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Endocrine Unit Phase 1 > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What does ACTH stimulate?

A

Secretion of Cortisol, aldosterone, and androgens

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2
Q

What are the functions of cortisol?

A

increases BP (upregulation of alpha adrenergic R in arterioles, vasoconstriction), regulates metabolism (SNS hormone, increases insulin resistance, gluconeogenesis, lipolysis, proteolysis), decreased inflammatory response, bone production, fibroblast activity

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3
Q

What are the functions of aldosterone?

A

Na+ retained from K, water follows, treats low BP (hypovolemia) + increases K+ secretion (hyperkalemia)

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4
Q

What are causes of primary acute adrenal insufficiency?

A

massive adrenal hemorrhage (Watershouse-Friderichsen Syndrome) due to Neisseria Meningitis blood infection

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5
Q

What are causes of chronic primary adrenal insufficiency? What is the pathophysiology?

A

Addison Disease: autoimmune destruction of adrenal gland or by infection w/ HIV, Tb, or other

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6
Q

What are the types of adrenal insufficiencies?

A

Primary - acute and chronic

Secondary

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7
Q

What are causes of secondary adrenal insufficiency?

A

pb with anterior pituitary, ACTH secretion, chronic use of exogenous glucocorticoids, autoimmune destruction of PG/, traumatic brain injury of PG/, pituitary hemorrhage

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8
Q

What are the general sxs of adrenal insufficiency?

A

weakness, fatique, weight loss, muscle aches, hypoglycemia, orthostatic hypotension

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9
Q

What are the sxs seen w/ low aldosterone?

A

salt-craving, low BP, hypoglycemic episodes leading to dizziness and falls

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10
Q

What are sxs of primary acute adrenal insufficiency?

A

gingival (hyperpigmentation of skin and mucosal surfaces), hyponatremia, hyperkalemia, metabolic acidosis, high eosinophil counts (w/ addison disease)

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11
Q

What are sxs seen with secondary adrenal insufficiency?

A

no increased skin pigmentation since low ACTH (and low POMC), no hyperkalemia or metabolic acidosis since aldosterone production preserved, regulated by RAAS

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12
Q

What regulates Aldosterone production?

A

RAAS

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13
Q

When is serum cortisol highest? What does it mean if it is low?

A

morning, adrenal gland dysfunction

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14
Q

What is ACTH stimulation test? When is it used?

A

if borderline-low morning cortisol, give synthetic, compare cortisol levels, should see ACTH, x increase if 2ndary AI (not adrenal pb). If 0-25% increase: primary AI or chronic 2ndary due to adrenal atrophy

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15
Q

What happens w/ chronic AI to adrenal gland?

A

can atrophy

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16
Q

What imaging modality should be used to dx primary AI? What should be seen?

A

CT = atrophy, hemorrhage, infection

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17
Q

What imaging modality should be used to dx secondary AI?

A

look for cause of pituitary insufficiency

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18
Q

What infectious test should be done in all primary AI dx? What hormone deficiencies should be screened for in secondary AI?

A

HIV testing since common cause of primary AI, consider other infections like Tb. Screen for prolactin, TSH, etc to see ndary AI

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19
Q

What is tx for acute primary AI?

A

IV cortisol to increase BP, IV dexamethasone to replace steroids, IV saline and dextrose to treat hypotension and hypoglycemia

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20
Q

What is tx for chronic primary AI?

A

Oral glucocorticoids (short-acting hydrocortisone and long-acting dexamethasone or prednisone)

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21
Q

How should secondary AI be treated?

A

oral glucocorticoids (short-acting hydrocortisone and long-acting dexamethasone or prednisone)

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22
Q

What should be kept in mind when providing long-term glucocorticoid therapy?

A

never stop suddenly, avoid acute AI (steroid withdrawal), taper off for weeks-months instead

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23
Q

How do you treat hyperkalemia and hyponatremia seen w/ AI? When is it given?

A

fludrocortisone (synthetic mineralocorticoids), given if pt remains hypotensive while taking glucocorticoid tx

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24
Q

What is Cushing Syndrome? What is seen w/ it?

A

Hypercortisolism mainly, decreased wound healing, slower bone formation, increased infections, 2ndary form of diabetes

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25
Q

What are the 2 categories of causes of Cushing?

A

exogenous/iatrogenic (most common, meds taken for lupus or arthritis) or endogenous (abnormal adrenal gland or high ACtH)

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26
Q

What causes primary hypercortisolism (Cushing)?

A

adrenal adenoma producing cortisol (beign neoplastic overgrowth), bilateral hyperplasia, adrenal carcinoma (rare)

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27
Q

What causes secondary hypercortisolism?

A

pituitary adenoma (most common), paraneoplastic syndrome (cancer)

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28
Q

What population is most at risk for pituitary adenoma causing Cushing disease?

A

women and prepubertal boys

29
Q

What is Cushing disease vs Cushing syndrome?

A 
disease = caused by pit. adenoma, increased ACTH secretion
Syndrome = affects associated w/ hypercortisolism, multiple causes
30
Q

What are sxs seen w/ Cushing syndrome?

A

moon face, emotional disturbances, cardiac hypertrophy, high BP, steroid-induced acne, buffalo hump, thin, wrinkled skin, hirsutism, obesity/weight gain + abdominal striae, proximal muscle weakness, osteoporosis and osteopenia, skin ulcers, amenorrhea, erectile dysfunction –> hyperglycemia, hypertriglyceridemia, frequent infections, DVT

31
Q

How do you measure cortisol levels?

A 
24h urine (free cortisol) test
late night salivary cortisol
low-dose dexamethasone suppression test (ACTH suppressed or elevated in response to exogenous steroid admission)
32
Q

What should we see during low dose dexamethasone suppression test?

A

serum cortisol doesn’tdecrease even when synthetic steroid given

33
Q

How do you differentiate between pituitary gland or ectopic cancer causing hypercortisolism and high ACTH?

A

high-dose dexamethasone test (8mg) = high ACTH, and high cortisol, both suppressed –> pituitary. Not suppressed –> cancer
CRH stimulation test = give CRH, see higher ACTH and cortisol –> pituitary, no change –> cancer

34
Q

What imaging modality should be used for lung cancer, carcinoid tumors, and other ectopic sources of hypercortisolism?

A

Chest and abdominal CT

35
Q

What is tx for hypercortisolism (Cushing syndrome)? Caused by exogenous drug, adrenal adenoma, pit. adenoma, bilateral adrenal hyperplasia, ectopic cancer?

A

exogenous = lower/stop drug
adenomas = remove surgerically
Bilateral adrenal hyperplasia = metyrapone, ketoconazole, mitotane, inhibit synthesis of cortisol
Cancer = surgery or chemo

36
Q

Where does aldosterone act?

A

collecting ducts of K

  • Na+ reabsorbed by epithelial Na+ channels ENaCs
  • K+ secreted by Na+-K+-ATPase due to influx of Na+ from ENaCs
  • H+ secreted from H+-ATPase in intercalated cells (high blood pH)
37
Q

If angiotensin II increases, what happens to aldosterone?

A

increases, regulated by RAAS

38
Q

What is seen w/ hyperaldosteronism?

A

hypokalemia, metabolic alkalosis, resistant HTN, increased ANP secretion due to initial volume expansion

39
Q

What is ANP? What does it do? When is it secreted?

A

peptide hormone synthesized and secreted by atrial cardiac myocytes in response to atrial wall stretching, promotes renal Na+ and H2O loss → counters aldosterone effects, secreted w/ hyperaldosteronism

40
Q

What are hypokalemia sxs?

A

muscle weakness, cardiac changes (T-wave inversions, prominent U waves)

41
Q

What are the causes of primary hyperaldosteronism?

A

bilateral hyperplasia of gland, adrenal adenoma (benign, Conn Syndrome), glucocorticoid remediable hyperaldosteronism (rare, genetic abnormality)

42
Q

What happens in glucocorticoid-remediable hyperaldosteronism? What is the tx?

A

rare genetic abnormality where aldosterone synthase hyperactivity. Tx = give glucocorticoids

43
Q

What are the causes of secondary hyperaldosteronism?

A

renal artery stenosis, edematous disorders (CHF, cirrhosis, chronic renal failure, nephrotic syndrome), juxtaglomerular tumors

44
Q

What can renal artery stenosis lead to? How?

A

Secondary hyperaldosteronism, impaired blood flow thyrough renal arteries stimulates release of renin

45
Q

How do edematous disorders result in hyperaldosteronism?

A

low renal blood flow, associated w/ edema, can cause high aldosterone levels

46
Q

What happens w/ juxtaglomerular tumors? What does it result in?

A

produce renin, results in hyperaldosteronism

47
Q

What is a normal plasma aldosterone:renin activity level? What is seen w/ primary aldosteronism? Secondary aldosteronism?

A 
normal = 10
primary = >30 since increased aldosterone negatively feedbacks on renin
Secondary = high aldosterone and high renin = ratio near normal
48
Q

How should hyperaldosteronism be confirmed? What should be seen?

A

Aldosterone suppression test, orally administer Na+ and Cl- followed by renin and aldosterone: will see renin and aldosterone levels will not lower

49
Q

How is renal artery stenosis supposed to be dx? Tx?

A

CT angiography or Doppler sonography, tx: renal artery stenosis

50
Q

What meds can be given to treat hyperaldosteronism?

A

competitive aldosterone R antagonists (K+ sparing diuretics spironolactone and eplerenone)

51
Q

What is spironolactone? MOA? What is it used for? Side effects?

A

K+ sparing diuretic, competitive aldosterone R antagonist used to treat hyperaldosteronism. Acts on collecting tubule by binding and inactivating R = reduces K+ loss and improving BP. Can see painful breast swelling (gynecomastia)

52
Q

What is congenital adrenal hyperplasia? What do you see?

A

family of different enzyme deficiencies involved in production of adrenal hormones, autosomal recessive = results in hyperplastic/enlargened adrenal gland

53
Q

Why does adrenal gland enlargen with congenital adrenal hyperplasia?

A

lack of cortisol hormone leads to high ACTH = promotes growth w/ increase in adrenal size

54
Q

What is the most common type of CAH? What does it lead to? What is it caused by?

A

Deficiency of enzyme 21-hydroxylase = decreased cortisol and aldosterone, increased androgenic (DHEA, androstenedione, testosterone) + buildup of progesterone and 17-OH progesterone. Caused by mutation in CYP21A2 gene

55
Q

What happens w/ high levels of androgens? Low levels?

A

high = virilization of external genitalia, low = feminization

56
Q

What are androgens (testosterone, androstenedione) converted to in peripheral tissues?

A

Estradiol

57
Q

What are the types of 21-hydroxylase deficiency CAH?

A

classic-saltwasting (deficiency) and non-saltwasting type (partial 21-OH deficiency)

58
Q

What is seen with saltwasting CAH?

A

severe dehydration, hypotension, more feedings of infant initially, develop poor feeding and adrenal crisis eventually, hyponatremia, hyperkalemia, mental status changes and vomiting due to electrolyte imbalances

59
Q

What are the sxs of non-saltwasting CAH?

A

no genital ambiguity at birth, no adrenal crisis, increased androgen features later w/ premature onset of puberty, short stature, hirsutism in teen girls, polycystic K disease, abnormal menstrual period

60
Q

What are sxs seen w/ CAH?

A

genital ambiguity for girls via virilization of external genitalial, enlarged clitoris w/ or w/o partial fusion of labioscrotal folds, can have testes or uterus, hyperpigmentation due to increased ACTH and MSH

61
Q

How is CAH diagnosed?

A

increased 17-OH-progesterone

62
Q

What is the tx for CAH?

A

IV fluid resuscitation w/ Na+ containing fluids, electrolyte regulation, cortisol + mineralocorticoid administration

63
Q

Are adrenal masses usually symptomatic?

A

No, usually discovered incidentally on abdominal CT/MRI

64
Q

What is shape and size of adrenal adenoma? CT attenuation? What is seen on contrast CT, MRI?

A

<4cm, regular shape and borders, CT attenuation <10 HU, Contrast CT: contrast washed out quickly w/ >50% after 10min injection, MRI + isointense w/ liver on T1 and T2

65
Q

What is shape and size of adrenal malignancy (carcinoma)? CT attenuation? What is seen on contrast CT, MRI?

A

> 4cm, irregular, can have calcifications, local invasion, necrosis. CT attenuation > 20 HU. CT contrast = increased blood vessels means <50% washed out 10min after injection. MRI = hypointense w/ liver on T1, hyperintense on T2

66
Q

What should all adrenal adenomas be screened for?

A

cortisol (Cushing) and catecholamine hypersecretion

67
Q

What is a pheochromocytoma? Sxs? How do you dx it? What is Tx?

A

Adrenal mass causing catecholamine hypersecretion = HTN difficult to control w/ meds, headaches, increased sweating, high metanephrine levels, tx w/ surgery

68
Q

What should be done before surgery for pheochromocytoma?

A

removal of mass can precipitate severe hypertensive crisis so 2 weeks before surgery, start on alpha blockers to normalize BP, 2-3 days before, start on beta blocker to prevent HTN, right before start on glucocorticoids to prevent adrenal crisis

69
Q

What are the hereditary primary adrenal carcinoma’s

A

Li-Fraumeni, Beckwith-Wiedemann, MEN1 syndromes

Endocrine Unit Phase 1 (5 decks)

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