Thyroid-Related Hypertension, Endocrine Hypertension Syndromes, Hypertension - Full Vignette with Ex

Описание: A 28-year-old pregnant woman with chronic kidney disease and hypertension presents to the emergency department with weeks of worsening headaches, palpitations, heat intolerance, unintentional weight loss, and a noticeably enlarged thyroid. Her blood pressure remains dangerously high despite medication. What underlying endocrine or systemic processes could explain her severe, refractory hypertension in the context of these symptoms and abnormal thyroid labs?

VIDEO INFO
Category: Thyroid-Related Hypertension, Endocrine Hypertension Syndromes, Hypertension
Difficulty: Moderate - Intermediate level - Requires solid foundational knowledge
Question Type: Differential Physical History
Case Type: Pregnant Patient

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QUESTION
A 28-year-old G2P1 woman at 18 weeks gestation presents to the emergency department with 3 weeks of worsening, throbbing bitemporal headaches, palpitations, heat intolerance, and an unintentional 4-kg weight loss despite increased appetite. She has noticed fine hand shaking when buttoning clothes....

OPTIONS
A. Thyrotoxicosis due to Graves disease
B. Pheochromocytoma associated with multiple endocrine neoplasia type 2
C. Superimposed early-onset pre-eclampsia on chronic hypertension
D. Renovascular hypertension secondary to fibromuscular dysplasia

CORRECT ANSWER
A. Thyrotoxicosis due to Graves disease

EXPLANATION
Suppressed thyroid-stimulating hormone, markedly elevated free thyroxine, a diffusely enlarged hypervascular thyroid with a bruit, and a thyroid-stimulating immunoglobulin (TSI) index of 450 % (reference less than 140 %) together point to newly diagnosed Graves disease causing overt thyrotoxicosis. Excess thyroid hormone raises blood pressure by up-regulating beta-adrenergic receptors, increasing cardiac output, widening pulse pressure, and secondarily activating the renin-angiotensin-aldosterone system. Normal pregnancy physiology (human chorionic gonadotropin cross-stimulation of the TSH receptor, plasma-volume expansion, and low systemic vascular resistance) amplifies these effects, so long-standing chronic hypertension and chronic kidney disease rapidly escalate into a hypertensive emergency that responds only partially to pregnancy-approved beta-blockade. Definitive control of blood pressure therefore requires treatment of the underlying hyperthyroidism, making Thyrotoxicosis due to Graves disease the most coherent single diagnosis.

Pheochromocytoma associated with multiple endocrine neoplasia type 2 is unlikely because 24-hour urinary total metanephrines are within the pregnancy-adjusted reference range and the patient lacks classic paroxysmal spells. Superimposed early-onset pre-eclampsia on chronic hypertension would require new proteinuria, thrombocytopenia, liver test abnormalities, or other organ dysfunction after 20 weeks-or, when it occurs before 20 weeks, an association with molar pregnancy or antiphospholipid antibody syndrome-none of which are present. Renovascular hypertension secondary to fibromuscular dysplasia is unsupported: renal Doppler study shows normal kidney sizes, normal peak systolic velocities, and no wave-form abnormalities, and the aldosterone-to-renin ratio is normal, indicating that renovascular activation is not occurring. These three alternatives do not simultaneously account for the biochemical, historical, and physical findings as parsimoniously as Graves disease does.


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