Diabetes insipidus

Introduction

Diabetes insipidus (DI) is a condition which causes frequent urination. The reduction in production or release of ADH results in fluid and electrolyte imbalance caused by increased urinary output. Depending on the cause, Diabetes insipidus may be transient or life long condition. In its clinically significant forms, diabetes insipidus is a rare disease.

 

 

Definition

Diabetes insipidus (DI) is a group of conditions associated with a deficiency of secretion of anti-diuretic hormone characterized by the chronic excretion of abnormally large volumes (more than 50 mL/kg) of dilute urine.
 

Incidence

The true prevalence of DI is unknown, but it is usually underdiagnosed because the symptoms and signs are benign and many patients ignore them or are unaware of them. It commonly occur in older adults.
 

Types

• · Central (neurogenic) DI: it occurs when any lesion of the hypothalamus or posterior pituitary interferes with ADH synthesis, transport or release.
• · nephrogenic DI: it results from the decreased renal response to ADH despite presence of adequate ADH.
• · Primary polydipsia(dispogenic DI): excessive water intake caused by structural lesion in thirst center or psychologic disorder.
• · Gestational DI.
• Causes
• · Central (neurogenic) DI: Multiple causes include brain tumour, head injury, brain surgery, CNS infections.
• · nephrogenic DI: Caused by lithium therapy, renal damage, or hereditary renal disease.
• · Primary polydipsia(dispogenic DI): excessive water intake caused by structural lesion in thirst center or psychologic disorder.

Pathophysiology
The decrease in ADH results in fluid and electrolyte imbalances caused by increased urinary output and increased plasma osmolality. Tubular reabsorption of water reduces due to decreased tubular permiabilityto the water. This results in excessive urination which affects activities of daily living and interrupts sleep when nocturia occurs. Distended bladder leads to back flow of urine and hydronephrosis may develope as a complication. This will eventually leads to renal insufficiency.
Serum osmolality increases due to excessive urine output. Serum sodium level elevates in order to compensate for the fluid loss. severe thirst develops by osmoreceptor stimulation in response to the hypernatrmia. Patent intakes fluid to replace the loss. If hypernatremia persists restlessness, reduction in reflexes and seizures may develope. Cardiac output decreases and tachycardia develops if fluid volume is not restored. It will lead to hypotension and finally to hypovolemic shock.
 

Clinical manifestations

• Diabetes insipidus is characterized by increased thirst and increased urination. The primary character of DI is polyuria, excretion of large quantities of urine ( 5-20L per day)with a very low specific gravity(less than 1.005) and urine osmolality of < 100mmol/kg. In partial DI urine output may be lower(2-4L per day).
• Polydipsia (excessive intke of fluids) is also a characteristic feature of DI. Patient compensate for fluid loss by drinking great amount of water. The patient with central DI favours cold or iced drinks. Nocturia occurs due to frequent tendency to urinate which interrups sleep of the patient.
• Central DI usually occurs suddenly with excessive fluid loss. DI usually has a triphastic pattern: the acute phase with abrupt onset of polyuria, an interphase where urine volume apparently normalizes, and a third phase where DI is permanent.
• If fluid loss is not compensated, severe fluid volume de ficit results. This deficit is manifested by weight loss, hypotension, tachycardia with decreased cardiac output, poor tissue turgor, irritability, mental dullness. Hypovolemic shock may develop if fluid volume is not restored.

Diagnostic studies

• · Complete history collection regarding cause and origin of Diabetes Insipidus. Hourly intake and output should be recorded.
• · Physical examination: frequent monitoring of vital signs, body weight, skin turgor, level of consciousness are necessary.
• · Urine specific gravity less than 1.005 indicates Diabetes Insipidus.
• · Urine osmolality less than 100mmol/kg indicates Diabetes Insipidus..
• · Serum osmolality greater than 295mmol/kg indicates Diabetes Insipidus.

Water deprivation test:

Use to find cause of polyuria. All fluids are withheld for 8 to 16 hours. During the test patient’s blood pressure, weight and urine osmolality are assessed hourly. ADH is administered IV or subcutaneously and urine osmolality is measured one hour later. In central DI the rise in urine osmolality after vasopressin exceeds 9%. In nephrogenic DI there is no response to ADH.

Treatment

Goal: maintenance of fluid and electrolyte balance.

Pharmacological management.

• · Fluid replacement: hypotonic saline is administered intravenously.
• For central diabetes Insipidus-

Hormone replacement:

• Desmopressin acetate(DDAVP) can be administered orally,intravenously or as nasal spray.
• Aqueous vasopressin( pitressin)
• Vasopressin tenate
• Chlorpropamide( diabinese)
• Carbamazepine (tegretol)

For nephrogenic diabetes insipidus-

• Dietary measures: limiting sodium intake to less than 3 g per day help to reduce urine output.
• Thiazide diuretics: they are able to slow glomerular filtration rate and allows the kidney to reabsorb more water. E.g. hydrochlorothiazide (hydroDiuril), chlorothiazide (Diuril).
• Indomethacin (indocin).

 

Nursing diagnosis

1. Fluid volume deficit related to excessive urinary output as manifested by increased thirst and weight loss.
2. Sleeping pattern disturbances, insomnia related to nocturia as manifested by verbalization of patient about interrupted sleep
3. Activity intolerance related to fatigue and frequent urination as manifested by weakness and fatigue of the patient.
4. Anxiety related to course of disease and frequent urination as manifested by verbalization of anxious questions.
5. Ineffective coping related to frequent urination as manifested by verbalization of negative feeling by the patient.
6. Risk for complications related to excessive loss of fluid from the body as manifested by hypotension and weight loss.
7. Knowledge deficit regarding management of diabetes insipidus as manifested by verbalization of doubts by the patient.

Interventions

1. Fluid volume deficit related to excessive urinary output as manifested by increased thirst and weight loss.
Ø Assess the fluid level of the patient
Ø Monitor vital signs frequently
Ø Restrict oral fluid intake.
Ø Administer hypotonic saline intravenously.
Ø Administer medications if ordered.
 
2. Disturbed sleeping pattern, insomnia related to nocturia as manifested by verbalization of patient about interrupted sleep.
Ø Assess the sleeping pattern of the patient
Ø Give psychological support.
Ø Advice the patient to restrict oral fluids
Ø Provide calm and quiet environment.
 
3. Activity intolerance related to fatigue and frequent urination as manifested by fatigue and weakness of the patient.
Ø Assess the activity status of the patient
Ø Give psychological support to the patient.
 
4. Anxiety related to course of disease and frequent urination as manifested by verbalization of anxious questions.
Ø Assess the anxiety level of the patient.
Ø Explain the patient about the disease and treatment.
Ø Provide calm and quiet environment.
Ø Divert the attention of the patient by talking about different matter.
 
5. Ineffective coping related to frequent urination as manifested by verbalization of negative feeling by the patient.
Ø Assess the coping ability of the patient
Ø Explain the patient about the disease and treatment
Ø Give psychological support.
 
6.Risk for complications related to excessive loss of fluid from the body as manifested by hypotension and weight loss.
Ø Assess the fluid volume of the patient
Ø Monitor vital signs frequently.
Ø Take immediate measures to restore fluid volume such as IV fluid therapy
Ø Administer medications as ordered.
 
7. Knowledge deficit regarding management of diabetes insipidus as manifested by verbalization of doubts by the patient
Ø Assess the knowledge level of the patient.
Ø Explain the management of diabetes insipidus to the patient.
 
Summary
Diabetes insipidus cause frequent urination, even at night, which can disrupt sleep. Patient feels excessive thirst by the stimulation of osmoreceptor response. Because of the excretion of abnormally large volumes of dilute urine, patient may quickly become dehydrated if do not drink enough water. It can be treated with fluid replacement and hormone replacement therapy.

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Acromegaly(Gigantism)

Anterior pituitary gland produces Growth Hormone which stimulate the growth of bodily tissues. Hyperpituitarism, also called acromegaly and gigantism. It results in longitudinal growth of long bones. These children may grow as tall as 8 feet. In adults excessive Growth Hormone cause acromegaly. Because this develops after epiphyseal closure in adults, the bones are unable to grow longer. Instead, the bones increase in size and width.
 

Definition

Acromegaly is the overgrowth of the bones and soft tissues due to excessive secretion of the growth hormone.

Incidence

Acromegaly is uncommon; only three to four cases are diagnosed per million people each year. It develops very gradually and may not be recognized until it has been present for many years. hyperpituitarism occurs equally among men and women. The mean age at diagnosis is about 40-60 years.

 

Causes

It is caused by prolonged, excessive secretion of growth hormone (GH). The most common cause of acromegaly is a benign tumour (adenoma) of the somatotroph cells, which produce growth hormone. These cells are within the anterior pituitary gland, located in the middle of the head just below the brain.
 

Pathophysiology

In adults excessive Growth Hormone cause overgrowth of bones and tissues. Because this develops after epiphyseal closure in adults, the bones are unable to grow longer. Instead, the bones increase in size and width. It results in structural changes of the skeletal system. It develops gradually, usually during the third and fourth decades of the life. Individuals experience enlargement of hands and feet. The fingertips develop a tufted or clubbed like appearance. The enlargement of bones and cartilage may cause mild joint pain to deforming, clipping arthritis.
Changes in physical appearance occur with thickening and enlargement of bony and soft tissue on the face and head. Enlargement of mandible causes jaw to jut forward. The paranasal and frontal sinuses enlarges. Enlargement of soft tissue around eyes, nose and mouth results in hoarsening of facial structures. Enlargement of tongue results in speech difficulties, and the voice deepens as a result of the hypertrophy of the vocal cords.
 

Overproduction of growth hormone -- Enlargement of viscera without increase in height -- fingertips develop a tufted or clubbed like appearance -- mild joint pain to deforming, clipping arthritis -- Enlargement of mandible -- The paranasal and frontal sinuses enlarges --- Enlargement of soft tissue around eyes, nose and mouth -- Change in facial structures

 

Clinical manifestations

Excessive growth of soft tissue, cartilage, and bone in the face, hands and feet.
Face and head — Facial features (nose, lips, ears, and forehead) become broader and larger the tongue enlarges, the space between the teeth increases, and the lower jaw grows, resulting in an under bite and extended lower jaw.
headache may be present.
Facial hair growth increases, which may be especially bothersome to women.
Throat — Excessive soft tissue growth of the throat and voice box can lead to a hoarse voice or sleep apnoea (a condition in which a person stops breathing temporarily during sleep, causing lowered levels of oxygen and disrupted sleep).
Hands and feet — The hands and feet enlarge, often requiring patients to wear larger sized rings, gloves, and shoes. Overgrowth of tissues in the wrist can compress nerves to the hands, leading to tingling or pain in the fingers (called carpal tunnel syndrome).
Skin — The skin may thicken, and skin tags may appear. Excessive sweating, even while resting, is common.
Bones — Overgrowth of the ends of bones can damage neighbouring cartilage and lead to arthritis.
Tumors — Patients with acromegaly have an increased risk of noncancerous (benign) tumors, especially if growth hormone levels are not controlled. Benign tumors of the uterus (fibroids) are more common in acromegaly. Polyps of the colon are more common, and can become cancerous if not surgically removed.
Heart — The incidence of heart disease is increased, likely due to enlargement of the heart muscle, which impairs functioning of the muscle (called cardiomyopathy). High blood pressure is more common in acromegaly. Some people have problems with their heart valves. Heart failure may occur if acromegaly is uncontrolled.
Diabetes — Higher blood glucose levels may be a direct result of excessive growth hormone production, which causes insulin resistance. Diabetes is more common in people with acromegaly, and people with previously diagnosed diabetes may require higher doses of medication.
Life expectancy may be reduced by approximately 10 years, especially when growth hormone levels are uncontrolled and diabetes and heart disease are present. Patients with controlled hormone levels generally have a normal life expectancy.

Diagnostic studies

· If acromegaly is suspected based upon a person's appearance, the diagnosis must be confirmed by measurement of IGF-1 and growth hormone levels. The blood level of IGF-1 can be determined in a single blood sample drawn at any time of day.
· Growth hormone must be measured by taking several samples of blood, drawn before and after drinking a glucose (sugar) solution. In acromegaly GH concentration do not fall.
· Plasma GH evaluation.
· MRI: Once excessive growth hormone secretion has been confirmed, magnetic resonance imaging (MRI) is indicated for identification, localisation ane determination of extension of the pituitary tumour.
· CT scanning may also be used to locate the tumour.
· A complete ophthalmologic examination, including visual fields to assess pressure of macroadenoma on optic nerves.

Treatment

Patients with acromegaly are treated to avoid the risk of complications, even if there are no obvious symptoms. The goal of therapy is to lower the level of growth hormone and IFG-1 in the blood. If therapy is successful, the soft tissue changes will regress over a period of several months and the risk of early death returns to normal. Sometimes, initial treatment is not entirely successful and additional treatment is needed.
There are three main forms of treatment: surgery, medications, and radiation therapy.
 

Surgery

Surgery offers the chance of a cure if the somatotroph adenoma can be completely removed. Surgery is also the first choice of treatment when the adenoma is very large and impairing or threatening vision.
During surgery, a small incision is made in the nose. The incision is extended through the sphenoid sinus, allowing the surgeon to visualize and remove the adenoma. An endoscope (a thin, lighted tube with a camera) may be used to ensure that the adenoma has been removed completely. Alternately, the entire procedure may be performed using the endoscope.
Surgery is usually effective in reducing growth hormone levels, although levels do not always return to normal. The chance that the growth hormone levels will be normal after surgery is directly related to the size of the adenoma before surgery. The levels of growth hormone and IGF-1 will return to normal in about eighty percent of people with small adenomas (less than 1 cm [0.5 inch]). On the other hand, only about 30 percent of people who have larger adenomas that extend beyond the pituitary will have normal hormone levels after surgery.
If the adenoma is completely excised, the blood GH level falls to normal within hours after surgery and the blood IGF-1 level returns to normal within weeks to months.

Medications

There are three classes of medications used to treat acromegaly:

• Somatostatin analogs (octreotide or lanreotide)
• Dopamine agonists, especially cabergoline
• Growth hormone receptor antagonist (pegvisomant)

Somatostatin analogs — Somatostatin analogs inhibit secretion of growth hormones from the growth hormone-secreting cells of the pituitary.
Ø Octreotide (Sandostatin) is made in short-acting and long-acting forms. The short-acting form is given three times a day by injection, and the long-acting form is given every four weeks by injection.
Ø Lanreotide (Somatuline) is available in a long-acting form that is injected every four weeks.
These medications can be used as an initial treatment, especially when an adenoma is too large to remove completely with surgery. They can also be used as secondary treatment for people who have remaining adenoma tissue and an elevated blood growth hormone concentration after transsphenoidal surgery.
· Growth hormone receptor antagonist — Growth hormone receptor antagonists block the effects of growth hormone by binding to the hormone receptor, decreasing IGF-1 production and thereby decreasing growth effects. Pegvisomant (Somavert®) is given daily by injection.
· Dopamine agonists — Dopamine agonists may inhibit growth hormone secretion and therefore decrease IGF-1 levels, although they are not usually as effective as other classes of medications. They can be taken orally and may be more convenient than other forms of treatment.

Radiation therapy

Radiation therapy has been used for many years for treatment of pituitary adenomas, including somatotroph adenomas. Radiation can be delivered in one of several ways:

A linear accelerator
A cobalt source (gamma radiation)
A cyclotron (proton beam)

Radiation can be given as a single large dose or in multiple smaller doses. Whatever the source and number of doses, the radiation is directed stereotactically (three-dimensionally) to the adenoma by a computerized program.
Radiation therapy is usually effective in stopping or even reversing adenoma growth, and in decreasing growth hormone and IGF-1 production. However, the decline in growth hormone secretion (and clinical improvement) is very slow. Even 10 to 15 years after radiation, only a small percentage of patients achieve a normal blood growth hormone level.
Complications of treatment
The chance of serious complications, such as worsening of vision, hormonal imbalance, meningitis, nasal leakage, or very rarely, death, is less than 5 percent. The chance of damage to the pituitary gland is about 7 percent; Within 10 years after treatment, about 50 percent of patients treated with pituitary radiation develop a deficiency of one or more pituitary hormones, including the hormones that control the thyroid gland, adrenal glands, and ovaries or testicles.
 

Nursing diagnosis

1. Disturbed body image related to enlargement of body parts as manifested by enlarged hands, feet and jaw.
2. Disturbed sensory perception related to enlarged pituitary gland as manifested by protrusion of eye balls .
3. Fluid volume deficit related to polyuria as manifested by excessive thirst of the patient.
4. Disturbed sleeping pattern related to soft tissue swelling as manifested by verbalization of the patient about insomnia.
5. Anxiety related to change in appearance and treatment as manifested by verbalization of the patient about body appearance.
6. Ineffective coping related to change in appearance as manifested by verbalization of negative feeling about the change in appearance.
7. Knowledge deficit regarding development of disease and treatment as manifested by repeated questions by the patient regarding disease and treatment.

Interventions
1. Disturbed body image related to enlargement of body parts as manifested by enlarged hands, feet and jaw.

o Assess the body changes of the patient.
o Give psychological support.

2. Disturbed sensory perception related to enlarged pituitary gland as manifested by protrusion of eye balls.

o Assess the sensory perception status of the patient
o Administer medications if ordered

3. Fluid volume deficit related to polyuria as manifested by excessive thirst of the patient.

o Assess the fluid and electrolyte status of the patient.
o Provide more oral fluids to the patient.
o Administer IV fluids if ordered.

4. Disturbed sleeping pattern related to soft tissue swelling as manifested by verbalization of the patient about insomnia.

o Assess the sleeping pattern of the patient.
o Provide comfortable position to the patient.
o Provide calm and quiet environment.

5. Anxiety related to change in appearance and treatment as manifested by verbalization of the patient about body appearance.

o Assess the anxiety level of the patient
o Explain the patient about progressive features of the disorder
o Divert the attention of the patient by talking.

6. Ineffective coping related to change in appearance as manifested by verbalization of negative feeling about the change in appearance.

o Assess the coping ability of the patient.
o Provide psychologic support to the patient.

7. Knowledge deficit regarding development of disease and treatment as manifested by repeated questions by the patient regarding disease and treatment.

o Assess the knowledge level of the patient regarding features and treatment of the disorder.
o Explain the patient about progressive features of the disorder.
o Clarify patient’s doubts and questions regarding hyperpituitary disorder.

Technorati Tags: anterior pituitary gland,excessive secretion,Hyperpituitarism,Acromegaly,Gigantism,nursing management,nursing managment

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Assessment of Endocrine System

Hormones affect every body system and organs, causing great diversity in the signs and symptoms of endocrine dysfunction. Endocrine dysfunction may result from excessive or deficient hormone secretion, transport abnormalities, an inability of the target tissue to respond to a hormone or inappropriate stimulation of the target tissue receptor.

 

Subjective Data

The lack of clear cut manifestations of endocrine problems requires a conscientious and detailed heath history.
 

1.Health Information

· past health history :- The patient should be questioned about general state of health and previous and current endocrine abnormalities.
· medications :- The patient should be questioned about the use of all medications and dietary supplements.
· surgery or other treatment :- Nurse should enquire about previous surgery, chemotherapy or radiotherapy
 

2.Functional health patterns

Heredity
Heredity plays a major role in a major role in the occurrence of endocrine problems. The patient should be questioned about endocrine conditions in family members.
Nutritional or metabolic pattern
Reported change in appetite and weight can indicate endocrine dysfunction. Weight loss with increased appetite may indicate huperthyroidism or diabetes mellitus. Weight loss with decreased appetite may indicate hupopituitarism or hypocortisolism. Weight gain indicate hypothyroidism. Difficulty in swallowing or a change in neck size indicate thyroid disorder or inflammation.
The patient should be questioned about dietary intake. This record should be examined for foods that contain thyroid- inhibiting substances.
Elimination pattern
Increased thirst and urination can indicate Diabetes Mellitus or Insipidus. Frequent defecation may indicate hyperthyroidism. constipation is also seen in patients with diabetes mellitus, hypothyroidism, hypoparathyroidism or hypopituitarism.
Sleep-rest pattern
The patient with diabetes will complain of nocturia which can severely disrupt normal sleep patterns. The hyperthyroid patient may complain about inability to sleep. The hypothyroidism and hypopituitarism patient may sleep all the time, yet still being fatigued.
Cognitive-perceptual pattern
A patient with an endocrine dysfunction will frequently manifest apathy and depression. Memory deficits and an inability to concentrate are common in endocrine disorders.
Objective Data
Most endocrine glands are inaccessible to direct examination.

Physical Examination

1.Vital signs

Variations in temperature may associated with thyroid dysfunction. Cardiovascular changes such as bradicardia , tachycardia, hypotension or hypertension maybe seen with endocrine problems.

2.Height and weight

Changes in weight may be associated with endocrine problems. Growth pattern abnormalities suggest problems associated with growth hormone. Thyroid disorders and diabetes mellitus are example for disorders that can affect body weight.

3.Integument

The nurse should note the colour and text of the skin, hair, and nails. The hair distribution should be noted on the head, face,trunk, and extremities. Dull brittle hair, excessive hair growth or hair loss indicates endocrine dysfunction.

4. Head

The size of the head should be examined. Facial features should be symmetric. Eyes should be inspected for position shape and eye movement.

5. Neck

When inspecting the thyroid gland first observation should be made in the normal position, then in slight extension, and then as the patient swallows some water. The trachea should be in midline and neck should appear symmetric. If there is no noticeable enlargement of the thyroid gland, palpation can be done. Water should be available for the patient t swallow as a part of the examination. There are two types of thyroid palpation.

For anterior palpation the nurse stands in front of the patient, with patient’s neck flexed. The thumb is placed over the cricoid cartilage and moved over the isthmus as the patient swallows. Then each lateral lobe is palpated before and while the patient swallows water.

For posterior palpation , examiner stands behind the patient. With thumb of both hands rest on nape of the neck of the patient, uses the index and middle fingers for the thyroid isthmus and for the anterior surfaces of the lateral lobes. The thyroid is palpated for size shape, symmetry, tenderness and for any nodules.

6. Extremities

The size ,shape, symmetry, and general proportion of hand and feet should be noted. Muscle strength and deep tendon reflexes should be noted. In the upper extremities, the presence of tremors is assessed by placing a piece of paper in the outstretched fingers, palm down.

Diagnostic studies

Pituitary studies

Ø Growth hormone (GH) (somatotrophin) Ø Somatomedin C Ø Growth hormone Stimulation test. Ø Water deprivation test Radiologic studies- Ø MRI:

Ø <5ng/ml in men, <10ng/ml in women, values >50ng /ml suggest acroegaly. Ø normal values are 135-250ng/ml Ø IGF-1 low level- GH deficiency, high level-GH excess . Ø measures GH secretion in response to insulin. Baseline blood levels for GH, glucose obtains before administration of IV insulin GH should rise twofold over baseline. Response is subnormal in GH deficiency. Ø use to find cause of polyuria. ADH is administered IV or subcutaneously. In central DI, urine osmolality increases after ADH administration. In nephrogenic DI there is no response to ADH. Ø useful in identification of tumour involving hypothalamus or pituitary.

Thyroid function tests

Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. TFTs may be requested if a patient is thought to suffer from hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid), or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy.

Ø Thyroid – stimulating hormone(TSH) Ø Thyroxine(T4) Ø Triiodothyronin(T3) Ø Free T4 Ø T3 resin uptake Radiological studies Ø Radioactive iodine uptake Ø Thyroid scan

Ø normal 0.3-5.4mu/L Ø 51-142nmol/L. useful in evaluating thyroid function Ø 65-195ng/dl. Helpful in diagnosing hyperthyroidism. Ø 1-3.5ng/dl Ø indirectly measures binding capacity of thyroid- binding Globulin. Normal 25%-35%. Ø patient is given radioactive iodine orally or IV. The uptake by the thyroid gland is measured with a scanner at intervals of 2to 4 hours and at 24 hours. Normal values are 3%-19% for 2-4 hours and 11%-30% for 24 hours. Ø radioactive isotops are given orally or IV. In scan benign nodules appear as warm spots. Malignant tumors appear as cold spots.

 

Parathyroid studies

Ø Parathyroid hormone(PTH) Ø Total serum calcium Ø Serum phosphate

Ø measures PTH level in serum. Ø normal 9-11 mg/dl. Hypercalcemia indicate hyperparathyroidism Ø hyperphosphatemia indicates hypopaathyroidism. Normal 2.8-4.5 mg/dl.

 

Adrenal studies

Ø Cortisol Ø Aldosterone Ø Adrenocorticotropic hormone(ACTH) Radiological studies Ø Computed tomography (CT)

5-25mg/dl at 8am,10mg/dl at 8pm. 5-20ng/dl <80pg/ ml-morning, <50pg/dl-evening. use to detect tumour and size of tumour mass.

 

Pancreatic studies

Serum studies Ø Fasting blood sugar(FBS) Ø Oral glucose tolerance Urine studies Ø Glucose Ø Ketones Radiologic studies Ø Computed tomography(CT)

Ø measures circulating glucose level. Normal 70-110mg/dl. Ø patient drinks 75g of glucose, samples for glucose are drawn immediately,and at 30,60,120 minutes. Normal values: <200mg/dl at 30,60 min. and <140mg/dl at 1 hr. Ø normal value is negative. Ø normal value is negative. Ø used to identify tumors or cysts.

Technorati Tags: hormone secretion,thyroid disorder,endocrine,endocrine problems,diagnosis

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