Adrenalcortical Dx

Front 1

What are the two parts of the Adrenal Glands?

Back 1

Adrenal medrulla-inner 20%
Adrenal cortex-outer area

Front 2

What hormones does the adrenal medulla secrete?

Back 2

epinephrine & norepinephrine

Front 3

What hormones does the adrenal cortex secrete?

Back 3

glucocorticoids (cortisol)
mineralcorticoid (aldosterone)
androgenic hormone (androgens)

Front 4

What steriod substance are the adrenal cortex hormones synthesized from?

Back 4

cholesterol

Front 5

What are the 3 layers of the adrenal cortex and which secretes which type of hormone?

Back 5

-Zona glomerulosa (15%): thin layer under capsule secretes aldosterone, but contains aldosterone synthase; controlled by angiotensin II & K+
-Zona fasciculata:(75%)middle & widest layer, secretes cortisol, androgens, estrogens; controlled by ACTH
-Zona reticularis: (10%) deep layer, secretes androgens, estrogens, glucocorticoids; controlled by ACTH

Front 6

What hormone accounts for 95% of glucocorticoids released by adreanl cortex?

Back 6

Cortisol (hydrocortisone)

Front 7

What type of effects does cortisol have?

Back 7

-Carbohydrate metabolism
-Protein metabolism
-Fat metabolism
-Inflammation & immunity
-Bone & calcium metabolism
-Vascular reactivity

Front 8

What is the HPA?

Back 8

Hypothalamic-Pituitary-Adrenal Axis (HPA): hormonal circuit

Front 9

What is the regulation/mechanism for control of cortisol?

Back 9

Corticotropin releasing factor (CRF) from hypothalamus to Adrenocorticotropin homrone (ACTH) from anterior pituitary to adrenal cortex to release cortisol
Negative feedback inhibits further release

Front 10

What is the daily cortisol production and the maximum release under stress?

Back 10

15-25mg/day
up to 250mg/day

Front 11

Which hormone accounts for 90% of all mineralcorticoid activity?

Back 11

Aldosterone, secreted from zona glomerulosa, affects fluids/electrolytes

Front 12

What is the daily aldosterone production rate?

Back 12

0.15mg/day

Front 13

What are the renal & circulatory effects of aldosterone?

Back 13

Aldosterone acts on collecting tubule prinicpal cells to increase reabsorption of Na+ with secretion of K+ & H+, net effect is fluid retention, hypokalemia, metabolic alkalosis, increased B/P

Front 14

What happens with excess aldosterone and too little aldosterone?

Back 14

Excess: hypokalemia, muscle weakness, metabolic alkalosis

Too little: hyperkalemia, cardiac toxicity d/t large Na+ loss, Cl- loss = decreased ECF = dehydration, shock

Front 15

What effect does aldosterone have on sweat glands?

Back 15

Stimulates sodium and potassium transport in sweat glands, salivary glands, intestinal epithelial cells = reabsorption of sodium and the secretion of potassium by the ducts

Front 16

What are the 4 main physiologic stimulants of aldosterone release?

Back 16

-Hyperkalemia-most potent
-Angiotnesin II-most potent
-Hyponatremia
-ACTH

Front 17

What are the causes of Cushing's syndrome/disease?

Back 17

-Iatrogenic-exogenous administration of glucocorticoids most common cause of Cushing’s syndrome
-Endogenous Cushing’s syndrome d/t to 4 pathogenic disorders:
1. Anterior pituitary tumor-“Cushing’s disease” adenoma of anterior pituitary which secretes large amounts of ACTH
2. Adrenal tumor-“Adrenal Cushing’s Syndrome” autonomous cortisol production via adrenal tumor
3. Ectopic Cushing’s Syndrome-ectopic secretionof ACTH by a tumor elsewhere in body, mostly with small cell lung cancer
4. Abnormal function of hypothalamus-causes high level of corticotrophin releasing factor/hormone = excess ACTH = excess cortisol

Front 18

S/S of Cushing's:

Back 18

HTN, wt. gain, truncal obesity, moon face, buffalo hump, decreased muslce mass, weakness, hyperglycemia, glucosuria, polydipsia, osteoporosis,loss of collagen-thin frail skin, poor wound healing, modd swings, insomnia,

Front 19

What diagnositic lab tests are used for Cushing's?

Back 19

24 hour urine cortisol, dexamethasone suppression test (should depress ACTH = ↓cortisol levels), ACTH level (↑ with anterior pituitary dx & ectopic Cushing’s)

Front 20

How does one treat Cushing's?

Back 20

: transphenoidal microadenomectomy-85-90% resection of anterior pituitary; pituitary radiation, surgical removal of adrenal glands, decrease exogenous glucocorticoid use

Front 21

Anesthetic management of Cushing's:

Back 21

-Consider physiologic effects of excessive cortisol secretion, evaluate systemic blood pressure, evaluate electrolytes & glucose, surgical stimulation increases cortisol, may need to decrease muscle relaxants d/t muscle weakness, normalized increased intravascular fluid volume-spironolactone, osteoporosis & positioning, regional anesthesia difficulty d/t vertebral body collapse, may need postoperative ventilation, ↑ risk of infection d/t immunosuppression

Front 22

What are the physiologic effects of excess Cortisol secretion?

Back 22

-systemic hypertension
-hyperglycemia
-skeletal muscle weakness
-osteoporosis
-obesity
-menstrual disturbances
-poor wound helaing
-susceptibility to infection

Front 23

What are the causes of hyperaldosteronism?

Back 23

Primary hyperaldosteronism / Conn’s Syndrome:
1.Hypersecretion of aldosterone from adrenal adenoma
2.Hyperplasia of adrenal cortices, women > men
-Secondary hyperaldosteronism-presnet when there is a secondary aldosterone rise d/t ↑ renin production=renin producing tumor, renovascular HTN

Front 24

S/S of Conn's disease?

Back 24

-nonspecific & may be aysmptomatic;
-HTN & H/A: aldosterone induced Na+ retention & subsequent increase in ECF volume, may be resistant to treatment;
-Hypernatremia
-Hypokalemic metabolic alkalosis
-skeletal muscle weakness/cramps d/t low K+

Front 25

Diagnosis of Conn's disease?

Back 25

hypokalemia, ↓plasma renin in primary hyperaldosteronism but ↑ in secondary, systemic HTN, elevated plasma levels of aldosterone

Front 26

Treatment of Conn's:

Back 26

supplemental K+, restore intravascular fluid volume=spironalactone, antihypertensive meds, excision of adrenal tumor, adrenalectomy

Front 27

Anesthetic management of Conn's:

Back 27

preoperative correction of hypokalemia & b/p, avoid intraoperative hyperventilation (↓K+ further), ABG’s & electrolyte monitoring intraop, consider CVP

Front 28

Hypoadrenalism

Back 28

Primary Adrenalcortical insufficiency = Addison’s disease: lack of cortisol & aldosterone d/t destruction of adrenal cortex or adrenal atrophy. Causes: atrophy from autoimmunity, destruction of adrenal cortex by adrenal hemorrhage in anticoagulated patients, sepsis, accidental or surgical trauma, tuberculosis
-Secondary adrenal insufficiency: causes-adrenal cortex suppression d/t glucocorticoid therapy (leading cause), ACTH deficiency d/t hypothalamic & pituitary dysfunction

Front 29

S/S of hypoadrenalism

Back 29

reflect glucocorticoid & mineralcorticoid deficiency, mineralcorticoid more preserved in secondary causes; weakness, fatigue, ↓ appetite, wt loss, vomiting, abd pain, ↓ glucose, hyponatremia, hyperkalemia, mild acidosis, hypovolemia, hypotension, oligomenorrhea, ↑ melanin formation in skin

Front 30

Diagnosis of hypoadrenalism:

Back 30

injection of synthetic ACTH to evaluate plasm cortisol levels pre-injection, @ 30 & 60 min. Normally cortisol level rises to at least 7mg/dl; abnormal if no response

Front 31

Treatment of hypoadrenalism:

Back 31

untreated with total adrenal destruction death within days to weeks, typically oral replacement with prednisone 5mg q am & 2.5mg q pm OR hydrocortisone 20mg q am & 10mg q pm; mineralcorticoid replacement 0.05mg-0.2mg qd of fludrocortisone

Front 32

Anesthetic management of hypoadrenalism:

Back 32

provide exogenous corticosteriod supplementatiion, consider avoiding etomidate

Front 33

Addison's Crisis/Adrenal Crisis:

Back 33

-Life threatening hypocortisolism, occurs with minor stress, undiagnosed Addisons’s, abrupt withdrawal from long-term glucocorticoids
-S/S: severe hypotension, hemodynamic instability, acute circulatory collapse
-Treatment: cortisol 100mg IV followed by infusion at 10mg/hr, D5NS or colloid, inotropic

Front 34

Surgery & Hypothalamic Pituitary Adrenal Axis (HPA) suppression:

Back 34

corticosteroid supplementation should be provided for patients being treated for chronic hypocortisolism (prednisone 5mg) longer than 2 weeks in the last 6-12mos prior to undergoing surgical procedures

Front 35

Treatment for HPA suppression:

Back 35

Plan A: hydrocortisone 25mg IV q 4 hours x 24 hours
Plan B: hydrocortisone 100mg IV q 8 hours beginning the night before or morning of surgery for the 1st 24 hours