Hormonal Regulation

adrenal glands

one on top of each kidney

medulla

secrete catecholamines like epinephrine and norepinephrine; increases blood flow to major organs in fight or flight; divert from nonessential organs

cortex

secretes cortisol, aldosterone, and androgens/estrogens

adrenal insufficiency

can be caused by decreased secretion of CRH from hypothalamus, decreased secretion of ACTH from anterior pituitary gland, or decreased secretion of glucocorticoids or mineral corticoids from adrenal cortex

primary adrenal insufficiency

addison’s disease; autoimmune destruction of the adrenal glands

secondary insufficiency

decreased secretion of ACTH from pituitary gland

tertiary insufficiency

dysfunction of the hypothalamus

addison’s disease

darkened and bronzed pigmentation, weight loss, fatigue, abdominal pain, nausea, gastroenteritis, decreased axillary and pubic hair; excretion of sodium and retention of potassium

AM cortisol test

differentiate between primary and secondary insufficiency and diagnose in general

> 19

normal AM cortisol

< 3

diagnostic for adrenal insufficiency from AM cortisol labs

> 100

diagnostic of primary adrenal insufficiency via serum ACTH

CT scan

assess size of adrenal gland; small - autoimmune and large - infectious process

hydrocortisone sodium succinate

50 - 100 mg IV to treat addison’s disease

dexamethasone

4-12 mg IV to treat addison’s disease

Addisonian crisis

acute adrenal insufficiency; life threatening; give isotonic fluids, IV glucocorticoids, BG stabilization, and place in recumbent position

high sodium, high protein, and low potassium

diet to follow for addison’s disease

cushing’s disease

excess of cortisol with same primary, secondary, and tertiary reasons; females 5x more likely to develop

fluid retention

cause of moon face and buffalo hump seen in cushing’s disease

virilization

male sex characteristic development

24 hour urine cortisol

collect urine for 24 hours to monitor cortisol levels

10 - 55

normal cortisol levels in 24 hour cortisol test

overnight dexamethasone suppression test

1-8 mg PO at night and draw plasma cortisol in the AM labs

< 5

normal DST test result

high potassium, protein, calcium, and vitamin D

diet for cushing’s disease

iodine

thyroid gland uses most of body’s supply; when it is low then hormone production is low

T3

rapid metabolism regulation

T4

slow metabolism regulation

calcitonin

produced by thyroid when blood calcium is high; lowers calcium by promoting storage in bones

0.7 - 2.0

normal free T4 levels

RAIU

test to see how quickly thyroid absorbs iodine

5.4 - 11.5

normal range for T4

260 - 480

normal range for T3

Hashimoto’s disease

autoimmune thyroiditis; immune-mediated thyroid destruction; hypothyroidism

primary hypothyroidism

dysfunction of thyroid gland itself

secondary hypothyroidism

originates from the pituitary gland

tertiary hypothyroidism

hypothalamic dysfunction

central hypothyroidism

thyroid deficiency due to failure of pituitary, hypothalamus, or both

neonatal hypothyroidism

deficiency present at birth

myxedema

severe, long-standing hypothyroidism

hypothyroidism

puffy face, slow pulse, enlarged heart, weight gain, peripheral edema, muscle weakness, cold intolerance, deep voice, gastric atrophy

myxedema coma

priority is thyroid hormone replacement with levothyroxine IV; maintain airway, IV fluids (NS or D5NS); passive rewarming with blankets; avoid sedative and opioids

levothyroxine

synthetic thyroid hormone T4; slowly titrated; taken in morning

low calorie, high fiber

diet for hypothyroidism; prevent weight gain and constipation

high TSH

hypothyroidism

low TSH

hyperthyroidism

goiter

seen in Hashimoto’s disease frequently

Graves disease

autoimmune hyperthyroidism; women 8x more likely than men; protruding eyes, headaches, thick skin on shins, and diffuse goiter

hyperthyroidism

goiter, sweating, heat intolerance, fine tremor in hands, increased appetite, tachycardia, palpations, high urine output; pulses, thrill or bruit over thyroid arteries

radioactive iodine

commonly used for Graves disease; destroys thyroid tissue

iodine toxicity

brown mucosa, burning, laryngeal swelling, shock

PTU

blocks synthesis of T3 and T4; monitor for cardiac issues, transition to hypothyroidism, rash, N/V

methimazole

inhibits synthesis or thyroid hormone; more toxic than PTU, take once in the morning

sodium iodide

suppress release of thyroid hormone; give 1 hour after PTU or methimazole; watch for edema, hemorrhage, or GI upset

potassium iodide

suppress release of thyroid hormone; DC if rash or iodine toxicity begins

SSKI

suppress release of thyroid hormone; mix with glass of juice or milk; give by straw to prevent staining of teeth

beta blocker

monitor cardiac status, hold for bradycardia or decreased CO; mask symptoms of hyperthyroidism

AFIB

pt at high risk for this when having hyperthyroidism

small, frequent meals

diet with Grave’s disease/hyperthyroidism

thyroid storm

severe, sudden onset hyperthyroidism; reduce fever and HR, prevent vascular collapse; IV fluids with dextrose, humified O2