Endocrine Lecture 3: Adrenal Gland Flashcards
Adrenal Anatomy:
The Cortex of the adrenal gland refers to the ____, the Medulla refers to the ____.
Outer “bark” = Cortex
inner region = Medulla
The Adrenal Medulla is directly connected to the _____ branch of the nervous system via nerves.
Sympathetic
The Adrenal Medulla releases ______, which are responsible for activation of our fight or flight responses.
Catecholamines
What cells in the adrenal medulla are responsible for creating catecholamines?
Chromaffin cells
Catecholamines are derived from what substance?
Tyrosine
What are the 4 catecholamines that are produced in the Adrenal Medulla?
DOPA [Aromatic L-amino acid decarboxylase (AADC or AAAD), also known as DOPA decarboxylase]
Dopamine
Epinephrine
Norepinephrine
_____ is the principal product of the Adrenal Medulla and is ONLY made in the Adrenal Medulla.
Epinephrine
Of the catecholamines made in the Arenal Medulla, 80% is ______ and 20% is ______ . Only a scant amount of ____ is made in the Adrenal Medulla as well.
80%= Epinephrine
20%= Norepinephrine
scant amount = Dopamine
Norepinephrine and Dopamine are primarily made elsewhere in the body.
Epinephrine and Norepinephrine have strong alpha-1 effects which results in ______?
Arterial vasoconstriction most importantly
- Bronchoconstriction
- Inhibits insulin secretion
- Stimulates glycogenolysis (↑blood sugar) and gluconeogenesis
- Mydriasis-eyes open wide
- GI relaxation
- Activation increases intracellular Ca (neurotransmitter release)
- Smooth muscle contraction
Epinephrine has stronger beta-1 effects which results in ____ and _____.
Increased HR
and
Contractility
Beta-1 (Target for Beta blockers)
-↑HR, ↑Conduction velocity, ↑myocardial contractility (inotropy)
Norepinephrine is converted to Epinephrine by what enzyme?
Phenylethanolamine N-Methyltransferase (PNMT)
PNMT expression is regulated by ________, which accounts for ______’s role in affecting BP.
Glucocorticoids (cortisone)
_________ is a tumor either caused by adrenal medullary hyperplasia or extra-adrenal chromatin tissue
Pheochromocytoma
Pheochromocytoma tumors make and release _______ in an unregulated fashion.
Catecholamines
Symptoms of pheochromocytoma include:
paroxysmal HTN tachycardia HA sweating anxiety tremor glucose intolerance
T/F: Most pheochromocytoma (85-90%) are solitary tumors localized to a single adrenal gland (usually the R side)
True
10-15% of Pheochromocytomas are extra-medullary, of these most are found in the _______.
Abdomen
Diagnosis of Pheochromocytoma is made by testing _____ for the presence of _______.
Urinary Vanillymandelic acid (VMA) through a 24 hour urine collection.
Both Epi and Norepi are degraded into VMA
The introduction of alpha adrenergic antagonist preoperatively reduces the incidence of _______
preoperative blood pressure fluctuations MI CHF Dysrhythmias CVA
Alpha blockers phenoxybenzamine or parson should be started _____ days prior to surgery to normalize BP.
10-14 days before surgery
Once alpha blockage is established, beta blockage can begin. Why is this?
Beta blockage is delayed B/C of the risk of unopposed alpha mediated vasoconstriction.
When arteries do relax, volume expansion is necessary.
What medications should be avoided intraoperatively to prevent provocation of pheochromocytomas?
Histamine releasing agents
metoclopramide
glucagon
When a Pheochromocytoma tumor is removed, ______ can happen.
abrupt hypotension
(as catecholamine levels drop and alpha and beta blockade are unopposed), blood resuscitation may be required sometimes pressers are needed.
Following removal of pheochromocytoma tumor removal, catecholamine levels return to normal after a few days and about ____% of patients become normotensive within _____ days.
75%
10 days
T/F: Medullary Hyposecretion= not a serious physiologic problem.
TRUE
The SNS compensates for cardiovascular regulation.
Other regulatory hormones compensate for metabolic effects.
What are the 3 zones/layers of the adrenal cortex? (from outer to inner)
Zona glomerulosa (outer)
Zona Fasciculata (middle)
Zona reticularis (inner)
What is produced in each of the zones/layers of the adrenal cortex?
Zona glomerulosa (outer)= mineralocorticoid (Aldosterone)
Zona Fasciculata (middle)= glucocorticoid (Cortisol)
Zona reticularis (inner)= Androgens (Androstenedione)
The primary mineralocorticoid produced in the zona glomerulosa is ______. What are it’s primary functions?
Aldosterone
Aldosterone effects salt and water balance and therefore BP. Aldosterone effects the distal convoluted tubule and collecting ducts of the nephrons. It causes water and sodium retention and excretion of potassium and hydrogen.
If unopposed = HTN, extracellular fluid expansion, hypokalemia, and alkalosis.
Aldosterone is primarily regulated by the renin-angiotensin system and by potassium levels.
The primary glucocorticoid produced in the zona fasciculata is _______.
Cortisol
- named glucocorticoid b/c it has effects of glucose metabolism
- essential for life and regulates a variety of CV, metabolic, immunologic, and homeostatic functions.
- regulates gluconeogenesis (formation of glucose in the liver as proteins are converted into carbohydrates.)
- High cortisol levels have anti-inflammatory effects. (useful in autoimmune diseases or allergic reactions)
The primary Androgen produced in the zona reticular is _____.
Androstenedione
All of the steroid hormones produced in the Adrenal Cortex are synthesized from ______.
Cholesterol
Conn’s syndrome is ______.
Hyperaldosteronism- Primary
Caused by aldosterone secreting tumors or hyperplasias.
Dx: low renin from negative feedback. Tx: surgical
s/s: HTN, extracellular fluid expansion, hypokalemia, and alkalosis.
Secondary Hyperaldosteronism
- Caused by CHF, cirrhosis w/ ascites & nephrosis
- ECF list to extravascular space
- total body volume overload and intravascular volume depletion, triggers release of renin by kidneys. exacerbates fluid retention and Na retention.
Hypoaldosteronism/Adrenal insufficiency:
- Na lost in urine, K retained
- plasma volume decreases, hypotension & hyperkalemia may lead to circulatory collapse
Almost any stress (physical or neurogenic) can use an immediate release of ______ from the anterior pituitary gland followed by greatly increased secretion of cortisol (glucocorticoids)
ACTH
Adrenalcorticotropic Hormone
ACTH stimulates cortisol secretion almost entirely.
ACTH release is controlled by corticotropin-releasing hormone (CRH) from the hypothalamus.
High cortisol levels causes negative feedback loop and inhibits ACTH and CRH release
CRH, ACTH, and cortisol are released in relation to circadian rhythms with higher levels in the AM.
Cushing Disease:
Cushings syndrome:
Cushing disease= ACTH secreting tumor of the pituitary causing high cortisol levels
Cushings syndrome= sequela of symptoms caused by excessive cortisol secretion.
Cushing syndrome symtoms:
Integument: thin skin, stria, poor healing, bruising, acne
Bone: inhibition of GI Ca absorption, decreased serum Ca, increased PTH, decreased bone formation, osteoporosis
muscle: wasting, weakness, fatiguability
Endocrine: impaired glucose tolerance, amenorrhea, turncal obesity, moon mace, buffalo hump
Renal: salt/water retention, hypokalemia from mineralocorticoid activity and excessive glucocorticoids
CV: HTN
CNS: moody
Addison’s Disease/Adrenal insufficiency:
Results from failure to produce adrenocortical hormones (mineralocorticoids and glucocorticoids)
- Primary: adrenal nonfunction= autoimmune
- Secondary: hypothalamic or pituitary nonfunction (shock/sepsis)
Symptoms of Addison’s disease:
Lack of glucocorticoids: Hypoglycemia, fatigue, weakness, WT loss, anorexia
hyper pigmentation of skin d/t increased ACTH
severe deterioration to stress
lack of mineralocorticoids: dehydration, polyuria, hypotension, low sodium, hyperkalemia, metabolic acidosis
Risk of cardiovascular collapse (Addisonian Crisis)
What is an Addisonian Crisis and how is it treated?
Risk of cardiovascular collapse from lack of adrenocorticol hormones (mineralocorticoids and glucocorticoids-cortisol)
Tx: give cortisol
Death in 4 days - 2 weeks if untreated.
Etomidate is a induction drug used often times for hemodynamically unstable patients, why is Etomidate contraindicated for patients with adrenal insufficiency/ addison’s disease?
Etomidate causes profound suppression of cortisol for at least 24 hours and contribute to deterioration of patient. Can cause profound hypotension.
