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Diseases » Hyperglycemia » Diagnosis
 

Diagnosis of Hyperglycemia

Hyperglycemia Diagnosis: Book Excerpts

Diagnosis of Hyperglycemia: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Hyperglycemia:

Diagnostic Tests for Hyperglycemia: Online Medical Books

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


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

ALKALINE PHOSPHATASE ELEVATION: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. What is the calcium level? If this is increased, one should look for primary hyperparathyroidism and bone metastasis. These two findings can be further differentiated with parathyroid hormone (PTH) assay. If calcium is decreased, the patient may have vitamin D deficiency, malabsorption syndrome, Fanconi's syndrome, or other renal diseases.
  2. Are there abnormalities of liver function tests? If the calcium is normal but liver function tests are abnormal, think of liver disease, obstructive jaundice, and liver metastasis. If the patient is not pregnant, sepsis, Paget's disease, osteogenic sarcoma, gynecologic malignancies, and liver and bone metastasis may be considered.
  3. What is the phosphate level? In the face of a low calcium level, a low phosphate level will help distinguish vitamin D deficiency, malabsorption syndrome, and Fanconi's syndrome from other renal diseases in which the phosphate level will be high.
  4. Is there a high 5'-nucleotidase or γ -glutamyltransferase level? This will help distinguish liver disease from Paget's disease, metastatic bone disease, and osteogenic sarcoma.

DIAGNOSTIC WORKUP

The workup should include a CBC, sedimentation rate, urinalysis, chemistry panel, protein electrophoresis, liver profile, PTH assay, skeletal survey, bone scan, CT scan of the abdomen, alkaline phosphatase isoenzymes, acid phosphatase, and a PSA to rule out prostatic carcinoma.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

ASPARTATE AMINOTRANSFERASE ELEVATION: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is the patient receiving heparin therapy? As many as 27% of patients taking heparin have an elevated aspartate aminotransferase [AST, or serum glutamine-oxaloacetic transaminase (SGOT)], and 60% have an elevated alanine aminotransferase (ALT).
  2. Are the results of liver function tests abnormal? This indicates that the elevated AST is due to liver disease.
  3. Is the creatine phosphokinase (CPK) elevated? An elevated CPK would indicate that the elevated AST is related to muscle damage or disease or a myocardial infarction. Further differentiation of these two conditions is made by ordering CPK isoenzymes and an EKG.
  4. What is the arm-to-tongue circulation time? This is increased in congestive heart failure.
  5. Is the serum amylase elevated? This would point to pancreatitis as the cause of the AST elevation. If all of the above related tests are normal, the AST elevation is most likely due to liver disease or renal infarction.

DIAGNOSTIC WORKUP

Additional tests to order that will help pin down the diagnosis include a CBC, serum amylase, chemistry panel, lactic acid dehydrogenase (LDH) isoenzymes, γ -glutamyltransferase, urinalysis, serial EKGs, pulmonary function tests, chest x-ray, flat plate of the abdomen, electromyography (EMG), liver biopsy, and muscle biopsy. Consultation with a cardiologist or hepatologist would be prudent before ordering expensive diagnostic tests.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

LACTIC DEHYDROGENASE ELEVATION: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. What is the level of creatine phosphokinase isoenzyme containing M and B subunits (MB-CPK) ? An elevated MB-CPK combined with elevated LDH is most likely due to a myocardial infarction, although myocarditis and pericarditis can produce a similar picture.
  2. What is the AST level? If the MB-CPK or CPK are not also increased, an elevation of both the LDH and AST would point to liver disease.
  3. What are the serum and urine creatine levels? If these are elevated, muscle disease must be considered likely.
  4. What does the lung scan show? If positive, a lung scan separates pulmonary infarction from the other conditions in this group.

DIAGNOSTIC WORKUP

The diagnostic workup should include a CBC, urinalysis, chemistry panel, sedimentation rate, ANA, urine and serum creatine, urine myoglobin, serial EKGs, blood gas analysis, LDH isoenzymes, chest x-ray, lung scan, EMG, and cardiology and neurology consults. A liver scan, CT scan of the abdomen and liver, and muscle biopsy may be necessary.

 

» 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

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

ASPARTATE AMINOTRANSFERASE, ALANINE AMINOTRANSFERASE, AND LACTIC DEHYDROGENASE ELEVATION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Obviously, the first condition to rule out is myocardial infarction. This is done by ordering serial MB-CPKs (MB isoenzyme of creatine phosphokinase) and ECGs. Serum cardiac troponin levels may also be helpful. Next, determine if the patient is on heparin, because this may elevate the alanine aminotransferase (ALT) level. Various muscle diseases (dermatomyositis, muscular dystrophy, muscle trauma, etc.) may be excluded by ordering CPK enzymes also, particularly the MM (MM isoenzyme of creatine phosphokinase) fraction. Liver disease can be revealed through by a liver profile, CT scan of the abdomen, and gallbladder ultrasonography.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

ALKALINE PHOSPHATASE ELEVATION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

If the elevated alkaline phosphatase level is related to liver disease, the clinical examination will often show jaundice or hepatomegaly. If it is related to bone disease, the clinical examination will show bone pain, pathologic fracture, or bone mass. A liver profile will also help diagnose a liver disorder, but a CT scan of the abdomen may be necessary. A skeletal survey will usually reveal bony metastasis and other disorders of the bone, but a bone scan may be necessary to show early metastasis to the bone. A serum parathyroid hormone (PTH) level will help diagnose primary hyperparathyroidism whereas secondary hyperparathyroidism (rickets, etc.) will require the specialized tests listed below.

» 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

ALKALINE PHOSPHATASE ELEVATION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

If the elevated alkaline phosphatase level is related to liver disease, the clinical examination will often show jaundice or hepatomegaly. If it is related to bone disease, the clinical examination will show bone pain, pathologic fracture, or bone mass. A liver profile will also help diagnose a liver disorder, but a CT scan of the abdomen may be necessary. A skeletal survey will usually reveal bony metastasis and other disorders of the bone, but a bone scan may be necessary to show early metastasis to the bone. A serum parathyroid hormone (PTH) level will help diagnose primary hyperparathyroidism, whereas secondary hyperparathyroidism (rickets, etc.) will require the specialized tests listed below.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007


 » Next page: Signs of Hyperglycemia

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