hodgkin lymphoma).
Lambert-Eaton vs myasthenia gravis
| Feature | Lambert-Eaton | Myasthenia Gravis |
|---|---|---|
| Antibody target | Presynaptic P/Q Ca²⁺ channel | Postsynaptic ACh receptor |
| Tumor | Small cell lung cancer | Thymoma |
| Weakness with use | IMPROVES | WORSENS |
| Ocular/bulbar signs | Uncommon | Ptosis, diplopia, classic |
| Autonomic symptoms | Present: dry mouth, impotence | Absent |
| Reflexes | ↓, and improve after exercise | Normal |
| Response to AChE inhibitors | Poor | Good, pyridostigmine |
Skin and bone
Musculoskeletal and cutaneous syndromes
- Dermatomyositis: proximal weakness with Gottron papules and a heliotrope rash, from adenocarcinomas, especially ovarian. Antibody is anti-Jo1.
- Acanthosis nigricans: hyperpigmented velvety plaques in the axilla and neck, from gastric adenocarcinoma and other visceral malignancy.
- Sign of Leser-Trélat: sudden onset of multiple seborrheic keratoses, from GI adenocarcinoma.
- Hypertrophic osteoarthropathy: clubbing, arthralgia, periostosis of tubular bones, from lung adenocarcinoma.
A smoker with a central lung mass has a serum calcium of 13.5 mg/dL and a suppressed PTH. Which histologic type is most likely, and what is the tumor secreting?
Squamous cell carcinoma, secreting PTHrP. Small cell lung cancer is the one that secretes ACTH and ADH instead.
How it's tested
The purest mechanism question: a chronic smoker with a central lung mass, hypercalcemia, and a suppressed PTH has squamous cell carcinoma secreting PTHrP. PTHrP acts at the PTH receptor to raise calcium, and that calcium feeds back to shut off the real parathyroids, so PTH is low while calcium is high. That is what distinguishes it from primary hyperparathyroidism, where both are high.
Note the standard pairing to memorize: squamous cell gives hypercalcemia via PTHrP; small cell gives SIADH, Cushing via ACTH, and Lambert-Eaton.
Go deeper
First Aid "Paraneoplastic syndromes" table; Pathoma Ch. 3; Boards & Beyond. Anchor the two central-lung culprits (SCLC = ACTH/ADH/Lambert-Eaton; Squamous = PTHrP hypercalcemia), plus RCC → EPO polycythemia and the antibody syndromes (Lambert-Eaton = presynaptic Ca channel vs myasthenia gravis = postsynaptic ACh receptor, thymoma).
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