Adrenals Flashcards

1
Q

Describe the HPA (hypothalamic pituitary axis)

A

Primary organ: target organ
Secondary: Pituitary
Tertiary: hypothalamus

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2
Q

What are the hormones of the adrenals

A

zona Glomerulosa: Mineralocorticoids (Aldosterone)
zona Fasciculata: Glucocorticoids (cortisol)
zona Reticularis: Adrenal androgens (DHEA)
Medulla: catecholamines (epi/NE)

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3
Q

What does aldosterone do

A

controls body fluid volume!
Increase reabsorption of Na and H2O
Increase excretion of K+ and H+

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4
Q

Describe cortisol secretion

A

Pulsatile, diurnal under control of ACTH

Secreted mainly in the morning, around 8-9AM

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5
Q

What stimulates the hypothalamus to release CRH (then ACTH then cortisol)

A

Stress!
trauma, pain, hypoglycemia, hemorrhage
Mineralocorticoids mediate the long-term stress response

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6
Q

What can long term high dose glucocorticoid therapy cause

A

adrenal atrophy

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7
Q

What does primary overproduction of cortisol by the adrenals cause

A

ACTH secretion inhibition (negative feedback)

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8
Q

What are the functions of cortisol

A
Protect against hypoglycemia 
Decrease insulin sensitivity 
Anti-inflammatory 
Suppress immune system 
Maintain vascular responsiveness to NE/Epi 
Inhibit bone formation 
Promote increase in GFR
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9
Q

How does cortisol protect against hypoglycemia

A

Gluconeogenesis in liver
Proteolysis
Lipolysis

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10
Q

How is cortisol anti-inflammatory

A

Inhibits production of inflammatory mediators; histamine, leukotrienes, prostaglandins

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11
Q

What is DHEA

A

Little significance in men

Women: major source of androgens! causes early development of pubic and axillary hair, and masculinization

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12
Q

What are the physiologic effects of the catecholamines

A
Epi/NE
Increase rate and force of heart contraction 
Vasoconstriction  
Dilate Bronchioles 
Stimulate lipolysis in fat cells 
Increase metabolic rate 
Pupil dilation 
Inhibit "non-essential" processes (GI secretions)
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13
Q

In other words, Epi/NE mediate

A

Short term stress response

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14
Q

What are the principles of endocrine testing

A

Hypofunction: do a stimulation test
Hyperfunction: do a suppression test

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15
Q

What are the possible results of a serum total cortisol

A

> 10: unlikely to have adrenal insufficiency
3-10: inconclusive
<3: very likely to have adrenal insufficiency

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16
Q

How do you preform a 24 hour urinary free cortisol test

A

Discard first morning void
Collect for next 24 hours (including void at end of 24 hours)
record last voiding time
Keep urine cool during collection (high temp alters results)
If urine is lost, start over the next day

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17
Q

What does a 24 hour urinary free cortisol test measure

A

quantity of free cortisol collected

Ideal for suspected hypercortisolism

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18
Q

What is the purpose of a Plasma ACTH test

A

Differentiate primary, secondary, and tertiary source of cortisol imbalance
-You collect it with a serum cortisol, as it has the same diurnal variation

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19
Q

What does the ACTH stimulation test assess

A

The source of adrenal insufficiency (cortisol deficiency)

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20
Q

How do you preform an ACTH stimulation test

A

Get baseline plasma cortisol level
Give 250 mg IV short acting Cosyntropin (synthetic ACTH)
Measure plasma cortisol at 30 and 60 min

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21
Q

What are the possible results of an ACTH stimulation test

A

Cortisol level doubles: normal adrenal fxn

Cortisol level subnormal: Adrenal Insufficiency

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22
Q

What is the Dexamethasone suppression test

A

Get baseline plasma cortisol
Give 1mg DXM (synthetic steroid) PO at 11PM
Measure plasma cortisol at 8AM

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23
Q

What are the possible results of the dexamethasone suppression test

A

Cortisol level no change: excess cortisol production (steroid can’t even suppress it)
Cortisol level suppressed: normal adrenal fxn

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24
Q

Prolonged exposure to elevated cortisol results in

A

Cushing’s Syndrome!

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25
Q

What are the MCC of Cushing’s syndrome

A

Exogenous: chronic excess corticosteroids
Endo: Pituitary adenoma (cushing’s disease)- W:M 10:1
(endo can also be 2/2 adrenal hyperplasia, sdrenocortical tumor, neuroendocrine tumor, small cell lung cancer, and ovarian cancer)

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26
Q

What are the physical manifestations of Cushing’s Syndrome

A

HTN
central obesity (moon face, buffalo hump)
Insulin resistance (overt DM)
Purple striae >1cm wide
easy bruising
androgen excess (hirsutism, acne, irreg menses)
severe fatigue and proximal muscle weakness
osteoporosis
impaired wound healing
infections
psych- depression, paranoia

27
Q

If you have clinical suspicion for Cushing’s syndrome, how can you test for it and what will your results be

A

24 hour free urine cortisol: high
midnight salivary cortisol level: high on 2 separate nights
DXM suppression: no change in cortisol level
Plasma ACTH: <20 is an adrenal tumor- >80 at 8am is a pituitary adenoma (ACTH dependent)

28
Q

How do you manage Cushing’s syndrome

A

If 2/2 pituitary tumor: get an MRI
If 2/2 ectopic ACTH secreting tumor: get CXR to r/o lung mass, and pelvic u/s to r/o ovarian mass
If 2/2 pituitary tumor: is there a palpable abd mass? get CT abdomen
If 2/2 exog steroids: taper to lowest possible therapeutic dose

29
Q

What are treatments for Cushing’s syndrome

A

Pituitary adenoma: Transspheniodal resection
Adrenal tumor: adrenalectomy
Adrenal hyperplasia: meds
Ectopic ACTH syndrome: target source of ectopic production

30
Q

Medical management of Cushing’s Syndrome includes

A
Adrenolytic agents (Mitotane): permanently destroys adrenocortical cells! medical adrenalectomy 
Adrenal enzyme inhibitors
31
Q

What are the adrenal enzyme inhibitors used in Cushing’s syndrome

A

Ketoconazole: antifungal, cortisol reduction in higher doses (ADE liver toxic!!)
Metyrapone: inhibits cortisol synthesis, mostly a combo drug

32
Q

What can cause Primary adrenal insufficiency

A

MC in USA: Addison’s disease (AI cortical destruction) causing mineral/glucocorticoid deficiency
MC in world: Tuberculosis
-Also: congenital enzyme deficiencies, infection, surgery (adrenalectomy)

33
Q

What can cause Secondary adrenal insufficiency

A

Insufficient ACTH secretion

Long term exogenous steroid= HPA suppression= abrupt med withdrawal= Addison’s crisis

34
Q

What causes tertiary adrenal insufficiency

A

insufficient CRH secretion

35
Q

Clinical manifestations of adrenal insufficiency are

A

Insidious onset, non-specific Sx: weakness, fatigue, anorexia, weight loss
*Hyperpigmentation (creases, pressure areas, and nipples)
Hypotension
Hypoglycemia
Salt cravings
GI complaints

36
Q

What drives hyperpigmentation

A

ACTH

37
Q

Clinical manifestations of Addison’s Crisis (2ndry insuff) are

A
Extremely low cortisol 
Sudden onset Hypotension
acute abd/back pain 
vomiting 
diarrhea
dehydration 
AMS 
electrolyte abnormalities
38
Q

What initial diagnostic studies should you get for adrenal insufficiency, and what are results

A

CMP: hyperkalemia, hypercalcemia, hyponatremia
CBC: Eosinophilia

39
Q

If initial CBC and CMP are suspicious, what other labs can you get

A

Anti-adrenal antibodies, indicating AI if primary insufficiency (Addison’s)
AM plasma cortisol: abn low
Plasma ACTH: if high, primary. if low, second/tertiary
ACTH stimulation test: cortisol level does not change

40
Q

Review of what to do if you suspect Addison’s disease

A

Get a CBC, CMP

Get a plasma ACTH, plasma cortisol, and ACTH stimulation test

41
Q

When would you need a radiograph of the adrenals

A

CT: For secondary causes, to eval possible infection or malignancy; Not needed for primary adrenal insufficiency
MRI: pituitary if secondary insufficiency (hypothalamus or pituitary)

42
Q

How do you treat Adrenal insufficiency

A

Primary: Glucocorticoids (hydrocortisone) AND mineralocorticoids (fludrocortisone) replacement
1/3: Glucocorticoids only (hydrocortisone)

43
Q

What changes can be made to adrenal insufficiency meds

A

Increase dose in stressful times
Give DHEA to women
Taper long term steroids to prevent 2/3 adrenal insuff

44
Q

How do you treat an adrenal crisis

A

IV steroics
Correct electrolytes (Volume resuscitation)
50% dextrose to correct hypoglycemia
when stable, look for the underlying cause

45
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism
MCC adrenocortical adenoma
also 2/2 cortical hyperplasia

46
Q

How does primary hyperaldosteronism present

A
HTN 
Hypokalemia 
Muscular weakness 
Paresthesias 
Paresthesias 
HA 
Polyuria and Polydipsia
47
Q

What should the work up for primary hyperaldosteronism include

A

Elevated plasma and urine aldosterone
low plasma renin (RAAS)
CT scan of adrenals to eval adrenal adenoma

48
Q

How do you manage primary hyperaldosteronism

A

Surgically remove adenoma

Spironalactone, anti-HTN

49
Q

What is a pheochromocytoma

A

Tumor arising from chromaffin cells in adrenals, MC in medulla;
Secretes catecholamines (epi/NE)
10% are malignant

50
Q

What are the clinical manifestations of a pheochromocytoma

A

Paroxysmal Palpitations (tachycardia)
HA
Episodic sweating
Paroxysmal/sustained HTN (very high, 200/100 levels)

51
Q

When I say “refractory hypertension” you say…

A

PHEOCHROMOCYTOMA!

52
Q

What is a Pheochromocytoma attack

A

+/- displacement of abd contents (lift, bend)
Lasts 30-40 min
Increases in frequency and severity over time

53
Q

Other Sx of pheochromocytoma include

A
pallor 
nausea 
tremor 
fatigue
anxiety
epigastric pain 
hypertensive retinopathy (from prolonged HTN)
54
Q

When should you suspect a pheochromocytoma

A
Classic paroxsymal attacks 
Refractory HTN, HTN <20 y/o 
Idiopathic DCM 
Abdominal mass 
Fhx 
Adrenal mass 
MEN2 
Neurofibromatosis
55
Q

How do you diagnose a pheochromocytoma

A

1st*Metanephrine 24 hour urine screen (catecholamine metabolite)
Clonidine suppression
MRI abdomen and pelvis
MIBG (radio-isotope) to ID extra-renal tumors

56
Q

What does Clonidine usually do to catecholamines

A

It causes them to decrease

If you have a pheochromocytoma, they do not decrease

57
Q

How do you treat pheochromocytomas

A

Give alpha blocker (phenoxybenzamine) to control BP
Give beta blocker (propanolol) to control HR
Surgical resection

58
Q

What is an adrenal incidentaloma

A

Mass >1cm discovered incidentally by radiographs (abd CT)
MC in obese, hypertensive, diabetic patients
Most are non-functional

59
Q

What must you ask yourself when you find an adrenal mass

A

Is it malignant (<4cm, lipid rich, rapid contrast wash out)

Is it functioning

60
Q

How do you work up an adrenal incidenteloma

A

Get a plasma cortisol, serum ACTH, serum DHEA, and plasma aldosterone

  • Do they have Sx of cushing’s? (if yes, get 24 hr urine free cortisol) (if no, do DXM suppression)
  • Are you susp of pheo? (24 hr metanephrine, catecholamines)
61
Q

When would you order a fine needle aspiration/biopsy

A

If you have a known primary malignancy elsewhere and are evaluating an adrenal incidenteloma

62
Q

When DON’T you need a FNA

A

If you have evidence of a pheo (dont want to release the contents)
Known widespread mets

63
Q

How do you treat an adrenal incidenteloma

A

If pheo/carcinoma: Surgery
If underlying dz: pharm intervention
If benign in imaging:>2cm resect, <2cm repeat imaging at 6, 12, and 24 mo; test DXM suppression q4 years