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APEX > Endocrine > Flashcards

Endocrine Flashcards

1
Q

How does the hypothalamus communicate with the anterior pituitary gland?

A

Hormones are released into the hypophyseal portal vessels. Transported along the pituitary stalk.

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2
Q

How does the hypothalamus communicate with the posterior pituitary gland?

A

Supraoptic nuclei - ADH
Paraventricular nucleus - PITOCIN (OXYTOCIN)

Travel along pituitary stalk via nervous system

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3
Q

Where is the pituitary gland located? What is another name for the anterior and posterior pituitary gland?

A

Resides in the sella turcica.

Ant pit = adenohypophysis
Post pit = neurohypophysis

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4
Q

What hormones are released from the anterior pituitary gland?

A

FLAT PiG

FSH
LH
ACTH
TSH
Prolactin
ignore
GH

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5
Q

What is the function of FSH

A

girls - ovarian follicle growth
both boys & girls - germ cell maturation

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6
Q

LH function

A

girls - ovulation
males - testosterone production

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7
Q

ACTH function

A

adrenal hormone release

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8
Q

SIADH vs DI causes

A

SIADH = TBI, cancer, noncancerous lung dx, carbamazepine
DI = pituitary surgery, TBI, SAH

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9
Q

SIADH treatment

A

fluid restriction
demeclocycline (decreases responsiveness to ADH)
sodium

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10
Q

DI treatment

A

DDAVP or vasopressin
supportive

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11
Q

Anesthetic implications for acromegaly

A

DAW
Subglottic narrowing
Turbinate enlargement
OSA
HTN, CAD, rhythm disturbances
Glucose intolerance
Sk. muscle weakness

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12
Q

T4

A

Directly released from the thyroid
-T4 = delivery vehicle
-lots of protein binding
-less potent
-1/2 life = 7 days

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13
Q

T3

A

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

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14
Q

How does iodine deficiency affect T3 and T4

A

TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize T3&T4.

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15
Q

How does the thyroid hormone affect MAC?

A

IT DOES NOT

Hyperthyroidism = increased CO = decreased rate of inhalational induction

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16
Q

What is the most common etiology of hyperthyroidism

A

Graves = #1
MG
Goitor
Carcinoma
Preggo
Pituitary Adenoma
Amio

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17
Q

What is the most common cause of hypothyroidism

A

Hashimoto’s thyroiditis
-iodine
-HPA dysfunction
-neck radiation
-thyroidectomy
-amio

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18
Q

List 3 thionamides that can be used to treat hyperthyroidism. What is MOA

A

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

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19
Q

What are the contraindications to radioactive iodine

A

Pregnancy
Breast feeding mothers

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20
Q

When is it ok for hyperthyroid pt to undergo surgery?

A

never if elective
if emergent, admin a BB, potassium, glucocorticoid, PTU

21
Q

What anesthetic agent should be avoided in the hyperthyroid pt?

A

Sympathomimetics, anticholinergics, ketamine, pancuronium

22
Q

Discuss thyroid storm

A

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

23
Q

when does hypocalcemia present s/p thyroidectomy

A

6-12 hours

prolonged QT, hypotension, tetany, changes in mental status, laryngospasm

24
Q

Zones of adrenal glands

A

GFR

Zona glomerulosa (salt) - mineralocorticoids
Zona fasciculata (sugar) - glucocorticoids
Zona reticularis (androgens)

25
Q

How much cortisol is produced per day

A

15 - 30 mg/day

Normal = 12 mcg/dL

Surgery - 100 mg/day, 30 - 50 mcg/dL

26
Q

Which steroids has no glucocorticoid effects/

A

ALDOSTERONE
-mineralocorticoid effect = 3000x
-DOA = 24 hours

27
Q

Which steroids have no mineralocorticoid effects?

A

Decadron (25x glucocorticoid effect) = 0.75 mg = 36 - 54h DOA
Betamethasone (25x) = 0.75 = 36 - 54h
Triamcinolone (5x) = 4 = 12 - 36h

28
Q

Conn’s Syndrome

A

TOO MUCH ALDOSTERONE
-Primary - increased from adrenal gland
-Secondary - increased renin or aldosterone tumor

HTN, Hypokalemia, Metabolic Alkalosis (H+ wasting)

29
Q

What is the difference btw Cushing’s syndrome and disease?

A

SYNDROME = too much cortisol
DISEASE = too much ACTH

30
Q

How does Cushing’s Syndrome present? Why?

A

-Cortisol has glucocorticoid, mineralocorticoid, and androgenic effects. So Cushing presents with an excess of all 3 things.

31
Q

Adrenal insufficiency causse

A

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)

32
Q

Adrenal insuffiency presentation

A

muscle weakness
hotn
hypoglycemia
hyponatremia
hyperkalemia
metabolic acidosis

Treated with 15 - 30 mg cortisol equivalent

33
Q

When do we do stress steroids?

A

Must be on a steroid for > 3 weeks
> 5 mg/day

34
Q

4 endocrine hormones produced by the pancreases

A

alpha = glucagon
beta = insulin
delta = somatostatin
PP = pancreatic polypeptide

35
Q

What conditions increase insulin release

A

anything that raises blood glucose

PNS - post meal
SNS
glucagon
cortisol
GH
catechols
beta agonists

36
Q

what conditions decrease insulin release

A

anything that reduces blood glucose

insulin
volatiles
beta agonists

37
Q

what conditions stimulate glucagon

A

anything that reduces blood glucose
-hypoglycemia, stress, trauma, sepsis, beta agonists

while insulin and somatostatin decrease glucagon release

38
Q

somatostatin

A

GH inhibiting hormone

REGULATES ENDOCRINE HORMONE OUTPUT

inhibits insulin & glucagon
inhibits splanchnic blood flow, gastric motility, and gall bladder contraction

39
Q

Pancreatic polypeptide

A

INHIBITS EXOCRINE HORMONE SECRETION
GASTRIC ACID SECRETION
GALLBLADDER CONTRACTION
GASTRIC MOTILITY

40
Q

moa for Biguanides

A

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

41
Q

Sulfonylureas

A

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

42
Q

Meglitinides

A

Stimulate insulin secretion from beta cells.

REPAGLINIDE & NATEGLINIDE

Hypoglycemia risk

43
Q

Thiazolidinediones

A

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.

44
Q

Alpha-glucosidase inhibitors

A

Slows digestion and absorption of carbs from GI tract.

ACARBOSE, MIGLITOL

NO HYPOGLYCEMIA

45
Q

Glucagon-like peptide 1 receptor agonist

A

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.

46
Q

Dipeptidyl-peptidase-4 inhibitors

A

Increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells

LIPTINS

hypoglycemia risk duh

47
Q

Amylin agonists

A

decrease glucagon release from alpha cells and reduce gastric emptying

PRAMLINTIDE

risk of hypoglycemia if admin’d with insulin
may cause n&v

48
Q

what drugs extend the hypoglycemic effects of insulin

A

MAO, salicylates, tetracycline

APEX (18 decks)

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