Endocrine 1 Flashcards by Hannah Hutchison

Gigantism and acromegaly are usually caused by

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

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gigantism vs acromegaly

gigantism - childhood
acromegaly - adulthood

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dx acromegaly

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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tx acromegaly

surgical removal or radiation

octreotide or lanreotide can suppress GH

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Addison’s disease is also called

primary adrenal insufficiency

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what is adrenocortical insufficiency

disorder where the adrenal gland does not produce enough hormones

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what is secondary adrenocortical insufficiency

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

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causes of secondary adrenocortical insufficiency

history of exogenous glucocorticoid use
Sheehan

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what is primary adrenocortical insufficiency

adrenal gland destruction (lack of cortisol AND aldosterone)

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causes of primary adrenocortical insufficiency

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

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

autoimmune - MC in US

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sx adrenocortical insufficiency

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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baseline labs adrenocortical insufficiency

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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CT scan for adrenocortical insufficiency

autoimmune - small non calcified adrenal glands (atrophy)

infection - calcification of hemorrhage (TB)

METS or hemorrhage - b/l adrenal enlargement

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screening tests adrenocortical insufficiency

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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tx adrenocortical insufficiency

glucocorticoid replacement - hydrocortisone; dexamethasone

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

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what is Cushing’s syndrome

symptoms and signs related to excess cortisol

what are the 4 main causes of Cushing’s syndrome

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

sx Cushing’s syndrome

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

PE Cushing’s syndrome

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

lab findings in Cushing’s

hyperglycemia
dyslipidemia
leukocytosis
hypokalemia
metabolic alkalosis

screening tests Cushing’s

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

differentiating tests Cushing’s

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

what imaging should you do for cushing’s

based on suspected cause

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

tx Cushing's

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

what is diabetes insipidus (DI)

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

2 types of DI

central - no production of ADH (MC type) nephrogenic - partial or complete renal insensitivity to ADH; MC due to lithium and hypercalcemia

sx DI

polyuria + polydipsia neuro sx of hypernatremia - weakness, myalgias, confusion, lethargy

PE DI

may be normal Dehydration HypoTN

Labs DI

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

Dx DI

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

tx central DI

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

tx nephrogenic DI

correct underlying cause hydrochlorothiazide, indomethacin, or amiloride if sx persist amiloride is an alternative for lithium-induced DI when lithium use is continued

what is the dawn phenomenon

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

tx for dawn phenomenon

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

what is the somogyi effect

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

tx somogyi effect

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

dx diabetes

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%

treatment goal A1C

< 7%

treatment goal blood sugar for meals

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