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45 Cards in this Set
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T3RU decrease, T4 elevated
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excess thyroxine binding (estrogen use)
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T3RU increased, T4 decreased
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Reduced binding states (malnutrition)
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May be asymptomatic, or exhibit thyroid dysfunction, known as a
“hot” nodule |
Thyroid Nodule
Description Solitary thyroid lesion. Pathology Most common benign lesion: follicular adenoma. Most common malignant nodule: papillary cancer. History of irradiation: very important to ask. Increased chance of malignancy if young. Poor outcome—male gender, over 40 years old, distant metastases, large primary tumor over 1.5 cm in diameter, extrathyroidal invasion |
Diagnosis
History and physical exam, needle aspiration or thyroid scan (most malignant nodules are nonfunctioning, cold), ultrasound and surgical removal. Treatment Steps 1.Cyst: aspirate/follow. 2.Carcinoma: surgical/radioiodine (131I) |
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Description/Symptoms
Enlarged thyroid gland. May be asymptomatic or cause compressive symptoms secondary to large gland size. |
Goiter
Diagnosis History and physical exam, T4 normal, TSH may be normal or slightly elevated, ultrasound examination. No autoimmune antibodies present. Pathology Inadequate iodine or excessive iodine. Lithium use, familial goiter, adolescent goiter |
Treatment Steps
1. Levothyroxine. 2.If inadequate iodine in iodine deficiency countries, give iodine. 3.Surgery (rare). |
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Description
Thyroid gland inflammation |
Thyroiditis
May have type I diabetes |
Diagnosis
History and physical exam, thyroid scan, lab (thyroid peroxidase au- toantibodies-autoimmune), elevated T4 and T3RU, in de Quervain’s. de Quervain’s: Elevated sed rate, biopsy |
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Description
Thyroid gland inflammation thyroid pain/erythema/dysphagia, and fever. |
Acute suppurative
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Treatment Steps
antibiotics. |
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Description
Thyroid gland inflammation lethargy, migratory neck pain, fever, malaise, may be asymptomatic. |
de Quervain’s
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Treatment Steps
aspirin/NSAIDs, pred- nisone |
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Description
Thyroid gland inflammation goiter. Serum antithyroid antibodies may be present |
Hashimoto’s—goiter.
Although can cause transient hyperthyroidism, more often causes hypothyroidism requiring treatment with thyroxin Most common type of thyroiditis. Autoimmune etiology |
Treatment Steps
thyroxine. |
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Description
Thyroid gland inflammation tracheal compression/sclerosing fibrosis (rare). |
Riedel’s—tracheal compression/sclerosing fibrosis (rare).
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Treatment Steps
thyroxine. |
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Description
Thyroid gland inflammation Painles |
Painless thyroiditis (postpartum).
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Treatment Steps
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Symptoms
Dry skin, lethargy, umbilical hernia, slow teething/sexual development |
Congenital Hypothyroidism (Cretinism)
Pathology Thyroid absent, or ineffective hormone secreted due to enzyme deficiency (familial goiter) |
Diagnosis
History and physical exam, elevated TSH, low T4, bone stippling, and delayed maturation Treatment Steps Levothyroxine (synthetic L-thyroxine) |
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Symptoms
Fatigue, myxedema of tissue, cold intolerance, dry skin, lateral eye- brow thinning, constipation, lethargy, bradycardia, carpal tunnel syndrome, depression, menorrhagia. |
Adult Hypothyroidism
Description Failure of the thyroid gland. Usually idiopathic (see Fig. 3–2). Two to three percent of general population. Subclinical hypothyroidism can occur. Pathology The two most common causes are autoimmune thyroid disease (Hashimoto’s thyroiditis) and prior treatment of hyperthyroidism (including thyroidectomy and prior radioactive iodine for Graves’ disease). Other less common causes include postpartum necrosis of the pituitary gland (Sheehan’s syndrome), use of antithyroid med- ications (propothiouracil and methimazole), iodine deficiency or excess, and other medications (amiodarone, lithium). |
Diagnosis
Elevated TSH, low T4, low free T4. Treatment Steps Levothyroxine. Low dose if history of heart disease. Follow TSH lev- els approximately every 6–8 weeks and adjust dose of levothyroxine accordingly |
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congenital goiter and
deafness |
Pendred syndrome
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Symptoms
Anxiety, tremors, diarrhea, weight loss, heat intolerance, diaphoresis, palpitations, insomnia, menstrual irregularities. 1) symptoms of hyperthyroidism as well as goiter & ophthalmopathy, which can manifest as eye changes ranging from proptosis and lid retraction to diplopia and, rarely, visual loss |
Hyperthyroidism/Thyrotoxicosis/Graves’ Disease
Pathology Causes of an overactive thyroid gland are many, but most people think first of Graves’ disease (see below). Other causes: See Table 3–1. 1)=Graves a type of autoimmune hy- perthyroidism caused by circulating antibodies, known as thyroid- stimulating immunoglobulins (TSIs). The TSIs bind to the TSH receptor, causing excess production of thyroxine and growth of thyroid gland. CAUSES OF HYPERTHYROIDISM • Graves’ disease • Thyrotoxicosis factitia (surreptitious ingestion of thyroxine, commonly in persons attempting to lose weight). On boards, this is often a young woman, and is described as a nurse or a patient with a family member with hypothyroidism, which would mean she would have some access to thyroxine. • Subacute thyroiditis (which is often self-limited) • Hydatidiform mole • Toxic multinodular goiter |
Diagnosis
Physical findings may include tremor, tachycardia, goiter, onycholy- sis. Thinning of hair may occur. High-output congestive heart failure (CHF) is rare but can occur. Labs show a depressed TSH (classically “undetectable,” which is < 0.01) and an elevated free T4. (Although classically thyroid panels will include testing for total thyroxine, T3 and T3 resin uptake (T3RU), the findings of an elevated free T4 with low TSH are diagnostic.) Treatment of Hyperthyroidism Treatment varies with etiology; can include: • β-Blockers may be used to help with symptoms (tremor, tachycar- dia). • Antithyroid medications used in certain cases (propylthiouracil, methimazole). • Radioactive iodine or subtotal thyroidectomy |
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Symptoms
Hyperthermia (very high fever), delirium, nausea, vomiting, abdominal pain. Diagnosis Physical exam findings can include diaphoresis, tachycardia, hyper- tension in early stage, hypotension and shock in later stages, signs of high-output heart failure. Labs:Elevated T4, elevated free T4, and T3-RIA. TSH suppressed. |
Thyroid Storm
Description Severe thyrotoxicosis. Usually in individuals inadequately treated or new-onset hyperthyroidism. This is a medical emergency. Pathology Thyroid storm can be precipitated by multiple causes in individuals who already have hyperthyroidism, including infection/sepsis, trauma, surgery, radioactive iodine therapy, medications (pseu- doephedrine, anticholinergics). Rarely, thyroid storm can be the presentation of a patient with new-onset hyperthyroidism. |
Treatment Steps
1.Supportive care (control of hyperthermia, arrhythmias, hyper- or hypotension). 2. β-Blockers will help minimize symptoms. 3.Glucocorticoids to minimize peripheral conversion of T4 to T3. |
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his refers to abnormal finding on thyroid testing that occurs in the
setting of a sick, usually hospitalized patient. The thyroid function abnormalities can vary, but the most common are low T3 and ele- vated reverse T3. |
Euthyroid Sick Syndrome
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These abnormalities should reverse as the patient
improves |
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Symptoms
Polyuria, polyphagia, polydipsia, hyperglycemia, urine/blood ketones |
Diabetes Mellitus Type 1
Description Absolute insulin deficiency, due to autoimmune islet cell antibodies. Pathology No insulin production by pancreatic β cells under stimuli. A result of genetic predisposition to pancreatic immune and/or environmental injury. Human leukocyte antigen markers common. |
Diagnosis
Two or more fasting plasma glucose levels over 126 mg/dL. May have islet cell antibodies and human leukocyte antigen (HLA) present, low C-peptide. Treatment Steps 1.Insulin (see Table 3–2). 2.Diet (monitor carbohydrates and be consistent with snacks/tim- ing of meals), exogenous insulin. 3.Exercise—aerobic, approximately 30 minutes three times per week |
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Symptoms
Polyuria, polydipsia, blurred vision. May be asymptomatic, skin/ vaginal infections noted |
Diabetes Mellitus Type 2
Description Most commonly due to insulin resistance. Occasionally due to insulin secretory defect Pathology Increased hepatic glucose production, decreased peripheral glucose utilization. Insulin resistance |
Diagnosis
Two or more fasting plasma glucose levels over 126 mg/dL, or ran- dom glucose over 200 mg/dL × 2 with polyuria, polydipsia, polypha- gia. Finally, although not commonly performed, a level ≥ 200 mg/dL 2 hours after a 75-g glucose load is diagnostic of diabetes. Treatment Steps 1.Diet (restrict calories and carbohydrates to reach ideal body weight) and patient education. 2. Oral agents (secretagogue, biguanides, α-glucosidase inhibitors, glitazone) (see Table 3–3). 3.Exercise. 4.Insulin alone or in combination with oral agents. |
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Symptoms
Lethargy, nausea/vomiting, polyuria, abdominal pain, confusion, Kussmaul’s respiration, dehydration, fruity breath. Diagnosis History and physical exam, elevated glucose (400–600 mg/dL), ke- tonuria/ketonemia, low pH on arterial blood gas (ABG), metabolic acidosis with increased anion gap. |
Diabetic Ketoacidosis
Pathology May be the presentation of a new-onset diabetic. May result from in- fection/illness/not taking insulin, stress, hyperthyroidism; is associated with lack of insulin. Severe complication: cerebral edema. Potassium will fall during treatment if not replaced |
Treatment Steps
1. Insulin (continuous infusion 5–10 U/hr or 0.1 U/kg/hr). 2. Correction of fluid/electrolyte abnormality. Use isotonic saline to start; check glucose, electrolytes frequently. 3. Replace potassium as necessary and monitor blood pressure (BP), electrocardiogram (ECG), and electrolytes. |
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Symptoms
Severe dehydration, lethargy, confusion, coma. Pathology Elevated glucose without ketosis resulting in cellular fluid loss. |
Hyperosmolar Coma
Description Extracellular hyperosmolality associated with hyperglycemia. |
Treatment Steps
1. Fluids—water (hypotonic saline). 2. Insulin (lower doses required than in ketoacidosis). 3.Treat infection, malignancy, and other underlying illness. |
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Symptoms
Coma, confusion, hyperventilation. Diagnosis History and physical exam [critically ill diabetic with complication(s)], elevated plasma lactate, negative ketonuria, positive anion gap. |
Lactic Acidosis
Description Excess lactic acid in the blood, may be combined with diabetic ketoacidosis. Pathology Overproduction or inadequate removal of lactic acid, noted rarely with biguanides. |
Treatment Steps
1. Treat etiology. 2.Sodium bicarbonate. 3.Supportive. |
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Symptoms
Lethargy, diplopia, headache, in A.M.or when fasting. Diagnosis History and physical exam, typical hypoglycemic symptoms, blood glucoseunder 40 mg/dL, response to glucose. Elevated serum in- sulin level during hypoglycemic episode. Elevated proinsulin level, and lack of C-peptide suppression. |
Hypoglycemia, Pancreatic β-cell Tumors
Description Fasting hypoglycemia; insulinoma, Addison’s disease, hypopitu- itarism. Reactive hypoglycemia (postprandial): treat with frequent meals, reduced simple carbohydrates. Pathology Islets of Langerhans adenoma most often; usually benign. |
Treatment Steps
1. Surgical excision of insulinoma; preop give diazoxide (Pro- glycem). 2. Emergency therapy: give 50 mL 50% dextrose IV. |
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Symptoms
Often asymptomatic and found on routine blood work (elevated cal- cium). Occasionally kidney stones, bone pain/lesions (osteitis fi- brosa cystica). Symptoms of elevated calcium (memory loss, depres- sion, proximal muscle weakness, nausea, weight loss, polyuria). |
Primary Hyperparathyroidism
Pathology Etiology unknown; single chief cell adenoma most common. Hyper- plasia in multiple endocrine neoplasia (MEN) syndromes. |
Diagnosis
Elevated serum calcium, and elevated intact parathyroid hormome (iPTH). May see subperiosteal bone resorption on x-ray. Parathyroid scan may localize an adenoma. Treatment Steps 1. Surgical resection; for parathyroid adenoma: parathyroid neck exploration. 2.If severe hypercalcemia is present, medical therapy—saline, furosemide, calcitonin, pamidronate. |
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Symptoms
Symptoms of hypocalcemia (positive Chvostek’s and Trousseau’s signs), circumoral paresthesia, tetany, cataracts, intracranial calcifi- cations, laryngeal stridor, seizure |
Hypoparathyroidism
Description Decreased parathyroid hormone amount or effect. Can include thyroid surgery or genetic. |
Diagnosis
History and physical exam, hyperphosphatemia, hypocalcemia, nor- mal renal function, parathyroid hormone (PTH), and urinary cyclic adenosine monophosphate (cAMP) level. Treatment Steps Vitamin D and calcium. |
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Symptoms
Polyuria, nocturia, thirst. May crave ice. Diagnosis History and physical exam, routine urinalysis and labs, urine specific gravity under 1.005, urine osmolality under 250, water loss more than 3 L/day |
Diabetes Insipidus
Description Water-loss syndrome. Nephrogenic vasopressin resistant: kidney Pathology Insufficient antidiuretic hormone (ADH), or lack of response to ADH, resulting from pituitary injury, tumor, or other disorder (tuberculosis, sarcoid, etc.). Drugs—demeclocycline, lithium (nephrogenic). does not respond to vasopressin. Neurogenic vasopressin respon- sive/central: inadequate vasopressin. |
Diagnosis
History and physical exam, routine urinalysis and labs, urine specific gravity under 1.005, urine osmolality under 250, water loss more than 3 L/day. Water-Deprivation Test—Vasopressin injection followed by plasma/urine osmolality studies. Nephrogenic Diabetes Insipidus—Cannot concentrate urine (not responsive to vasopressin). Primary Polydipsia—No urine osmolality change (or minimum increase) after injection. Central Diabetes Insipidus—Urine osmolality greater than plasma osmolality (responsive to vasopressin) Treatment Steps Antidiuretic hormone replacement (pitressin tannate, 1-deamino-8-D- arginine vasopressin [DDAVP]), subcutaneous or oral. |
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Symptoms
Confusion, lethargy, seizures, coma. Diagnosis Hyponatremia, serum hypo-osmolality, urine hyperosmolarity |
Syndrome of Inappropriate Secretion
of Antidiuretic Hormone (SIADH) Pathology Associated with malignant/nonmalignant lung disease, other tumors, endocrinopathy, central nervous system (CNS) disease, drugs. |
Treatment Steps
1. Fluid restriction. 2.Demeclocycline and/or hypertonic saline in certain cases. |
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Symptoms
Lack of TSH: hypothyroid symptoms. Lack of adrenocorticotropic hormone (ACTH): adrenocortical insufficiency symptoms (hypoten- sion, nausea/vomiting, confusion). Lack of gonadotropins: impo- tence/amenorrhea. Evidence of lack of prolactin and/or growth hor- mone. |
Panhypopituitarism
Description Reduced or lacking pituitary hormone secretion. Affecting single or several hormones. Pathology Infarction (Sheehan’s syndrome), tumor, infection, trauma, and other causes; use of clofibrate, vincristine, vinblastine, chlorpropamide. |
Diagnosis
History and physical exam, thyroid functions, serum testosterone, growth hormone, insulin-like growth factor (IGF)-1, endocrine stimulation testing. Treatment Steps Replacement of appropriate hormone deficiency (glucocorticoids, thyroxine, estrogen, testosterone, growth hormone). |
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Symptoms
As Adult—Enlarging hands/feet, coarse features, deep voice, wide teeth, large tongue, joint pain, hypertension, headache, hyperhydrosis |
Acromegaly
Description Excessive growth hormone secretion postpuberty, from a pituitary adenoma. |
Diagnosis
Clinical features, labs, and magnetic resonance imaging (MRI) of the brain. • IGF-1 levels are elevated in acromegaly and it is a sensitive screen- ing test for acromegaly • Glucose suppression test: An oral glucose load is given (1.75G/kg, maximum dose 75G). Failure to suppress serum growth hormone (GH) levels to < 5 ng/dL is diagnostic of acromegaly. • Random measurements of GH are not useful because GH is se- creted in a pulsatile fashion. • MRI can confirm the presence of a pituitary adenoma Treatment Steps 1.Surgical (transsphenoidal) to resect a pituitary adenoma. May be curative. 2.Radiation and medications are used if surgery not curative 3.Medications (bromocriptine, octreotide, cabergoline). Goal is normalization of GH. |
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Symptoms
Patients can present with severe hypotension (shock), which can be mistaken for septic shock. Other symptoms include fever, nausea, vomiting, abdominal pain, fatigue, weakness, and hypoglycemia |
Adrenocortical Insufficiency––Acute
Description Abrupt lack of adrenocortical hormones Pathology Trauma, infection, gland necrosis, glucocorticoid withdrawal (in steroid-dependent patient). COSYNTROPIN STIMULATION TEST • Can be done at any time of day. • First, check baseline plasma cortisol level. • Inject (IV or IM) 250 mg of cosyntropin (synthetic ACTH). • Check repeat plasma cortisol level 30 minutes later. • Normal response is a plasma cortisol level > 20 µg/dL. • Note: There is also a low- dose cosyntropin (1 µg) test that can be used, but the traditional test utilizes 250 µg |
Diagnosis
One needs to have a high clinical suspicion as it is often mistaken for other illnesses. Cosyntropin testing (see Cram Facts). Often, steroids are given empirically (particularly if patient is not responding to other treatments) and clinical response to steroids is virtually diagnostic. Treatment Steps 1. Hydrocortisone sodium succinate 100 mg IV, infusion, then taper. 2.Fludrocortisone as mineralocorticoid supplement may be indicated. |
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Symptoms
Lethargy, skin pigmentation, hypotension, nausea/vomiting, dehy- dration, salt craving. |
Adrenocortical Insufficiency––Chronic
Pathology Most often autoimmune (Addison’s disease) and history of long-term glucocorticoid use as etiology. Other causes: human immunodefi- ciency virus (HIV), cytomegalovirus, hemorrhage, tuberculosis (TB). |
Diagnosis
History and physical exam, hyponatremia, hyperkalemia, low plasma cortisol, ACTH stimulation test. Treatment Steps Usually both hydrocortisone (glucocorticoid), and fludrocortisone (mineralocorticoid) needed. |
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Symptoms
Centripetal obesity, striae/bruising, hypertension, hirsutism, weak- ness, osteoporosis, supraclavicular fat pad, buffalo hump, moon facies, facial plethora. |
Cushing’s Syndrome
Description Clinical state caused by glucocorticoid overabundance. Pathology Most commonly iatrogenic. Other causes: Cushing’s disease most common (pituitary adenoma), also adrenal tumor, or ectopic ACTH hypersecretion. |
Diagnosis
Clinical, overnight dexamethasone suppression test, 24-hour urine for free cortisol, elevated urine 17-hydroxysteroids. Treatment Steps 1.Iatrogenic––use smallest effective steroid dose possible. 2.Cushing’s disease––surgery/radiation. 3.Medications include ketoconazole, metyrapone, mitotane |
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Symptoms
Hirsutism, amenorrhea, deep voice, acne, enlarged clitoris (ambigu- ous genitalia as newborn) |
Adrenogenital Syndrome
Description Virilizing female disorder Pathology In child: usually due to congenital adrenal hyperplasia (21-hydroxy- lase deficiency) (see Cram Facts). In adult: ovarian disease (polycystic ovary), or adrenal disease (attenuated forms). |
Diagnosis
History and physical exam, high urinary 17-ketosteroids, ultrasound, laparoscopy, high l7-hydroxyprogesterone Treatment Steps 1.Surgical excision (if tumor). 2.Estrogen spironolactone, metformin (for polycystic ovary syn- drome). 3.For congenital adrenal hyperplasia, give glucocorticoid replace- ment/possible mineralocorticoid replacements. |
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Symptoms
May be asymptomatic or show evidence of hypokalemic symptoms, weakness, hypertension. |
Hyperaldosteronism
Pathology Aldosterone overproduction by zona glomerulosa, from adenoma (Conn’s syndrome), or hyperplasia. Pseudohyperaldosteronism: Liddle syndrome, (?)renal tubule defect results in hyperaldosteronism symptoms without excess aldosterone production. Overindulgence in licorice may cause hyperaldosteronism-like picture |
Diagnosis
History and physical exam, sodium retention, hypokalemia, hyper- tension, low plasma renin, elevated plasma/urine aldosterone. Differential diagnosis between adenoma and hyperplasia: after salty diet, A.M. plasma aldosterone over 20 ng/dL in adenoma; under 20 ng/dL in hyperplasia Treatment Steps Adrenalectomy, give spironolactone preop. |
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Diagnosis by high levels of
11-deoxycortisol or 17- hydroxyprogesterone. |
Congenital adrenal
hyperplasia: due to 11- or 21-β-hydroxylase deficiency (most common). |
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Symptoms
Episodes of headache, flushing, diaphoresis, diplopia, weight loss, paroxysmal hypertension. |
Pheochromocytoma
Description Catecholamine-producing chromaffin cell tumor Pathology Tumor, may be intra-adrenal or extra-adrenal. May be familial or sporadic. |
Diagnosis
History and physical exam, tachycardia, 24-hour urinary vanillylman- delic acid (VMA), or metanephrines, serum catecholamines. Urinary catecholamines may be elevated by Aldomet and other meds. MRI. Treatment Steps 1. Surgical excision (difficult procedure). 2. Give phenoxybenzamine preop, hydration. |
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Symptoms
Ambiguous genitalia. |
True Hermaphroditism
Pathology Ovarian and testicular tissue present (ovatestes). |
Diagnosis
History and physical exam, chromosome studies, histologic evalua- tion of ovatestes tissue. Treatment Steps Varies with age and genitalia development. |
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Diagnosis
Amenorrhea, negative pregnancy test, elevated follicle-stimulating hormone (FSH) and leutinizing hormone (LH) |
Premature Ovarian Failure
Description Cessation of menses in a woman younger than age 35. Pathology Autoimmune (antiovarian antibodies) |
Treatment Steps
Supportive treatment. Hormone therapy controversial. |
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Symptoms
No menses, abnormal flow of milk from breasts. If pituitary tumor present, may have visual field cut or headache. |
.Amenorrhea/Galactorrhea
See also Chapter 13 for amenorrhea. Pathology Most common cause is a pituitary adenoma that produces excess prolactin. Galactorrhea can be an uncommon side effect of some medications (haloperidol, thorazine). |
Diagnosis
Clinical, elevated prolactin level, MRI of head with gadolinium (reveals pituitary adenoma). Treatment Steps 1.Surgery/radiation to resect adenoma. 2.Medications include bromocriptine, cabergoline. |
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Serum Gonadotropins Prepubertal (low)
Serum Gonadal Steroids Low Patient usually has short stature for chronologic age but appropriate height and growth rate for bone age. Adrenarche and gonadarche are delayed. |
Constitutional delay
in growth and adolescence |
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Serum Gonadotropins Prepubertal (low)
Serum Gonadal Steroids Low patient usually has normal height and growth rate. Adrenarche may be normal in spite of absent gonadarche |
Hypogonadotropic
hypogonadism Patient may have anosmia (Kallmann syndrome) or other associated pituitary hormone deficiencies. If gonodotropin deficiency is isolated, patient usually has normal height and growth rate. Adrenarche may be normal in spite of absent gonadarche (serum dehydroepiandrosterone [DHEA] sulfate may be pubertal). |
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Serum Gonadotropins
Serum Gonadal Steroids |
Hypergonadotropic
hypogonadism Patient may have abnormal karyotype and stigmas of Turner’s or Klinefelter’s syndrome. |
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Symptoms
Hepatomegaly, skin pigmentation, cardiomegaly, pancreatic disease (diabetes mellitus). |
Hereditary Hemochromatosis
Description Hereditary disorder of iron excess. Autosomal recessive inheritance. Also known as bronze diabetes. |
Diagnosis
May be diagnosed due to screening of family members with the disease. Genetic testing is available. Labs include abnormal aspartate transaminase (AST) and alanine transaminase (ALT), elevated iron, ferritin, and percentage of saturation. Liver biopsy may be indicated. Treatment Steps 1. Phlebotomy. 2. Deferoxamine. |
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Screening test: In pregnant women who are not high risk for GDM,
a glucose tolerance test is given at 26–28 weeks. Serum glucose is checked after a 50-g glucose load. If this initial screening test is abnormal, a 3-hour (100-g) glucose tolerance test is given. (Fasting glucose should be < 95, 1 hour < 180 mg/dL, 2 hours < 155 mg/dL, 3 hours < 140 mg/dL.) In women who are at higher risk for GDM, screening should be done in the first trimester. This includes women with GDM in a prior pregnancy, maternal age > 35 years, prior unexplained fetal demise, prior infant weighing less than 4,000 g, obesity, or strong family history of type 2 diabetes. |
Gestational Diabetes
Description Gestational diabetes mellitus (GDM) refers to abnormal levels of hyperglycemia occurring in pregnant women. (It does not address pregnant women who have preexisting diagnoses of type I or type II diabetes mellitus.) Women are often asymptomatic and diagnosis is made during prenatal screenin COMPLICATIONS OF GDM • Fetal macrosomia • Shoulder dystocia • Miscarriage/stillbirth • Birth defects • Neonatal polycythemia • Neonatal hypoglycemia |
family history of type 2 diabetes.
Treatment Steps 1. Diabetic diet, counseling with a nutritionist. 2. Insulin in certain cases |
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Symptoms
Diarrhea, flushing, bronchospasm, and heart valve lesions. |
Carcinoid Syndrome
Description Serotonin-secreting, argentaffin cell tumor Pathology Tumors from enterochromaffin cells. Pulmonary and gastrointestinal (GI) tract sites common. |
Diagnosis
History and physical exam, urinary 5-hydroxyindoleacetic acid (5-HIAA). Treatment Steps 1. Surgery. 2. Cyproheptadine. |
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Description/Symptoms
Mast cell disorder causing flushing, vomiting, diarrhea, tachycardia, hypotension, syncope, in episodic attacks. |
Mastocytosis
Diagnosis History and physical exam, may have urticaria pigmentosa, histamine and histamine metabolite studies, skin/bone marrow biopsy. May show Darier’s sign (stroking skin lesion results in elevated/erythematous reaction: dermographism Pathology Release of mast cell mediators (heparin, histamine, enzymes). Cutaneous and systemic types. |
Treatment Steps
Epinephrine, antihistamines (block both H1 and H2 receptors), and antiprostaglandins |
