Endocrine 4 Flashcards

(45 cards)

1
Q

_________ are bone cells that promote bone deposition

A

Osteoblasts

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2
Q

__________ are bone cells that promote bone resorption

A

Osteoclasts

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3
Q

Osteoblasts add Ca2+ to the bone which

A

reduces the ionized Ca2+ concentration in the blood

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4
Q

Describe the process for decreased Ca2+ levels

A

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

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5
Q

Describe the process for increased Ca2+ levels

A

thyroid gland releases calcitonin–> osteoclast activity is inhibited–> Ca2+ reabsorption in the kidneys decreases–> ca2+ level in blood decreases

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6
Q

After the parathyroid gland is removed, a decline in ________ indicates successful removal

A

PTH level

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7
Q

Signs and symptoms of hypoparathyroidism include

A

hypotension
myocardial depression
long QT interval
tetany
seizures
paresthesias
muscle spasms
abdominal cramping

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8
Q

Signs and symptoms of hyperparathyroidism include

A

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

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9
Q

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

A

Zona fasciculata- glucocorticoids
zona glomerulosa- mineralocorticoids
zona reticularis- androgens
adrenal medulla- catecholamines

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10
Q

The adrenal gland is divided into

A

the cortex and the medulla

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11
Q

The cortex synthesizes and releases 3 classes of steroids:

A

mineralocorticoids (aldosterone)
glucocorticoids (cortisol)
androgens (sex hormones)

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12
Q

The medulla synthesizes and releases 2 cathecolamines:

A

epinephrine (80%)
norepinephrine (20%)

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13
Q

Aldosterone release is caused by

A

RAAS activation
hyperkalemia
hyponatremia

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14
Q

Aldosterone stimulates the kidney to

A

conserve sodium and water and excrete potassium and hydrogen

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15
Q

_________ increases cortisol production

A

Stress

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16
Q

Increased cortisol initiates

A

gluconeogenesis, protein catabolism, and fatty acid mobilization

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17
Q

Cortisol mitigates ____________ by reducing cytokine release

A

the inflammatory cascade

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18
Q

Cortisol imrpoves

A

myocardial performance

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19
Q

The zona glomerulosa secretes

A

mineralocorticoids

20
Q

The zone fasciculata secretes

A

glucocorticoids

21
Q

The zona reticularis secretes

22
Q

The medulla secretes

A

catecholamines

23
Q

Cortisol production is

24
Q

Normal serum cortisol levels are

25
Cortisol is required for the vasculature to respond to
the vasoconstrictive effects of catecholamines
26
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
27
What are the hemodynamic effects of cortisol?
cortisol improves myocardial performance by increasing the number and sensitivity of beta receptors on the myocardium
28
Order each drug in terms of its glucocorticoid potency dexamethasone aldosterone methylprednisolone aldosterone
dexamethasone methylprednisolone cortisol aldosterone
29
_________ has equal glucocorticoid and mineralocorticoid effects
Cortisol
30
______ does NOT have glucocorticoid effects
aldosterone
31
_________ is an analog of cortisol, making it a good choice to treat adrenocortical insufficiency (Addison's disease)
Prednisone
32
The following do NOT have mineralocorticoid effects
dexamethasone betamethasone triamcinolone
33
Triamcinolone is commonly adminsitered
in the epidural space to treat lumbar disc disease
34
Triamcinolone is unique because it is associated with
a higher incidence of skeletal muscle weakness & more likely to cause sedation and anorexia
35
What are the 3 most relevant endogenous steroids?
cortisol aldosterone cortisone
36
Primary hyperaldosteronism is caused by
excessive aldosterone release
37
Primary hyperaldosteronism is known as
Conn's syndrome
38
Etiologies of primary hyperaldosteronism include
aldosteronoma pheochromocytoma primary hyperthyroidism
39
_____________________ causes a syndrome that highly resembles hyperaldosteronism
Long-term licorice ingestion
40
Anesthetic considerations for the patient with Conn's syndrome inclue
hypertension & hypokalemia
41
What's the difference between primary and secondary hyperaldosteronism?
primary: aldosterone release from adrenal gland secondary: stimulus from extra-renal location
42
Clinical features of Conn's syndrome include
hypertension hypokalemia metabolic alkalosis (H+ wasting)
43
Treatment of Conn's syndrome includes
removal of aldosterone secreting tumor aldosterone antagonists (spironolactone or eplerenone) potassium supplementation Na+ restriction
44
S/sx of hypokalemia include
muscle weakness/cramping increased sensitivity to non-depolarizing NMBs U wave on EKG avoid hyperventilation
45
Name a cause of secondary hyperaldosteronism
renovascular hypertension