endocrine- adrenal glands Flashcards
where are the adrenal glands?
sit adjacent to the kidney
- adrenal medulla= less problems
- adrenal cortex= most endocrine problems
adrena medulla secretes?
epinephrine and norepinephrine, which target most cells and activate SNS
adrenal cortex secretes? (3)
3 groups of hormones:
- glucocorticoids (eg cortisol)
- mineralocorticoids (eg aldosterone)
- gonadocorticoids (eg androgens)
explain glucocorticoids briefly
secreted in response to stress, target most cells to decrease inflammation, alters metabolism of proteins and fats, suppress immune response
-corticosteroids (prednisone, cortisone) treat chronic inflammation
explain mineralocorticoids briefly
chief: aldosterone, targets kidneys to increase sodium reabsorption and increase fluid retention which increases BV and increases BP
explain gonadocorticoids briefly
androgens are male sex hormones (testosterone)
-very small amount is released from adrenal glands (in men and women), but most is produced in testes, so if excess women will see more effects
ACTH=
adrenocorticotropic hormone produced and released by anterior pituitary, stimulates cortex to release cortisol
what could potentially cause hypersecretion?
hyperplasia of cells that secrete these hormones—> excess hormones being secreted
tumor (more cells, more secretion)
cortisol tumor or hyperplasia=
increased cortisol production—> decreased ACTH due to negative feedback loop
pituitary tumor or hyperplasia=
excessive ACTH production, resulting in excessive cortisol production
ectopic tumors=
in location in body that is not the gland, but does some function of gland
ex. malignancy in lung produces ACTH like substance which stimulates cortisol production, but negative feedback look is not suppressing this ACTH like substance, so cortisol levels keep rising
- paraneoplastic syndrome
what is cushings syndrome?
a common disease with excess cortisol production (glucocorticoid, hypersecretion)
- cortisol catabolizes (breaks down proteins—> leading to weakened muscles)
- proteins have NO stores in body as glucose and lipids do, only exist in structured forms with functions
gluconeogenesis in cushings syndrome?
- production of CHO from non-CHO source
- results in increased glucose in blood, altered glucose metabolism
- prolonged hyperglycemia
- insulin resistance
- impaired glucose tolerance, can develop DM
cushings- cortisol: hypokalemia and hypertension?
no affect on mineralocorticoid release!!!
excess cortisol results in cortisol taking on some of aldosterones functions?!!?!?
-so now there is na+ and water retention, excess K+ excretion
visual manifestations with cushings?
- rounded moon face (excess lipid deposit within body causing fat deposition in face, neck, and abdomen
- buffalo hump: deposits on shoulders
what manifestations occur if androgen secretion is elevated in cushings?
- buffalo hump: fat deposits on shoulders
- facial hair and male balding pattern
- females looking masculine
diagnosis of cushings syndrome?
- 24 h urine cortisol: urine sample analyzed for cortisol
- late night cortisol (secretion of cortisol is usually low at night, so if its high that is off)
- dexamethasone test: similar function to cortisol so when administered, ACTH levels should decrease due to negative feedback- if not then there is hypersecretion of ACTH
- CT and MRI scan for an adrenal tumor (producing cortisol), or pituitary tumor (producing ACTH) or an ectopic tumor!
treatment of cushings syndrome?
- eradicate tumor
- ectopic tumor: enzyme inhibitors to suppress hormone it produces + chemo
- irradicate pituitary (radiation therapy) second line
- adrenalectomy–> 2 adrenal glands, one can be removed but LAST resort
what is Conn syndrome?
primary hyperaldosteronism
-RARE—> usually only encountered in the hospital on an endocrine unit
etiology of Conns? (3)
- mostly caused by a cortical adenoma (tumor in cortex)
- idiopathic hyperplasia of cortex
- renin secreting tumor in the kidney (renin converts angiotensinogen into angiotensin I, which is converted by ACE into angiotensin II. this produces aldosterone. Over stimulation of RAAS= increased aldosterone production!)
manifestations of Conns?
- hypertension… aldosterone causes vasoconstriction, and retention of Na+, increased BV and BP
- hypokalemia due to excretion of K+
- alkalosis, aldosterone normally excretes H+, so if too much is being excreted than there is a loss of H, increased pH
treatment of Conns?
excise adenoma if possible unilateral adrenalectomy for adenoma -aldosterone receptor antagonist -restrict Na+ intake antihypertension drugs if it occurs
what is Addisons disease?
decreased production of aldosterone (main mineralocorticoid) and cortisol (glucocorticoid) in cortex—> primary cortical deficiency!!
- impacts both mineralocorticoids and glucocorticoids
- slight deficiency of androgens (affects females a lil bit more)
adrenal cortex has a functional reserve, meaning?
if there is damage to cortex, it is still able to function, but if function is lost over 90%, cortex is damaged
etiology of addisons?
usually classic autoimmunity- antibodies are targeting self antigens in cortex
-could be a non-secretory, non-functional tumor (damages tissue)
side effect of long term steroid use: decreased ACTH released because steroids inhibit it–> decreased ACTH= less aldosterone and cortisol secreted
manifestations of addisons?
- hypovolemia (na+ and h20 are excreted because function of aldosterone is to retain it)
- decreased CO—> hypotension, hypoxia, fatigue
- hyperkalemia (not enough K+ excreted)
- poor stress response (general adaptive syndrome… adrenal gland is involved in this)
- poor appetite and weight loss
- atrophic adrenal gland
why does hyperpigmentation occur in addisons?
-hyperpigmentation d/t lack of feedback—> aldosterone/cortisol is not secreted, ACTH is not triggered to stop secreting. ACTH is broken down into A.As which can join to form MSH (melanocyte stimulating hormone) which produces melanin, increase in pigment—> darker skin
what is the acute complication of addisons?
and addisonian crisis!!!
-deficiency of cortisol resulting from untreated addisons + added physical or mental stress, adrenal cortex cannot cope!!! loss of functional reserve
treatment of acute addisons?
-bring cortisol to normal levels, IV fluids stat and IV glucocorticoids
treatment of chronic addisons?
hormone replacement d/t deficiency of hormones
