TOP 100 SECRETS IN ENDOCRINOLOGY

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1. Type 1 diabetes is caused by the autoimmune destruction of pancreatic beta cells resulting in an
absolute deficiency of insulin; type 2 diabetes is the consequence of a combination of insulin
resistance and progressive beta cell failure.(2). Diabetic patients should be treated to standards that
are based upon scientific evidence:hemoglobin A1C < 7%, LDL cholesterol < 100 mg/dL, blood
pressure < 130/80 mm Hg.(3). Microvascular complications of diabetes mellitus are directly related
to hyperglycemia and result from the formation of advanced glycation end products, polyol
accumulation, protein kinase C activation, accrual of intracellular glucosamine, and oxidative stress.
(4). The propensity for developing vascular disease in type 2 diabetes is likely related to insulin
resistance and the pathological clustering of dyslipidemia and hypertension inherent in this condition.
(5). Intensive insulin therapy, or basal/bolus therapy, mimics normal pancreatic insulin secretion;
basal insulin is the amount required to regulate hepatic glucose production between meals, while
bolus insulin is given to match mealtime carbohydrate intake, using a carbohydrate to insulin ratio
and a hyperglycemic correction factor with each meal.
(6). Insulin is the best medication for managing hyperglycemia in hospitalized patients; in intensive
care patients, intravenous insulin infusions are superior to subcutaneous insulin regimens in
achieving quick and appropriate glycemic control.(7). Sliding scale regular insulin regimens in
hospitalized patients cause more hyperglycemia and hypoglycemia than do scheduled target-based
regimens of basal insulin and short acting insulin analogs; sliding scale regular insulin regimens
should be abandoned.( . Women who develop gestational diabetes have approximately a 50% risk
of developing type 2 diabetes mellitus within 5 to 10 years.(9). Normalizing the A1C in diabetic
women prior to pregnancy and during the first 10 weeks of organogenesis can reduce the fetal major
malformation rate from 25% to 2–3%.(10). Elevated LDL cholesterol and low HDL cholesterol are
major risk factors for coronary artery disease (CAD); serum triglyceride levels over 150 mg/dl also
promote CAD, while levels greater than 1000 mg/dl increase the risk of developing acute
pancreatitis.
11. Metabolic syndrome is a major CAD risk factor complex, consisting of any 3 of the following:
abdominal obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and
hyperglycemia.These secrets are 100 of the top board alerts. They summarize the concepts,principles,
and most salient details of pathology.12. Obesity, defined as a body mass index (BMI) > 30 kg/m2, is
associated with an increased risk of developing related medical illnesses, including diabetes mellitus,
hypertension,coronary artery disease, pulmonary emboli, sleep apnea, and osteoarthritis.13. Diet and
exercise to alter energy balance are the mainstays of obesity management, but sibutramine, orlistat
and phentermine are currently FDA approved medications that can be used to help overweight and
obese patients lose weight. 14. Adequate intake of calcium (1000–1500 mg/day) and vitamin D
(800–1200 units/day), regular exercise, smoking cessation, and limitation of alcohol and caffeine
consumptionshould be advised for all people who want to prevent osteoporosis and for all patients
who are being treated with medications for osteoporosis.15. Medical therapy for osteoporosis should
be given to all patients who have sustained a fragility fracture and to all patients who have a 30% risk
of having a hip fracture or 20% risk of any major fracture according to the World Health
Organization (WHO) fracture risk assessment tool (FRAX).
16. Medications that have been shown to significantly reduce the risk of osteoporotic fractures fall
into two main categories: anti-resorptive agents and anabolic agents.17. Glucocorticoid induced-
osteoporosis results from both suppressed bone formation and enhanced bone resorption, accounting
for the rapid bone loss often seen in glucocorticoid treated patients.18. Treatment is recommended
for all postmenopausal women regardless of initial BMD and for men or premenopausal women with
a BMD T-score 1.0 when they are being treated or will be treated with 5 mg/day of prednisone (or
equivalent) for 3 months.19. The forearm is the most important site for bone mass measurement in
patients with hyperparathyroidism.20. Osteomalacia and rickets result from inadequate or delayed
mineralization of bone.
16. Medications that have been shown to significantly reduce the risk of osteoporotic fractures fall
into two main categories: anti-resorptive agents and anabolic agents.17. Glucocorticoid induced-
osteoporosis results from both suppressed bone formation and enhanced bone resorption, accounting
for the rapid bone loss often seen in glucocorticoid treated patients.18. Treatment is recommended
for all postmenopausal women regardless of initial BMD and for men or premenopausal women with
a BMD T-score 1.0 when they are being treated or will be treated with 5 mg/day of prednisone (or
equivalent) for 3 months.19. The forearm is the most important site for bone mass measurement in
patients with hyperparathyroidism.20. Osteomalacia and rickets result from inadequate or delayed
mineralization of bone.
21. The causes of osteomalacia and rickets fall into 3 categories: 1) abnormal vitamin D
supply,metabolism or action; 2) abnormal phosphate supply or metabolism; and 3) a small group of
disorders in which there is normal vitamin D and mineral metabolism.22. Paget’s disease is
characterized by abnormal bone architecture resulting from an imbalance between osteoclastic bone
resorption and osteoblastic bone formation.23. Bisphosphonates are the most effective treatment for
Paget’s disease of bone.24. Although there are over 30 major causes of hypercalcemia,
hyperparathyroidism and hypercalcemia of malignancy account for > 90%; measuring a serum
parathyroid hormone (PTH) level will reliably differentiate these two disorders.25. Calcimimetics are
medications that bind to the calcium sensor-receptor and suppress the secretion of PTH; cinacalcet is
FDA approved for the treatment of secondary hyperparathyroidism and parathyroid carcinoma and,
though not FDA approved in primary hyperparathyroidism, has been shown to significantly lower
serum calcium and PTH levels in patients with this condition.
26. Primary hyperparathyroidism is associated with hypercalcemia, osteoporosis, nephrolithiasis, and
symptoms associated with these conditions.27. The recommendations for surgery in patients with
asymptomatic hyperparathyroidism are as follows: serum calcium > 1 mg/dl above the upper normal
limit, hypercalciuria > 400 mg per 24 hours, decreased creatinine clearance < 70% of age matched
normal persons, reduced bone density with T-Score < 2.5, age < 50 years, and calcium
nephrolithiasis.28. Hypercalcemia of malignancy is most often due to tumor production of
parathyroid hormone–related peptide (PTHrp), which binds to PTH/PTHrp receptors to stimulate
bone resorption and inhibit renal calcium excretion, causing hypercalcemia.29. Hypocalcemia is a
frequent problem in intensive care settings and is often a result of intravenous medications and/or
transfusions.30. Calcitriol (1,25-dihydroxyvitamin D) is the treatment choice for hypocalcemia in
patients with hypoparathyroidism or renal failure.
31. Kidney stones form because of supersaturation of urinary stone precursors (such as calcium and
oxalate), insufficient stone inhibitors (such as citrate), abnormal urine pH, or insufficient urine
volume.32. Therapy of kidney stones includes daily intake of 2 liters of fluid, increased intake of
citrate containing drinks, 1000 to 1200 mg of calcium, and no more than 2300 mg of sodium and
1g/kg ideal body weight protein; excessive calcium, oxalate, vitamin D and grapefruit juice should
also be avoided.33. Replacement with thyroid hormone alone in a hypothyroid patient with
coexistent primary or secondary adrenal deficiency may precipitate an acute adrenal crisis. 34.
Aldosterone deficiency generally does not occur in hypopituitarism because the principalphysiologic
regulator of aldosterone secretion is the renin-angiotensin system, not ACTH from the hypothalamic-
pituitary system.35. Non-functioning pituitary tumors produce symptoms primarily by mass effects,
resulting in compression of the optic chiasm, invasion of the cavernous sinuses, erosion into the bony
sella turcica, and compression or destruction of the pituitary stalk or gland causing hypopituitarism.
36. Treatment for non-functioning pituitary tumors 1.0 cm in size is transphenoidal surgery with
subsequent close monitoring for recurrence or regrowth; radiation therapy may be a useful adjunctive
therapy for incompletely resected tumors.37. A prolactin level over 200 ng/ml is almost always
indicative of a prolactin-secreting tumor, except when found during late pregnancy.38. Prolactin
elevation often causes galactorrhea and amenorrhea in women and hypogonadism in men; another
important consequence of elevated prolactin is decreased bone mineral density, which is not always
completely reversible.39. Acromegaly is caused by a pituitary tumor that secretes excess growth
hormone, which causes damage to bones, joints, the heart, and other organs, and is associated with
considerable morbidity and excess mortality.40. The best screening test for acromegaly is a serum
IGF-1 level.
41. Glycoprotein-secreting pituitary tumors include gonadotropinomas (LH or FSH secreting) and
TSHomas (TSH secreting); these tumors are frequently quite large.42. Hyperthyroid patients with
detectable serum TSH levels should always be evaluated for inappropriate TSH secretion (either a
TSHoma or thyroid hormone resistance).
43. Cushing’s syndrome screening tests (urinary cortisol, salivary cortisol, overnight 1 mg
dexamethasone suppression test) can be misleading, and repeated testing or more extensive
confirmatory testing is often needed.
44. Most patients with Cushing’s syndrome have a small pituitary tumor producing ACTH.45. Rapid
changes in body water or distribution can cause severe neurological dysfunction and are reflected
clinically by hyponatremia or hypernatremia; treatment requires a clear understanding of changes in
plasma sodium, plasma osmolality, and effective circulating volume.
46. Identification of growth abnormalities in children requires accurate height measurements and
plotting against appropriate standards.47. Growth abnormalities in children are most commonly due
to normal growth variants or chronic medical problems; hormonal abnormalities are less common
causes.
48. Chronic abuse of supraphysiologic growth hormone doses may lead to features of acromegaly:
osteoarthritis, irreversible bone and joint deformities, increased vascular, respiratory and cardiac
abnormalities, hypogonadism, diabetes mellitus and abnormal lipid metabolism.49. Spontaneous or
easily-provoked hypokalemia in a hypertensive patient should suggest the possibility of primary
hyperaldosteronism.50. The best screen for primary hyperaldosteronism is a plasma aldosterone /
plasma renin activity (PA/PRA) ratio > 20; most cases of primary hyperaldosteronism are due to
bilateral adrenal hyperplasia (idiopathic hyperaldosteronism).
51. Episodic headache, diaphoresis and palpitations in a hypertensive patient suggest
pheochromocytoma.52. Pheochromocytomas are 10% bilateral, 10% extra-adrenal, 10% familial,
10% malignant.53. Features suggesting that an adrenal tumor is malignant are size > 6 cm, evidence
of local invasion or metastases to the liver or lung, and high levels of urinary 17
ketosteroids,homovanillic acid, or plasma dopamine.54. Incidentally discovered adrenal masses
should be evaluated for evidence of malignancy(size >6 cm or progressive growth) and excess
hormone secretion (cortisol, aldosterone,androgens, catecholamines).55. Adrenal insufficiency
should be suspected in outpatients who have received supraphysiologic doses of glucocorticoids for
> 1 month, ICU patients who are hemodynamically unstable despite aggressive fluid resuscitation or
have septic shock, or any patient with signs or symptoms suggesting adrenal insufficiency.
56. Adrenal crisis should be treated aggressively using normal saline with 5% dextrose,intravenous
glucocorticoids (dexamethasone if treating before drawing random cortisol and ACTH,
hydrocortisone afterwards), other supportive care, and a search for the precipitating illness.57.
Congenital adrenal hyperplasia (CAH), the most common inherited disease, is a group of autosomal
recessive disorders, the most frequent of which is 21-hydroxylase deficiency;the most serious
consequences of CAH are ambiguous genitalia in females at birth,neonatal salt-wasting, premature
puberty and short stature as an adult.58. The radioactive iodine uptake (RAIU) is used primarily to
determine whether patients withthyrotoxicosis have a high RAIU disorder or a low RAIU
disorder.59. A thyroid scan is used to distinguish among the 3 types of high RAIU thyrotoxicosis
(Graves’ disease, toxic multinodular goiter, toxic nodule) and to determine whether thyroid nodules
are non functioning (cold), eufunctioning (warm), or hyperfunctioning (hot).60. Older patients with
thyrotoxicosis may not have classical hyperadrenergic symptoms and signs, but may instead present
with weight loss, depression, or heart disease (worsening angina pectoris, atrial fibrillation,
congestive heart failure); this picture is often referred to as apathetic thyrotoxicosis.
61. Radioiodine treatment may worsen eye disease in patients with significant proptosis or periorbital
inflammation due to Graves’ ophthalmopathy; if radioiodine is used, patients should stop smoking
and should take a course of oral corticosteroids immediately after the radioiodine treatment.62.
Levothyroxine is the preferred initial treatment for hypothyroidism; healthy young patients can be
started at a dose of 1.6 ug/kg/day but in patients over age 60 and in those with coronary artery
disease, a starting dose of 25 ug a day is preferable.63. The goal TSH for treatment of primary
hypothyroidism is between 0.5 and 2.0 mU/L.64. Amiodarone-induced thyroid disease (AITD) may
be due to iodine-induced hyperthyroidism (Type 1 AITD) or destruction-induced thyroiditis (Type 2
AITD).65. Women with Type 1 diabetes mellitus have a threefold greater risk of developing
postpartum thyroid disorders than do non-diabetic TPO antibody positive women.
66. Fine needle aspiration (FNA) of thyroid nodules is a safe outpatient procedure with an accuracy
of 90% to 95% in determining malignancy.67. Toxic thyroid adenomas are almost never
cancerous.68. Thyroglobulin is the best tumor marker for monitoring differentiated thyroid
cancer.69. Suppression of TSH, a thyroid cancer growth factor, with levothyroxine is an important
therapeutic intervention in patients with differentiated thyroid cancer.70. Thyroid storm is treated
with anti-thyroid drugs, cold iodine, beta blockers, stress glucocorticoid doses, and management of
any precipitating factors.
71. Myxedema coma is treated with rapid repletion of the thyroid hormone deficit with levothyroxine
þ/ liothyronine, glucocorticoids and treatment of any precipitating causes.72. The euthyroid sick
syndrome is not a thyroid disorder, but is instead a group of changes in serum thyroid hormone and
TSH levels that result from cytokines and inflammatory mediators produced in patients with non-
thyroidal illnesses.73. The euthyroid sick syndrome appears to be an adaptive response to reduce
tissuemetabolism and preserve energy during systemic illnesses and therefore treatment withthyroid
hormone is not currently recommended for this condition.74. Postpartum thyroiditis occurs in 5% of
normal women and 25% of women with Type 1 diabetes mellitus.75. On average, a women’s thyroid
hormone replacement dose for hypothyroidism will increase by 25 to 50 mg per day during
pregnancy, often during the first trimester.
76. The symptoms of hypothyroidism often mimic those of depression, while those of
hyperthyroidism may be confused with mania or depression.77. About 20% of patients admitted to
the hospital with acute psychiatric presentations,including schizophrenia and major affective
disorders, but rarely dementia or alcoholism,may have mild elevations in their serum T4 levels, and
less often their T3 levels.78. Central precocious puberty occurs more frequently in girls than boys;
the condition is often idiopathic in girls while boys with central precocity have a much higher
incidence of underlying CNS pathology.79. Hypogonadism should be characterized as primary (a
disorder of the testes) or secondary (a disorder of the hypothalamic-pituitary unit); a reduction in
testicular volume (<20 ml) is the most common manifestation of hypogonadism and is seen in nearly
all cases of longstanding hypogonadism.
80. The diagnosis of hypogonadism is confirmed with a correctly-obtained serum testosterone
measurement or semen analysis; measurement of serum LH and FSH levels then helps to determine
whether the hypogonadism is primary (testicular) or secondary (pituitary or hypothalamic).
81. The specific cause of impotence can be diagnosed in 85% of men.82. The anti-hypertensive
medications that are least likely to cause impotence are ACE inhibitors, angiotensin receptor
blockers, and calcium channel blockers.83. Cysts on ovarian ultrasound do not always signify a
diagnosis of PCOS.84. A serum testosterone > 200 ng/dl or a DHEAS > 1000 ng/ml in a hirsute
patient suggests the presence of an androgen producing ovarian or adrenal tumor.85. Primary
hypothyroidism can cause amenorrhea, galactorrhea, pituitary enlargement and mildly elevated
serum prolactin levels, and thus can mimic a prolactinoma.86. Many medications and painful lesions
of the chest wall can cause galactorrhea.87. The common causes of hirsutism are PCOS, CAH,
idiopathic/familial hirsutism, and medications.88. The common causes of virilization are androgen
secreting ovarian or adrenal tumors and CAH.89. Side effects of anabolic-androgenic steroid abuse
include fluid retention, testicular atrophy,oligospermia, azoospermia, gynecomastia, cholestatic
hepatitis, pelioses hepatis, benign and malignant hepatic tumors as well as reduced HDL and higher
LDL cholesterol levels.
90. MEN 1, which consists of hyperplasia and/or tumors of the pituitary gland, pancreatic islets and
parathyroid glands, results from a mutation inactivating the Menin tumor suppressor gene on
chromosome 11.91. The MEN 2 syndromes, which consist of pheochromocytomas and medullary
thyroid carcinoma associated with hyperparathyroidism (MEN 2A) or mucosal neuromas (MEN 2B),
result from mutations in the Ret tumor suppressor gene; genetic testing for these conditions is now
clinically available.92. Autoimmune polyendocrine syndrome type 1 (APS-1) is a syndrome marked
by hypoparathyroidism, adrenal insufficiency and mucocutaneous candidiasis.93. Autoimmune
polyendocrine syndrome type 2 (APS-2) consists of adrenal insufficiency,thyroid dysfunction and
diabetes mellitus type 1.94. Fasting hypoglycemia often produces neuroglycopenic symptoms and is
frequently due to an organic disorder or surreptitious use of insulin or oral hypoglycemic
medications.95. Insulinomas most often cause fasting hypoglycemia with neuroglycopenic
symptoms.
96. Most patients with carcinoid syndrome have extensive liver metastases that either impair the
metabolic clearance of mediators secreted by the primary tumor or that secrete the mediators directly
into the hepatic vein. 97. A carcinoid crisis can be precipitated when a patient with a carcinoid tumor
is given anadrenergic medication or a monoamine oxidase inhibitor; effective treatment is
available.98. Mucormycosis is more common during diabetic ketoacidosis because the fungi are
thermotolerant, grow well in an acid pH, grow rapidly in the presence of high glucose, and are one of
the few types of fungi that can utilize ketones as a food substrate.99. The most common cause of
acanthosis nigricans is diabetes mellitus associated with insulin resistance and obesity.100. Aging is
associated with losses of muscle mass and bone mass and with increases in fatmass, which
may be associated with parallel age-related declines in the production of growth hormone
and sex steroid hormones and increased cortisol secretion.