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Lab Findings in Endocrine System Disease
Pituitary Tumours Aldosteronism  Diabetes Mellitus Hypoglycemia
Anterior Pituitary Insufficiency   Pheochromocytoma   Klinefelter's Syndrome Secondary Testicular Failure
    Testicular Tumors Acromegaly Turner's Syndrome Diabetes Insipidus
 Polycystic Ovary Syndrome (Stein-Leventhal Syndrome) Syndrome of Inappropriate Secretion of Antidiuretic Hormone  Secondary Ovarian Failure Hyperthyroidism
 Ovarian Tumors Carcinoma of the Thyroid Zollinger-Ellison Syndrome Hypothyroidism
Polycystic Ovary Syndrome (Stein-Leventhal Syndrome) Hyperparathyroidism Hashimoto's Disease Hypoparathyroidism 
Cushing's Syndrome Precocious Puberty Ectopic Hormone Production Adrenocortical Insufficiency

The Endocrine System
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PITUITARY TUMOURS

Link to Image source
Pituitary: Macro view of the pituitary gland. This and the following pituitary slides are stained with Masson's trichome wherein nuclei and other basophilic structures (may include cytoplasm) are blue, collagen is green or blue, and cytoplasm (nonbasophilic) are red. Notice the lightly-stained neurohypophysis and darker-stained adenohypophysis.

LABORATORY FINDINGS
 

  • Increased plasma PRL (>300 ng/ml) - this finding is more diagnostic than are tests designed to stimulate or suppress PRL secretion
  • Diminished PRL increase following administration of thyrotropin-releasing hormone (TRH) or phenothiazines, such as chlorpromazine or perphenazine

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ANTERIOR PITUITARY INSUFFICIENCY
GONADOTROPIC HORMONES
THYROID-STIMULATING HORMONE
ADRENOCORTICOTROPIC HORMONE
GROWTH HORMONE
LABORATORY FINDINGS
 
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ACROMEGALLY

Click here for enlarged view

LABORATORY FINDINGS

Diagnostic Studies
 

  • Increased serum GH, which is not suppressed by oral administration of glucose;  there is suppression of GH by glucose in normal persons.
  • GH is increased in response to TRH administration;  there is no such increase in normal persons.
Other Laboratory Findings
 
  • Increased serum phosphorus due to increased renal tubular phosphate reabsorption
  • Increased serum alkaline phosphatase reflects increased bone formation.
  • Increased serum and urine calcium reflect increased intestinal absorption of calcium.
  • Increased serum and urine creatinine reflect an increased rate of tissue synthesis.
  • Diabetes mellitus occurs in 10% of patients and there is impaired glucose tolerance in 50% of patients;  these occur as a result of the antagonistic effect of GH on insulin.

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DIABETES INSIPIDUS

LABORATORY FINDINGS
 

Diagnostic Studies
 
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SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE

LABORATORY FINDINGS
 



HYPERTHYROIDISM

Click here for enlarged image

LABORATORY FINDINGS

Diagnostic Studies
 

  • Increased serum T4 - this may be normal
  • Increased resin T3 uptake - this measures the availability of unbound binding sites for T4 and T3 on T4 - binding proteins;  this may be normal even more often than is T4.
  • Increased free T4 index - this is the product of T4 X resin T3 uptake;  this usually parallels absolute free T4 concentration.
  • Increased serum T3 - measurement of this hormone is indicated when the free T4 index is normal or borderline and clinical suspicion of hyperthyroidism is high.
  • Increased free T3 index - this is the product of T3 X resin T3 uptake;  this usually parallels absolute free T3 concentration.
  • Minimal or absent increase in TSH following IV administration of TRH - this reflects pituitary suppression by increased T4 and T3 and indicates thyroid autonomy.  Autonomy means that thyroid function is independent of pituitary regulation, but does not necessarily imply clinical thyrotoxicosis.
  • Presence of thyroid-stimulating immunoglobulins such as LATS in patients with Graves' disease
Other Laboratory Findings
 
  • Increased serum glucose due to increased intestinal absorption and gluconeogenesis
  • Decreased serum cholesterol and triglycerides due to increased utilization


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HYPOTHYROIDISM

Diagnostic Studies
 

  • Decreased serum T4, resin T3 uptake, and free T4 index - the degree of depression of these indices depends on the extent of destruction of the thyroid gland.
  • Increased serum TSH - this is the single most important diagnostic laboratory test for primary hypothyroidism.  This might be elevated, even with a normal free T4 index.  TSH is low or undetectable in cases of secondary hypothyroidism.
Other Laboratory Findings
 
  • Increased serum cholesterol and triglycerides reflect decreased utilization.
  • Increased serum creatinine phosphokinase (CPK), lactate dehydrogenase (LDH), and serum glutamic-oxaloacetic transaminase (SGOT) - myxedema of skeletal muscles causes leakage of these enzymes through the muscle membranes into capillaries
  • Flat glucose tolerance curve due to decreased gastric emptying and diminished cellular utilization of gtlucose
  • Anaemia, usually normocytic due to decreased erythropoietin production, decreased tissue oxygen needs, or impaired marrow function.  Microcytic anaemia might follow increased menstrual blood loss.  The occasional occurrence of macrocytic anaemia is due to vitamin-B12 or folate deficiency.
  • Achlorhydria and parietal cell antibodies occur in up to 40% of patients.

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HASHIMOTO'S DISEASE

Link to Image source
This slide shows a diffuse lymphocytic and plasma cell infiltrate around the follicular structures of the thyroid gland. The appearances are those of Hashimoto's thyroiditis. This is an autoimmune disease which produces a diffuse goitre. Serum anti-thyroglobulin and anti-microsomal antibodies are raised. The natural history of the disease results in diffused fibrosis and hypothyroidism. The risk of thyroid lymphoma is increased

LABORATORY FINDINGS
 

  • Increased serum antithyroglobulin and antimicrosomal antibodies.  Microsomal antibody titers correlate with the degree of lymphocytic infiltrate in the thyroid gland.  Thyroglobulin antibodies correlate with the degree of thyroid fibrosis and occur in the chronic stage of the disorder.  Children often do not have elevated antibody titers.
  • Increased TSH characteristically reflects primary hypothyroidism;  this occurs before the free T4 index decreases.
  • Free T4 index is normal early in the disease but decreases as the disease progresses and more of the thyroid gland is destroyed.

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SUBACUTE THYROIDITIS

LABORATORY FINDINGS
 


CARCINOMA OF THE THYROID

Link to image source
Papillary thyroid carcinoma, . The majority of this tumor showed features of the follicular variant of papillary carcinoma. Note the prominent intranuclear inclusions at the center of the field. H&E, x200

LABORATORY FINDINGS
 

  • Biopsy of the thyroid gland is required for definitive diagnosis.
  • Increased serum calcitonin - characteristic finding in medulary carcinoma.  An increased level may occur only following stimulation by calcium or pentagastrin infusion.  These stimulation tests should be performed on relatives of patients with medullary carcinoma to facilitate early recognition of the disease at a stage when it might be curable.
  • Increased serum thyroglubulin - this occurs in many patients with untreated papillary and follicular carcinomas;  it might also be elevated in Graves' disease and in subacute thyroiditis.  The major use of this assay is in the follow-up of patients with thyroglobulin-secreting thyroid carcinoma.  Very low or undectable postoperative thyroglobulin levels indicate complete removal of the tumour.  Persistence of elevated thyroglobulin indicates that residual thyroid carcinoma probably remains.  Thyroglobulin is also elevated when metastases develop.

Papillary Carcinoma of the Thyroid

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CUSHING'S SYNDROME
Cushing's Syndrome is an excess of cortisol in the body that results in a variety of changes, which are discussed in more detail below.
How does it occur?
Cortisol is a hormone normally produced by the adrenal glands to help regulate various processes in the body. There are multitude of causes that can result in higher than normal levels of cortisol in the body. The production of cortisol is directly controlled by another hormone called ACTH, which is made in the pituitary. The levels of ACTH in turn are controlled higher up in the brain by the hypothalamus. By understanding this pathway of hypothalamus > pituitary (ACTH) > cortisol (made by the adrenal gland), one can see how an increase at any of these levels can result in elevated cortisol.
Tumors in the brain that overproduce ACTH, thereby causing excess cortisol production, is a common cause of Cushing's syndrome. There are other tumors in the body, such as lung tumors, that can also overproduce ACTH.
Tumors in the adrenal gland can lead to overproduction of cortisol directly. The most common cause of Cushing's syndrome is from long-term steroid medication usage. Steroids are used to treat many diseases and chronic therapy with them can lead to Cushing's syndrome.
Symptoms?
The symptoms are wide ranging as cortisol has many effects on the body. High levels of cortisol can cause increased weight most notably in the face ("moon facies"), chest and the back ("buffalo hump").
Other findings include diabetes, muscle weakness, fatigueability, osteoporosis leading to bone fractures, easy bruisability, high blood pressure, irritability and emotional instability, purplish lines on the skin (esp. the abdomen), menstrual changes and virilizing signs.

LABORATORY FINDINGS

Diagnostic Studies

Low-Dose Dexamethasone Test

Table 6-1
DISORDER PLASMA ACTH SUPPRESSION OF URINARY STEROIDS
Cushing's disease Normal or slightly elevated To <50% of baseline values
Ectopic ACTH syndrome Markedly elevated None
Adrenal tumour Low or undetectable None

High-Dose Dexamethasone test
 

Table 6-1 indicates the differential laboratory findings.

Other Laboratory Findings
 


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ADRENOCORTICAL INSUFFICIENCY

Fig. 1 Hyperpigmentation (adrenocortical insufficiency), sparse head hair and totally absent body hair (hypothyroidism).
Link to image (English/German site)

LABORATORY FINDINGS

Diagnostic Studies

Rapid ACTH Stimulation Test Using Cosyntropin (synthetic ACTH)

  • A lack of increase in plasma cortisol following cosyntropin injection indicates adrenocortical insufficiency.
Differentiation of Primary From Secondary Adrenocortical Insufficiency
 
  • Increased plasma ACTH indicates primary insufficiency.
  • Normal or low plasma ACTH indicates secondary insufficiency.
Other Laboratory Findings

Primary Adrenocortical Insufficiency

  • Presence of adrenal antibodies occurs in 50% to 70% of patients with nontuberculous Addison's disease.
Effects of mineralcorticoid deficiency:
 
  • Decreased serum sodium due to loss in urine;  this finding might be obscured by associated dehydration
  • Increased serum potassium
  • Increased blood urea nitrogen (BUN) and creatinine due to decreased blood volume and dehydration
Effects of glucocorticoid deficiency:
 
  • Normocytic, normochromic anaemia - this finding might be obscured by associated dehydration
  • Decreased neutrophils, increased lymphocytes, increased eosinophils
Secondary Adrenocortical Insufficiency
 
  • Adrenal effects are only those of glucocorticoid deficiency (listed above), because the mineralocorticoid, aldosterone, is not effected by diminished ACTH secretion.
  • Decreased GH, gonadotropins, and possibly TSH reflect pituitary insufficiency.

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ALDOSTERONISM

LABORATORY FINDINGS

Diagnostic Studies
 

Other Laboratory Findings
 
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PHEOCHROMOCYTOMA

Link to Image source

Pheochromocytoma, Adrenal Pheochromocytoma (Cut Surface)
Mottled brown tan mass is the neoplasm filling up the adrenal medulla.
  • Blue arrow points to residual normal medulla.
  • Yellow arrows point to golden yellow adrenal cortex.
  • Black discoloration around the specimen is india ink applied to assess the margins of the specimen.
Image Contrib. by: Hartford Hospital
Description by: Melinda Sanders, M.D. ( 423-6151)

LABORATORY FINDINGS

Diagnostic Studies
 

  • Increased 24-hour urine metanephrines - this is the best single screening test; metanephrines might be elevated even between hypertensive attacks.
  • Increased plasma norepinephrine (noradrenalin) - this is not suppressed by clonidine hydrochloride. This is the best definitive test and should be done regardless of urinary metanephrine excretion if the entire clinical picture is strongly suggestive of pheochromocytoma.
  • Increased urine metanephrine - creatinine ratio (> 2.2 mcg/mg)
Other Laboratory Findings
 
  • Increased serum and urine glucose due to catecholamine - induced suppression of insulin secretion and acceleration of glucose production

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KLINEFELTER'S SYNDROME

LABORATORY FINDINGS
 

Three sex chromosomes are associated with Klinefelter rather than the expected 2 - XXY. These individuals are males with some development of breast tissue normally seen in females. Little body hair is present, and such person are typically tall, with or without evidence of mental retardation. Males with XXXY, XXXXY, and XXXXXY karyotypes have a more severe presentation, and mental retardation is expected.

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SECONDARY TESTICULAR FAILURE

LABORATORY FINDINGS
 


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TESTICULAR TUMOURS

LABORATORY FINDINGS
 

Seminomas are radiosensitive Stage I and II disease treated by inguinal orchidectomy plus Radiotherapy to ipsilateral abdominal and pelvic nodes ('Dog leg') or
Surveillance
Stage IIC and above treated with chemotherapy
Teratomas are not radiosensitive Stage I disease treated by orchidectomy and surveillance Chemotherapy (BEP = Bleomycin, Etopiside, Cisplatin) given to: Stage I patients who relapse Metastatic disease at presentation

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TURNER'S SYNDROME

LABORATORY FINDINGS
 

Only 1 sex chromosome is present -X0, or X_. The expected Y chromosome is missing. Turner syndrome is associated with underdeveloped ovaries, short stature, webbed/.bull neck, and broad chest. Individuals are sterile, and lack expected secondary sexual characteristics. Mental retardation typically not evident.

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POLYCYSTIC OVARY SYNDROME
(STEIN-LEVENTHAL SYNDROME)

LABORATORY FINDINGS
 

Polycystic Ovaries: Link to Image Source

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SECONDARY OVARIAN FAILURE

LABORATORY FINDINGS
 


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OVARIAN TUMOURS

LABORATORY FINDINGS

Feminising Ovarian Tumours
 

Masculinising Ovarian Tumours
  Ovarian Fibroma: Link to image source

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DIABETES MELLITUS

LABORATORY FINDINGS

Diagnostic Studies
 

Other Laboratory Findings
  Laboratory Findings in Ketoacidosis
 
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HYPOGLYCEMIA

LABORATORY FINDINGS

Insulin-Producing Islet Cell Tumour

Symptoms of hypoglycemia occur while fasting and are accompanied by plasma glucose <45 mg/dl and an inappropriately high plasma insulin level (>10 U/ml).  In about 50% of patients, overnight fasting produces the characteristic findings.  Some patients require as much as a 72-hour fast, followed by exercise, to demonstrate hypoglycemia and hyperinsulinemia and establish the diagnosis.

Postprandial (Reactive) Hypoglycemia

Plasma glucose below 45 mg/dl and appropriate symptoms occur 2-4 hours after eating but not during fasting.  The glucose frequently returns to normal spontaneously.  The 5-hour glucose tolerance test is an artificial situation and is not recommended for establishing the diagnosis.  A standard meal may be used in an attempt to produce postprandial hypoglycemia.  Blood sugar should be drawn at the time symptoms occur.  It is not necessary to measure serum insulin levels.

Other Laboratory Findings
 


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ZOLLINGER-ELLISON SYNDROME

LABORATORY FINDINGS

Diagnostic Studies
 

Other Laboratory Findings
 
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HYPERPARATHYROIDISM

LABORATORY FINDINGS

Diagnostic Studies
 

0.22 HCT + 0.76 Cl - 1.5 Caex - 1.9 P - 7.44*


*HCT    =    haematocrit
 Cl    =        chloride
 Caex    =    the difference between the total serum calcium and the upper limits of normal in a given laboratory
 P        =    phosphorus
      The formula is not useful in separating hyperparathyroid patients from normal patients.  Patients who are vomiting or using diuretics might be misclassified using
        this formala.
 

Other Laboratory Findings
 

Increased serum PTH, which must be correlated with serum calcium:
  Radioimmunoassay of PTH might help in the patient with borderline elevation of serum calcium, unresolved metabolic bone disease, or recurrent calcium stone formation, but is not usually needed to diagnose hyperparathyroidism.

A major cause of variability of PTH might help in the patient with borderline elevation of serum calcium, unresolved metabolic bone disease, or recurrent calcium stone formation, but is not usually needed to diagnose hyperparathyroidism.

A major cause of variability in PTH determinations is that the available immunoassays measure different portions of the PTH.  Some assays measure carboxy-terminal fragments and intact PTH, whereas others measure the amino-terminal portion of the PTH molecule.  The latter is the biologically active region of the molecule.  In a study of 29 patients with hypercalcemia.  Raisz et al had serum PTH assaays done by four commercial laboratories and observed, "....we found considerable variation in the frequency of elevated values (of PTH) in hyperparathyroidism and the degree to which the assay discriminated between primary hyperparathyroidism and hypercalcemia of malignancy......it is still necessary to use multiple tests in the different diagnosis of hypercalcemia."


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HYPOPARATHYROIDISM

LABORATORY FINDINGS
 


PRECOCIOUS PUBERTY

LABORATORY FINDINGS
 

Girls Boys ECTOPIC HORMONE PRODUCTION

LABORATORY FINDINGS

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