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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
Q

How do you tx pheochromocytoma?

A

start with alpha blocker (phentolamin) then give BB

then after a few weeks surgery (adrenalectomy)

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26
Q

Why do we not biopsy adrenal tumors?

A

you could potentially spread the cancer if it was cancer

could cause HTN crisis and KILL THE PT d/t epi and norepi release

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27
Q

What activities, foods, medications, can precipitate pheochromocytoma sxs?

A 
exercise 
change in position 
pregnancy 
surgery 
urination
food with tyramine
TCA 
Opioids
metoclopramide
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28
Q

What do you do if the pheochormocytoma is not resectable?

A

tumor mass reduction
alpha blockade for sxs
chemotherapy
nuclear medicine

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29
Q

Hirsutism

A

unwanted male pattern hair growth in women
can be a sing of hyperandrogenism
>70% PCOS

excessive androgens

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30
Q

Hypertrihocis

A

diffusely increasing total body hair
rare
can be drug induced of d/t systemic illness such as anorexia, hypothyroidism, malnutrition

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31
Q

Virilization

A

male physical characteristics caused by testosterone > 150

seen with hirsutism

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32
Q

What are the two most common causes of hirsutism?

A

PCOS

non-classic congenital adrenal hyperplasia (CAH)

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33
Q

What will you see of PE for a pt with hirsuitism?

A 
evidence of virilization 
BMI
Skin findings 
-bruising
-strie
-acanthosis
34
Q

Congenital Adrenal Hyperplasia

A

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
Q

Is congenital adrenal hyperplasia recessive or dominant?

A

recessive

36
Q

What are the signs and sxs of congenital adrenal hyperplasia?

A

severe:
adrenal crisis
virilization in infancy

mild:
late onset
hirsutism

ambiguous genitalia
clitoral enlargement
fusion of labial folds

37
Q

How do you dx 21 hydroxylase deficiency?

A

congenital adrenal hyperplasia

elevated 17OH progesterone

38
Q

17OH progesterone

A

will be elevated in congenital adrenal hyperplasia

dx

39
Q

Where are the adrenal glands located?

A

retroperitoneal cavity above each kidney posteromedial surface

40
Q

What is the precursor for adrenal steroidogeneis?

A

cholesterol

41
Q

Primary vs secondary adrenal problem

A 
primary = gland itself (addisons)
secondary = problem at the pituitary gland (failure of ACTH secretion)

secondary MC

42
Q

What hormone stimulates the pituitary gland to release ACTH?

A

CRH from the hypothalamus

43
Q

When is cortisol the highest?

A

about an hour before you wake up, assuming you wake up around 7 or 8

44
Q

Addison’s disease

A

primary adrenal insufficiency

most common cause in western world is autoimmune adrenalitis –loss of cortical cells - medulla intact

45
Q

What is the most common cause of primary adrenal insufficiency?

A

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
Q

How does the path of infectious primary AI differ from autoimmune AI?

A

infectious - calcifications

autoimmune - atrophy

47
Q

How can ketoconazole affect the adrenals?

A

inhibit cortisol synthesis leading to primary AI

48
Q

What labs would you see for primary AI?

A

high ACTH
low cortisol

glucocorticoid AND mineralocorticoid deficiency

49
Q

What are the sxs of chronic primary AI?

A 
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
Q

What sxs are specific to primary AI?

A

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
Q

What laboratory findings would you see with primary AI?

A

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
Q

What is the treatment for primary AI?

A

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
Q

In primary AI what drugs do we use to replace cortisol?

A

prednisone or hydrocortisone or dexomethasone

54
Q

In primary AI what drugs do we use to replace aldosterone?

A

fludrocortisone

55
Q

What do you tell your primary AI pt to do if they become sick?

A

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
Q

How do you dx adrenal insufficiency?

A

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
Q

What is adrenal crisis?

A

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
Q

What is the clinical manifestation of adrenal crisis?

A 
shock and hypotension out of proportion with their illness 
abdominal pain 
N/V
fever, lethargy 
coma, confusion

LIFE THREATENING EMERGENCY

59
Q

What do you do for a pt in adrenal crisis?

A

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
Q

How do you dx adrenal insufficiency?

A

AM cortisol <3ug/dl

normally cortisol would be highest in the morning

61
Q

Cosyntropin

A

ACTH stimulation test

measure basal, 30 min and 60 min cortisol

these assess adrenal reserve but not direct pituitary/hypothalamic function

62
Q

Secondary AI causes

A

exogenous glucocotricoids
pituitary disorders
-tumors, apoplexy, infarction
granulomatous disease (TB, sarcoid)

63
Q

What lab values would you expect for secondary AI?

A

Low ACTH

Low cortisol

64
Q

Why must pts on long term steroids be tapered off slowly?

A

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
Q

Which steroids are deficient in primary and secondary AI?

A

primary - glucocorticoids and mineralocorticoids

secondary - glucocorticoids only

66
Q

What are the signs and sxs of secondary AI?

A

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
Q

Primary vs secondary aldosteronism

A

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
Q

What are the clinical features of primary aldosteronism?

A

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
Q

Who do we screen for primary aldosteronism?

A

HTN with OSA
HTN with adrenal incidentaloma
resistant HTN despite 3 medications

70
Q

How do you dx primary aldosteronism?

A

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
Q

What is the treatment for primary aldosteronism?

A

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
Q

How do you treat bilateral idiopathic hyperplasia?

A

mineralocorticoid antagonists

  • spironolactone (SE: painful gynecomastia)
  • eplerenone

sodium restricted diet

73
Q

Cushing Syndrome

A

excess glucocorticoids

Cushings disease: ACTH secreting pituitary adenoma

74
Q

Cushings Disease

A

ACTH secreting pituitary adenoma

75
Q

Cushingoid habitus

A 
central obesity 
moon face
supraclavicular fat 
dorsal fat pad 
wide (>1cm) purple striae
76
Q

What are the signs and sxs of Cushings Syndrome?

A

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
Q

What is the initial test of choice for Cushings Syndrome?

A

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
Q

ACTH dependent Cushings

A

Cushings disease (pituitary adenoma)
ectopic ACTH
ectopic CRH

79
Q

ACTH independent Cushings

A

adrenal adenoma
exogenous steroids

pregnancy
obesity

80
Q

How do you determine if the ACTH Dependent Cushings syndrome is pituitary or ectopic?

A

high dose dexamethasone suppression test

ectopic ACTH will have no suppression on cortisol

81
Q

Where do we see ectopic ACTH production?

A

small cell lung cancer

bronchial carcinoid

Clin Med - Endocrine (13 decks)

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