TABLE IV-114 Risk Factors for Active Tuberculosis Among Persons Who Have Been Infected With Tubercle Bacilli 32 page

X-16. The answer is B. (Chap. 340) This patient presents with acute central diabetes insipidus (DI) in the context of AMML. MRI will most likely demonstrate a chloroma (myeloid tumor often seen in AMML) in the posterior pituitary, particularly given his history of other extra–bone marrow tumor nodules. The urine is dilute due to the ADH deficiency leading to hypernatremia. The altered mental status is likely due to the hypernatremia, which typically develops in central DI as water intake cannot keep up with urine output, which can exceed 5 L/d. Immediate replacement of ADH in the form of desmopressin will confirm the diagnosis of central DI if urine output drops and will provide symptomatic relief. Desmopressin may be administered nasally or intravenously with rapid onset of action. Hydrochlorothiazide is used in nephrogenic DI to increase proximal sodium and water reabsorption. ATRA is used to treat acute promyelocytic leukemia, not AMML. Hydrocortisone would be the therapy of choice for acute Addisonian crisis, not central DI. Lithium is a well-known cause of nephrogenic DI.

X-17. The answer is B. (Chap. 341) Nutritional and maternal iodine deficiencies are common in many parts of the developing world and, when severe, can result in cretinism. Cretinism is characterized by mental and growth retardation but is preventable by administration of iodine and/or thyroid hormone early in life. Concomitant selenium deficiency can contribute to the neurologic manifestations. Iodine

supplementation of bread, salt, and other foods has markedly decreased the rates of this disease. Beriberi disease is a nervous system ailment caused by a thiamine deficiency in the diet. Scurvy is due to vitamin C deficiency. Folate deficiency in pregnant women is associated with an increased risk preterm labor and a number of congenital malformations, most notably involving the neural tube. Folate supplementation can lower the risk of spina bifida, anencephaly, congenital heart disease, cleft lips, and limb deformities. Vitamin A deficiency is a common cause of blindness in the developing world.

X-18. The answer is E. (Chap. 341) T₄ is secreted from the thyroid gland in approximately 20-fold greater quantities than T₃. Both hormones are bound to plasma proteins including albumin, transthyretin, and thyroxine-binding protein. Thyroxine-binding protein has a high affinity for T₄; thus despite its low

concentration it carries 80% of the plasma hormone. It is followed by albumin and then transthyretin. Pregnant women may be euthyroid with elevated levels of total T₄ because of the increase in thyroid-binding globulin. T₃ is less protein bound than T₄. Unbound hormone is thought to be biologically

available to tissues, and normalization of the unbound fraction is the primary goal of homeostatic mechanisms. Measurement of free T₄ is biologically more relevant than total T₄. Thyroid peroxidase is

an enzyme within the thyroid involved in the organification of iodine.

X-19. The answer is C. (Chap. 341) There are a number of conditions associated with normal thyroid function, but hyperthyroxinemia. Although some of these are associated with clinical hyperthyroidism, many simply have elevated levels of total T₄ and normal conversion to T₃ and thus are clinically

normal. Anything that increases liver production of thyroid-binding globulin will produce elevated total T₄ levels and normal free T₄ and T₃ levels. In this category are pregnancy, estrogen-containing oral

contraceptives, cirrhosis, and familial excess thyroid-binding globulin production. Familial dysalbuminemic hyperthyroxinemia results in an albumin mutation and increased T₄ with normal free T₄

and T₃ levels. Sick-euthyroid syndrome occurs during acute medical and psychiatric illness. In this

syndrome, there is transiently increased unbound T₄ and decreased TSH. Total T₄ and T₃ may be

decreased, particularly later in the course of disease.

X-20. The answer is D. (Chap. 341) Iodine deficiency remains the most common cause of hypothyroidism worldwide. It is present at relatively high levels even in the developed world including Europe. In areas of iodine sufficiency, autoimmune disease (Hashimoto’s thyroiditis) and iatrogenic hypothyroidism (treatment of hyperthyroidism) are the most common causes.

X-21. The answer is B. (Chap. 341) There are a number of important effects of thyroid hormone (or its absence) on the cardiovascular system. Importantly, hypothyroidism is associated with bradycardia and reduced myocardial contractility, and thereby reduced stroke volume. Increased peripheral resistance may be accompanied by systemic hypertension, particularly diastolic hypertension in hypothyroidism. Pericardial effusions are found in up to 30% of patients with hypothyroidism, though they rarely cause decreased cardiac function. Finally, in hypothyroid patients, blood flow is directed away from the skin and thus produces cool extremities.

X-22. The answer is B. (Chap. 341) The most common cause of hypothyroidism in the United States is autoimmune thyroiditis, as it is an iodine-replete area. Although earlier in the disease, a radioiodine uptake scan may have shown diffusely increased uptake from lymphocytic infiltration, at this point in the

disease when the infiltrate is “burned out” there is likely to be little found on the scan. Likewise, a thyroid ultrasound would only be useful for presumed multinodular goiter. Antithyroid peroxidase antibodies are commonly found in patients with autoimmune thyroiditis, while antithyroglobulin antibodies are found less commonly. Antithyroglobulin antibodies are also found in other thyroid disorders (Graves’ disease, thyrotoxicosis) as well as systemic autoimmune diseases (SLEs). Thyroglobulin is released from the thyroid in all types of thyrotoxicosis with the exception of factitious disease. This patient, however, was hypothyroid, and thus serum thyroglobulin levels are unlikely to be helpful.

X-23. The answer is D. (Chap. 341) An increase in TSH in a patient with hypothyroidism that was previously stable in dosing for many years suggests either a failure of taking the medication, difficulty with absorption from bowel disease, or medication interaction or drug-drug interaction affecting clearance. Patients with normal body weight taking more than 200 μg of levothyroxine per day who have elevated TSH strongly suggests noncompliance. Such patients should be encouraged to take two tablets at one time on the day they remember, to attempt to reach the weekly target dose; the long drug half-life makes this practice safe. Other causes of increased thyroxine requirements include malabsorption, such as with celiac disease or small bowel surgery, estrogen therapy, and drugs that interfere with T₄ absorption (e.g., ferrous sulfate and cholestyramine) or clearance, such as lovastatin,

amiodarone, carbamazepine, and phenytoin.

X-24. The answer is A. (Chap. 341) The patient has myxedema coma. This condition of profound hypothyroidism most commonly occurs in the elderly, and often a precipitating condition may be identified such as myocardial infarction or infection. Clinical manifestations include altered level of consciousness, bradycardia, and hypothermia. Management includes repletion of thyroid hormone through IV levothyroxine, but also supplementation of glucocorticoids because there is impaired adrenal reserve in severe hypothyroidism. Care must be taken with rewarming as it may precipitate cardiovascular collapse. Therefore, external warming is indicated only if the temperature is below 30°C. Hypertonic saline and glucose may be used if hyponatremia or hypoglycemia is severe; however, hypotonic solutions should be avoided as they may worsen fluid retention. Because the metabolism of many substances is markedly reduced, sedation should be avoided or minimized. Similarly, blood levels of drugs should be monitored when available.

X-25. The answer is A. (Chap. 341) Patients with Graves’ disease produce thyroid-stimulating immunoglobulins. They subsequently produce higher levels of T₄ compared with the normal population.

As a result, many patients with Graves’ disease are mildly iodine deficient, and T₄ production is

somewhat limited by the availability of iodine. Exposure to iodinated contrast thus reverses iodine deficiency and may precipitate worsening hyperthyroidism. Additionally, the reversal of mild iodine deficiency may make I-125 therapy for Graves’ disease less successful because thyroid iodine uptake is lessened in the iodine-replete state.

X-26. The answer is C. (Chap. 341) Hyperthyroidism is associated with a number of cardiovascular complications including tachycardia, palpitations, high cardiac output with bounding pulse, widened pulse pressure, and aortic systolic murmur. This may lead to worsened angina in predisposed patients. Atrial fibrillation is more common in patients greater than 50 years of age, and treatment of thyroid state alone will lead to the reversal of atrial fibrillation in half of patients, suggesting underlying cardiac

disorder in the remainder of unconverted patients.

X-27. The answer is B. (Chap. 341) Although lid retraction can occur in any type of hyperthyroidism, Graves’ disease is associated with specific eye signs that are thought to be due to the interaction of autoantibodies with periorbital muscles. The onset of Graves’ ophthalmopathy may occur before or after hyperthyroidism, and rarely may not be associated with hyperthyroidism at all, but simply the effects of the presence of autoantibodies on the periorbital muscles. Subtle features are eye grittiness, discomfort, and excess tearing. Proptosis occurs in one-third of patients and may result in corneal abrasion if there is a failure of closure of the eyelids, particularly during sleep. The most serious manifestation is compression of the optic nerve at the apex of the orbit, which can lead to papilledema and permanent vision loss if left untreated.

X-28. The answer is C. (Chap. 341) The main antithyroid drugs used in the treatment of Graves’ disease are propylthiouracil, carbimazole, and the active metabolite of carbimazole, methimazole. All act to inhibit the function of thyroid peroxidase. While propylthiouracil also reduces the peripheral conversion of T₄ to T₃, this is not its major mechanism of action and is not responsible for the majority

of the drug’s utility in the therapy of Graves’ disease.

X-29. The answer is C. (Chap. 341) Sick-euthyroid syndrome can occur in the setting of any acute, severe illness. Abnormalities in the levels of circulating TSH and thyroid hormone are thought to result from the release of cytokines in response to severe stress. Multiple abnormalities may occur. The most common hormone pattern is a decrease in total and unbound T₃ levels as peripheral conversion of T₄ to

T₃ is impaired. Teleologically, the fall in T₃, the most active thyroid hormone, is thought to limit

catabolism in starved or ill patients. TSH levels may vary dramatically, from 0.1 to above 20 mU/L, depending on when they are measured during the course of illness. Very sick patients may have a decrease in T₄ levels. This patient undoubtedly has abnormal thyroid function tests as a result of his

injuries from the motor vehicle accident. There is no indication for obtaining further imaging in this case. Steroids have no role. The most appropriate management consists of simple observation. Over the course of weeks to months, as the patient recovers, thyroid function will return to normal.

X-30 and X-31. The answers are E and B, respectively. (Chap. 341) Subacute thyroiditis, also known as de Quervain’s thyroiditis, granulomatous thyroiditis, or viral thyroiditis, is a multiphase illness that occurs three times more frequently in women than men. Multiple viruses have been implicated, but none have been definitively identified as the trigger for subacute thyroiditis. The diagnosis can be overlooked in patients as the symptoms mimic pharyngitis, and it frequently has a similarly benign course. In this patient, Graves’ disease is unlikely given her elevated TSH and negative antibody panel. Autoimmune hypothyroidism should be considered; however, the tempo of her illness, the tenderness of the thyroid on examination, and her preceding viral illness make this diagnosis less likely. Ludwig’s angina is a potentially life-threatening bacterial infection of the retropharyngeal and submandibular spaces, often caused by preceding dental infection. Cat-scratch fever is a usually benign illness that presents with lymphadenopathy, fever, and malaise. It is caused by Bartonella henselae and is frequently transmitted from cat scratches that penetrate the epidermis. It will not cause an elevated TSH. Subacute thyroiditis can present with hypothyroidism, thyrotoxicosis, or neither. In the first phase of the disease, thyroid inflammation leads to follicle destruction and release of thyroid hormone. Thyrotoxicosis ensues. In the second phase, the thyroid is depleted of hormone and hypothyroidism

results. A recovery phase typically follows in which decreased inflammation allows the follicles to heal and regenerate hormone.

X-32. The answer is B. (Chap. 341) Subacute thyroiditis, also known as de Quervain’s thyroiditis, granulomatous thyroiditis, and viral thyroiditis, is characterized clinically by fever, constitutional symptoms, and a painful, enlarged thyroid. The etiology is thought to be a viral infection. The peak incidence is between 30 and 50 years of age, and women are affected more frequently than men. The symptoms depend on the phase of the illness. During the initial phase of follicular destruction, there is a release of thyroglobulin and thyroid hormones. As a result, there is increased circulating T₄ and T₃,

with concomitant suppression of TSH. Symptoms of thyrotoxicosis predominate at this point. Radioiodine uptake is low or undetectable. After several weeks, thyroid hormone is depleted and a phase of hypothyroidism ensues, with low unbound T₄ levels and moderate elevations of TSH.

Radioiodine uptake returns to normal. Finally, after 4–6 months, thyroid hormone and TSH levels return to normal as the disease subsides. Patient A is consistent with the thyrotoxic phase of subacute thyroiditis except for the increased radioiodine uptake scan. Patient C is more consistent with Graves’ disease with suppression of TSH, an elevated uptake scan, and elevated thyroid hormones as a result of stimulating immunoglobulin. Patient D is consistent with a neoplasm. Patient E is consistent with central hypothyroidism.

X-33. The answer is E. (Chap. 341) Thyroid nodules are found in 5% of patients. Nodules are more common with age, in women, and in iodine-deficient areas. Given their prevalence, the cost of screening, and the generally benign course of most nodules, the choice and order of screening tests have been very contentious. A small percentage of incidentally discovered nodules will represent thyroid cancer, however. A TSH should be the first test to check after detection of a thyroid nodule. A majority of patients will have normal thyroid function tests. In the case of a normal TSH, fine-needle aspiration or ultrasound-guided biopsy can be pursued. If the TSH is low, a radionuclide scan should be performed to determine if the nodule is the source of thyroid hyperfunction (a “hot” nodule). In this case, this is the best course of action. “Hot” nodules can be treated medically, resected, or ablated with radioactive iodine. “Cold” nodules should be further evaluated with a fine-needle aspiration. Four percent of nodules undergoing biopsy are malignant, 10% are suspicious for malignancy, and 86% are indeterminate or benign.

X-34. The answer is C. (Chap. 342) The adrenal gland has three major functions: glucocorticoid synthesis, aldosterone synthesis, and androgen precursor synthesis. Glucocorticoid synthesis is controlled by the pituitary secretion of ACTH. The primary stimulus for aldosterone synthesis is the renin-angiotensin-aldosterone system, which is independent of the pituitary. Thus, morning cortisol secretion and release of cortisol in response to stress are regulated by the pituitary gland, while regulation of sodium retention and potassium excretion by aldosterone is independent of the pituitary and would be preserved in this patient.

X-35. The answer is A. (Chap. 342) Cushing’s syndrome is a constellation of features that result from chronic exposure to elevated levels of cortisol from any etiology. Although the most common etiology is ACTH-producing pituitary adenoma, which accounts for 75% of Cushing’s syndrome, 15% is due to ectopic ACTH syndromes such as bronchial or pancreatic tumors, small cell lung cancer, and others. ACTH-independent Cushing’s syndrome is much more rare. Adrenocortical adenoma underlies 5–10%

of cases, and adrenocortical carcinoma is present in 1% of Cushing’s cases. McCune-Albright syndrome is a genetic cause of bone abnormalities, skin lesions (cafe au lait), and premature puberty, particularly in girls. Interestingly, it is caused by a sporadic in utero mutation, not an inherited disorder, and thus will not be passed onto progeny.

X-36. The answer is B. (Chap. 342) Conn’s syndrome refers to an aldosterone-producing adrenal adenoma. Although it accounts for 40% of hyperaldosterone states, bilateral micronodular adrenal hyperplasia is more common. Other causes of hyperaldosteronism are substantially more rare, accounting for less than 1% of disease. The hallmark of Conn’s syndrome is hypertension with hypokalemia. Because aldosterone stimulates sodium retention and potassium excretion, all patients should be hypokalemic at presentation. Serum sodium is usually normal because of concurrent fluid retention. Hypokalemia may be associated with muscle weakness, proximal myopathy, or even paralysis. Hypokalemia may be exacerbated by thiazide diuretics. Additional features include metabolic alkalosis that may contribute to muscle cramps and tetany.

X-37. The answer is B. (Chap. 342) Incidental adrenal masses are often discovered during radiographic testing for another condition and are found in approximately 6% of adult subjects at autopsy. Fifty percent of patients with a history of malignancy and a newly discovered adrenal mass will actually have an adrenal metastasis. Fine-needle aspiration of a suspected metastatic malignancy will often be diagnostic. In the absence of a suspected nonadrenal malignancy, most adrenal incidentalomas are benign. Primary adrenal malignancies are uncommon (<0.01%), and fine-needle aspiration is not useful to distinguish between benign and malignant primary adrenal tumors. Although 90% of these masses are nonsecretory, patients with an incidentaloma should be screened for pheochromocytoma and hypercortisolism with plasma free metanephrines and an overnight dexamethasone suppression test, respectively. When radiographic features suggest a benign neoplasm (<3 cm), scanning should be repeated in 3–6 months. When masses are larger than 6 cm, surgical removal (if more likely to be primary adrenal malignancy) or fine-needle aspiration (if more likely to be metastatic malignancy) is preferred.

X-38. The answer is A. (Chap. 343) When the diagnosis of pheochromocytoma is entertained the first step is measurement of catecholamines and/or metanephrines. This can be achieved by urinary tests for vanillylmandelic acid, catecholamines, fractionated metanephrines, or total metanephrines. Total metanephrines have a high sensitivity and therefore are frequently used. A value of three times the upper limit of normal is highly suggestive of pheochromocytoma. Borderline elevations, as this patient had, are likely to be false positives. The next most appropriate step is to remove potentially confounding dietary or drug exposures, if possible, and repeat the test. Likely culprit drugs include levodopa, sympathomimetics, diuretics, tricyclic antidepressants, and alpha and beta blockers (labetalol in this case). Sertraline is an SSRI antidepressant, not a tricyclic. Alternatively, a clonidine suppression test may be ordered.

X-39. The answer is E. (Chap. 343) Complete removal of the pheochromocytoma is the only therapy that leads to a long-term cure, although 90% of tumors are benign. However, preoperative control of hypertension is necessary to prevent surgical complications and lower mortality. This patient is presenting with encephalopathy in a hypertensive crisis. The hypertension should be managed initially with IV medications to lower the mean arterial pressure by approximately 20% over the initial 24-hour period. Medications that can be used for hypertensive crisis in pheochromocytoma include

nitroprusside, nicardipine, and phentolamine. Once the acute hypertensive crisis has resolved, transition to oral α-adrenergic blockers is indicated. Phenoxybenzamine is the most commonly used drug and is started at low doses (5–10 mg three times daily) and titrated to the maximum tolerated dose (usually 20–30 mg daily). Once alpha blockers have been initiated, beta blockade can safely be utilized and is particularly indicated for ongoing tachycardia. Liberal salt and fluid intake helps expand plasma volume and treat orthostatic hypotension. Once blood pressure is maintained below 160/100 mmHg with moderate orthostasis, it is safe to proceed to surgery. If blood pressure remains elevated despite treatment with alpha blockade, addition of calcium channel blockers, angiotensin receptor blockers, or angiotensin-converting enzyme inhibitors should be considered. Diuretics should be avoided, as they will exacerbate orthostasis.

X-40. The answer is C. (Chap. 344) The risk of both type 1 and type 2 diabetes mellitus is rising in all populations, but the risk of type 2 diabetes is rising at a substantially faster rate. In the United States, the age-adjusted prevalence of diabetes mellitus is 7.1% in non-Hispanic whites, 7.5% in Asian Americans, 11.8% in Hispanics, and 12.6% in non-Hispanic blacks. Comparable data are not available for individuals belonging to American Indian, Alaska Native, or Pacific Islander populations, but the prevalence is thought to be even higher than in the non-Hispanic black population.

X-41. The answer is E. (Chap. 344) Glucose tolerance is classified into three categories: normal glucose tolerance, impaired glucose homeostasis, and diabetes mellitus. Normal glucose tolerance is defined by the following: fasting plasma glucose below 100 mg/dL, plasma glucose below 140 mg/dL following an oral glucose challenge, and hemoglobin A1C less than 5.6%. Abnormal glucose homeostasis is defined as fasting plasma glucose 100–125 mmol/dL or plasma glucose 140–199 following oral glucose tolerance test or hemoglobin A1C of 5.7–6.4%. Actual diabetes mellitus is defined by either a fasting plasma glucose above 126 mg/dL, glucose of 200 mg/dL after oral glucose tolerance test, or hemoglobin A1C of 6.5% or above.

X-42. The answer is E. (Chap. 344) Because the patient has symptoms, she is not being screened for diabetes mellitus. For screening, the fasting plasma glucose or hemoglobin A1C is recommended. Because the patient has symptoms, a random plasma glucose of greater than 200 mg/dL is adequate to diagnose diabetes mellitus. Other criteria include fasting plasma glucose above 126 mg/dL or hemoglobin A1C above 6.4% or 2-hour plasma glucose above 200 during an oral glucose tolerance test. C peptide is a useful tool to determine if the normal cleavage of insulin from its precursor is occurring. A normal C-peptide level with hypoglycemia suggests surreptitious insulin use, and a low C-peptide with hyperglycemia suggests pancreatic failure.

X-43. The answer is B. (Chap. 344) Risk factors for type 2 diabetes mellitus include family history of diabetes mellitus, including parent or sibling, BMI greater than 25 kg/m², physical inactivity, race/ethnicity, previously identified impaired fasting glucose or hemoglobin A1C 5.7–6.4%, systemic hypertension, history of gestational diabetes or delivery of a baby greater than 4 kg, HDL less than 35 mmol/L and/or triglyceride level greater than 250 mg/dL, polycystic ovarian disease or acanthosis nigricans, and history of cardiovascular disease.

X-44. The answer is A. (Chap. 344) Type 1 diabetes mellitus often has a more severe presentation with diabetic ketoacidosis and often presents in younger individuals compared with type 2 diabetes; however, there are some cases where the distinction of type 1 from type 2 is not straightforward. There

is HLA-DR3 localization preferences for type 1 diabetes; several haplotypes are present in 40% of children with type 1 diabetes mellitus, but it is still the minority. Immunologic destruction of the beta cell is the primary cause of disease in type 1 diabetes, and islet cell antibodies are commonly present. GAD, insulin, IA/ICA-512, and ZnT-8 are the most common targets. Commercially available assays for GAD-65 autoantibodies are widely available and can demonstrate antibodies in more than 85% of individuals with recent-onset type 1 diabetes. These autoantibodies are infrequently present in type 2 diabetes; mellitus at 5–10%. There may be some residual insulin in the plasma in early type 1 diabetes; thus this will not distinguish the two conditions reliably. Polymorphisms of the peroxisome proliferator-activated receptor γ-2 have been described in type 2 diabetes mellitus, but cannot distinguish the two conditions.

X-45. The answer is C. (Chap. 344) Type 2 diabetes mellitus is preceded by a period of impaired fasting glucose or impaired glucose tolerance, and a number of agents and interventions have been studied in this period to prevent progression to frank diabetes mellitus. The Diabetes Prevention Program demonstrated that intensive lifestyle changes including diet and exercise prevented or delayed the development of diabetes mellitus by 58% compared to placebo. Metformin was used in the same study and prevented the development of diabetes by 31%. Other drug therapies have been studied and showed delayed progression including alpha-glucosidase inhibitors, thiazolidinediones, and orlistat, though none are approved for this purpose, and the American Diabetes Association recommends only metformin for therapy in impaired glucose tolerance. Sulfonylureas, such as glyburide, stimulate glucose secretion and have not been shown to delay progression to type 2 diabetes.

X-46. The answer is E. (Chap. 344) Diabetic ketoacidosis and hyperglycemic hyperosmolar state exist on a spectrum, with diabetic ketoacidosis being more common in patients with type 1 diabetes mellitus, but it does occur with some frequency in patients with type 2 diabetes. Both conditions include hyperglycemia, dehydration, absolute or relative insulin deficiency, and acid-base abnormalities. Ketosis is more common in diabetic ketoacidosis. In diabetic ketoacidosis, glucose normally ranges from 250 to 600 mg/dL, while it is frequently 600–1200 mg/dL in the hyperglycemic hyperosmolar state. Sodium is often mildly depressed in ketoacidosis and is preserved in the hyperosmolar state. Potassium is normal to elevated in diabetic ketoacidosis and normal in hyperglycemic hyperosmolar patients. Magnesium, chloride, and phosphate are normal in both conditions. Creatinine may be slightly elevated in diabetic ketoacidosis, but is often moderately elevated in the hyperglycemic hyperosmolar state. Plasma ketones may be slightly positive in hyperosmolar patients, but are always strongly positive in diabetic ketoacidosis. Because hyperosmolarity is the hallmark of hyperglycemic hyperosmolar patients, they have an osmolarity of 330–380 mosm/mL, while patients with diabetic ketoacidosis have a plasma osmolarity ranging from 300 to 320 mosm/mL. Serum bicarbonate is markedly depressed in diabetic ketoacidosis and normal or slightly depressed in the hyperosmolar state. Arterial pH is depressed at less than 7.3 in ketoacidosis and more than 7.3 in the hyperosmolar state. Finally, the anion gap is wide in diabetic ketoacidosis and normal to slightly elevated in the hyperglycemic hyperosmolar state.

X-47. The answer is C. (Chap. 344) Diabetic retinopathy is the leading cause of blindness in adults aged 20–74 years in the United States. Blindness is the result of macular edema and progressive retinopathy, which can be divided into nonproliferative and proliferative retinopathy. Nonproliferative retinopathy tends to occur in the first and early second decades after diagnosis and is characterized by

retinal vascular microaneurysms, blot hemorrhages, and cotton-wool spots. Neovascularization is the hallmark of proliferative retinopathy and occurs in response to retinal hypoxemia. Newly formed vessels occur in the retina and, because they are fragile, rupture easily and cause vitreous hemorrhage, fibrosis, and ultimately retinal detachment.

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