A
General effect of thyroid hormones on the body
increased metabolic state
The only compound that contributes to negative feedback in the hypothalamic-pituitary-adrenal axis:
Cortisol
Net serum effect of Vitamin D action
This is due to an increase in which compound being produced:
(Double points)
Hyper-pigmentation; a-MSH
Increased serum calcium has this effect on neuromusculature
The enzyme in the kidney responsible for creating the active form of vitamin D
1a-hydroxylase
At high concentrations, cortisol can begin to mimic the effects of this:
Mineralocorticoids (Aldosterone)
A deficiency in all three classes of Adrenal hormones is called:
Primary adrenal insufficiency or Addison's disease
Iodine enters thyroid follicular cells via this enzyme
Bonus: this enzyme can be competitively inhibited by what compounds
NIS (sodium/iodine symporter)
Bonus answer: Perchlorate anions, thiocyanate
The enzyme the transports free cholesterol from the cytoplasm of a cell to the matrix of the mitochondria, where it is acted upon by Cholesterol desmolase and turned to pregnenolone
StAR (Steroidogenic Acute Regulatory protein)
decrease
Defects in this trans-membrane protein can lead to high PTH levels in the presence of high serum calcium concentrations
Bonus: The name of the disease in which this protein^^^ is widely inactivated throughout the body
CaSR
Bonus: Familial benign hypocalciuric hypercalcemia
Name the 3 layers of the adrenal gland cortex and what type of compounds they secrete (Name all for full points):
Glomerulosa - Mineralocorticoids (Aldosterone)
Fasciculata - glucocorticoids (Cortisol)
Reticularis - Androgens (DHEA)
Myxedema, goiter, and Hypercholesterolemia can be seen in which condition:
Hypothyroidism
Excess cortisol levels cause blood glucose levels to do this:
increase
Two potential enzyme deficiencies that could cause adrenogenital syndrome (Congenital adrenal hyperplasia)
21B-hydroxylase (most common), 11B-hydroxylase (only decreases glucocorticoid levels)
Angiotensin II increases aldosterone levels by acting on which enzyme:
Aldosterone Synthase
High levels of thyroxine binding globulin will have this effect on total T3/T4, and Free T3/T4 respectively:
Bonus: Which condition can cause an increase in TBG
Increase total, no change in Free
Bonus: High estrogen, pregnancy
Three ways to manage primary hyperthyroidism
PTU (inhibits thyroid peroxidase), surgical resection, radioactive iodine (gets taken up into the thyroid cells and kills them)
three effects of PTH in the kidney
increased 1a-hydroxylase activity (more VitD), decreases Na/Pi symporter in proximal tubule (less serum phosphate), increases calcium reabsorption in distal tubule
The reason the an 11B-hydroxylase deficiency presents with hypertension, hypokalemia, and hypernatremia
DOC is still being produced in this disorder, which is a semi-potent mineralocorticoid. Increases in levels of DOC can mimic hyperaldosteronism
This hormone is increased in response to high serum phosphate levels. It's effects in the kidney are to reduce 1a-hydroxylase and Na+/Pi+ symporter activity
FGF-23
The three enzymes in the gut that are up-regulated in the presence of Vit D
calbindin, Ca-ATPase (PMCA), Na+/Pi+ symporter
Apparent Mineralocorticoid excess syndrome:
Cortisol is not inactivated in the kindeys (no conversion to cortisone), thus it can act as a mineralocorticoid (aldosterone) and increase sodium retention while also increasing secretion of H+ and K+
The expected TSH levels in someone with Hashimoto's Thyroiditis
High TSH