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49 Cards in this Set
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H/P = frequently asymptomatic; symptoms of hypercalcemia may be present (e.g., bone pain, nausea and vomiting, mental status changes, renal stones, constipation, weakness, increased risk of fracture)
Labs = increased Ca2+, decreased phosphate, increased urine Ca2+, increased PTH Radiology = decreased bone density on dual x-ray absorptiometry (DXA) scan |
Primary hyperparathyroidism
Excess PTH secretion, leading to hypercalcemia and osteopenia Most cases result from single adenoma; remaining cases mostly occur with hyperplasia of all four glands; parathyroid cancer is rare Decreased Ca2+ with increased PTH suggests a hyperparathyroidism secondary to malnutrition, malabsorption, renal disease, or calcium-wasting drugs. “bones,” “stones,” “groans,” and “psychiatric overtones” of hypercalcemia in cases of hyperparathyroidism |
Treatment = surgical resection (i.e., parathyroidectomy) of single adenoma; for four-gland hyperplasia, all glands are removed, and a portion of one gland is implanted in the muscle of forearm to maintain some PTH production; treat hypercalcemia with IV fluids and bisphosphonates
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H/P = tingling in lips and fingers, dry skin, weakness, abdominal pain, tetany, dyspnea; possible tachycardia, seizures, movement disorders, cataracts, dental hypoplasia, positive Trousseau's (i.e., carpal spasm when blood pressure cuff inflated) and Chvostek's signs (i.e., tapping of facial nerve causes spasm)
Labs = decreased Ca2+, increased phosphate, decreased PTH |
Hypoparathyroidism
PTH deficiency caused by surgical removal of parathyroids (most common) or autoimmune degeneration of glands (uncommon), leading to hypocalcemia |
Radiology = x-rays may demonstrate osteosclerosis or increased bone density
Treatment = Ca2+ and vitamin D supplementation |
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H/P = symptoms of hypocalcemia, short stature, seizures, poor mental development in children
Labs = decreased Ca2+, increased phosphate, increased PTH; administration of PTH causes no change in serum or urine Ca2+ |
Pseudohypoparathyroidism
Hypocalcemia resulting from tissue nonresponsiveness to PTH Associated with developmental and skeletal abnormalities (e.g., Albright's hereditary osteodystrophy) |
Treatment = Ca2+ and vitamin D supplementation
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H/P = polyuria, polydipsia, polyphagia, weight loss; more rapid onset than type II DM
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Diabetes mellitus (DM) type I (juvenile onset diabetes, insulin-dependent diabetes)
Loss of ability to produce insulin most likely caused by autoimmune destruction of β-islet cells Association with human leukocyte antigens HLA-DR3, HLA-DR4, and HLA-DQ genotypes Usually diagnosed <13 yr of age Complications = diabetic ketoacidosis (DKA), hypoglycemia (secondary to excess insulin administration), retinopathy, neuropathy, nephropathy, atherosclerosis |
Labs = hyperglycemia, glycosuria (i.e., glucose in urine), serum and urine ketones, increased hemoglobin A1c (indicates hyperglycemia over prior 3 months and used to monitor adequacy of control)
Treatment = scheduled insulin injections or continuous insulin infusion via insulin pump; monitoring of serum glucose at home to guide insulin and dietary adjustments; close multidiscipline follow-up to monitor development of complications |
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H/P = asymptomatic in early stages with gradual onset of symptoms; polyuria, polydipsia, polyphagia; symptoms related to complications can present before actual diagnosis
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Diabetes mellitus type II (adult onset diabetes, non–insulin-dependent diabetes)
Development of tissue resistance to insulin, leading to hyperglycemia and gradual decrease in the ability of β-islet cells to produce insulin Risk factors = family history, obesity, lack of exercise Historically diagnosed after age 40 yr, but mean age of diagnosis is decreasing Complications = hyperosmolar hyperglycemic nonketotic coma (HHNK), retinopathy, nephropathy, neuropathy, atherosclerosis |
Labs = hyperglycemia, glycosuria (i.e., glucose in urine), serum and urine ketones, increased hemoglobin A1c (indicates hyperglycemia over prior 3 months and used to monitor adequacy of control)
Treatment = Initial therapy focuses on nutrition (reduced calorie intake, carbohydrate control and consistency), exercise, and weight loss Metformin is frequently the first oral agent prescribed (see Table 5-4) If hemoglobin A1c remains >7 after 2–3 months of monotherapy, add sulfonylurea and/or thiazolidinedione If patient begins to exhibit signs of decreased insulin production or if hemoglobin A1c is consistently >8.5, add insulin regimen Close monitoring of blood glucose levels is important to directing therapy |
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H/P = weakness, polyuria, polydipsia, hyperventilation, abdominal pain, vomiting; dry mucous membranes, decreased skin turgor, fruity odor on breath, Kussmaul respirations (i.e., slow, deep breathing); mental status changes develop with worsening dehydration
Labs = glucose 300–800 mg/dL (rarely >1,000), decreased Na+, decreased K+, decreased phosphate, high anion gap metabolic acidosis, serum and urine ketones |
Diabetic ketoacidosis (DKA)
Extremely low insulin and glucagon excess cause degradation of triglycerides into fatty acids and eventual conversion into ketoacids Occurs in patients with DM type I who do not take prescribed insulin or those who have infections, high stress, myocardial infarction (MI), or high alcohol use |
Treatment = intravenous (IV) fluids, insulin, KCl; treat underlying disorder (success of treatment may be confirmed by decreasing ketone levels)
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H/P = polyuria, polydipsia, dehydration, mental status changes; seizures and stroke can occur in severe cases
Labs = glucose >800 mg/dL (frequently >1,000), no acidosis |
Hyperosmolar hyperglycemic nonketotic coma (HHNK)
Extremely high glucose with profound dehydration Occurs in patients with DM type II with lengthy infections, stress, or illness; insulin production is sufficient to prevent DKA |
Treatment = IV fluids, insulin, correction of electrolyte abnormalities; treat underlying disorder
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H/P = progressive vision loss, premature cataracts; retinal changes seen on funduscopic examination (e.g., arteriovenous nicking, hemorrhages, edema, infarcts)
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Diabetic retinopathy
Vascular occlusion and ischemia, with or without neovascularization in retina, leading to visual changes Associated with microaneurysms, hemorrhages, infarcts, & macular edema Background retinopathy (no neovascularization) makes up most cases; proliferative retinopathy (with neovascularization) has increased risk of hemorrhages Complications = vision loss, early cataracts and glaucoma, retinal detachment |
Treatment = control diabetes, anti-hypertension (HTN) therapy, annual follow-up with ophthalmology, laser photocoagulation for neovascularization, injection of intervitreal corticosteroids to reduce macular edema
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H/P = develops after several years with DM (20+); lab abnormalities may appear well before symptoms; symptoms and signs of renal insufficiency (e.g., HTN, uremia) develop as renal function deteriorates
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Diabetic nephropathy
Intercapillary glomerulosclerosis, mesangial expansion, and basement membrane degeneration that develops after long-term DM Slightly greater risk in DM type I than in DM type II Initially presents with proteinuria; renal insufficiency later develops with nephrotic syndrome Complications = end-stage renal disease |
Labs = hypoalbuminemia, increased creatinine (Cr), increased blood urea nitrogen (BUN); urinalysis shows proteinuria; electron microscopy shows basement membrane thickening and Kimmelstiel-Wilson nodules in glomeruli
Treatment = control diabetes; angiotensin-converting enzyme inhibitor (ACE-I) or angiotension receptor blocker (ARB) to decrease blood pressure, low-protein diet, infection prevention; dialysis may eventually be required |
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Sensory neuropathy begins in feet and progresses in stocking-glove pattern; symptoms include paresthesias, neural pain, and decreased vibratory and pain sensation
Motor neuropathy may be distally or proximally distributed and may be characterized by weakness or loss of coordination Autonomic neuropathy can cause postural hypotension, impotence, incontinence, and diabetic gastroparesis (i.e., delayed gastric emptying) |
Diabetic neuropathy
Neural damage and conduction defects leading to sensory, motor, and autonomic nerve dysfunction Complications = Charcot joints, diabetic foot ulcers; amputation may be needed to treat progressive infections and deformity |
Treatment = control diabetes; neural pain can be treated with tricyclic antidepressants, phenytoin, carbamazepine, or gabapentin; narcotics or tramadol can be considered for persistent neural pain; patients should be taught how to perform regular foot examinations
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Increased risk of coronary artery disease and peripheral vascular disease (PVD), leading to increased risk of MI, distal ischemia, and ulcer formation secondary to poor healing and infection
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Atherosclerosis
Incidence greatly increased in diabetic patients secondary to microvascular disease Complications = MI (frequently silent), PVD, poor healing of trauma and infections |
Treatment = control HTN and hyperlipidemia; daily aspirin (ASA) therapy
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H/P = faintness, weakness, diaphoresis, and palpitations because of responsive excess secretion of epinephrine (attempt to mobilize glycogen); headache, confusion, mental status changes, decreased consciousness because of inadequate supply of glucose to the brain
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Hypoglycemia
Inadequate blood glucose that can result in an inadequate supply of glucose to tissues and brain damage |
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Hypoglycemia and symptoms improve with carbohydrate meal
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Reactive Hypoglycemia
Decrease in serum glucose after eating (postsurgical or idiopathic) |
Treatment=Frequent small meals
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Hypoglycemia
Increased insulin in presence of hypoglycemia, adjustment of drug regimen reduces symptoms |
Iatrogenic (excess insulin) Hypoglycemia
Excess insulin administration or adverse effect of sulfonylurea or meglitinide use |
Treatment=Adjust insulin regimen, consider different oral hypoglycemic drug
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Hypoglycemia
Increased insulin in presence of hypoglycemia, may be detected on CT or MRI |
Insulinomaa
β-islet cell tumor producing excess insulin |
Treatment=Surgical resection if able to locate
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Hypoglycemia
Lab abnormalities and history associated with particular etiology |
Hypoglycemia
Fasting Underproduction of glucose because of hormone deficiencies, malnutrition, or liver disease |
Treatment=Proper nutrition, enzyme replacement
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Hypoglycemia
History of alcohol use, serum ethanol >45 mg/dL |
Alcohol-induced
Glycogen depletion and gluconeogenesis inhibition by high concentrations of alcohol |
Treatment=Proper nutrition, stopping high quantity alcohol use
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Hypoglycemia
Low serum cortisol; site of defect determined by ACTH activity tests; possible other comorbid endocrine abnormalities |
Pituitary/adrenal insufficiency
Decreased cortisol production leads to insufficient hepatic gluconeogenesis in response to hypoglycemia |
Treatment=Cortisol replacement
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H/P = weight loss, increased appetite, heat intolerance, anxiety, diaphoresis, palpitations, increased bowel frequency; staring or lid lag, tremor, tachycardia, increased pulse pressure, warm skin, hyperreflexia, possible atrial fibrillation
Labs = decreased TSH, increased total T4, free T4, total T3, and T3 resin uptake |
Hyperthyroidism
Excess production of thyroid hormones Multiple causes, but Graves' disease is most common Complications = thyroid storm |
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H/P = existing symptoms of hyperthyroidism, severe diaphoresis, vomiting, diarrhea; tachycardia, fever, mental status changes
Labs = increased T4 and T3, decreased TSH |
Thyroid storm
Severe hyperthyroidism induced by infection, surgery, or stress in patients with preexisting hyperthyroidism Complications = 25%–50% mortality |
Treatment = similar to treatment of hyperthyroidism, but higher doses of medications given in greater frequency; β-blockers, thionamides, IV sodium iodine (helps block thyroid hormone release), hydrocortisone (inhibits conversion of T4 to T3); surgery or radioablation when patient is stable
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Hyperthyroidism
Exophthalmos, pretibial myxedema, painless goiter; TSI found in serum; high uptake on thyroid scan |
Graves' disease
Autoimmune TSI antibodies bind to TSH receptors in thyroid and stimulate thyroid hormone production |
Treatment=Thionamides (methimazole, PTU) achieve euthyroidism in many cases; radioablation with radioactive iodine or subtotal thyroidectomy for definitive cure; atenolol can be used for symptomatic relief
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Hyperthyroidism
Thyroid scan shows increased uptake at site(s) of nodule(s) |
Toxic adenoma (Plummer's disease)/toxic multinodular goiter
Single or multiple hyperactive nodules produce excess thyroid hormones |
Treatment=Thionamides, radioactive iodine, or surgical resection
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Hyperthyroidism
Painful goiter, mild symptoms of hyperthyroidism, neck pain, fever; increased ESR; decreased uptake on thyroid scan |
Subacute thyroiditis (de Quervain's thyroiditis)
Enlarged thyroid due to possible viral stimulus |
Treatment=Self-limited; NSAIDs and β-blockers to treat symptoms; thyroid replacement may be needed if hypothyroidism occurs during gland recovery
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Hyperthyroidism
Painless goiter; low uptake on thyroid scan; biopsy shows inflammation |
Silent thyroiditis
Temporary thyroiditis that may follow pregnancy |
Treatment=Self-limited; β-blockers to treat symptoms
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Hyperthyroidism
No goiter in cases of hyperthyroidism; normal thyroid scan |
Factitious hyperthyroidism Excess thyroid hormone ingestion
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Treatment=Stop excess ingestion
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H/P = weakness, fatigue, decreased exercise capacity, Cold intolerancE, Weight gaiN, constipation, irregular menstruation, DepressioN, hoarseness; hyporeflexia, bradycardia, dry skin, edema, Painless goiteR
Labs = increased TSH, decreased total T4, decreased free T4, antimicrosomal and antithyroglobulin antibodies; lymphocytic infiltrates and fibrosis seen on biopsy |
Hashimoto's thyroiditis
Most common cause of hypothyroidism Autoimmune condition characterized by chronic thyroiditis; most commonly in middle-aged women Symptoms of hyperthyroidism can be seen in early Hashimoto's thyroiditis |
Radiology = decreased uptake on thyroid scan (i.e., “cold scan”)
Treatment = life-long levothyroxine replacement |
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H/P = nontender nodule in anterior neck, dysphagia, hoarseness; possible cervical lymphadenopathy
Labs = biopsy provides diagnosis; thyroid hormones normal or decreased Radiology = US used to determine size and local extension; thyroid scan may differentiate hot from cold nodule (malignant nodules more likely to be cold) |
Thyroid nodules
usually benign and increase in frequency with age Evaluated with TSH levels, thyroid function tests, ultrasound (US), and fine needle aspiration (FNA) with biopsy |
Treatment =
Benign small cystic nodules may be observed Benign solid nodules treated with surgery, radioablation, and postoperative levothyroxine to stop thyroid hormone overproduction and decrease risk of malignant conversion Malignant tumors require surgical resection (lobectomy for nonanaplastic tumors <1 cm diameter, total thyroidectomy for larger tumors) and radioiodine ablation Radiation therapy for tumors with local extension; chemotherapy for metastatic tumors Thyroid replacement (levothyroxine) needed after surgery |
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H/P = Amenorrhea and galactorrheA (women); decreased libido, erectile dysfunction, and GynecomastiA (men); bilateral hemianopsia can result from mass effect of tumor in sella turcica
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Hyperprolactinemia
Excess prolactin secretion by anterior pituitary Can result from pregnancy, prolactinoma, drugs that block dopamine synthesis (e.g., phenothiazines, risperidone, haloperidol, methyldopa, verapamil), dopamine-depleting drugs, or hypothalamic damage Causes decreased LH and FSH secretion, galactorrhea (i.e., milk secretion), and amenorrhea in women Causes gynecomastia in men |
Labs = increased prolactin; if adenoma, prolactin >300 ng/mL and TRH administration causes no additional prolactin secretion
Radiology = magnetic resonance imaging (MRI) may detect pituitary tumor Treatment = dopamine agonists (e.g., cabergoline, bromocriptine, pergolide), stopping offending agents; transsphenoidal surgery and radiation therapy should be performed in refractory cases |
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H/P = enlargement of hands and feet, coarsening of facial features (e.g., enlargement of nose, jaw, and skin folds), thickened skin, increased body hair growth, joint pain (caused by osteoarthritis), neural pain (because of nerve entrapment); changes may be gradual
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Acromegaly
Excess secretion of GH by anterior pituitary caused by adenoma Heart, lungs, spleen, liver, and kidneys become enlarged and can cause symptoms secondary to dysfunction Complications = cardiac failure, DM, spinal cord compression, vision loss secondary to pressure of tumor on optic nerve |
Labs = increased GH, increased GH 1–2 hr following 100 g glucose load (GH decreases in normal cases)
Radiology = computed tomography (CT) or MRI may detect tumor; x-rays may demonstrate increased bone density Treatment = surgical resection of adenoma; dopamine agonists or octreotide to lessen effects of GH; radiation therapy may be useful in cases unresponsive to surgical or medical treatment |
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Labs =
LH/FSH: decreased LH, FSH, estrogen (women), and testosterone (men); menstruation does not occur following administration of medroxyprogesterone GH: decreased GH; no increase in GH after administration of insulin TSH: decreased TSH, T4, and T3 uptake Prolactin: decreased prolactin (most noticeable postpartum) ACTH: decreased ACTH; cortisol does not increase following administration of insulin (normally should increase at least 10 µg/dL), ACTH and 11-deoxycortisol do not increase following administration of metyrapone |
Hypopituitarism
Deficiency of all anterior pituitary hormones caused by tumor, hemorrhagic infarction (i.e., pituitary apoplexy), surgical resection, trauma, sarcoidosis, tuberculosis, postpartum necrosis (i.e., Sheehan syndrome), or dysfunction of the hypothalamus Some pituitary hormones are kept in storage, and target organs may maintain some autonomous function, so symptoms specific to deficiency of each type of hormone appear at various times Remember the order in which symptoms of hormone deficiencies develop in panhypopituitarism by the mnemonic Good Luck Finding Treatment (for) Pituitary Accidents: GH → LH → FSH → TSH → Prolactin → ACTH. |
Treatment = treat underlying cause, if possible; treatment depends on which hormones are deficient
GH: recombinant hormone replacement therapy LH/FSH: testosterone replacement in men; estrogen-progesterone pill for women; gonadotropin-releasing hormone (GnRH) can be used in men or women desiring fertility TSH: levothyroxine Prolactin: no need to treat (women will be unable to lactate) ACTH: hydrocortisone, dexamethasone, or prednisone |
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/P = weakness, depression, menstrual irregularities, polydipsia, polyuria, increased libido, impotence; HTN, Acne, increased hair growtH, central obesity, “Buffalo humP” (i.e., hunchback-like hump on back), “Moon facieS” (i.e., rounded face caused by increased fat deposition), Purple striaE on abdomen
Labs = hyperglycemia, glycosuria, decreased K+ |
Cushing's syndrome
Syndrome of excess cortisol caused by excess corticosteroid administration, pituitary adenoma (i.e., Cushing's disease), paraneoplastic ACTH production, or adrenal tumor Complications = increased risk of mortality from cardiovascular or thromboembolic complications; increased infection risk, avascular necrosis of hip, hypopituitarism or adrenal insufficiency after surgery |
Treatment = adjust corticosteroid dosing in cases of excess administration; surgical resection or pituitary irradiation for pituitary tumors; surgical resection for nonpituitary or adrenal tumors; octreotide may improve symptoms in paraneoplastic syndromes; cortisol replacement may be needed after surgery
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H/P = polyuria, headache, weakness, paresthesias; recalcitrant HTN, tetany
Labs = decreased K+, mildly increased Na+, metabolic alkalosis, decreased renin (Conn's syndrome only), increased 24-hr urine aldosterone |
Hyperaldosteronism
Excess aldosterone secretion caused by unilateral adrenal adenoma (i.e., Conn's syndrome) or increased renin-angiotensin system activity secondary to low blood pressure in kidney |
Radiology = CT or MRI may detect adrenal mass
Treatment = surgical resection of tumor; treat underlying disorder causing renin-angiotensin system hyperactivity; spironolactone improves hypokalemia until definitive therapy administered |
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H/P = weakness, Fatigue, anorexia, weight loss, nausea and vomiting (more common in primary disease), myalgias, arthralgias, decreased libido (women), memory impairment, depression, mild psychosis; hypotension, possible Increased skin pigmentation (because of feedback influence of melanocyte-stimulating hormone [MSH])
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Adrenal insufficiency
Mineralocorticoid (i.e., aldosterone) or glucocorticoid (i.e., cortisol) deficiency caused by adrenal disease or ACTH insufficiency Addison's disease (primary insufficiency): autoimmune destruction of adrenal cortices caused by autoimmune disease, infection, or hemorrhage; can occur with other endocrine autoimmune processes P.121 Secondary corticoadrenal insufficiency: due to decreased ACTH secondary to chronic corticosteroid use (adrenal atrophy) or insufficient ACTH production by pituitary Tertiary corticoadrenal insufficiency: because of insufficient corticotropin-releasing hormone (CRH) secretion by hypothalamus Complications = Addisonian crisis (i.e., severe weakness, fever, mental status changes, and vascular collapse caused by stress and increased cortisol need; treat with IV glucose and hydrocortisone or vasopressors), secondary insufficiency caused by excess cortisol replacement |
Labs =
Decreased Na+ and increased K+ secondary to low aldosterone, eosinophilia, decreased cortisol Increased ACTH with Addison's disease, decreased ACTH with secondary insufficiency Decreased cortisol that increases following ACTH analogue administration in secondary or tertiary insufficiency, but not in Addison's disease Treatment = treat underlying disease; glucocorticoid replacement (e.g., hydrocortisone, dexamethasone, or prednisone), mineralocorticoid replacement (may not be needed in secondary or tertiary disease), dehydroepiandrosterone (DHEA), and hydration to achieve adequate volume status; titrate cortisol levels for periods of stress (increased need) and to avoid exacerbating secondary adrenal insufficiency |
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H/P = amenorrhea (women), ambiguous genitalia (men); HTN
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Congenital adrenal hyperplasia (CAH)
17-α-hydroxylase deficiency Deoxycorticosterone overproduction; cortisol, androgen, and estrogen deficiencies |
Labs = decreased K+, increased Na+, decreased androgens, decreased 17-α-hydroxyprogesterone
Treatment = cortisol replacement to achieve ACTH suppression; most children raised as females; estrogen-progesterone replacement given to genotypic females at puberty; genotypic males may have reconstructive surgery of genitals |
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H/P = ambiguous genitalia (female infants), virilization (women), macrogenitosomia and precocious puberty (men); dehydration and hypotension in more severe cases
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Congenital adrenal hyperplasia (CAH)
21-α-hydroxylase deficiency (Usually) partial deficiency of enzyme resulting in excess androstenedione, insufficient cortisol and aldosterone |
Labs = decreased Na+, increased K+, increased androgens
Treatment =cortisol replacement therapy for ACTH suppression; fludrocortisone for mineralocorticoid replacement; reconstructive genital surgery |
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H/P = ambiguous genitalia (female infants), virilization (women), macrogenitosomia and precocious puberty (men); HTN (secondary to deoxycorticosterone)
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Congenital adrenal hyperplasia (CAH)
11-β-hydroxylase deficiency Enzyme deficiency resulting in excess deoxycorticosterone, deoxycortisol, and androgens and insufficient cortisol and aldosterone |
Labs = increased deoxycorticosterone, increased deoxycortisol, increased androgens
Treatment=cortisol replacement (hydrocortisone or dexamethasone) for ACTH suppression; anti-HTN may be required for persistent HTN |
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H/P = sudden palpitations, chest pain, diaphoresis, headache, anxiety; Intermittent tachycardia, HTn
Labs = increased 24-hr urinary catecholamines and metanephrines; increased plasma-free metanephrines; increased 24-hr urinary vanillylmandelic acid (VMA) (test performed infrequently because of limited sensitivity/specificity) |
Pheochromocytoma
Adrenal medulla tumor that secretes epinephrine and norepinephrine, leading to stimulation of sympathetic nervous system; rarely extra-adrenal in location |
Treatment = surgical resection; α- and β-blockers used before and during surgery to control blood pressure
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Hyperparathyroidism, hypercalcemia, possible Zollinger-Ellison syndrome, various pituitary disorders (e.g., acromegaly, Cushing's syndrome, galactorrhea)
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MEN I / Wermer syndrome
Parathyroid Pancreas (islet cell tumors) Pituitary Ps: Parathyroid, Pancreas, Pituitary |
Treatment=Subtotal parathyroidectomy, surgical resection of pancreatic tumor or octreotide, surgical resection of pituitary tumor
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Medullary carcinoma, increased calcitonin, hyperparathyroidism, hypercalcemia, increased serum and urine catecholamines
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MEN IIa / Sipple syndrome
Medullary thyroid Pheochromocytoma Parathyroid Cs: Carcinoma of thyroid (medullary), Catecholamine excess (pheochromocytoma), Calcium excess (hyperparathyroidism) |
Treatment=Total thyroidectomy, surgical resection of pheochromocytoma, subtotal parathyroidectomy
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Medullary carcinoma, increased calcitonin, hyperparathyroidism, hypercalcemia, Marfanoid body habituS, mucosal nodules
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MEN IIb
Medullary thyroid Pheochromocytoma Mucosal neuroma 3 Ms: Medullary thyroid carcinoma, Medulla of adrenal tumor (pheochromocytoma), and Mucosal neuromas. |
Treatment=Total thyroidectomy, surgical resection of pheochromocytoma
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H/P = frequently asymptomatic if mother has normal thyroid function; poor feeding, lethargy, large fontanelles that remain open, thick tongue, constipation; umbilical hernia, poor growth, hypotonicity, dry skin, hypothermia, prolonged JaundicE
Labs = decreased T4, increased TSH |
Cretinism
Congenital hypothyroidism caused by severe iodide deficiency or hereditary disorder of thyroid hormone synthesis that leads to abnormal mental development and growth retardation |
Radiology = x-ray shows poor bone development; thyroid scan shows decreased uptake with malformed thyroids and increased uptake with iodide deficiency
Treatment = levothyroxine started soon after birth to avoid permanent developmental delays |
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Thyroid Carcinoma
Begins as slow-growing nodule; eventually metastasizes to local cervical lymph nodes |
Papillary
affect Columnar cells of gland Most common form (78% cases); most common in younger patients; follicular variant (17% cases) is most common varian |
Prognosis Good; few recurrences; follicular type has slightly worse prognosis (50% 10-yr survival)
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Thyroid Carcinoma
Produces calcitonin; may present with other endocrine tumors (MEN IIa and IIb) |
Medullary
affect Parafollicular C cells 4% of thyroid cancers |
Worse in older patients; metastases common at diagnosis
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Thyroid Carcinoma
Very aggressive; local extension causes hoarseness, dysphagia |
Anaplastic
Poorly differentiated neoplasm 1% of thyroid cancers |
Poor Prognosis
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Hormone Deficiency in Hypopituitarism
Growth failure and short stature in children |
GH
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Hormone Deficiency in Hypopituitarism
Infertility, - libido, and - pubic hair; amenorrhea and genital atrophy in women; impotence |
LH, FSH
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Hormone Deficiency in Hypopituitarism
fatigue and cold intolerance |
TSH
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Hormone Deficiency in Hypopituitarism
No postpartum lactation |
Prolactin
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Hormone Deficiency in Hypopituitarism
fatigue, weight loss, - appetite, and poor response to stress; - skin pigment |
ACTH, MSH
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