Endocrine 4 Flashcards
_________ are bone cells that promote bone deposition
Osteoblasts
__________ are bone cells that promote bone resorption
Osteoclasts
Osteoblasts add Ca2+ to the bone which
reduces the ionized Ca2+ concentration in the blood
Describe the process for decreased Ca2+ levels
parathyroid glands release PTH–> osteoclasts release Ca2+ from bone–> Ca2+ is reabsorbed by the kidneys–> Ca2+ absorption in the small intestine increases vitamin D synthesis–> Ca2+ level in blood increases
Describe the process for increased Ca2+ levels
thyroid gland releases calcitonin–> osteoclast activity is inhibited–> Ca2+ reabsorption in the kidneys decreases–> ca2+ level in blood decreases
After the parathyroid gland is removed, a decline in ________ indicates successful removal
PTH level
Signs and symptoms of hypoparathyroidism include
hypotension
myocardial depression
long QT interval
tetany
seizures
paresthesias
muscle spasms
abdominal cramping
Signs and symptoms of hyperparathyroidism include
hypertension
short QT interval
confusion
lethargy
psychosis
bone pain
osteopenia
pathologic fractures
muscle weakness
anorexia
N/V
abdominal pain
peptic ulcer disease
pancreatitis
polyuria
polydipsia
kidney stones
Match each region of the adrenal gland with the class of hormones it produces:
zona glomerulosa
adrenal medulla
zona reticularis
zona fasciculata
androgens
catecholamines
mineralocorticoids
glucocorticoids
Zona fasciculata- glucocorticoids
zona glomerulosa- mineralocorticoids
zona reticularis- androgens
adrenal medulla- catecholamines
The adrenal gland is divided into
the cortex and the medulla
The cortex synthesizes and releases 3 classes of steroids:
mineralocorticoids (aldosterone)
glucocorticoids (cortisol)
androgens (sex hormones)
The medulla synthesizes and releases 2 cathecolamines:
epinephrine (80%)
norepinephrine (20%)
Aldosterone release is caused by
RAAS activation
hyperkalemia
hyponatremia
Aldosterone stimulates the kidney to
conserve sodium and water and excrete potassium and hydrogen
_________ increases cortisol production
Stress
Increased cortisol initiates
gluconeogenesis, protein catabolism, and fatty acid mobilization
Cortisol mitigates ____________ by reducing cytokine release
the inflammatory cascade
Cortisol imrpoves
myocardial performance
The zona glomerulosa secretes
mineralocorticoids
The zone fasciculata secretes
glucocorticoids
The zona reticularis secretes
androgens
The medulla secretes
catecholamines
Cortisol production is
15-30 mg/day
Normal serum cortisol levels are
12 mcg/dL
Cortisol is required for the vasculature to respond to
the vasoconstrictive effects of catecholamines
How does cortisol production change in response to perioperative stress?
major perioperative stress can increase cortisol production upwards of 100 mg/day with a serum level up to 30-50 mcg/dL
What are the hemodynamic effects of cortisol?
cortisol improves myocardial performance by increasing the number and sensitivity of beta receptors on the myocardium
Order each drug in terms of its glucocorticoid potency
dexamethasone
aldosterone
methylprednisolone
aldosterone
dexamethasone
methylprednisolone
cortisol
aldosterone
_________ has equal glucocorticoid and mineralocorticoid effects
Cortisol
______ does NOT have glucocorticoid effects
aldosterone
_________ is an analog of cortisol, making it a good choice to treat adrenocortical insufficiency (Addison’s disease)
Prednisone
The following do NOT have mineralocorticoid effects
dexamethasone
betamethasone
triamcinolone
Triamcinolone is commonly adminsitered
in the epidural space to treat lumbar disc disease
Triamcinolone is unique because it is associated with
a higher incidence of skeletal muscle weakness & more likely to cause sedation and anorexia
What are the 3 most relevant endogenous steroids?
cortisol
aldosterone
cortisone
Primary hyperaldosteronism is caused by
excessive aldosterone release
Primary hyperaldosteronism is known as
Conn’s syndrome
Etiologies of primary hyperaldosteronism include
aldosteronoma
pheochromocytoma
primary hyperthyroidism
_____________________ causes a syndrome that highly resembles hyperaldosteronism
Long-term licorice ingestion
Anesthetic considerations for the patient with Conn’s syndrome inclue
hypertension & hypokalemia
What’s the difference between primary and secondary hyperaldosteronism?
primary: aldosterone release from adrenal gland
secondary: stimulus from extra-renal location
Clinical features of Conn’s syndrome include
hypertension
hypokalemia
metabolic alkalosis (H+ wasting)
Treatment of Conn’s syndrome includes
removal of aldosterone secreting tumor
aldosterone antagonists (spironolactone or eplerenone)
potassium supplementation
Na+ restriction
S/sx of hypokalemia include
muscle weakness/cramping
increased sensitivity to non-depolarizing NMBs
U wave on EKG
avoid hyperventilation
Name a cause of secondary hyperaldosteronism
renovascular hypertension
