Thyroid/ Parathyroid Flashcards
What are the distinguishing features of Grave’s disease?
- Nervousness
- Palpitations
- Weight loss
- Fine resting tremor
- Dyspnea on exertion
- Difficulty concentrating
- Tachycardia
- Hypertension
- Heat insensitivity
- Exophthalmos
- Dry skin
- Amenorrhea
- Atrial fibrillation (irregular heart rate)
What is the most appropriate imaging in suspected Grave’s?
- Nuclear medicine thyroid scan with uptake
What is the definitive nonsurgical treatment of Grave’s?
- Thyroid ablation with radioactive iodine and often times thyroid hormone replacement
Describe the pathophysiology behind Grave’s disease.
- Autoimmune thyroid disorder where autoantibodies agains TSH receptors on the thyroid gland result in hyper functioning of the gland
What is common the demographic for Grave’s disease?
- Reproductive age females
What are the treatments for Grave’s disease?
- Antithyroid drugs => propylthiouracyl and methimazole
- Beta blockers to block the peripheral effects of excessive thyroxine
Who is radioactive iodine contraindicated in the treatment of Graves/hyperthyroidism?
- Pregnant women (these patients undergo thyroidectomy)
- Breastfeeding women
- Children
What are the most dangerous consequences of thyroid storm?
- Altered mental status, coma, seizures
What are the symptoms of thyroid storm?
- Fever
- Confusion
- restlessness
- Psychotic behavior
- Tachycardia
- Elevated BP
- Dyspnea on exertion
- Peripheral vasoconstriction
- Cerebral or cardiac ischemia
- Altered mental status, coma, seizures
What lab results would indicate hyperthyroidism?
- High free thyroxine
- Low TSH
How would Graves differ from thyroiditis on radio nucleotide imaging?
- Grave’s => Diffuse hyperactivity with large amounts of uptake due to presence of new hormone
- Thyroiditis => patchy uptake with overall reduced activity, reflecting the release of existing hormone rather than over production
How do propylthiouracil and methimazole work?
- PTU => inhibit the organification of iodine AND prevents the peripheral conversion of T4=> T3
- Methimazole => inhibit the organification of iodine
What is the most risky potential side effect of PTU and methimazole?
- Agranulocytosis
What is the treatment in thyroid storm?
- PTU
- Beta blockers
- Hydrocortisone to prevent adrenal crisis
What symptoms are observed in patients who are hypothyroid?
- Lethargy
- Weight gain
- Hair loss/thinning
- Dry skin
- Slowed mentation or forgetfulness
- Constipation
- Cold intolerance
- Depressed affect
- Low BP
- Bradycardia
- Myxedema
- Diminished relaxation of reflexes
What is the most common cause of hypothyroidism in the U.S.?
- Hashimoto thyroiditis
How would labs be different in primary hypothyroid and secondary hypothyroid?
- Primary hypothyroid => elevated TSH and low free thyroxine
- Secondary hypothyroid => lower TSH; work up to see if hypothalamic or pituitary in etiology (TRH test)
What are thyroid nodules associated with?
- Iodine deficiency
- Ingestion of goitrogens
- Increased number of pregnancies
Which type of thyroid nodule is rarely malignant?
- Hyperfunctional(hot) nodules are rarely malignant
How should nonfunctioning nodules be biopsied?
- Fine needle aspiration
Differentiate hyperparathyroidism from secondary hyperparathyroidsim, and tertiary hyperparathyroidism.
- Hyperparathyroidism: Elevated parathyroid hormone usually due to excess production by the parathyroid, leading to hypercalcemia
- Secondary hyperparathyroidism: Parathyroid glands overproduce PTH to respond to low serum calcium levels (could be due to low calcium intake or vitamin D)
- Tertiary hyperparathyroidism: Elevated PTH in patients who have renal failure
What are the cause of hypercalcemia?
- increase in calcium resorption from bone
- decreased renal excretion of calcium
- increase absorption form the GI tract
What is the role of calcitonin in calcium homeostasis?
- Calcitonin responds to increased levels of calcium and attempts to lower calcium through renal excretion and by opposing osteoclast activation
- Calcitonin in produced by the parafollicular cells of the thyroid
What is the role of PTH in calcium homeostasis?
- PTH responds to low levels of calcium by promoting osteoclast activation and increases calcium resorption from the kidneys
- PTH increases serum calcium levels but decreases phosphate levels (promotes phosphate excretion renal)
- PTH increases calcitriol (Vit D) levels which act in the GI tract to promote calcium and phosphate absorption
What is the most common cause of hypercalcemia?
- Hyperparathyroidism (in the ambulatory patient)
- Cancer is second
What are the 5 main etiologies of hypercalcemia?
- PTH related
- Malignancy
- Renal failure
- High bone turnover
- Vit D
What are the classic signs of hypercalcemia?
- Stones (nephrolithiasis)
- Bones ( bone pain)
- Psychiatric groans (poor concentration, weakness, fatigue, stupor, coma)
- Abdominal moans (abdominal pain, constipation, nausea, vomiting, pancreatitis, anorexia)
- Shortened QT
- Arrhythmias
What are examples of primary hyperparathyroidism?
- MEN I or II ( multiple endocrine neoplasia)
What types of cancers cause hypercalcemia?
- lung tumors (tumor secretes PTH-rP)
- squamous carcinoma of the head and neck
- renal carcinoma
- breast cancer
- multiple myeloma
- prostate cancer
How does vitamin A lead to hypercalcemia?
- Vitamin A (and analogs used to treat acne) causes increased bone resorption
How does granulomatous disease cause hypercalcemia?
- Granulomatous disease (TB, sarcoidosis, hodgkin disease) cause extra renal conversion of Vit D to calcitriol
Describe the labs of a patient with renal failure causing tertiary hyperparathyroidism.
- Hypocalcemia
- Hyperphosphatemia
- Low vitamin D levels
- can lead to increased PTH and hypercalcemia if left untreated
What medications are associated with hypercalcemia?
- Thiazides and Li+
