Flashcards in thyroid and parathyroid Deck (39):
what stimulates the parathyroid glands to release PTH
low serum calcium
what form of calcium is sensed?
where does the increase in calcium come from?
the bone, intestine, and kidney
how does the kidney respond to PTH?
it increases its secretion of phosphate, retains calcium, produces 1, 25 hydroxyvit D, which stimulates the intestinal absorption.
how does VIt D increase calcium?
stimulates intestinal absorption and stimulates osteoclasts.
how is vit D regulated?
tightly, through the action of calcium, PTH and phosphorus
what are the most common causes of hypercalcemia?
hyperparathyroidism and malignancy
what is the first step in diagnosing hyperthyroidism
PTH levels! always first
PTH levels in primary hyperparathyroid?
high or normal
primary hyperparathyroidism characteristics and statistics ?
3:1 women, more common when 60. typically caused by hyper secretion in one or more glands. solitary adenoma 80% of the time. less common that all glands are hypertrophied.
how is primary hyperPT diagnosed on labs?
elevated calcium, elevated or normal PTH, low phosphorus, elevated urine calcium.
secondary hyperPT characteristics
perceived low calcium concentration. can occur in renal disease due to phosphate retention and lack of 1-alpha hydroxylase activity in the kidney thus a deficiency of activated Vit D.
how does high phosphorus effect the PTH system?
it will stimulate PTH secretion
what do you have to prescribe sometimes in renal disease, due to phosphorus and why?
low phosphate diet, phosphate binders, replacement of activated Vit D and dialysis.
can vitamin D deficiency cause hyperPT
yes. very common actually. need to replace sometimes.
tertiary hyperPTism characteristics and causes
PT becomes autonomous after prolonged hyperPTism. this is similar to primary, in that the gland is hyper secreting. this is different from secondary in the sense that the calcium in high, not low.
the PTH levels will be high in effort to counteract. can be caused by destruction of the parathyroid, or failure to produce. characterized by the level of PTH
PTH produced is insufficient to meet demands or is unable to function properly. usually there is a low serum calcium and low PTH.
similar to hypo but the PTH is elevated. there is a resistant state.
thyroid disease characteristics and demographics
most prevalent endocrine disorder. usually a slow and insidious process, often vague symptoms not understood by the patient. often misdiagnosed.
failure to secrete adequate amounts of hormone.
destruction of the thyroid or interference with hormone synthesis.
hypothalamic or pituitary disease.
labs for primary hypothyroidism
high TSH, low T4
labs for secondary hypothyroid
T4 low but TSH low or normal.
common causes of primary hypothyroidism
hashimotos. idiopathic (usually old hash), irradiation of the thyroid, surgical removal, fibrous thyroiditis, iodine deficiency, drug therapy, infiltrative diseases
causes of secondary hypothyroid
pituitary or hypothalamic tumor, congenital hypopituitarism, pituitary necrosis
apathetic facies, lack of eyebrows, bilateral ptosis.
risk factors for hypothyroid
age (men > 60, women >35), sex (female), goiter, history of thyroid dysfunction, family history, head/neck/thyroid surgery, autoimmune disease, drug, hypercholesterolemia
treatment for hypothyroid
levothyroxine aiming to normalize TSH.
hyper metabolic state caused by increased availability of hormone.
clinical features of hyperthyroid
nervousness, irritability, sweating, goiter, rapid HR, bulging eyes, warm moist palms, infertility, weight loss, first-trimester miscarriage. difficulty sleeping.
causes of hyperthyroidism
diffuse toxic goiter (graves), diffuse multinodular goiter, toxic adenoma.
autoimmune disorder, favors women 8:1, thyroid stimulating antibodies to the TSH receptor causes hypertrophy and hyper secretion.
ophthalmic disorder graves
true infiltrative eye disease, results in periorbital edema, conjunctival swelling and congestion, limited upward and lateral gaze, keratitis.
viral or bacterial etiology
De Quervains subacute thyroiditis
lymphocytic (painless, subacute), post-partum thyroiditis,
labs for primary hyperthyroid
suppressed TSH levels, high T4 and T3. increased radioactive iodine uptake.