Adrenal glands Flashcards by Jacob Martinez

adrenal cortex vs medulla location

medulla middle
cortex outer layer

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adrenal cortex layers

GFR
Salt Sugar sex
Glomerulosa aldosterone
Fasciculata glucocorticoids- cortisol
Reticularis sex hormones DHEA

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What is the primary mineral corticoid?

aldosterone

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What is the primary glucocorticoid

cortisone

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What mainly activates aldosterone

hyperkalemia
RAAS

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Where does aldosterone work (specifically)

Principal cells of the distal convoluted tubule and collecting ducts

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Effects of aldosterone

NA and water retention
Excretion of K and H

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If unopposed, aldosterone leads to

htn/ ECF expansion
hypokalemia
alkalosis

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4 main controllers of aldosterone secretion

potassium- potent controller
RASS (at2) - potent
sodium
ACTH- minor/ no effect

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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

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Conns syndrome is __

Primary hyperaldosteronism

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Conns syndrome is caused by

aldosterone secreting tumor, hyperplasia

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Conns syndrome effects (symptoms, labs, abg)

increased ecf volume, htn, hypokalemia, metabolic alkalosis

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how to diagnose conns syndrome

low renin from negative feedback

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secondary hyperaldosteronism is caused by ___

chf
cirrhosis with ascites
nephritis

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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

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symptoms of hypoaldosteronism/ adrenal insufficiency

na lost in urine
hyperkalemia
plasma volume decreases and hotn. hyperkalemia may lead to circulatory collapse

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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

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long term stress response

retention of sodium, increased bp and volume
proteins/ fats broken down into energy
increased blood glucose
immune suppression

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what can cause hyperaldosteronism

not a pituitary tumor
liver n kidney damage

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primary vs secondary hyperaldosteronism diagnosis/ renin levels

primary- low renin
seondary- high renin

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skip 16-23

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anesthesia and addisons

cortisol before induction

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addisons results from___

failure to produce adrenocortical hormones- glucocorticoids and mineralcorticoids

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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