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AP + Phys > Adrenal glands > Flashcards

Adrenal glands Flashcards

1
Q

adrenal cortex vs medulla location

A

medulla middle
cortex outer layer

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2
Q

adrenal cortex layers

A

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

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3
Q

What is the primary mineral corticoid?

A

aldosterone

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4
Q

What is the primary glucocorticoid

A

cortisone

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5
Q

What mainly activates aldosterone

A

hyperkalemia
RAAS

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6
Q

Where does aldosterone work (specifically)

A

Principal cells of the distal convoluted tubule and collecting ducts

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7
Q

Effects of aldosterone

A

NA and water retention
Excretion of K and H

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8
Q

If unopposed, aldosterone leads to

A

htn/ ECF expansion
hypokalemia
alkalosis

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9
Q

4 main controllers of aldosterone secretion

A

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

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10
Q

RAAS system

A

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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11
Q

Conns syndrome is __

A

Primary hyperaldosteronism

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12
Q

Conns syndrome is caused by

A

aldosterone secreting tumor, hyperplasia

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13
Q

Conns syndrome effects (symptoms, labs, abg)

A

increased ecf volume, htn, hypokalemia, metabolic alkalosis

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14
Q

how to diagnose conns syndrome

A

low renin from negative feedback

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15
Q

secondary hyperaldosteronism is caused by ___

A

chf
cirrhosis with ascites
nephritis

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16
Q

secondary hyperaldosteronism effects/ symptoms, labs

A

ECF lost to extravascular space
intravenously depleted despite total body overload, triggers renin release
exacerbates fluid retention and na retention

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17
Q

symptoms of hypoaldosteronism/ adrenal insufficiency

A

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

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18
Q

Short term response to stress

A

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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19
Q

long term stress response

A

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

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20
Q

what can cause hyperaldosteronism

A

not a pituitary tumor
liver n kidney damage

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21
Q

primary vs secondary hyperaldosteronism diagnosis/ renin levels

A

primary- low renin
seondary- high renin

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22
Q

skip 16-23

A
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23
Q

anesthesia and addisons

A

cortisol before induction

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24
Q

addisons results from___

A

failure to produce adrenocortical hormones- glucocorticoids and mineralcorticoids

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25
Q

primary vs secondary addisons disease

A

primary- mostly autoimmune adrenal nonfunction, pituitary adrenal axis stays intact
secondary- hypothalamic or pituitary dysfunction from removal or chronic administration

26
Q

treatment of primary vs secondary addison disease

A

primary- treatment is to replace glucocorticoid and mineralcorticoid deficiency
secondary- treat crisis w cortisol

27
Q

symptoms of secondary addisons disease

A

hypoglycemia, fatigue, weak. weight loss, anorexia, hyperpigmentation, severe deterioration to stress

28
Q

how to treat addisonian crisis

A

cortisol to treat cardiovascular collapse

29
Q

symptoms of low mineralcorticoids

A

dehydration
polyuria
hypotension
hyponatremia
hyperkalemia
met acidosis
deat in 4 days to 2 weeks if untreated

30
Q

symptoms of adrenal crisis

A

profound fatigue
dehydration
vascular collapse dt hotn
renal shut down- hyperK, hypoNA

31
Q

symptoms of addisons disease

A

bronze skin
hair on women
gi disturbances
weakness
hypoglycemia
postural hypotension
weight loss

32
Q

periop glucocorticoids

A

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

33
Q

Induction drug for hemodynamically unstable

A

etom

34
Q

how does etom affect cortisol

A

suppresses for 24 hours and can cause hotn and adrenal insuffciciency

35
Q

etom should be used sparingly in what population

A

septic shock

36
Q

What bridges the endocrine and sympathetic nervous system

A

adrenal medulla

37
Q

where are catecholamines made specifically

A

chromaffin cells in the adrenal medulla

38
Q

what are catecholamines derived from

A

tyrosine

39
Q

4 catecholamines

A

dopa, dopamine, norepi, epi

40
Q

what is the output of the adrenal medulla

A

80% epi
20% nor epi

41
Q

what will trigger fight or flight

A

pain
fear
hemorrhage
cold and heat
hypoglycemia
hotn
exercise

42
Q

effects of fight or flight

A

increase co to heart and skeletal muscle
decrease blood flow to kidneys, skin, and mucosa
glucose and fatty acid mobilization for energy
increased respiration

43
Q

what converts norepi to epi and what is it helped by

A

pnmt
phenylethanolamine n methyltransferase
expression is influenced by glucocorticoids (cortisol) which helps blood pressure

44
Q

what causes pheochromocytoma

A

tumor caused by adrenal medullary hyperplasia or extra adrenal chormaffin tissue

45
Q

pheo symptoms

A

paroxysmal htn
tachy
sweating
headache
anxiety
tremor
glucose intolerance

46
Q

where is the tumor in pheo

A

most in a single gland, the right
10% in abdomen/ extra adrenal sites
10% are malignant

47
Q

who is at risk for pheo

A

either gender
30,40,50s
half are incidental findings
40% have MEN multiple endocrine neoplasia
50% have men type 2

48
Q

how to diagnose pheo

A

urinary Vanillylmandelic acid (VMA) as norepi and epi are degraded to it

49
Q

COMT and MAO

A

Metabolize catecholamines
MAO- present in liver, kidneys, gi tract that catalyzes oxidative deamination

50
Q

benefit of alpha blockers in pheo

A

alpha blocker reduces bp lability, mi, chf, dysrhthmias, cva

51
Q

when should alpha blockers be started for pheo

A

10-14 days to normalize bp
THEN start bb
ensure fluid status is good bc of dilation

52
Q

anesthetic plan for pheo

A

intra op tee
geta
a line
cvc

53
Q

what meds provoke pheochromocytomas

A

histamine releasing agents- reglan and glucagon

54
Q

how soon do catecholamines return to normal after surgery

A

several days
75% become normotensive within 10 days

55
Q

what stimulates cortisol secretion

A

acth almost entirely
from crf in the hypothalamus

56
Q

glucocorticoids and glucose

A

elevates bg dt glucose formation in liver and decreased utilization of glucose
stimulates gluconeogensis- formation of carbs from protein in liver

57
Q

what can cause acth (cortisol) release

A

trauma
infection
heat/ cold
surgery
catecholamine injection

58
Q

cortisol inlfammation

A

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

59
Q

What is cushings n its caused

A

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

60
Q

cushings syndrome symptoms

A

thin skin, easy bruising
osteoperosis from increased bone resorption
muscle wasting
moon face, buffalo hump

61
Q

what is the primary androgen

A

testosterone

AP + Phys (38 decks)

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