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Diagnosis of Impaired glucose tolerance

Diagnostic Test list for Impaired glucose tolerance:

The list of medical tests mentioned in various sources as used in the diagnosis of Impaired glucose tolerance includes:

Impaired glucose tolerance Diagnosis: Book Excerpts

Diagnosis of Impaired glucose tolerance: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Impaired glucose tolerance:

Diagnostic Tests for Impaired glucose tolerance: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Impaired glucose tolerance.


GLYCOSURIA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Was the test used specific for glucose? Glucose oxidase tests (Clinistix, etc.) are specific for glucose, whereas other tests (Benedict's, etc.) are not. Thus, the latter will give false positives for lactose, fructose, galactose, and salicylates.
  2. What is the blood sugar? If the blood sugar is elevated or a glucose tolerance test is positive, one should suspect diabetes mellitus. If these tests are normal, one should suspect renal glycosuria, pregnancy, or renal tubular acidosis.

DIAGNOSTIC WORKUP

The investigation of glycosuria should include a glucose tolerance test, chemistry panel, and electrolyte panel. If there are clinical features of an endocrine disorder, the various tests for these disorders should be ordered.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

HYPERGLYCEMIA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. What is the free T 4 ? If this is elevated, think of hyperthyroidism.
  2. What is the plasma cortisol? If this is elevated, think of Cushing's syndrome.
  3. What is the plasma growth hormone? If this is elevated, think of acromegaly or gigantism.
  4. What is the 24-hr urine catecholamine level? If this is high, think of a pheochromocytoma.

If all of the above tests are normal, diabetes mellitus is usually the diagnosis, although some of these patients could have a glucagonoma or pancreatic disease. Certain drugs can cause a spurious hyperglycemia also.

DIAGNOSTIC WORKUP

Further workup may include a CBC, urinalysis, chemistry panel, glucose tolerance test, plasma cortisol, free T 4 , TSH, plasma and urine catecholamines, skull x-ray, vanillylmandelic acid (VMA) , and endocrinology consult.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Hyperglycemia: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Impaired fasting glucose
  • Medications
    –Corticosteroids are a common cause
    –Common medications include growth hormone, estrogen (including oral contraceptives), nicotinic acid, salicylates and NSAIDs, thiazide and loop diuretics, phenytoin, and epinephrine
  • Diabetes mellitus type I
    –Diabetic ketoacidosis
  • Diabetes mellitus type II
  • Pancreatic disease
    –Acute or chronic pancreatitis
    –Pancreatectomy
    –Pancreatic carcinoma
    –Hemochromatosis
    –Cystic fibrosis
    • Increased counter-regulatory hormones associated with acute disease
      –Myocardial infarction
      –Stroke or other neurologic disease
      –Renal insufficiency
      –Hepatic insufficiency
  • Acromegaly
  • Cushing's syndrome
  • Pheochromocytoma
  • Hyperthyroidism (thyroid storm)
  • Glucagonoma
  • Gestational diabetes
  • Amyloidosis

Workup and Diagnosis

  • History and physical examination
    –Symptoms of hyperglycemia include fatigue, polyuria, polyphagia, polydipsia, and stomach discomfort
    –Complete medication history is essential
    –Examination is most commonly normal, but patients occasionally present with acanthosis nigricans (hyperpigmented, velvety lesions commonly on the back of the neck and/or axilla), or necrobiosis lipoidica diabeticorum (atrophic, shiny, erythematous or pale macules on anterior shins).
    –Complicating problems of diabetes (end-organ dysfunction) involve many systems (e.g., diabetic retinopathy, peripheral neuropathy, diabetic nephropathy, hypertension, coronary artery disease)
  • Initial presentation may be dramatic, with greatly elevated glucose and significant electrolyte abnormalities
  • Both type I and type II result in elevated levels of insulin
    –In type I disease, exogenous insulin is often abnormally elevated
    –In type II disease, endogenous insulin is often abnormally elevated
  • C-peptide is increased in type II and decreased in type I

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Hyperglycemia: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Type I diabetes mellitus
    –Most common form of diabetes in children
    –Prevalence: 1.9/1,000
    –Autoimmune-mediated destruction of pancreatic islets (β-cells)
    –Absolute insulin deficiency
    –Often presents with ketosis and DKA
  • Type II diabetes mellitus
    –Increasing prevalence in children, especially among obese
    –In children, onset usually in mid-puberty
    –More frequent in blacks, Hispanics, Pacific Islanders, Asians, and Native Americans (Pima Indians)
    –Strong association with family history of type II diabetes
    –Insulin resistance and inadequate insulin secretion results in relative insulin deficiency
    • Maturity-onset diabetes of the young (MODY)
      –Infrequent
      –Autosomal dominant disease
      –Onset usually between 9 and 25 years old
      –Genetic defects in enzymes or nuclear transcription factors involved in islet cell development or the regulation of insulin secretion
    • Drug- or chemical-induced diabetes
      –Glucocorticoids, β-adrenergic agonists, phenytoin, asparaginase, cyclosporine, tacrolimus, vacor, pentamidine, diazoxide, nicotinic acid, thyroid hormone, thiazides
  • Other endocrinopathies: Cushing disease, acromegaly, pheochromocytoma
  • Exocrine pancreatic diseases
    –Cystic fibrosis
    –Hemochromatosis
  • Pancreatectomy
  • Physiological stress (trauma, infection)
  • Infections
    –CMV
    –Congenital rubella
  • Genetic syndromes: Prader-Willi syndrome, Down syndrome, Turner syndrome, Klinefelter syndrome, Wolfram syndrome

Workup and Diagnosis

  • History
    –Classic symptoms: Polyuria, polydipsia, weight loss
    –Also polyphagia, nocturia, secondary enuresis, intermittent blurry vision
    –Nausea, vomiting, abdominal pain with ketoacidosis
    –Mental status changes with severe acidosis and dehydration
    –Family history of DM, autoimmune, endocrinopathy
  • Physical exam
    –Vital signs, weight, body mass index
    –Ketoacidosis: Funduscopic exam (blurred optic discs with cerebral edema), Kussmaul respirations, fruity odor to breath, tachycardia/hypotension/poor perfusion, severe dehydration, mental status changes
    –Type II diabetes: Obesity and acanthosis nigricans
  • Diagnostic criteria for diabetes
    –Random plasma glucose >200 mg/dL
    –Fasting plasma glucose >126 mg/dL
    –Or 2-hour plasma glucose during the oral glucose tolerance test >200 mg/dL
    –Lab abnormalities must be present on two different days or in the presence of symptoms of diabetes (polyuria, polydipsia, weight loss)
  • Other tests
    –HbA1c, urinalysis for glucose and ketones
    –If suspect DKA, check electrolytes and blood gas
    –To help distinguish type I from type II diabetes, check fasting insulin, C-peptide, and β-cell autoantibodies

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

GLYCOSURIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The investigation of glycosuria should include a glucose tolerance test, chemistry panel, and electrolyte panel. A clinical history of polyuria, polyphagia, weakness, and weight loss will be helpful. If there are clinical features of one of the endocrine diseases listed above, various tests for these disorders and an endocrinology consult should be ordered.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

HYPERGLYCEMIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Obviously, the first thing to do is repeat the blood sugar after fasting. If the result is borderline, a glucose tolerance test should be done. Clinical evaluation for a history of diabetes, hypertension (Cushing disease and pheochromocytoma), protruding jaw and increasing hat size (acromegaly), polyuria, polydypsia, and weight loss (diabetes mellitus and hyperthyroidism) is important. Further workup depends on which endocrine disorder is being considered.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

Diabetes insipidus: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Urinalysis reveals almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that of plasma) and low specific gravity (less than 1.005).

CONFIRMING DIAGNOSIS Diagnosis requires evidence of vasopressin deficiency, resulting in the kidneys’ inability to concentrate urine during a water deprivation test.

In this test, after baseline vital signs, weight, and urine and plasma osmolalities are obtained, the patient is deprived of fluids and observed to make sure he doesn’t drink anything surreptitiously. Hourly measurements then record the total volume of urine output, body weight, urine osmolality or specific gravity, and plasma osmolality. Throughout the test, blood pressure and pulse rate must be monitored for signs of orthostatic hypotension. Fluid deprivation continues until the patient loses 3% of his body weight (indicating severe dehydration). When urine osmolality stops increasing in three consecutive hourly specimens, patients receive 5 units of aqueous vasopressin subcutaneously (S.C.).

Hourly measurements of urine volume and specific gravity continue after S.C. injection of aqueous vasopressin. Patients with pituitary diabetes insipidus respond to exogenous vasopressin with decreased urine output and increased specific gravity. Patients with nephrogenic diabetes insipidus show no response to vasopressin.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Diabetes mellitus: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

According to the American Diabetes Association (ADA), DM can be diagnosed if any of the following exist:

❑ symptoms of diabetes (polyuria, polydipsia, and unexplained weight loss) plus a random (non-fasting) blood glucose level greater than or equal to 200 mg/dl accompanied by symptoms of diabetes.

❑ a fasting blood glucose level (no caloric intake for at least 8 hours) greater than or equal to 126 mg/dl.

❑ a plasma glucose value in the 2-hour sample of the oral glucose tolerance test greater than or equal to 200 mg/dl. This test should be performed after a glucose load dose of 75 g of anhydrous glucose.

If results are questionable, the diagnosis should be confirmed by a repeat test on a different day. The ADA also recommends the following testing guidelines:

❑ Test every 3 years: people age 45 or older without symptoms

❑ Test immediately: people with the classic symptoms

❑ High-risk groups should be tested frequently: Individuals with impaired glucose tolerance usually have normal blood levels unless challenged by a glucose load, such as a piece of pie or glass of orange juice. Two hours after a glucose load, the glucose level ranges from 140 to 199 mg/dl. These individuals have an abnormal fasting glucose level between 110 and 125 mg/dl. Because the fasting plasma glucose test is sufficient to make the diagnosis of diabetes, it replaces the oral glucose tolerance test. (See Classifying blood glucose levels.)

An ophthalmologic examination may show diabetic retinopathy. Other diagnostic and monitoring tests include urinalysis for acetone and blood testing for glycosylated hemoglobin (Hb A1C), which reflects recent glucose cortisol.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Hereditary fructose intolerance: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

A dietary history often suggests hereditary fructose intolerance.

Confirming diagnosis  A fructose tolerance test (using glucose oxidase or paper chromatography to measure glucose levels) usually confirms the diagnosis. However, liver biopsy showing a deficiency in fructose-1-phosphate aldolase may be necessary for a definitive diagnosis.

Supportive values may include decreased serum inorganic phosphorus levels. Urine studies may show fructosuria and albuminuria.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Diabetes Mellitus: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 The initial presentation of DM can vary. Either type may present with the insidious onset of the symptoms associated with hyperglycemia (polyuria, polydipsia, and polyphagia) or with the abrupt onset of an acute complication [diabetic ketoacidosis (in type 1 DM) or nonketotic hyperglycemic-hyperosmolar coma (in type 2 DM)].

 A. Type 1 diabetes. Patients with type 1 DM typically present before the age of 18 years. The symptoms heralding the disease emerge gradually as hyperglycemia appears and becomes more frequent and profound. Physiologic stress (e.g., an acute illness or trauma), which increases the requirement for insulin, can unmask the insulinopenia and give the impression that the problem is acute. Enuresis may be a clue for polyuria in a child who was previously toilet-trained. Lethargy, weakness, and weight loss are other common features.

 B. Type 2 diabetes. Patients with type 2 DM usually present after the age of 40 years. The diagnosis is often made in an asymptomatic patient as a result of routine blood tests that reveal an elevation of plasma glucose. Other patients may present with the symptoms of hyperglycemia. The patient may have a history of recurrent skin infections or persistent vulvovaginitis. Other common symptoms include altered sensations in the extremities, nocturia, erectile dysfunction, and visual disturbances (Chapters 4.6, 5.1, 10.3, and 10.4). The use of glucocorticoids, β-adrenergic agonists, or thiazides can precipitate the symptoms of type 2 DM.

Physical examination

Patients often present with similar physical findings in both type 1 and type 2 DM, owing to hyperglycemia. In the young child, failure to grow and gain weight can occur with type 1 DM. The child may be ill appearing, lethargic, and often have signs of dehydration (tachypnea, tachycardia, and low blood pressure). Ketone production will produce a fruity odor on the patient’s breath. The patient with type 2 DM tends to be obese (especially upper body obesity) and may appear fatigued and have muscle weakness or decreased vision. The neurologic examination may reveal painful feet and numbness. Monilial infections may be found in the vagina and pubic areas.

» READ BOOK EXCERPT ONLINE »

Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Diabetes insipidus: Diagnosis
(Handbook of Diseases)

Urinalysis reveals almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that of plasma) and low specific gravity (less than 1.005). However, a diagnosis requires the water deprivation test to provide evidence of vasopressin deficiency, resulting in the kidneys’inability to concentrate urine.

Water deprivation test

In this test, after baseline vital signs, weight, and urine and plasma osmolalities are obtained, the patient is deprived of fluids and observed to make sure he doesn’t drink anything surreptitiously. Hourly measurements then record the total volume of urine output, body weight, urine osmolality or specific gravity, and plasma osmolality. Throughout the test, blood pressure and pulse rate must be monitored for signs of orthostatic hypotension.

Fluid deprivation continues until the patient loses 3% of his body weight (indicating severe dehydration). When urine osmolality stops increasing in three consecutive hourly specimens, the patient receives 5 units of aqueous vasopressin subcutaneously (S.C.).

Hourly measurements of urine volume and specific gravity continue after S.C. injection of aqueous vasopressin. Patients with pituitary diabetes insipidus respond to exogenous vasopressin with decreased urine output and increased specific gravity. Patients with nephrogenic diabetes insipidus show no response to vasopressin.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Diabetes mellitus: Diagnosis
(Handbook of Diseases)

In nonpregnant adults, diabetes mellitus is diagnosed with:

❑ at least two occasions of a fasting plasma glucose level greater than or equal to 126 mg/dl

❑ typical symptoms of uncontrolled diabetes and a random blood glucose level greater than or equal to 200 mg/dl

❑ a blood glucose level greater than or equal to 200 mg/dl at 2 hours after ingestion of 75 grams of oral dextrose.

Two tests are required for diagnosis; they can be the same two tests or any combination and may be separated by more than 24 hours.

An ophthalmologic examination may show diabetic retinopathy. Other diagnostic and monitoring tests include urinalysis for acetone and blood testing for glycosylated hemoglobin, which reflects glucose control over the past 2 to 3 months.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

GLYCOSURIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The investigation of glycosuria should include a glucose tolerance test, chemistry panel, and electrolyte panel. A clinical history of polyuria, polyphagia, weakness, and weight loss will be helpful. If there are clinical features of one of the endocrine diseases listed above, various tests for these disorders and an endocrinology consult should be ordered.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

HYPERGLYCEMIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Obviously, the first thing to do is repeat the blood sugar test after fasting. If the result is borderline, a glucose tolerance test should be done. Clinical evaluation for a history of diabetes, hypertension (Cushing disease and pheochromocytoma), protruding jaw and increasing hat size (acromegaly), polyuria, polydipsia, and weight loss (diabetes mellitus and hyperthyroidism) is important. Further workup depends on which endocrine disorder is being considered.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007


 » Next page: Signs of Impaired glucose tolerance

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