Pathophysiology for Endocrine Flashcards
What would lab results show in primary hyperparathyroidism?
high PTH
high serum Ca2+
low serum Pi
high vitamin D (active form)
hypercalcemia & hypophosphatemia (due to tumor on parathyroid gland so keeps producing PTH)
What would lab results show in 21B hydroxylase deficiency?
low cortisol
low mineralcorticoids
high androgens
high ACTH
extreme sexual characteristics, hyperkalemia & hypoglycemia
**most common enzyme deficiency
What would lab results show in 11B hydroxylase deficiency?
high mineralcorticoids (DOC) low cortisol low aldosterone high androgens high ACTH
**still have mineralcorticoids that increase Na+ reabsorb & increase K+ & H+ secretion (hypokalemia)
What would lab results show in 17alpha hydroxylase deficiency?
low androgens
low cortisol
high aldosterone
high ACTH
excess mineralcorticoids can cause increase in BP & hypokalemia
What would lab results show in primary hypercortisolism?
high cortisol
low ACTH
low CRH
due to overproduction of cortisol by adrenal gland (ACHT independent) so still get negative feedback of cortisol on pituitary
What would lab results show in secondary hypercortisolism?
high cortisol
high ACTH
low CRH
hyperpigmentation due to increased ACTH
What would lab results show in primary cortisol deficiency?
adrenal gland insufficiency:
low cortisol low aldosterone high CRH high ACTH hyperpigmentation
What would lab results show with steroid administration (exogenous glucocorticoids)?
low CRH
low ACTH
low cortisol
**w/ symptoms of excess
What would lab results show in secondary cortisol deficiency?
low cortisol
low ACTH
high CRH
normal aldosterone
What is the cause of Cushing’s disease? What would the lab results show?
pituitary tumor
high cortisol
high ACTH
low CRH
What is the cause of Addison’s disease?
primary adrenal insufficiency
autoimmune destruction of all zones of adrenal cortex (decreased synthesis of all hormones from cortex)
What would lab results show in primary hyperaldosteronism?
high aldosterone
low plasma renin
hypertension, hypokalemia
What is another name for primary hyperaldosteronism?
Conn’s syndrome (excessive release of aldosterone from adrenal cortex…issue @ zona glomerulosa)
CoNNNNNN (extra Na+)
What would lab results show in secondary hyperaldosteronism?
high aldosterone
high plasma renin
hypertension, hypokalemia (due to excessive renin secretion by juxtaglomerular cells in kidney)
What would lab results show in hypoaldosteronism?
low aldosterone
low plasma Na+
hypotension
*if affects glucocorticoid synthesis, will lead to decrease in cortisol production & cause increase in ACTH (hyperpigmentation)
What would lab results show if pt has pheochromocytoma?
adrenal medulla tumor that causes increase in production of catecholamines
high epi
high norepi
headaches, palpitations, sweating, hypertension
What can block synthesis of thyroid hormone & at which part of the process?
Perchlorate & Thiocynate: NIS (Na+ & I- co transport)
PTU: blocks all steps catalyzed by peroxidase (1st blocks organification of I)
Diodinase: mimics dietary I- deficiency b/c blocks recycling of MIT & DIT
mutation in PDS gene: affects Pendrin channel would block transport of I2 into lumen of follicle
What is Wolff-Chaikoff syndrome?
effect of high I- levels that inhibits organification & synthesis of thyroid hormones
What would lab results show with high TBG?
When would you see high TBG?
increased T4
decreased T3 resin uptake
occurs in pregnancy
What would lab results show with low TBG?
When would you see low TBG?
decreased T4
increased T3 resin uptake
hepatic failure
What would lab results show in Grave’s disease?
high serum T4/T3
low TSH
circulating thyroid-stimulating immunoglobs*
goiter & exopthalmos
pregnancy
What would lab results show in Hashimoto’s?
low serum T4/T3
high TSH
circulating TRG or TPO antibodies (impairs thyroid hormone synthesis)
goiter
What would lab results show in I- deficiency?
low serum T4/T3
high TSH
goiter
What would lab results show in Sheehan syndrome?
symptoms of hypothyroidism (disease of pituitary gland that blocks TSH secretion): low T4/T3 and low TSH
NO goiter b/c no TSH (pt also presents w/ issue in lactation, amenorrhea, etc)
What would lab results show in primary hyperparathyroidism?
high PTH
high serum Ca2+
low serum Pi
high vitamin D
adenoma on parathyroid gland causes unregulated secretion of PTH
hypercalcemia, hypophosphatemia
What would lab results show in secondary hyperparathryoidism? (if due to renal failure)
high PTH
low Ca2+
high Pi
low vitamin D
What would lab results show in secondary hyperparathyroidism? (if due to vit D deficiency)
high PTH
low serum Ca2+
low serum Pi
low vitamin D
What would lab results show in hypoparathyroidism?
low PTH
low serum Ca2+
high serum Pi
low vitamin D
hypocalcemia & hyperphosphatemia
What would lab results show in vitamin D deficiency?
high PTH low Ca2+ low Pi (serum) high Pi & cAMP (in urine) low active & precursor vit D in serum
What would lab results show in pseudo-hypoparathyroidism type 1a
high PTH
low Ca2+
high Pi
low vitamin D
PTH resistance (PTH cannot work @ its receptor to induce translation of its message via AC in bone & kidney cells)
What would lab results show in humoral hypercalcemia of malignancy?
low PTH
high Ca2+
low Pi
low vitamin D
tumor makes PTHrP that mimics PTH so leads to increase in Ca2+ that negatively feeds back onto endogenous PTH levels
What would lab results show in hypocalciuric hypercalcemia?
normal PTH
high serum Ca2+
low urine Ca2+
normal Pi & vitamin D
CaSR on PTH gland & in kidney can’t sense changes in Ca2+ so thinks that Ca2+ is low
What can cause issues in vitamin D metabolism?
dietary deficiency of vitamin D
deficit in synthesis of active vitamin D (no 1 alpha hydroxylase)
vitamin D resistance (@ its receptor)
What would lab results show in rickets?
low Ca2+ & low Pi
depends if @ 1 alpha hydroxylase or vitamin D receptor
What would lab results show in osteomalacia?
low Ca2+ & low Pi
bone pain/muscle weakness
bone tenderness
fracture
muscle spasms
What would lab results show for a pt with an ectopic-ACTH secreting tumor?
high cortisol
low ACTH (coming from pit)
low CRH
NO hyperpigmentation