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Internal Med EOR > Endocrine 1 > Flashcards

Endocrine 1 Flashcards

1
Q

Gigantism and acromegaly are usually caused by

A

pituitary adenoma that secretes excessive amounts of Growth Hormone (GH)

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2
Q

gigantism vs acromegaly

A

gigantism - childhood
acromegaly - adulthood

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3
Q

dx acromegaly

A

Diagnose by measuring IGF-1 and GH levels

IGF-1 levels are typically substantially elevated (3-fold to 10-fold)

Plasma GH levels measured by radioimmunoassay are typically elevated - Blood should be taken before the patient eats breakfast (basal state); in normal people, basal GH levels are < 5 ng/mL;The degree of GH suppression after a glucose load remains the standard and thus should be measured in patients with elevated plasma GH

CT or MRI to look for tumor

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4
Q

tx acromegaly

A

surgical removal or radiation

octreotide or lanreotide can suppress GH

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5
Q

Addison’s disease is also called

A

primary adrenal insufficiency

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6
Q

what is adrenocortical insufficiency

A

disorder where the adrenal gland does not produce enough hormones

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7
Q

what is secondary adrenocortical insufficiency

A

pituitary failure of ACTH secretion –> lack of cortisol only
aldosterone is intact

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8
Q

causes of secondary adrenocortical insufficiency

A

history of exogenous glucocorticoid use
Sheehan

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9
Q

what is primary adrenocortical insufficiency

A

adrenal gland destruction (lack of cortisol AND aldosterone)

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10
Q

causes of primary adrenocortical insufficiency

A

autoimmune - MC in US
infection (TB, HIV) - MC in developing countries
ketoconazole

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11
Q

what is the MC cause of primary adrenocortical insufficiency in the US

A

autoimmune - MC in US

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12
Q

sx adrenocortical insufficiency

A

sx due to lack of cortisol - weakness, myalgias, fatigue, weight loss, N/V, diarrhea, headache, sweating,

Hyponatremia and salt craving
Hypotension
Hypoglycemia
Hyperpigmentation

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13
Q

baseline labs adrenocortical insufficiency

A

8am ACTH, cortisol, and renin should be obtained. elevated renin, esp w primary

Elevated ACTH + low cortisol in primary; decreased ACTH + low cortisol in secondary

labs: hypoglycemia (MC in secondary), primary - hyponatremia, hyperkalemia, non-anion gap metabolic acidosis due to decreased aldosterone

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14
Q

CT scan for adrenocortical insufficiency

A

autoimmune - small non calcified adrenal glands (atrophy)

infection - calcification of hemorrhage (TB)

METS or hemorrhage - b/l adrenal enlargement

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15
Q

screening tests adrenocortical insufficiency

A

high dose 250 mcg ACTH (Cosyntropin) stimulation test

adrenal insufficiency - insufficient or absent rise in serum cortisol (<18 microg/dL) after ACTH administration

normal response is rise in serum cortisol after ACTH administration :)

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16
Q

tx adrenocortical insufficiency

A

glucocorticoid replacement - hydrocortisone; dexamethasone

mineralocorticoid replacement only in primary (Addison’s) - fludrocortisone

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17
Q

what is Cushing’s syndrome

A

symptoms and signs related to excess cortisol

18
Q

what are the 4 main causes of Cushing’s syndrome

A

long term high-dose glucocorticoid therapy MC overall cause

Cushing’s disease - pituitary gland ACTH overproduction - most common ENDOGENOUS cause of Cushing’s syndrome

ectopic ACTH producing tumor - small cell lung CA, medullary thyroid CA

Adrenal tumor (adenoma) - secretion of excess cortisol

19
Q

sx Cushing’s syndrome

A

proximal muscle weakness
weight Gian
HA
oligomenorrhea
erectile dysfunction
polyuria
osteoporosis
mental disturbances

20
Q

PE Cushing’s syndrome

A

Central (truncal) obesity
Moon facies
buffalo humo
supraclavicular fat pads
thin extremities
striar
hyperpigmentation
acanthuses nigricans
HTN

21
Q

lab findings in Cushing’s

A

hyperglycemia
dyslipidemia
leukocytosis
hypokalemia
metabolic alkalosis

22
Q

screening tests Cushing’s

A

3 options - at least 2 screening tests are performed

screening tests:
24 hour urinary free cortisol (2 measurements) - most specific
nighttime salivary cortisol (2 measurements)
low dose 1 mg overnight dexamethasone suppression test –> elevated cortisol or no suppression w low dose dexamethasone = Cushing’s syndrome

23
Q

differentiating tests Cushing’s

A

Baseline ACTH + high dose 8 mg dexamethasone suppression tests

Cushing’s disease - increased ACTH + suppression of cortisol w high-dose dexametheaseone - Cushings disease is the only 1 of the 4 major causes that suppresses w high dose testing

ectopic ACTH-producing tumor - increased ACTH + no suppression of cortisol w high dose dex

adrenal tumor and steroids - decreased ACTH + no suppression of cortisol w high-dose dex

24
Q

what imaging should you do for cushing’s

A

based on suspected cause

Pituitary MRI - Cushing’s disease
CT of abdomen - adrenal tumor
Chest imaging - ectopic ACTH producing lung tumor

25
Q

tx Cushing’s

A

corticosteroid use - gradual taper
Cushing disease - transsphenoidal resection
adrenal tumor - resection
ectopic tumor - resection if resectable; ketoconazole or Metyrapone if unresectable

26
Q

what is diabetes insipidus (DI)

A

inability of the kidney to concentrate urine leading to production of large amounts of dilute urine

27
Q

2 types of DI

A

central - no production of ADH (MC type)

nephrogenic - partial or complete renal insensitivity to ADH; MC due to lithium and hypercalcemia

28
Q

sx DI

A

polyuria + polydipsia

neuro sx of hypernatremia - weakness, myalgias, confusion, lethargy

29
Q

PE DI

A

may be normal
Dehydration
HypoTN

30
Q

Labs DI

A

increased serum osmolarity due to increased urinary free water loss

Decreased urine osmolality < 300 mOsm/kg
Decreased specific gravity < 1.005
Increased urine volume 3-20 liters in 24 h
Hypernatremia and dehydration if severe

31
Q

Dx DI

A

step 1 - screening
fluid deprivation test - established dx; normal response = progressive urine concentration; DI = continued production of large amounts of dilute urine (low urine osmolality)

step 2 - desmopressin (ADH/AVP) stimulation test - distinguishes central vs nephrogenic DI; normal response = progressive urine concentration (increase in urine osmolality) after ADH is given
central = reduction in urine output + > 50 % increase in urine osmolality; associated w urine osmolality of >/= 300 mOsm/kg after desmopressin
Nephrogenic = continued production of large amounts of dilute urine (well below 300 mOsm/kg, indicating lack of response to ADH

32
Q

tx central DI

A

desmopressin - synthetic ADH analog
low solute/low sodium/low protein diet

33
Q

tx nephrogenic DI

A

correct underlying cause
hydrochlorothiazide, indomethacin, or amiloride if sx persist

amiloride is an alternative for lithium-induced DI when lithium use is continued

34
Q

what is the dawn phenomenon

A

Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting

35
Q

tx for dawn phenomenon

A

Treat with bedtime injection of long-acting insulin (NPH) to blunt morning hyperglycemia, avoiding carbohydrate snacks late at night

36
Q

what is the somogyi effect

A

Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone

37
Q

tx somogyi effect

A

Treat with decreased nighttime long-acting insulin (NPH) dose or give bedtime snack

38
Q

dx diabetes

A

Random blood glucose level of > 200 mg/dL + diabetic symptoms
2 separate fasting (8 hours) glucose levels of > 126 mg/dL
2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
Hemoglobin A1c of > 6.5%

39
Q

treatment goal A1C

A

< 7%

40
Q

treatment goal blood sugar for meals

A

Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial

41
Q
A

Internal Med EOR (17 decks)

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