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Clin Med - Endocrine > Lecture 6 - Adrenal Disorders > Flashcards

Lecture 6 - Adrenal Disorders Flashcards

1
Q

Where is aldosterone produced?

A

zona glomerulosa

mineralocorticoids

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2
Q

Where is cortisol produced?

A

zona fasciculata

glucocorticoid

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3
Q

Where are androgen hormones produced?

A

zona reticularis

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4
Q

Primary vs secondary causes of gland problems?

A

Primary –the problem is the gland itself

Secondary - the level above the gland (whatever hormone is working on the gland)

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5
Q

Secondary adrenal gland issues means the problem is where?

A

The pituitary gland

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6
Q

When is cortisol level the highest?

A

about an hour before you wake up (assuming you wake up at 7 or 8)

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7
Q

Primary Adrenal Insufficiency

A

Addison’s disease

MC cause in developed countries = autoimmune adrenalitis

*autoimmune dz clump together so think about hypothryoidism or celiac disease

worldwide the most common reason is TB

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8
Q

What is the most common worldwide cause of Addison’s disease?

A

TB

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9
Q

What is the most common cause of Addison’s disease in US?

A

autoimmune

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10
Q

Which drugs can cause primary adrenal insufficiency?

A

Ketoconazole (antifungal - inhibits cortisol synthesisi)
Rifampin (increases cortisol metabolism)
Etomidate

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11
Q

What ACTH and cortisol levels would you expect to see in primary adrenal insufficiency?

A

ACTH - high
cortisol - low

(the pituitary is trying to stimulate the adrenal glands)

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12
Q

What is the treatment for Addison’s disease?

A

fludrocortsione (mineralocorticoid)

+

prednisone or hyrocortisone
(glucocorticoids)

all of these pts need to have a medic alert bracelet

send these pts home with extra glucocorticoids (IM and PO)

if they get sick they need to take 2 or 3 more times of their steroids to avoid adrenal crisis

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13
Q

What are the sxs in primary AI?

A 
weakness 
tiredness 
fatigue 
anorexia (loss of appetite) 
GI sxs (N,V, constipation, abdominal pain)

+/-
salt craving
postural dizziness
muscle or joint pains

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14
Q

What are the signs of primary AI?

A

weight loss (100% of pts)

hypotension
hyperpigmentation

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15
Q

Why do pts with primary AI have hyperpigmentation in the joints and friction areas?

A

increased production of pro-opiomelanocortin d/t increase pituitary production
this increases MSH – increases melanin

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16
Q

What lab findings do you see on primary AI pts?

A 
low sodium (low BP) 
high potassium 
anemia
volume loss
eosinophilia
elevated TSH
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17
Q

What are the sxs of adrenal crisis?

A

shock and hypotension out of proportion to their illness
abdominal pain
N/V
coma, confusion

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18
Q

What is the treatment for adrenal crisis?

A

IV access with large bore IVs
draw electrolytes, cortisol, ACTH, and do not delay while result return
NS boluses and IV hydrocortisone 100 mg IV q8h

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19
Q

Cosyntropin stimulation test

A

synthetic ACTH to test for adrenal insufficiency (if the labs were previously unclear)

you inject the drug
measure basal, 30 min, and 60 min cortisol levels
you should see a response >18 ug/dl

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20
Q

What is the most common cause of secondary adrenal insufficiency?

A

exogenous glucocorticoids

other causes could be pituitary disorders

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21
Q

What labs will you expect to see in secondary adrenal insufficiency?

A

low ACTH and low cortisol

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22
Q

Pheochromocytoma

A 
adrenal tumor (medulla - chromaffin cells) 
that secretes Norepi and epi (surprisingly 15% of these tumors are actually not in the adrenal gland - paraganglioma)

sxs: HTN, Palpitations, HA, Excessive sweating

dx:
24 hour urine metanephrine test (metabolite of epinephrine)

tx: start on alpha blocker, then add BB, then get surgery

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23
Q

What are the signs and sxs of pheochromocytoma?

A

HTN
Palpitations - tachycarida
HA (episodic)
Excessive Sweating

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24
Q

How do you dx pheochromocytoma?

A

best first test is plasma metanephrines (draw blood in supine position)

24 hour urine metanephrine test

then you need to LOCATE the tumor –CT/MRI as first choice since 85% are in the adrenal
if you can’t find it there then you get MIBG scan to locate the tumor

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25
How do you tx pheochromocytoma?
start with alpha blocker (phentolamin) then give BB | then after a few weeks surgery (adrenalectomy)
26
Why do we not biopsy adrenal tumors?
you could potentially spread the cancer if it was cancer could cause HTN crisis and KILL THE PT d/t epi and norepi release
27
What activities, foods, medications, can precipitate pheochromocytoma sxs?
``` exercise change in position pregnancy surgery urination food with tyramine TCA Opioids metoclopramide ```
28
What do you do if the pheochormocytoma is not resectable?
tumor mass reduction alpha blockade for sxs chemotherapy nuclear medicine
29
Hirsutism
unwanted male pattern hair growth in women can be a sing of hyperandrogenism >70% PCOS excessive androgens
30
Hypertrihocis
diffusely increasing total body hair rare can be drug induced of d/t systemic illness such as anorexia, hypothyroidism, malnutrition
31
Virilization
male physical characteristics caused by testosterone > 150 seen with hirsutism
32
What are the two most common causes of hirsutism?
PCOS non-classic congenital adrenal hyperplasia (CAH)
33
What will you see of PE for a pt with hirsuitism?
``` evidence of virilization BMI Skin findings -bruising -strie -acanthosis ```
34
Congenital Adrenal Hyperplasia
21 hydroxylase deficiency no/low aldosterone and cortisol autosomal recessive inheritance severe: adrenal crisis and virilization in infancy mild: late onset, hirsutism dx. elevated 17OH progesterone non-classic (late onset)
35
Is congenital adrenal hyperplasia recessive or dominant?
recessive
36
What are the signs and sxs of congenital adrenal hyperplasia?
severe: adrenal crisis virilization in infancy mild: late onset hirsutism ambiguous genitalia clitoral enlargement fusion of labial folds
37
How do you dx 21 hydroxylase deficiency?
congenital adrenal hyperplasia elevated 17OH progesterone
38
17OH progesterone
will be elevated in congenital adrenal hyperplasia dx
39
Where are the adrenal glands located?
retroperitoneal cavity above each kidney posteromedial surface
40
What is the precursor for adrenal steroidogeneis?
cholesterol
41
Primary vs secondary adrenal problem
``` primary = gland itself (addisons) secondary = problem at the pituitary gland (failure of ACTH secretion) ``` secondary MC
42
What hormone stimulates the pituitary gland to release ACTH?
CRH from the hypothalamus
43
When is cortisol the highest?
about an hour before you wake up, assuming you wake up around 7 or 8
44
Addison's disease
primary adrenal insufficiency most common cause in western world is autoimmune adrenalitis --loss of cortical cells - medulla intact
45
What is the most common cause of primary adrenal insufficiency?
Western world: autoimmune adrenalitis --destruction of cortical cells 75% adrenal antibodies 50% have associated autoimmune disease (Thyroid MC) Worldwide: infectious disease -TB, fungal infections Other: -metastatic cancer (lung, breast, stomach, colon) >90% of each adrenal gland needs to be affect -medications --ketoconazole (inhibits cortisol synthesis)
46
How does the path of infectious primary AI differ from autoimmune AI?
infectious - calcifications autoimmune - atrophy
47
How can ketoconazole affect the adrenals?
inhibit cortisol synthesis leading to primary AI
48
What labs would you see for primary AI?
high ACTH low cortisol glucocorticoid AND mineralocorticoid deficiency
49
What are the sxs of chronic primary AI?
``` sxs related to the lack of cortisol: weakness tiredness fatigue GI sxs - N/V/C/abdominal pain Salt craving Postural dizziness muscle or joint pains ```
50
What sxs are specific to primary AI?
these sxs are related to the lack of aldosterone and sex hormones and increase in ACTH: hyperpigmentation (d/t the increase in MSH from the pituitary) hypotension weight loss
51
What laboratory findings would you see with primary AI?
hyponatremia (d/t mineralocorticoid deficiency - aldosterone) increased ADH secretion d/t decrease aldosterone production hypekalemia -aldosterone in the nephron is supposed to excrete potassium, but here there is a deficiency in aldosterone anemia eonsionphilia elevated TSH (glucocorticoids (cortisol) suppress TSH)
52
What is the treatment for primary AI?
glucocorticoids (prednisone or hydrocortinose) + mineralocorticoids (fludrocortisone) ALL PTS MUST HAVE MEDICAL ALERT BRACELET send pts home with extra glucocorticoids IM as well as PO for sickness
53
In primary AI what drugs do we use to replace cortisol?
prednisone or hydrocortisone or dexomethasone
54
In primary AI what drugs do we use to replace aldosterone?
fludrocortisone
55
What do you tell your primary AI pt to do if they become sick?
take extra cortisol replacement hormone (prednisone or hydrocortisone or dexomethasone) since a normal persons body would respond to being sick by increasing their cortisol double or triple the dose when you are sick otherwise you could get adrenal crisis
56
How do you dx adrenal insufficiency?
ACTH stimulation test (with cosyntropin) normal response to ACTH stimulation test would be rise in cortisol for AI pts there is no increase in cortisol (cortisol <20)
57
What is adrenal crisis?
sudden worsening in AI (whether you knew you had it or not) d/t a "stressful" event such as trauma, surgery, volume loss, hypothermia, MI, fever, sepsis, hypoglycemia, steroid withdrawal normal response to stress is a 3 fold increase in cortisol but these pts don't have that ability to increase their cortisol unless they take more exogenously less common in secondary AI
58
What is the clinical manifestation of adrenal crisis?
``` shock and hypotension out of proportion with their illness abdominal pain N/V fever, lethargy coma, confusion ``` LIFE THREATENING EMERGENCY
59
What do you do for a pt in adrenal crisis?
LIFE THREATENING EMERGENCY - IV access with large bore iVS - draw electrolytes, glucose, cortisol, ACTH (could give dexamthesone before drawing labs since it doesn't cross over into lab assay) - give IV hydrocortisone 100mg every 8 hours and NS boluses
60
How do you dx adrenal insufficiency?
AM cortisol <3ug/dl normally cortisol would be highest in the morning
61
Cosyntropin
ACTH stimulation test measure basal, 30 min and 60 min cortisol these assess adrenal reserve but not direct pituitary/hypothalamic function
62
Secondary AI causes
exogenous glucocotricoids pituitary disorders -tumors, apoplexy, infarction granulomatous disease (TB, sarcoid)
63
What lab values would you expect for secondary AI?
Low ACTH | Low cortisol
64
Why must pts on long term steroids be tapered off slowly?
when you are on exogenous steroids for a long period of time your adrenals (zona fasiculata) atrophy. So when you remove the exogenous steroids your HPA axis hasn't had time to ramp up and start producing steroids again if not you could send them into adrenal crisis
65
Which steroids are deficient in primary and secondary AI?
primary - glucocorticoids and mineralocorticoids secondary - glucocorticoids only
66
What are the signs and sxs of secondary AI?
hyponatremia may be present (with volume expansion) d/t inappropriate ADH secretion --more mild than primary hypoglycemia ---when a pt presents with hypoglycemia we always check them for AI
67
Primary vs secondary aldosteronism
primary - bilateral adrenal hyperplasia or Conn's syndrome (adrenal aldosteroma) excessive aldosterone from zona glomerulosa secondary - due to increase in RENIN (commonly from artery stenosis)
68
What are the clinical features of primary aldosteronism?
hypernatremia hypokalemia metabolic alkalosis hypomagnsemia lack of edema d/t "aldosterone escape" - spontaneous diuresis HTN (low renin levels) --typically these pts are uncontrolled on 3 or more drugs increases risk of CV disease greatly
69
Who do we screen for primary aldosteronism?
HTN with OSA HTN with adrenal incidentaloma resistant HTN despite 3 medications
70
How do you dx primary aldosteronism?
measure aldosterone to renin ratio -ideally the pt is sitting for 15 minutes after being awake for 2 hours aldosterone >15-20 renin <1.6 aldo:renin >20 [be sure that your pts that are normally on spironolactone or eplerenone are not on them for 6 weeks prior to this test] confirmatory testing then done --3 day oral sodium loading test --load pt with 6g sodium for 3 days and then do 24 hour urine CT scan for adrenal carcinomas get adrenal venous sampling if you want to go to surgery
71
What is the treatment for primary aldosteronism?
goal: prevent morbidity and mortality associated with HTN, hypokalemia, renal toxicity surgery is curative only in unilateral dz you only need 1 adrenal gland---never take out both adrenal glands
72
How do you treat bilateral idiopathic hyperplasia?
mineralocorticoid antagonists - spironolactone (SE: painful gynecomastia) - eplerenone sodium restricted diet
73
Cushing Syndrome
excess glucocorticoids Cushings disease: ACTH secreting pituitary adenoma
74
Cushings Disease
ACTH secreting pituitary adenoma
75
Cushingoid habitus
``` central obesity moon face supraclavicular fat dorsal fat pad wide (>1cm) purple striae ```
76
What are the signs and sxs of Cushings Syndrome?
cushingoid habitus immunosupression - infection bone demineralization affective disorder - mania or depression glucose intolerance (can get DM) androgen effects hypercoagulable state (prone to DVTs and PEs)
77
What is the initial test of choice for Cushings Syndrome?
low dose dexamthasone OR 24 hour urine (or saliva) test then check cortisol levels if still high then check ACTH to determine if its dependent or independent
78
ACTH dependent Cushings
Cushings disease (pituitary adenoma) ectopic ACTH ectopic CRH
79
ACTH independent Cushings
adrenal adenoma exogenous steroids pregnancy obesity
80
How do you determine if the ACTH Dependent Cushings syndrome is pituitary or ectopic?
high dose dexamethasone suppression test ectopic ACTH will have no suppression on cortisol
81
Where do we see ectopic ACTH production?
small cell lung cancer | bronchial carcinoid

Clin Med - Endocrine (13 decks)

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