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Endocrinology > Endocrinology in the Clinical Setting > Flashcards

Endocrinology in the Clinical Setting Flashcards

1
Q

What is clinical endocrinology?3

A
  • the diagnosis and treatment of conditions resulting form alterations of normal hormone physiology.
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2
Q

How does an evaluation of a patient with an endocrine disorder differ?

A
  • history differs by asking about cold and heat intolerance.
  • physical must be focused around the thyroid gland and nail beds.
  • labs focused around hormones. If a certain level is high, we attempt to suppress it. If it does not go down, we know there is an issue.
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3
Q

What are the common endocrine disorders?

A
  • T1DM and T2DM
  • HYPERthyroidism
  • HYPOthyroidism
  • thyroid nodule
  • obesity
  • metabolic syndrome
  • gestational diabetes
  • prolactinoma
  • PCOS
  • osteoporosis (osteopenia)
  • HYPERparathyroidism
  • growth hormone deficiency
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4
Q

What are the UNcommon endocrine disorders?

A
  • HYPOparathyroidism
  • Addison’s disease
  • acromegaly
  • adrenal carcinoma
  • Klinefelter’s syndrome
  • Cushing’s disease
  • pheochromocytoma
  • hermaphroditism
  • osteomalacia (soft bones)
  • diabetes insipidus
  • craniopharyingioma
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5
Q

What are the symptoms of endocrine disorders?

A
  • weakness
  • tiredness
  • cold intolerance
  • fatigue
  • warm intolerance
  • dizziness
  • headache
  • blurred vision
  • depression
  • inability to concentrate
  • constipation
  • frequent bowel movements.
  • very nonspecific
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6
Q

Does treatment of endocrine conditions require interaction with other specialties?

A
  • YES often
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7
Q

** What are the 5 concerns in endocrinology?

A
  1. laboratory selection
  2. know the limitations of your test.
  3. utilize screening tests when appropriate.
  4. If the hormone level is elevated, try to suppress it. If the hormone level is low, try to stimulate it.
  5. Recall the influence of medications and nutritional state when interpreting laboratory results (thyroid, adrenal).
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8
Q

What is the most common pituitary tumor?

A
  • non-functioning pituitary adenoma

* found incidentally on imaging stuidies.

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9
Q

What is the most common pituitary secreting tumor?

A
  • prolactinoma
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10
Q

What are the types of malignant pituitary tumors?

A
  • functional and non-functional pituitary carcinomas
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11
Q

From where can metastases to the pituitary occur?

A
  • breast, lung, stomach, kidney
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12
Q

What are some pituitary cysts?

A
  • Rathke’s cleft cyst, mucocoeles, others
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13
Q

What is empty sella syndrome?

A
  • congenital defect of the sella due to herniation of the arachnoid and CSF into the sella, compressing and destroying the pituitary gland.
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14
Q

What are some developmental abnormalities of the pituitary?

A
  • cransiopharyngioma= can suppress ADH (vasporessin) and develop diabetes insipidus.
  • germinoma
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15
Q

What vascular tumor can disrupt the pituitary-hypothalamic axis?

A
  • hemangioblastoma
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16
Q

What are some other diseases that can disrupt the pituitary-hypothalamic axis?

A
  • malignant systemic diseases (hodgkin’s, non-hodgkin lymphoma, histiocytosis…)
  • granulmoatous diseases (sarcoidosis, wegner’s, TB…)
  • vascular aneurysms (intrasellar location)
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17
Q

What size is considered to be an enlarged pituitary gland?

A
  • 10mm or more
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18
Q

** What visual disturbance can an enlarged pituitary cause?

A
  • bitemporal hemianopsia= loss of peripheral vision
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19
Q

36 y/o female with bilateral galactorrhea and amenorrhea for the last few months, and previously had children. She has BMI of 31 and is on psychotropic medications (can elevate prolactin). Imaging is done, and finds a pituitary adenoma. How should we treat her?

A
  • start her on BROMOCRIPTINE= dopamine agonist (inhibits prolactin release) that will help to shrink the tumor.
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20
Q

What are the clinical features of hyperprolactinemia/ prolactinoma?

A
  • women may present with oligomenorrhea, amenorrhea, galactorrhea, or infertility.
  • men often have less symptoms.
  • both sexes may experience visual defects or headache due to mass effect.
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21
Q

What can increase levels of prolactin?

A
  • drugs
  • stress
  • pregnancy
  • pituitary and hypothalamic disqease.
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22
Q

How are prolactinomas treated?

A
  • 1st line= medically (BROMOCRIPTINE and CABERGOLINE). Take with food (bread) to help with side effects before bed.
  • major side effect is nausea and vomiting.
  • 2nd line= surgically
  • 3rd line= radiotherapy
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23
Q

What is acromegaly?

A
  • enlarged bones of hands, feet, and jaw, enlarged tongue, widely spaced teeth, and growth of visceral organs leading to dysfunction (ex. cardiac failure) due to a rare pituitary adenoma in adults causing excessive secretion of GH and thus IGF-1.
24
Q

What is the greatest contributor to mortality in acromegaly?

A
  • cardiovascular disease
25
Q

How do you diagnose acromegaly?

A
  • elevated GH and insulin growth factor-1 (IGF-1) levels

- lack of GH suppression by oral glucose.

26
Q

Is IGF-1 or GH, better when evaluating for acromegaly?

A
  • IGF-1 bc it has a longer half-life
27
Q

How do you treat acromegaly?

A
  • bromocryptine (dosage may be higher than for prolactinomas)
  • relieve signs and symptoms
  • surgical (transphenoidal or transfrontal approach)
28
Q

What are some causes of HYPOpituitarism?

A
  • pituitary adenomas (adults) or craniopharyngioma (children)
  • Sheehan syndrome= pregnancy-related infarction of the pituitary gland.
  • empty sella syndrome= congenital defect of the sella. Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland.
29
Q

What labs will you look for if you suspect hypopituitarism?

A
  • hyponatremia

- hyposmolality of serum with elevated urine osmolality (SIADH-llike syndrome)

30
Q

What is pituitary dwarfism?

A
  • impairment of GH secretion, causing short stature but pts are proportionate (aka they don’t have abnormally short limbs)
31
Q

Can empty sella syndrome occur secondary to Sheehan’s syndrome?

A
  • YES
32
Q

Do you need to treat empty sella syndrome with hormone replacement?

A
  • normally only necessary in PRIMARY empty sella syndrome, but not secondary.
33
Q

What is central diabetes insipidus?

A
  • ADH deficiency due to hypothalamic or posterior pituitary pathology (tumor, trauma, infection, or inflammation).
34
Q

What are the clinical featuers of central diabetes insipidus?

A
  • polyuria and polydipsia with risk of life-threatening dehydration.
  • hypernatremia and high serum osmolality.
  • low URINE osmolality (DILUTE) and low specific gravity.
35
Q

How do we diagnose central DI?

A
  • water deprivation test fails to increase URINE osmolality.
36
Q

How do you treat central DI?

A
  • desmopressin (ADH analog)
37
Q

What is nephrogenic DI?

A
  • impaired renal response to ADH due to inherited mutations or drugs (lithium and demeclocycline).
38
Q

What happens if you give desmopressin to a pt with nephrogenic DI?

A
  • no response
39
Q

What are the general features of hypercortisolism (Cushinoid appearance)?

A
  • gynecologic (amenorrhea)
  • cardiovascular
  • musculoskeletal
  • neuro/psychiatric
  • DM
40
Q

What are the clinical features of Cushing’s disease?

A
  • buffalo hump
  • SUPRAclavicular fat pad
  • truncal obesity
  • facial plethora (redness)
  • hirsutism
  • acne
  • violaceous striae
  • easy bruising
  • moon facies and plethora
41
Q

How do you diagnose Cushings?

A
  • 24-hour urine cortisol level (increased)
  • late night salivary cortisol level (increased)
  • low dose dexamethasone suppression test (suppresses cortisol in normal individuals but fails to suppress cortisol in all causes of Cushing).
42
Q

What does high dose dexamethasone suppression test allow us to distinguish in Cushings?

A
  • if it suppresses ACTH production (serum cortisol is lowered), then you have a PITUITARY adenoma.
  • if it does not suppress ACTH (serum cortisol remains high), then you have ECTOPIC ACTH production.
43
Q

What laboratory studies will you see with Cushings?

A
  • DM
  • glucose intolerance
  • hypercalciuria
  • renal calculi
  • hypokalemia
  • erythrocytosis
  • eosinopenia
44
Q

What is a very useful tool to evaluate ACTH?

A
  • petrosal sinus sampling
45
Q

How do you treat Cushing’s disease?

A
  • surgery (transfrontal pituitary resection, or bilateral adrenalectomy; nelson’s syndrome)
46
Q

Is ADRENAL Cushing’s ACTH dependent or independent?

A
  • ACTH INDEPENDANT (aka ACTH levels don’t affect cortisol).
47
Q

What will you see with Ectopic Cushing’s syndrome?

A
  • high cortisol
  • no suppression with LOW-dose dexamethasone.
  • high levels of ACTH
  • no suppression with HIGH-dose dexamethasone.
  • bilateral adrenal hyperplasia due to high ACTH levels.
  • very severe HYPOKALEMIA.
  • usually due to small cell carcinoma of the lung)
48
Q

** What will you see with adrenal INSUFFICIENT states (Addison’s disease)?

A
  • hypotension
  • hyperpigmentation
  • hyponatremia
  • hyperkalemia
  • positive antiadrenal antibodies
  • metabolic acidosis
  • weakness
49
Q

*** What are some primary causes of adrenal insufficiency?

A
  • idiopathic (Addison’s disease)
  • TB
  • fungal infections
  • adrenal hemorrhage
  • congenital adrenal hypoplasia
  • sarcoidosis
  • amyloidosis
  • metastatic neoplasia
50
Q

How do we treat people with adrenal insufficiency?

A
  • treat dehydration (normal saline IV)
  • do a rapid ACTH stimulation test (measure cortisol and aldosterone before and after; looking for a large rise in either. If they don’t rise, then you have adrenal cortical insufficiency).
  • IV hydrocortisone
  • Florinef= synthetic aldosterone
51
Q

What will you see in 21-hydroxylase deficiency?

A
  • decreased aldosterone
  • decreased cortisol
  • increased DHEA and thus estrones and testosterone
  • hyperpigmentation
  • HIRSUITISM
  • AMENORRHEA
  • salt wasting
  • can look like PCOS initially
52
Q

What is the most common type of congenital adrenal insufficiency (congenital adrenal hyperplasia)?

A
  • 21-YDROXYLASE deficiency
53
Q

What is Conn syndrome?

A
  • adrenal adenoma causing excess production of the hormone aldosterone by the adrenal glands resulting in low renin levels (from increased renal perfusion pressure, which downregulates renin).
  • treat with spironolactoneo or aldactone (antagonist to aldosterone).
54
Q

What labs will you see with Conn syndrome?

A
  • HTN
  • HYPOkalemia
  • metabolic alkalosis
  • surgically remove the adenoma
55
Q

What can cause secondary adrenal insufficiency (ACTH deficiency)?

A
  • after exogenous glucocorticoids
  • after the cure of Cushing syndrome
  • hypothalamic and pituitary lesions

Endocrinology (18 decks)

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