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Endorine > Adrenal Pathophysiology (5/16) > Flashcards

Adrenal Pathophysiology (5/16) Flashcards

1
Q

List diseases of the Zona Fasciculata

A

Cortisol Xs: Cushings

Cortisol Deficiency: Addison’s

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2
Q

List disease of Zona Glomerulosa

A

Primary Hyperaldosteronism

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3
Q

List disease of the Zona Reticularis

A

Androgen Excess

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4
Q

List disease of the adrenal medulla

A

Pheochromocytoma (tumor that secrete XS catecholamines)

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5
Q

Dfine Cushing’s Syndrome

A

Having excess cortisol secretion (regardless of cause/source)

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6
Q

What is the most common cause of cushings syndrome?

A

Iatrogenic from exogenous glucocorticoid use

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7
Q

What are the pathophys changes in HPA axis with cushings?

A
  1. Loss of diurnal variation of cortisol secretion (cortisol peaks are higher and taller)
  2. Autonomy from ACTH control (ie loss of feedback regulation)
  3. XS cortisol secretion
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8
Q

What is Cushing’s Disease?

A

Pituitary adenoma that secretes too much ACTH

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9
Q

What is ectopic ACTH syndrome

A

Ectopic ACTH is being produced by a tumor outside the pituitary. Most common in lung and bronchi. Very severe

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10
Q

What are some basic metabolic derangements due to XS corticosteroids?

A
  1. Carb metab: stimulates gluconeogenesis leading to hyperglycemia
  2. Fat metab: inc lipgenesis leads to inc FFAs and insulin resistance (obesity is the most common finding in Cushings)
  3. Protein metab: Inc gluconeo–>catabolism (uses muscle)
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11
Q

What is the most common finding in cushings?

A

Obesity (also diabetes, hypertension, menstrual abnormalities, muscle weakness etc)

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12
Q

What are some phyiscal effects of fat metab?

A

Dewlap (double chin), Buffalo hump (fat bad at back of neck), supraclavicular fat pads

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13
Q

What are some effects of cortisol excess?

A
  • Impaired immunity
  • Inc clotting factors
  • Cataract formation
  • Proximal myopathy
  • Osteoporosis
  • Redistribution of body fat
  • Hypertension, cardiomyopathy, inc thromboemobolic events
  • Thin skin, easy brusing, striae, acne, hyperpigmentation, hirsutism
  • Psychiatric disturbances
  • Hypokalemia
  • Inc testosterone in females
  • Menses abnormalities
  • Marked virillization in women worrisome for malginant adnreal tumor
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14
Q

Describe ACTh dependent cushings

A

Characterized by bilateral adrenal hyperplasia

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15
Q

Describe ACTH independent cushings

A

Adenoma makes cortisol

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16
Q

What do you measure if there is loss of diurnal variation cortisol secretion?

A

Measure late night salivary cortisol. Measures free cortisol. Beware of pts with night shift/disturbed sleep/wake cycle

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17
Q

What do you measure if there is autonomy from ACTH control?

A

1mg dexamethasone suppression test. DST measures loss of feedback inhibition. Dex is a synthetic glucocorticoid so it should suppress ACTH and cortisol levels. If it doesn’t, then you have ACTH being produced elsewhere or from an ACTH producing adenoma.

  • indicates inappropriate secretion, does not indicate source of cortisol
  • Dex is taken at 11pm and cortisol is measured at 8am
  • Normal: cortisol <2mcg/dL after dex
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18
Q

What do you measure if there is an excess of cortisol?

A

24 hr urinary free cortisol measurements. Cushings is more likely if cortisol >3x upper limit of normal

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19
Q

If a pts urine cortisol is markedly elevated and cortisol is elevated after DSH. ACTH is also elevated. What is the source of cushings?

A

Pituitary adenoma (inc ACTH, cortisol despite DST)

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20
Q

If ACTH is low

A

Cushings from adrenal source

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21
Q

If ACTH is normal or elevated

A

Pituitary or ectopic source

22
Q

ACTH is suppressed

A

Source is exogenous glucocorticoids

23
Q

How do we localize the source?

A

imaging

24
Q

How do we treat cushings?

A

Depends on source

  • Cure unilateral adrenal adenoma with adrenalectomy
  • Use ketoconazole, metyrapone or bilateral adrenalectomy if required
25
Q

How long does it take for symptoms to go away post treatment?

A

Up to 12 mo, not all sequelae completely resolve, esp psychiatric complications

26
Q

Name a disease of cortisol deficiency

A

Addison’s (adrenal cortical failure)

27
Q

How much of cortex is destroyed prior to presentation in addisons?

A

90%

28
Q

What hormone is elevated in addisons?

A

ACTH

29
Q

What ion deficiencies can you have?

A

Hyponatremia and hyperkalemia

30
Q

What bp abnormality will you have?

A

Hypotension

31
Q

What are the clinical characteristics of addison;s?

A 
Hyperpigmentation from increased ACTH
Weight loss
Muscle or joint pains
Fatigue
Nausea, abdominal pain
Hypoglycemia can occur
32
Q

What is the etiology of primary adrenal insufficiency (aka Addison’s)

A
  • Autoimmune destruction of 60% of the adrenal cortex
  • Infectious from TB, fungus, HIV etc
  • Bilateral hemorrhage/infarction: anticoag, trauma, embolic, meningococcemia etc=waterhouse-friderichsen syndrome
  • Metastatic cancer
  • Drugs, including those that inc cortisol metab
33
Q

How do we diagnose Addison’s?

A

-Early AM cortisol 20mcg/dL excludes adrenal failure.

34
Q

What is a good initial short term treatment?

A

Dexamethasone because it will not interfere with cortisol assay. If pt is hypotensive with a strong clinical suspicion, treat with glucocorticoids first and make the diagnosis later

35
Q

What is an adrenal crisis

A

Acute deficiency in cortisol and mineralocorticoids. CAn be life threatening and masquerade as other conditions

36
Q

What are the clinical characteristics of an adrenal crisis?

A

Hypotension, shock, fatigue, weakness, fever, lethargy, abdominal pain, anorexia, hypoglycemia

37
Q

What are some causes of adrenal crisis?

A
  • New primary adrenal failure
  • Known adrenal insufficiency with acute illness or under-replacement of meds
  • Acute withdrawal of high dose glucocorticoids
  • Pituitary apoplexy
38
Q

How do we treat adrenal crisis (short term)?

A
  • 1-3 liters saline IV over 12-24 hrs
  • Dexamethasone 4mg IV
  • Monitor electrolytes
  • Monitor bP
39
Q

What are the two types of polyglandular syndromes and why do we care?

A
  • We care because addisons can be associated with polyglandular syndromes
  • Type 1: hypoparathyroidism, mucocutaneous candidiasis, primary hypogonadism
  • Type 2: T1D, autoimmune thyroiditis, vitiligo, hypogonadism
40
Q

What is primary hyperaldosteronism?

A

Mineralocorticoid excess

41
Q

What are the associated issues with hyperaldosteronism?

A

Hypertension, hypokalemia (though it is possible that this is normal…still aldosterone causes the collecting duct transporters to secrete k+ in exchange for Na+), mild hyernatremia, metabolic alkalosis, muscle weakness

42
Q

What causes hyperaldosteronism?

A

Adrenal adenoma producing aldosterone or bilateral adrenal hyperplasia

43
Q

Who should be screened for primary hyperaldosteronism?

A
  • <30 y.o with hyperT, no obesity or fam hx
  • Persons with unexplained hypokalemia and hyperT
  • Persons with resistant hyperT
  • Persons with an adrenal incidentaloma and hyperT (ie find it accidentally)
44
Q

How do we diagnose hyperaldosteronism?

A
  • Early morning aldosterone:renin ratio
  • Ratio >20 suggestive, but not diagnostic
  • Aldosterone >15 and suppressed renin suggestive
  • Once biochemical diag is certain, do CT or MRI
  • If pos imaging, further testing req: salt loading to demonstrate inappropriate aldosterone secretion, *adrenal vein sampling prior to surgery
45
Q

What is adrenal vein sampling

A
  • MEasure aldo and cortisol concentrations in each vein and IVC
  • Distinguishes between uni adenoma and bilateral adrenal hyperplasia
  • For lateral dis, the aldosterone concentration needs to be 4x greater than the contralateral side
46
Q

What is the treatment of primary hyperaldosteronism?

A
  • Unilateral aldosterone secreting adenoma: surgical resection
  • Bilateral adrenal hyperplasia: mineralocorticoid antag
47
Q

What are the symp of androgen excess?

A
  • Woman: hirsutism, male pattern baldness, menstrual irreg

- Men: Gonadotrophin sec disrupted

48
Q

What is an adrenal adenoma relationship to androgen excess?

A

Adrenal adenomas rarely cause androgen xs, they usually cause cortisol xs

49
Q

What can cause androgen excess?

A
  • ACTH dependent cushings can cause elevation in testosterone and DHEAS
  • If you see a woman with acute onset virilization–>think this
50
Q

What does the adrenal medulla secrete?

A

Catecholamines

Endorine (24 decks)

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