Adrenal Flashcards
Adrenal glands AKA
suprarenal glands
The adrenals are responsible for releasing ________ hormones
stress
The adrenal has a cortex and medulla. Cortex means ________ and medulla means _______
outer / inner
The adrenal medulla is connected directly to the _____ via nerves
SNS
The adrenal medulla bridges the endocrine and ______
SNS
The adrenal medulla releases substances known as _________ which enter the circulation and act on distal tissues like other hormones
catecholamines
Catecholamines are made by _______ cells in the adrenal medulla and are all derived from ________
chromaffin / tyrosine
What are the 4 catecholamines
DOPA, Dopamine, Norepinephrine, epinephrine
Catecholamines activate the stress, or ______ response
fight or flight
__________ is the principal product of the adrenal medulla and is made only in the medulla
epineprhine
Epinephrine accounts for nearly ____% of the adrenal medulla’s output, the other _____% is norepinephrine, and a scant amount of dopamine also made here
80% / 20%
The fight or flight response demonstrates ______ control of adrenal medullary function
central
Epinephrine and norepi are released and act as hormones causing _______ activation
sympathetic
Sympathetic activation is mobilization of needed resources including increased ____ and ____ as well as ___________.
BP, HR and bronchodilation
The fight or flight response happens in response to
pain, fear, hemorrhage, cold, hypoglycemia, hypotension, heat, exercise
The FOF response acts by increasing CO to ____ and ______
heart and skeletal muscle
The FOF response decreases blood flow to the ____, ____ and _____
kidneys, skin and mucosa
The FOF utilizes ______ and _____ mobilization for energy
glucose and fatty acid
What happens to respirations during FOF?
increased
Epi and norepi differ in which ________ receptors they stimulate
adrenergic
Epi and norepi both have strong _______ effects which result in ARTERIAL vasosconstriction
alpha-1
Epinephrine has stronger _______ effects which increases HR and contractility more
beta-1
___________ is an enzyme necessary for conversion of norepinephrine to epinephrine
Phenylethanolamine Methyltransferase (PNMT)
PNMT expression is regulated by _________, which helps account for __________ role in affecting BP.
glucocorticoids (cortisone) / glucocorticoids
_________ is a tumor either caused by adrenal medullary hyperplasia or extra-adrenal chromaffin tissue. These tumors make _______ in an unregulated fashion.
pheocromocytoma / catecholamines
Symptons of Pheocromocytoma
paroxysmal HTN, tachycardia, headache, sweating, anxiety, tremor, and glucose intolerance
Most tumors (85-90%) are solitary tumors localized to a single _____ _______
adrenal gland (mostly RIGHT)
10% of tumors are extramedullary, of these 95% are in the _______
abdomen
Dx of pheocromocytoma
strong clinical symptoms, then biochemical testing, then imaging
______ ____ ______ levels help to make the diagnosis as both epinephrine and norepi are degraded into this
Urinary Vanillylmandelic acid (VMA)
Anesthetic considerations for someone with a pheocromocytoma have helped decrease perioperative mortality from 45% to __ -__%
0-3%
The introduction of ___ ________ ______ preoperatively reduces the incidence of periop BP fluctuations, MI, CHF, dysrhythmias and CVA associated with pheocromocytoma
alpha adrenergic anatagonists
The alpha blockers ______ or _______ should be started 10-14 days prior to surgery to normalize BP in someone with pheocromocytoma
phenoxybenzamine / prazosin
With pheocromocytoma, once adequate alpha blockade is established, ______ ________ can begin. _____ blockade is delayed because of the risk of unopposed alpha mediated vasoconstriction.
beta blockade / beta
When arteries relax, _______ expansion is necessary
volume
Anesthetic plan for someone with pheocromocytoma typically includes _______ with arterial line and central venous access.
GETA
PHEOCROMOCYTOMA Anesthetic considerations - Short acting vasocative agents are desirable as paroxysms of both _____ and ______ are common when the tumor is manipulated
hypotension / hypertension
What agents provoke pheocromocytomas, awaken the beast, and should be avoided?
histamine releasing drugs, metoclopramide, glucagon
What can happen when a pheo tumor is removed? What is the treatment?
abrupt hypotension / 1st fluids then vasopressors if needed
For pheocromocytoma, catecholamine levels return to normal several days after surgery and approximately ___% of patients become normotensive within ____ days postop.
75% / 10 days
T/F The physiologic effect of Medullary HYPOsecretion is not a serious problem
TRUE
Medullary hyposecretion is not a serious problem because the _______ compensates for CARDIOVASCULAR regulation and other regulatory hormones compensate for ________ effects
SNS / metabolic
The adrenal cortex mediates the stress response via production of substances known as _______ and _________, it is also a secondary site of ______ synthesis.
mineralcorticoid / glucocorticoid / androgen
What are the 3 zones of the adrenal cortex
zona glomerulosa, zona fasciculata, zona reticularis
The zona glomerulosa produces ________
mineralcortcoids
The zona fasciculata produces ________
glucocorticoids
The zona reticularis produces __________
androgens
The primary mineralcorticoid is _________
aldosterone
The primary glucocorticoid is ________
cortisol
The primary androgen is ________
androstendedione
All of the streroid hormones (aldosterone, cortisol, androstendedione) are syntesized from ______
cholesterol
Mineralcorticoids are named so because they control ________ also known as the electrolytes Na and K.
minerals
Aldosterone efffects ______ and _______ balalnce and therby effect _____ _____ regulation of BP
salt and water / long-term
Aldosterone effects the ______and _____ of the kidneys and causes retention of _____ and _____ and excretion of ______ and ______.
DCT / Collecting Ducts / sodium and water / potassium and hydrogen
If unopposed, __________ leads to HTN, ECF expansion, hypokalemia, alkalosis
aldosterone
Aldosterone works with the _______ for BP control
RAAS
RAAS - in brief
Hypovolemia triggers kidneys to secrete renin. Through a series of steps Angiotensin II is prodcued. Angiotensin II is a potent vasoconstrictor and also stimulates secretion of aldosterone. Aldosterone causes retention of sodium and water and excretion of potassium, and also increases BP.
Aldosterone is regulated primarily by what?
RAAS and potassium levels
T/F Adreanlcorticotropic Hormone (ACTH) and sodium levels do not exert much control over the release of aldosterone?
TRUE
Primary Hyperaldosteronsim AKA
Conn’s Syndrome
Conn’s syndrome causes
Caused by aldosterone secreting tymors or hyperplasias
Effects of Conn’s syndrome
increased ECF volume, hypertension, K+ depletion, and metabolic alkalosis
Diagnosis of Conn’s syndrome is made by?
low renin from negative feedback
Treatment for Conn’s syndrome
surgically remove the tumor
Secondary hyperaldosteronism is caused by what?
CHF, cirrhosis with ascites, and nephrosis
In secondary hyperaldosteronism, ECF is lost to the extravascular space. They will be intravascularly ______ _______ despite total body volume overload, which triggers release of ______ from the kidneys. This exacerbates fluid and Na retention.
volume depleted / renin
Hypoaldosteronism is from ________ insufficiency. What is this noted by?
adrenal / Na lost in urine and K retained.
With adrenal insufficiency (hypoalsdosteronism), plasma volume _________ and hypotension/hyperkalemia may lead to ________ ______
depletion / circulatory collapse
Glucocorticoids are named because of their effects on _____ _______
glucose metabolism
Cortisol is AKA
hydrocortisone
_______ is the principal glucocorticoid and is prodcued in the zona ________
cortisol / fasciculata
T/F Cortisol is essential for life and regulates a variety of cardiovascular, metabolic, immunologic, and homeostatic functions
TRUE
Glucocorticoids stimulate gluconeogensis. This causes formation of carbohydrate from protein by the ________. It also causes mobilization of amino acids from muscle. Muscles can become _______ in great cortisol excess.
liver/ weak
Glucocorticoids ________ glucose utilization by cells and ________ blood glucose concentration
decrease / elevates
The elevation of blood glucose by glucocorticoids is caused by what?
increased formation of glucose by the liver and decreased utilization of glucose by the tissue
Almost any stress (physical of nuerogenic) can cause an immediate release of ______ by the ANTERIOR PITUITARY gland followed by greatly increased secretion of ______
ACTH / Cortisol
Examples that can cause ACTH release
trauma, infection, heat/cold, surgery, catecholamine injection
It is unclear what benefit cortisol provides in stressful situations but is probably related to ______ of resources for immediate availability
mobilization
High levels of cortisol of have ________ effects
anti-inflammatory
Cortisol prevents the development of inflammation by stabilizing _______, decreasing capillary permeability, decreasing migration of WBCs into inflamed areas, and other effects. Cortisol also causes __________ of inflammation within hours to days.
lysosomes / resolution
ACTH stimulates _______ secretion almost entirely
cortisol
ACTH release is controlled by _______ from the _______
corticotropin releasing hormone (CRH) / hypothalmus
Physiologic stress causes release of both ____ and _____
ACTH and CRH
High cortisol levels cause ________ of ACTH and CRH release
inhibition
Cortisol release is caused by the __________ when it senses stress
hypothalmus
Cortisol helps to relieve the damaging nature of the _________ state
stressful
Cortisol provides direct ______ _______ to decrease its release
negative feedback
CRF, ACTH, and cortisol are released in relation to circadian rhythms with high levels in the _____________
morning
ACTH secreting tumor of the pituitary
Cushings Disease
caused by excessive cortisol secretion
cushings syndrome
Causes for Cushing’s syndrome
ACTH secreting ectopic tumor, overactive hypothalamic secretion of CRH, primary glucocorticoid secreting adrenal tumor, Iatrogenic (chronic administration)
Effect of Cushing’s syndrome on connective tissue
thin skin, easy bruising, stria, poor healing/collagen formation and inhibition of fibroblasts
Effect of Cushing’s syndrome on Bone
inhibition of GI Ca++ absorption, decreased serum Ca++, increased PTH, decreased bone formation, increased bone resorption leading to osteoporosis
Cushing’s effect on muscle
wasting, weakness, fatigability
Cushing’s effect on Fat
Truncal obesity, moon faces, buffalo hump
Cushing’s effect on Skin
Hirsutisim, acne from increased adrenal androgen secretion
Cushing’s effect on Endocrine
impaired glucose tolerance, amenorrhea
Cushing’s effect on Renal
salt/water retention, hypokalemia from mineralcorticoid activity of excess glucocorticoids
Cushing’s effect on cardiovascular
HTN
Cushing’s effect on CNS
euphoria, irritability, emotional lability, depression
This results from failure to produce adrenocortical hormones (glucocorticoids and mineralcorticoids)
Addison’s disease
Primary Addison’s
adrenal nonfunction - mostly autoimmune
Secondary Addison’s
hypothalamic or pituitary nonfunction
Causes of secondary Addison’s
adrenal atrophy, metastatic tumor, TB, Iatrogenic/acute withdrawal of glucocorticoid treatment or removal of cortisol secreting tumor
Symptoms of Addison’s dz (glucocorticoid deficiency)
hypoglycemia, fatigue, weakness, wt loss, anorexia, hyperpigmentation (primarily by increased ACTH), severe deteroiration to stress
What is addisonian crisis and how is it treated?
Cardiovascular collapse and treated with cortisol
Symptoms of Addison’s dz (mineralcorticoid deficiency)
dehydration, polyuria, hypotension, low Na, Retention of K, metabolic acidosis
How soon can one die from Addison’s dz if untreated
4 days to 2 weeks
________ doses of glucocorticoids are given in the perioperative period to patients who take chronic steroids
larger
What would you give to a patient who takes chronic steroids?
Hydrocortisone 50-100 mg IV (adults)
Etomidate causes profound suppression of cortisol for at least 24 hrs and can contribute to adrenal insufficiency and resultant _________. Etomidate should be used sparingly in patients with ______ shock for this reason. Etomidate has not been shown to increase mortality when used for RSI.
hypotension / septic / RSI
