Adrenal glands Flashcards
adrenal cortex vs medulla location
medulla middle
cortex outer layer
adrenal cortex layers
GFR
Salt Sugar sex
Glomerulosa aldosterone
Fasciculata glucocorticoids- cortisol
Reticularis sex hormones DHEA
What is the primary mineral corticoid?
aldosterone
What is the primary glucocorticoid
cortisone
What mainly activates aldosterone
hyperkalemia
RAAS
Where does aldosterone work (specifically)
Principal cells of the distal convoluted tubule and collecting ducts
Effects of aldosterone
NA and water retention
Excretion of K and H
If unopposed, aldosterone leads to
htn/ ECF expansion
hypokalemia
alkalosis
4 main controllers of aldosterone secretion
potassium- potent controller
RASS (at2) - potent
sodium
ACTH- minor/ no effect
RAAS system
drop in bp and drop in blood fluid
liver creates angiotensinogen
renin from the kidneys converts angiotensinogen to angiotensin 1
ACE from the lungs converts a1 to a2
A2 stimulates aldosterone
Conns syndrome is __
Primary hyperaldosteronism
Conns syndrome is caused by
aldosterone secreting tumor, hyperplasia
Conns syndrome effects (symptoms, labs, abg)
increased ecf volume, htn, hypokalemia, metabolic alkalosis
how to diagnose conns syndrome
low renin from negative feedback
secondary hyperaldosteronism is caused by ___
chf
cirrhosis with ascites
nephritis
secondary hyperaldosteronism effects/ symptoms, labs
ECF lost to extravascular space
intravenously depleted despite total body overload, triggers renin release
exacerbates fluid retention and na retention
symptoms of hypoaldosteronism/ adrenal insufficiency
na lost in urine
hyperkalemia
plasma volume decreases and hotn. hyperkalemia may lead to circulatory collapse
Short term response to stress
increased hr
increased bp
liver converts glycogen to glucose and releases to blood
dilation of bronchioles
decreased gi and urine output
increased metabolic rate
long term stress response
retention of sodium, increased bp and volume
proteins/ fats broken down into energy
increased blood glucose
immune suppression
what can cause hyperaldosteronism
not a pituitary tumor
liver n kidney damage
primary vs secondary hyperaldosteronism diagnosis/ renin levels
primary- low renin
seondary- high renin
skip 16-23
anesthesia and addisons
cortisol before induction
addisons results from___
failure to produce adrenocortical hormones- glucocorticoids and mineralcorticoids
primary vs secondary addisons disease
primary- mostly autoimmune adrenal nonfunction, pituitary adrenal axis stays intact
secondary- hypothalamic or pituitary dysfunction from removal or chronic administration
treatment of primary vs secondary addison disease
primary- treatment is to replace glucocorticoid and mineralcorticoid deficiency
secondary- treat crisis w cortisol
symptoms of secondary addisons disease
hypoglycemia, fatigue, weak. weight loss, anorexia, hyperpigmentation, severe deterioration to stress
how to treat addisonian crisis
cortisol to treat cardiovascular collapse
symptoms of low mineralcorticoids
dehydration
polyuria
hypotension
hyponatremia
hyperkalemia
met acidosis
deat in 4 days to 2 weeks if untreated
symptoms of adrenal crisis
profound fatigue
dehydration
vascular collapse dt hotn
renal shut down- hyperK, hypoNA
symptoms of addisons disease
bronze skin
hair on women
gi disturbances
weakness
hypoglycemia
postural hypotension
weight loss
periop glucocorticoids
50-100mg to adult patients if on chronic steroids
if on chronic steroids, they cant increase cortisol, and get cv collapse
pt can die from holding steroids on day of surgery
Induction drug for hemodynamically unstable
etom
how does etom affect cortisol
suppresses for 24 hours and can cause hotn and adrenal insuffciciency
etom should be used sparingly in what population
septic shock
What bridges the endocrine and sympathetic nervous system
adrenal medulla
where are catecholamines made specifically
chromaffin cells in the adrenal medulla
what are catecholamines derived from
tyrosine
4 catecholamines
dopa, dopamine, norepi, epi
what is the output of the adrenal medulla
80% epi
20% nor epi
what will trigger fight or flight
pain
fear
hemorrhage
cold and heat
hypoglycemia
hotn
exercise
effects of fight or flight
increase co to heart and skeletal muscle
decrease blood flow to kidneys, skin, and mucosa
glucose and fatty acid mobilization for energy
increased respiration
what converts norepi to epi and what is it helped by
pnmt
phenylethanolamine n methyltransferase
expression is influenced by glucocorticoids (cortisol) which helps blood pressure
what causes pheochromocytoma
tumor caused by adrenal medullary hyperplasia or extra adrenal chormaffin tissue
pheo symptoms
paroxysmal htn
tachy
sweating
headache
anxiety
tremor
glucose intolerance
where is the tumor in pheo
most in a single gland, the right
10% in abdomen/ extra adrenal sites
10% are malignant
who is at risk for pheo
either gender
30,40,50s
half are incidental findings
40% have MEN multiple endocrine neoplasia
50% have men type 2
how to diagnose pheo
urinary Vanillylmandelic acid (VMA) as norepi and epi are degraded to it
COMT and MAO
Metabolize catecholamines
MAO- present in liver, kidneys, gi tract that catalyzes oxidative deamination
benefit of alpha blockers in pheo
alpha blocker reduces bp lability, mi, chf, dysrhthmias, cva
when should alpha blockers be started for pheo
10-14 days to normalize bp
THEN start bb
ensure fluid status is good bc of dilation
anesthetic plan for pheo
intra op tee
geta
a line
cvc
what meds provoke pheochromocytomas
histamine releasing agents- reglan and glucagon
how soon do catecholamines return to normal after surgery
several days
75% become normotensive within 10 days
what stimulates cortisol secretion
acth almost entirely
from crf in the hypothalamus
glucocorticoids and glucose
elevates bg dt glucose formation in liver and decreased utilization of glucose
stimulates gluconeogensis- formation of carbs from protein in liver
what can cause acth (cortisol) release
trauma
infection
heat/ cold
surgery
catecholamine injection
cortisol inlfammation
high levels of cortisol are anti inflammatory
stabiulze lysosomes, decreases cap perm, decrease wbc into inflamed areas
cortisol also causes resoluaiton of inflammation within hours, healing is enhanced, useful in autoimmune , allergic, asthma
What is cushings n its caused
excess cortisol secretion
acth ectopic tumor
over active hypothalamic secretion of crh
primary glucocorticoid secreting adrenal tumor
chronic administration / iatrogenic
cushings disease- acth secreting tumor of the pituitary gland
cushings syndrome symptoms
thin skin, easy bruising
osteoperosis from increased bone resorption
muscle wasting
moon face, buffalo hump
what is the primary androgen
testosterone
