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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
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
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
H/P = polyuria, polydipsia, polyphagia, weight loss; more rapid onset than type II DM
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
H/P = asymptomatic in early stages with gradual onset of symptoms; polyuria, polydipsia, polyphagia; symptoms related to complications can present before actual diagnosis
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
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)
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
H/P = progressive vision loss, premature cataracts; retinal changes seen on funduscopic examination (e.g., arteriovenous nicking, hemorrhages, edema, infarcts)
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
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
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
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
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
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
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
Hypoglycemia
Inadequate blood glucose that can result in an inadequate supply of glucose to tissues and brain damage
Hypoglycemia and symptoms improve with carbohydrate meal
Reactive Hypoglycemia
Decrease in serum glucose after eating (postsurgical or idiopathic)
Treatment=Frequent small meals
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
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
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
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
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
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
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
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
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
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
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
Hyperthyroidism
No goiter in cases of hyperthyroidism; normal thyroid scan
Factitious hyperthyroidism Excess thyroid hormone ingestion
Treatment=Stop excess ingestion
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
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
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
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
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
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
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
/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
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
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])
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
H/P = amenorrhea (women), ambiguous genitalia (men); HTN
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
H/P = ambiguous genitalia (female infants), virilization (women), macrogenitosomia and precocious puberty (men); dehydration and hypotension in more severe cases
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

H/P = ambiguous genitalia (female infants), virilization (women), macrogenitosomia and precocious puberty (men); HTN (secondary to deoxycorticosterone)
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
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
Hyperparathyroidism, hypercalcemia, possible Zollinger-Ellison syndrome, various pituitary disorders (e.g., acromegaly, Cushing's syndrome, galactorrhea)
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
Medullary carcinoma, increased calcitonin, hyperparathyroidism, hypercalcemia, increased serum and urine catecholamines
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
Medullary carcinoma, increased calcitonin, hyperparathyroidism, hypercalcemia, Marfanoid body habituS, mucosal nodules
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
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
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)
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
Thyroid Carcinoma
Very aggressive; local extension causes hoarseness, dysphagia
Anaplastic
Poorly differentiated neoplasm
1% of thyroid cancers
Poor Prognosis
Hormone Deficiency in Hypopituitarism
Growth failure and short stature in children
GH
Hormone Deficiency in Hypopituitarism
Infertility, - libido, and - pubic hair; amenorrhea and genital atrophy in women; impotence
LH, FSH
Hormone Deficiency in Hypopituitarism
fatigue and cold intolerance
TSH
Hormone Deficiency in Hypopituitarism
No postpartum lactation
Prolactin
Hormone Deficiency in Hypopituitarism
fatigue, weight loss, - appetite, and poor response to stress; - skin pigment
ACTH, MSH