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DEMS IV > adrenal disorders > Flashcards

adrenal disorders Flashcards

1
Q

Causes of primary adrenal insufficiency

A
  1. Autoimmune destruction of adrenal gland: Addison’s Dz. 2. Infectious: TB, Fungi, HIV. 3. Infiltrative: Amyloid. 4. Hemorrhage. 5. Metastatic. 6. Metabolic*. 7. Surgery
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2
Q

causes of secondary adrenal insufficiency

A

Exogenous glucocorticoid withdrawal (common), cure of Cushings syndrome (less common), opioids, radiation, infectious, hypothalamic/pituitary lesions (uncommon)

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3
Q

Hormone levels in primary vs secondary adrenal insufficiency

A

primary: Cortisol, aldosterone and adrenal androgens are low, but ACTH and CRF are high. Secondary: cortisol, adrenal androgens, ACTH and CRF are all low, and aldosterone is nl

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4
Q

Signs/symptoms of adrenal insufficiency

A

Chronic: fatigue, weakness, myalgias, arthralgias, nausea, weight loss, salt craving, hypotension, tachycardia. Acute: above plus fever, hypotension, confusion

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5
Q

labs of adrenal insufficiency

A

hyponatremia, hypoglycemia, azotemia, anemia (hemodilution), eosinophilia (cortisol lowers eosinophils)

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6
Q

What are signs/sx/labs that show up in primary adrenal insufficiency only

A

Vitiligo, pigmentation, hyperkalemia

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7
Q

What causes hyponatremia in AI

A

Decreased cortisol causes decreased cardiac output and decreased vascular tone. This creates a relative hypovolemia which causes stimulation of ADH, increased free water reabsorption and hyponatremia

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8
Q

What causes hyperkalemia in primary AI

A

The adrenal cortex is damaged, so patients lack aldosterone which leads to decreased sodium reabsorption and decreased potassium excretion by the kidney.

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9
Q

What causes hyperpigmentation in primary AI

A

Increased production of POMC (an ACTH precursor in the pituitary). POMC is also used as a precursor for melanocyte stimulating hormone so elevated levels lead to hyperpigmentation. In secondary AI, this does not occur b/c ACTH levels and POMC levels are low.

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10
Q

What is polyglandular autoimmune syndrome (type 2)

A

Clustering of autoimmune adrenal insufficiency with the following: hypothyroid, and type 1 diabetes. HLA asssociated

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11
Q

What is polyglandular autoimmune syndrome (type 1)

A

Autoimmune insufficiency plus hypoparathyroidism, type 1 diabetes and mucocutaneous candidiasis. Associated with an autoimmune regulator gene

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12
Q

Proposed mechanism of polyglandular autoimmune syndrome (type 2)

A
  1. endocrine cell undergoes non-specific cellular damage (viral, toxin). 2. non-susceptible individual does not recognize the autoantigen or develops tolerance and the gland recovers. 3. a susceptible individual recognizes autoantigen as foreign leading to immune attack on the gland, with subsequent hypofunction
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13
Q

Best imaging tool for adrenal glands

A

CT

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14
Q

Compare normal vs abnormal adrenal glands on imaging

A

normal body size is 5-8mm, limb size is 2-3mm and total width is 2-3cm. Abnormal gland may be small atrophic +/- calcifications (autoimmune or metabolic) OR enlarged with hemorrhage or necrosis (infctious, hemorrhage or mets)

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15
Q

risk facors for adrenal insufficiency

A

other autoimmune diseases, coagulopathy/sepsis /trauma (adrenal hemorrhage), HIV/AIDS, known malignancy, recent glucocorticoid treatment/ withdrawal, recent complicated delivery (pituitary infarct), or head trauma (pituitary infarct).

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16
Q

Primary adrenal insufficiency diagnosis

A
  1. serum cortisol: 100pg/ml. 3. Adrenal CT scan: small adrenal gland if autoimmune or metabolic. Large if other causes
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17
Q

caveat to cosyntropin testing

A

If pituitary/hypothalamus injury is recent (2 weeks to 6 months), the adrenal gland may still respond to cosyntropin stimulation

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18
Q

Stages of primary adrenal insufficiency

A

stage 1: increased plasma renin activity and decreased or nl plasma aldosterone. Stage 2: stage 1 plus decreased cortisol response to ACTH. Stage 3: stage 2 plus increased plasma ACTH. Stage 4: clinically overt AI

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19
Q

Diagnosis of secondary adrenal insufficiency

A
  1. serum cortisol: <20ug/dl after 10-60 minutes following cosyntropin (synthetic ACTH). 2. Plasma ACTH nl or low. 3. Pituitary MRI shows pathology
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20
Q

Adrenal insufficiency treatment

A

Primary only: mineralocorticoid replacement with Fludrocortisone. Primary + Secondary: glucocorticoid replacement with hydrocortisone, prednisone and/or dexamethasone

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21
Q

Sx of primary aldosteronism

A

hypertension, hypokalemia and metabolic alkalosis due to elevated aldosterone secretion

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22
Q

prevalence of primary aldosteronism in hypertensive pts

A

0.10

23
Q

Levels of renin and angiotensin II in primary aldosteronism

A

Both are low due to negative feedback by aldosterone

24
Q

Types of primary aldosteronism

A
  1. aldosterone producing adenoma (34%). 2. idiopathic hyperaldosteronism aka bilateral adrenal hyperplasia (66%). 3. glucocorticoid-remediable hyperaldosteronism (rare). 4. aldosterone producing carcinoma (rare)
25
Q

What causes glucocorticoid-remediable hyperaldosteronism

A

a mutation which fuses the promoter of 11-B hydroxylase (involved in cortisol synthesis) with aldosterone synthase creating a hybrid glomerulosa/fasciculata layer which produces aldosterone under the positive control of ACTH. Autosomal dominant. glucocorticoid treatment will inhibit ACTH, thus decreasing aldosterone release

26
Q

Who should be screened for primary aldosteronism

A

hypertensive pts with hypokalemia (spontaneous or provoked by diuretics), severe HTN (>160/100), resistant HTN (>2 drugs), HTN earlier than 40 yrs, adrenal incidental adenoma, first degree relative with primary hyperaldosteronism

27
Q

Diagnosis of primary aldosteronism

A

Morning samples: Plasma aldosterone >15ng/dl AND Plasma aldosterone/ plasma renin activity ratio >20. Restrict spironolacton usage. Plasma renin activity = direct renin/8

28
Q

Primary aldosteronism confirmation tests

A

Sodium suppression testing: 1. Oral salt load -high NaCl diet for 3 days followed by a 24 hr urine aldosterone >12ug confirms diagnosis. 2. IV saline infusion- 2L NS over 4 hrs followed by plasma aldosterone >10ng/dl confirms diagnosis

29
Q

How do you determine whether primary aldosteronism is due to adenoma or hyperplasia

A

adenoma is likely if age >40, severe HTN, hypokalemia, plasma aldosterone > 25ng/dl, urine aldosterone >30ug/24hrs. 1. CT abdomen. 2. adrenal vein sampling: lateralization indicates adenoma, no lateralization indicates hyperplasia.

30
Q

Imaging of adrenal hyperplasia and adenomas

A

Anatomic: CT is best, MRI. Functional: PET, adrenocortical scintigraphy. Interventional: adrenal venous sampling

31
Q

compare imaging of adrenal hyperplasia vs adenoma

A

Hyperplasia: enlarged limbs of one or both glands, normal shape, can be multinodular. Adenoma: round/oval mass, CT shows homogenous low density

32
Q

What is adrenocortical scintigraphy

A

NP-59 is a cholesterol analog which binds to adrenal LDL receptors.

33
Q

Treatment of primary aldosteronism

A

If aldosterone producing adenoma: pre-operative aldosterone antagonists then unilateral adrenalectomy. If idiopathic hyperaldosteronism: medical management with spironolactone or eplerenone plus BP meds (Ca channel blocker, ACEI, ARB)

34
Q

What is a pheochromocytoma

A

tumor of the chromaffin cells in the adrenal medulla leading to excess NE and epi. Can also arise from extra-adrenal chromaffin tissue anywhere along the sympathetic chain in which case they are referred to as paragangliomas.

35
Q

Pheochromocytoma Sx

A

HTN, headaches, sweating, palpitations

36
Q

pheochromocytoma rul of 10s

A

10% are Malignant, 10% are Familial, 10% are Bilateral, 10% are Extra-Adrenal

37
Q

List familial syndromes associated with pheochromocytoma

A

MEN type 2A/2B (mutation of ret receptor causes constitutive activation of neuroendocrine cells), von Hipppel Lindau syndrome, Neurofibromatosis type 1, familial paragangliomas (SDH mutations)

38
Q

Who to screen for pheochromocytoma

A

hypertensive pts with spells of headaches, sweating and/or palpitations, severe HTN (>160/100), resistant HTN (>2 drugs), adrenal incidental adenoma, familial syndrome

39
Q

Pheochromocytoma screening tests

A
  1. urine metanephrines. 2. Urine catecholamines. 3. Plasma metanephrines. Urine tests are best screening tests but plasma metanephrines is best for high risk patients
40
Q

Pheochromocytoma false positives

A

levodopa, ethanol, TCA, anti-psychotics, acetaminophen, amphetamines, renal failure, sleep apnea, physical stress

41
Q

Endocrine principle of pheochromocytomas

A

a biochemical diagnosis must be established prior to the anatomic localization. This is especially true for many adrenal disorders since 5-10% of people will have an adrenal mass on CT scan, and a majority of these masses are non-functioning.

42
Q

Pheochromocytoma localization tests

A

Abd MRI (hyperintense on T2, heterogenous) or CT, PET scans, MIBG (localization for ectopic, recurrent and metastatic tumors). Not hard to find.

43
Q

Pheochromocytoma treatment

A

Preoperative: First alpha blockers (phenoxybenzamine, prazosin, terazosin, doxazosin), then beta blockers, OR calcium channel blockers alone. Adrenalectomy

44
Q

Causes of Cushings Syndrome

A
  1. 80% are endogenous- ACTH secreting pituitary tumor causes elevated cortisol and adrenal androgens. 2. 10% are ectopic ACTH secreting tumors causing elevated cortisol and adrenal androgens. 3. 10% are cortisol secreting adrenal tumors resulting in decreased ACTH, elevated cortisol and nl adrenal androgens
45
Q

Cushings Syndrome clinical features

A

Fatigue, weakness, weight gain, facial plethora, easy bruising, HTN, central obesity, purple stretch marks, muscle weakness, thin skin, hirsutism, hyperglycemia, hyperlipidemia

46
Q

Cushings syndrome screening

A
  1. elevated 24 hr urine cortisol. 2. Elevated bedtime salivary cortisol. 3. Following 1mg dexamethasone suppression test, cortisol is >1.8ug/dl
47
Q

Compare the results of a dexamethasone suppression test for the three different causes of Cushings syndrome

A
  1. If pituitary ACTH secreting tumor, DST results in suppression of ACTH and cortisol. 2. If ectopic ACTH secretic tumor, DST does not suppress ACTH/ cortisol. 3. If adrenal cortisol secreting tumor, DST does not suppress ACTH/cortisol
48
Q

Name conditions with hypercortisolism that is not Cushings

A

Pregnancy, depression, alcoholism, morbid obesity, diabetes (poorly controlled)

49
Q

Cushings syndrome localization

A

Pituitary MRI, chest CT, Abdominal CT, inferior petrosal sinus sampling

50
Q

Cushings syndrome treatment

A
  1. surgery. 2. ACTH secretion inhibitors- Cabergoline, pasireotide. 3. Cortisol synthesis inhibitors- ketoconazole, metyrapone, etomidate. 4. adrenolytic agents- mitotane. 5. cortisol receptor blockers- mefispristone
51
Q

What is an adrenal incidentaloma

A

Benign finding on abd imaging. Usually non functioning- most common hormone abnormality is cortisol secretion

52
Q

Adrenal incidentaloma imaging

A
  1. CT: if high lipid content/low HU it is benign. If low lipid content/high HU it is malignant. 2. PET: measure FDG uptake. If high it is malignant, if low it is benign
53
Q

Adrenal incidentaloma surgery

A

remove if >4.5cm, progressive growth or hormone secretion.

DEMS IV (26 decks)

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