Endocrine Flashcards
How does the hypothalamus communicate with the anterior pituitary gland?
Hormones are released into the hypophyseal portal vessels. Transported along the pituitary stalk.
How does the hypothalamus communicate with the posterior pituitary gland?
Supraoptic nuclei - ADH
Paraventricular nucleus - PITOCIN (OXYTOCIN)
Travel along pituitary stalk via nervous system
Where is the pituitary gland located? What is another name for the anterior and posterior pituitary gland?
Resides in the sella turcica.
Ant pit = adenohypophysis
Post pit = neurohypophysis
What hormones are released from the anterior pituitary gland?
FLAT PiG
FSH
LH
ACTH
TSH
Prolactin
ignore
GH
What is the function of FSH
girls - ovarian follicle growth
both boys & girls - germ cell maturation
LH function
girls - ovulation
males - testosterone production
ACTH function
adrenal hormone release
SIADH vs DI causes
SIADH = TBI, cancer, noncancerous lung dx, carbamazepine
DI = pituitary surgery, TBI, SAH
SIADH treatment
fluid restriction
demeclocycline (decreases responsiveness to ADH)
sodium
DI treatment
DDAVP or vasopressin
supportive
Anesthetic implications for acromegaly
DAW
Subglottic narrowing
Turbinate enlargement
OSA
HTN, CAD, rhythm disturbances
Glucose intolerance
Sk. muscle weakness
T4
Directly released from the thyroid
-T4 = delivery vehicle
-lots of protein binding
-less potent
-1/2 life = 7 days
T3
Triiodothyronine
Small amount is released from the thyroid.
In the target cell, T4 is converted to T3.
Less protein binding but more potent
Half-life is only 1 day
How does iodine deficiency affect T3 and T4
TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize T3&T4.
How does the thyroid hormone affect MAC?
IT DOES NOT
Hyperthyroidism = increased CO = decreased rate of inhalational induction
What is the most common etiology of hyperthyroidism
Graves = #1
MG
Goitor
Carcinoma
Preggo
Pituitary Adenoma
Amio
What is the most common cause of hypothyroidism
Hashimoto’s thyroiditis
-iodine
-HPA dysfunction
-neck radiation
-thyroidectomy
-amio
List 3 thionamides that can be used to treat hyperthyroidism. What is MOA
PTU, methimazole, carbimazole
-Inhibit thyroid synthesis by blocking iodine addition to the tyrosine residues.
-PTU also inhibits T4 - T3 conversion in the periphery
NEED 6 - 7 WEEKS FOR A EUTHYROID STATE
What are the contraindications to radioactive iodine
Pregnancy
Breast feeding mothers
When is it ok for hyperthyroid pt to undergo surgery?
never if elective
if emergent, admin a BB, potassium, glucocorticoid, PTU
What anesthetic agent should be avoided in the hyperthyroid pt?
Sympathomimetics, anticholinergics, ketamine, pancuronium
Discuss thyroid storm
most commonly occurs 6-18 hours following surgery or infection
Block synthesis (methimazole, carbimazole, PTU, potassium iodine) , block release (iodine), block conversion (PTU, propanolol, glucocorticoids), block beta receptors
when does hypocalcemia present s/p thyroidectomy
6-12 hours
prolonged QT, hypotension, tetany, changes in mental status, laryngospasm
Zones of adrenal glands
GFR
Zona glomerulosa (salt) - mineralocorticoids
Zona fasciculata (sugar) - glucocorticoids
Zona reticularis (androgens)
How much cortisol is produced per day
15 - 30 mg/day
Normal = 12 mcg/dL
Surgery - 100 mg/day, 30 - 50 mcg/dL
Which steroids has no glucocorticoid effects/
ALDOSTERONE
-mineralocorticoid effect = 3000x
-DOA = 24 hours
Which steroids have no mineralocorticoid effects?
Decadron (25x glucocorticoid effect) = 0.75 mg = 36 - 54h DOA
Betamethasone (25x) = 0.75 = 36 - 54h
Triamcinolone (5x) = 4 = 12 - 36h
Conn’s Syndrome
TOO MUCH ALDOSTERONE
-Primary - increased from adrenal gland
-Secondary - increased renin or aldosterone tumor
HTN, Hypokalemia, Metabolic Alkalosis (H+ wasting)
What is the difference btw Cushing’s syndrome and disease?
SYNDROME = too much cortisol
DISEASE = too much ACTH
How does Cushing’s Syndrome present? Why?
-Cortisol has glucocorticoid, mineralocorticoid, and androgenic effects. So Cushing presents with an excess of all 3 things.
Adrenal insufficiency causse
Primary - Addison’s (autoimmune) and adrenal glands don’t secrete enough steroid hormone
Secondary - decreased CRH or ACTH release (most commonly due to exogenous steroid use)
Adrenal insuffiency presentation
muscle weakness
hotn
hypoglycemia
hyponatremia
hyperkalemia
metabolic acidosis
Treated with 15 - 30 mg cortisol equivalent
When do we do stress steroids?
Must be on a steroid for > 3 weeks
> 5 mg/day
4 endocrine hormones produced by the pancreases
alpha = glucagon
beta = insulin
delta = somatostatin
PP = pancreatic polypeptide
What conditions increase insulin release
anything that raises blood glucose
PNS - post meal
SNS
glucagon
cortisol
GH
catechols
beta agonists
what conditions decrease insulin release
anything that reduces blood glucose
insulin
volatiles
beta agonists
what conditions stimulate glucagon
anything that reduces blood glucose
-hypoglycemia, stress, trauma, sepsis, beta agonists
while insulin and somatostatin decrease glucagon release
somatostatin
GH inhibiting hormone
REGULATES ENDOCRINE HORMONE OUTPUT
inhibits insulin & glucagon
inhibits splanchnic blood flow, gastric motility, and gall bladder contraction
Pancreatic polypeptide
INHIBITS EXOCRINE HORMONE SECRETION
GASTRIC ACID SECRETION
GALLBLADDER CONTRACTION
GASTRIC MOTILITY
moa for Biguanides
Inhibit gluconeogensis and glycogenolysis in the liver. Decrease peripheral insulin resistance.
I.e., metformin
*no hypoglycemia
*metabolic acidosis
*treats PCOS
metformin meets glucose and advises it to stay out of the blood
Sulfonylureas
Stimulate insulin secretion from pancreatic beta cells. Closes potassium channels.
-Glyburide, Glipizide, Glimepiride
Sulfonylureas summon insulin. They close the potassium gates in the haunted graveyard of the pancreas and chaant depolarizing spells that open calcium channels. This brings insulin back from the dead!
GLYBURIDE is more like GHOST BRINGER!
Risk of hypoglycemia, Avoid with sulfa allergies
Meglitinides
Stimulate insulin secretion from beta cells.
REPAGLINIDE & NATEGLINIDE
Hypoglycemia risk
Thiazolidinediones
Decrease peripheral insulin resistance and increase hepatic glucose utilization.
ROSIGLITAZONE, PIOGLITAZOME
Toxic to Heart & Liver
*does not cause hypoglycemia. Black box warning d/t CHF risk.
Alpha-glucosidase inhibitors
Slows digestion and absorption of carbs from GI tract.
ACARBOSE, MIGLITOL
NO HYPOGLYCEMIA
Glucagon-like peptide 1 receptor agonist
Increase insulin release from beta cells, decrease glucagon release from alpha cells, and prolong gastric emptying
EXENATIDE, LIRAGLUTIDE
Hypoglycemia risk!
A tide of insulin is secreted after GLP1RA reaches the receptor shores. Tides is an anagram for diet.
Dipeptidyl-peptidase-4 inhibitors
Increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells
LIPTINS
hypoglycemia risk duh
Amylin agonists
decrease glucagon release from alpha cells and reduce gastric emptying
PRAMLINTIDE
risk of hypoglycemia if admin’d with insulin
may cause n&v
what drugs extend the hypoglycemic effects of insulin
MAO, salicylates, tetracycline
