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1
Question:

A 25-year-old woman comes to the clinic due to a 3-month history of weight loss, irritability, insomnia, and palpitations.  Medical history is insignificant.  The patient is not currently taking any medications.  She does not use tobacco, alcohol, or recreational drugs.  Blood pressure is 155/70 mm Hg and pulse is 110/min.  Physical examination is significant for bilateral proptosis, lid retraction, warm skin, and fine tremor of the hands.  Which of the following is the most likely cause of this patient's hypertension?

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Explanation:

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Cardiovascular effects of thyrotoxicosis

Rhythm

  • Sinus tachycardia
  • Premature atrial & ventricular complexes
  • Atrial fibrillation/flutter

Hemodynamic effects

  • Systolic hypertension & ↑ pulse pressure
  • ↑ Contractility & cardiac output
  • ↓ Systemic vascular resistance
  • ↑ Myocardial oxygen demand

Heart failure

  • High-output failure
  • Exacerbation of preexisting low-output failure

Angina symptoms

  • Coronary vasospasm
  • Preexisting coronary atherosclerosis

This patient has systolic hypertension along with weight loss, tremor, and tachycardia.  The associated proptosis (due to expansion of retroorbital tissues) is a specific finding for thyrotoxicosis due to Graves disease.

Patients with thyrotoxicosis can develop cardiovascular complications due to the direct effects of excess thyroid hormone on the myocardium and vasculature, manifesting with the following hemodynamic changes:

  • Reduced systemic vascular resistance (SVR) results from direct vasodilatory effects of thyroid hormone on the endothelium (ie, peripheral vasodilation).  This decreases diastolic blood pressure.

  • Increased cardiac contractility and stroke volume result from both a direct effect of thyroid hormone on the myocardium and a reflexive response to peripheral vasodilation.  This increases pulse pressure to cause systolic hypertension.

  • Increased heart rate results from a direct effect of thyroid hormone and a reflexive response to peripheral vasodilation, and further contributes to increased cardiac output.

Cardiovascular complications of thyrotoxicosis include high-output heart failure, angina (due to increased myocardial oxygen demand), and tachyarrhythmias (eg, atrial fibrillation, atrial flutter).

(Choice A)  Long-standing hypercalcemia, as seen in hyperparathyroidism, is associated with hypertension, possibly due to effects on cardiac contractility and large artery compliance.  Thyrotoxicosis may cause hypercalcemia due to increased bone turnover, but this is generally mild and is not a significant contributor to hypertension.

(Choice C)  Increased synthesis of catecholamines is seen in certain neuroendocrine tumors (eg, pheochromocytoma), which manifest with systolic hypertension, tachycardia, and tremor, but not proptosis (which is specific for Graves disease).  Thyrotoxicosis causes increased systemic sensitivity to circulating catecholamines, but does not directly increase catecholamine synthesis.

(Choice D)  SVR is decreased in thyrotoxicosis.  In contrast, hypothyroidism (low thyroid hormone) is associated with increased SVR and elevated diastolic blood pressure.

(Choice E)  Nocturnal hypoventilation due to obstructive sleep apnea can raise blood pressure, and may be associated with symptoms including disordered sleep, irritability, and palpitations.  However, weight loss, proptosis, and tremor are more suggestive of thyrotoxicosis.

Educational objective:
Thyrotoxicosis involves direct effects of thyroid hormone on the cardiovascular system that lead to reduced systemic vascular resistance (decreased diastolic blood pressure), increased contractility and stroke volume (increased pulse pressure causing systolic hypertension), and increased heart rate.  Cardiovascular complications include high-output heart failure, angina (increased myocardial oxygen demand), and tachyarrhythmias (eg, atrial fibrillation).