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Endocrine system

Lecture 19

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Anatomy & Physiology

The endocrine system controls the cellular activity that regulates growth & body metabolism through the release of hormones.

The hormones are chemical messengers secreted by various glands.

These glands includes: hypothalamus, pituitary, thyroid, thymus, adrenal, pancreas, ovaries & testes.

The male embryo begins to secrete testosterone at 7-8 weeks of gestation, which cause the gonads to differentiate into testes.

On the other hand, the female embryo secretes estrogen, causing the gonads to differentiate into ovaries.

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Diagnostic procedure

CT scan.

MRI.

Thyroid scan.

ACTH stimulation test.

Adrenal ACTH suppression test.

Fasting glucose.

Hormones level.

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Disorders of the thyroid function

Hypothyroidism

Thyroid gland secrets triiodothyronine (T3) & thyroxine (T4) that stimulated by TSH from pituitary gland, that responsible in regulating the metabolic rate of the cells, body heat production, protein, fat, & carbohydrate metabolism in the cells.

Hypothyroidism is an disorder in which the levels of active thyroid hormones are decreased.

It may be congenital or acquired. It occur mostly in children with Down syndrome & more common in girls than in boys.

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When these hormones are not available to stimulate other hormones or specific target cells, growth is delayed & mental retardation develops.

Exposure to drugs as lithium, or to infection in thyroid gland ( Hashiomoto’s thyroiditis) would lead to the acquired form of hypothyroidism.

While in case of spontaneous gene mutation would lead to congenital hypothyroidism.

if hypothyroidism is not treated in infants, child will show a thickened wide tongue, thick lips, dull appearance in the few months of life.

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Other signs includes prolonged neonatal jaundice, hypotonia, respiratory distress, bradycardia, decreased pulse pressure, cool extremities, umbilical hernia, large posterior fontanel, poor feeding, lethargy, constipation, horse cry.

Older children show symptoms as adults includes: decreased appetite, bradycardia, cool skin, constipation, thin hair, or hair loss, sensitivity to cold temperature, abnormal menses, & goiter (a non tender enlarged thyroid gland).

Some children shows changes in normal growthpatterns with increase weight & decrease height velocity, delayed bone & dental age, muscle atrophy, & weakness.

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Diagnostic test

Congenital hypothyroidism is detected in newborn screening of T4 & TSH levels, which is mandatory in all hospitals.

When the T4 level is low, & elevated TSH level; it indicate that the problem originate in the thyroid not the pituitary.

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Clinical therapy If the problem in the low levels of T4 & TSH levels is

increased; then a synthetic thyroid hormone levothyroxine is prescribed.

The dose of hormone is increased as the child grows, to ensure a euthyriod state (thyroid hormone in appropriate balance).

Antithyroid antibodies are measured in children with goiter & suspected Hashiomoto’s thyroiditis.

To ensure adequate growth & prevent mental retardation, the hormone must be taken throughout life.

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Nursing managements

Teach the parents about the disease.

Explain how to administer the hormone which is available in only tablet form (crush tablet & put it in formula).

Educate parents that the child would experience sleep changes, behavioral disturbances during therapy.

Dress the child appropriately to prevent hypothermia.

Modify diet to decrease constipation if present.

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Hyperthyroidism

Is a disorder of excessive levels of circulating thyroid hormones. It is more common in adolescent female due to Grave’s disease.

Grave’s disease is an autoimmune disease in which immunoglobulins produced by the B lymphocytes stimulate over secretion of thyroid hormones, resulting in hyperthyroidism.

it also could result from thyroid tumors, thyroiditis, as well as pituitary adenomas.

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Clinical manifestations

Signs & symptoms are caused by hyperactivity of the sympathetic nervous system.

These includes: an enlarged non tender thyroid gland (goiter), prominent eyes (exophthalmos), eyelid lag, tachycardia, nervousness, restlessness, irritability, increased appetite with weight loss, tremor, weakness, insomnia, diaphoresis.

The disease is diagnosed by serum TSH, T3, T4 levels & thyroid scan. It reviled elevated T3, T4 & decreased TSH levels.

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Clinical therapy

The goal is to inhibit excessive secretion of the hormones.

Antithyroid drug therapy, radiation therapy, or surgery are usually used.

Methimazole & propylthiouracil are given to inhibit thyroid hormone secretion. This therapy have side effects such as skin rashes, urticaria, & lymphadenopathy.

Treatment continues for 18 months to 2 years, or until thyroid decrease in size.

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Beta-adrenergic blocking agents such as propranolol may be given to relive symptoms of tremors, tachycardia, & restlessness.

If drug treatment is not effective, radiation therapy using oral radioactive iodine is the nest treatment choice.

Nurses must focus on teaching the child & parents about the disorder & its treatment, promoting rest, providing emotional support.

Promote increase caloric intake by providing five or six meals.

Encourage the parents to provide cool environment & dress less clothes to their child.

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If surgery performed, the nurse postoperatively must elevate the head of the bed to 30 degrees & assess the child for bleeding, hoarseness, difficulty of breathing, & thyrotoxicosis.

Thyrotoxicosis is resulted from sudden release of the thyroid hormones into the blood stream during surgery.

The child would have fever, diaphoresis, tachycardia, palpitations, muscle weakness, hypertension, & tremors due to sympathetic nervous system hyperactivity.

Treatment include antithyroid drugs & propranolol. The heart & blood pressure needs to be monitored frequently.

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Disorders of pancreatic function

Pancreas secrete multiple hormones that includes insulin that facilitate the cellular glucose utilization, glucagon that increase blood glucose when levels are low by stimulating glycogenesis.

As well as somatostatin that inhibits insulin & glucagon secretion (help in regulation of pancreatic function).

Any dysfunction of these hormones will leads to

Type 1 Diabetes or, Type 2 Diabetes.

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Diabetes Mellitus Is a disorder of hyperglycemia resulting from

defects in insulin secretion, insulin action or both.Leading to abnormalities in carbohydrates, protein & fat metabolism.

It has two main types:

1. Type 1 diabetes: insulin dependent Diabetes Mellitus or juvenile diabetes.

2. Type 2 diabetes: non-insulin dependent diabetes mellitus.

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Type 1 diabetes mellitus:

It is multifactorial disease caused by autoimmune destruction of insulin producing pancreatic beta cellsin genetically predisposing individuals.

it believed that an virus can trigger the inflammatory process, resulting in development of islet cells serum antibodies.

Environmental factors are believed to lead to autoimmune destruction of the beta cells of islet of Langerhans.

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It has a familial tendencies, but does not show any specific pattern of inheritance. As the child inherit the susceptibility to the disease not the disease itself.

As insulin helps transport glucose into the cells so that the body can use it as an energy source. It also prevents the outflow of glucose from the liver to the general circulation.

If an autoimmune destruction of the cells continues, the secretion of insulin will decrease, leading to increase levels of glucose in the blood (hyperglycemia(>180 mg/dl), increase level of glucose in urine (glycosuria) and large amount of fluid are shifted out body due to the high osmosis of glucose & water excreted by urine leading to polyuria.

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When glucose is not available for the cells for metabolism, free fatty acid provide an alternative source of energy that produced by the liver.

The by-products of these fatty acids (ketone bodies) will accumulate in body resulting in a state of metabolic acidosis or Ketoacidosis.

The classic signs of type 1 diabetes are:

Polyuria, polydipsia, & polyphagia (excessive appetite).

In addition to fatigue, lethargy, weight loss, headache.

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Diagnostic tests

Diagnosis is based on the presence of classic symptoms & plasma glucose levels as follows:

1. Fasting blood glucose > 126 mg/dl, no caloric intake for at least 8 hours.

2. Two-hour plasma glucose > 200 mg/dl, during an oral glucose tolerance test.

3. Plasma glucose concentration > 200 mg/dl, taken at any time of day regardless of time of last meal.

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Clinical therapy Insulin therapy:

Child on insulin therapy need to be monitored every 4-8 times daily for his blood sugar, count carbohydrates consumed & anticipate exercise on the daily routine.

Also, HbA1c must be monitored every 3 months when the child is started on insulin therapy, to monitor the glucose control over period of 6-8 weeks prior the examination day.

Exercise program:

Physical activity is associated with increase insulin sensitivity. 30- 60 minutes daily is needed. Exercise improve allover well being

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durationpeakOnset Type

3-4 hour0.5-2 hour5-10 minRapid acting

6-8 hour2-5 hour½-1 hourShort acting

12-18 hour5-8 hour1-3 hourIntermediate acting

22-26 hour8-15 hour1.5-4 hourLong acting

20-24 hournone3-4 hourVery long acting

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Nutritional therapy:

Consumption of carbohydrate is needed according to the body need, age of the child & amount of insulin given to the child.

Younger school aged child can consume 2 -4 carbohydrate choice in one meal while adolescent can consume 4- 6.

Generally one unit of insulin can covers 8 grams of carbohydrate, so calculation can be easy.

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Nursing interventions Provide education:1. Assess the child’s & family learning needs. 2. Provide over view of DM as a chronic disease. 3. Teach parents about the insulin therapy. 4. Educate the child or family how to draw insulin and it

storage.5. Educate the child or family how self inject insulin.6. Inform them that rotating is important, to prevent

lipoatropy (loss of subcutaneous tissue) or hypertrophy (replacement of collagen instead of fat cells).

7. Educate about sites of injection8. Educate the parent what to do in sick day care.&

monitoring of BGL.

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Manage food intake:

1. 50-55 % the child calorie will be from carbohydrate, 15-20 % from proteins, 30% from fat.

2. Educate parents that eating t consistent intervals is important for glycemic control.

Provide emotional support:

1. As the diagnosis of DM is a shock for the family, it is important for nurses to help family in emotional expression & relive the sense of guilt that they usually feel.

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Hypoglycemia

It can be develop within minutes in children with type 1 DM, the symptoms occur rapidly.

It caused by:

1. insulin dose too high for food eaten.

2. Insulin injection into muscles.

3. Too much exercise for insulin dose.

4. Too few carbohydrate eaten.

5. Illness, stress.

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Rapid onset:

Irritability, nervousness, tremors, unsteady feeling, difficulty in concentration & specking, behavior changes, confusion.

Pallor, sweating, hunger, headache, dizziness, blurred vision, double vision, photophobia.

Hypoglycemia

Gradual onset:

Lethargy sleeplessness, slow response, confusion, deep rapid breathing, flushed skin, dry skin, dry mucus membrane, thirst, hunger, dehydration, weakness, abdominal pain, vomiting, nausea, blurred vision & shock.

Hyperglycemia

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Management:

Hypoglycemia needs urgent treatment, as shown previously of signs of both hypoglycemia & hyperglycemia. It is difficult to distinguish them.

So in emergent situation, give glucose to the child immediately in form of glucose tablet, sugar gel, drink high in sugar.

In hospital, administer an intravenous infusion of D5W and if the child become unconscious give glucagon injection to the child or increase infusion rate.

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Type 2 diabetes Is a disease that associated with obesity & insulin

resistance (an impairment of cell receptors on cell membrane, leading to inability to transfer sufficient amount of glucose into cells).

Risk factors for type 2 diabetes are obesity, low activity levels, high fat diet. Child with BMI > 85th

percentile. With an increased of body weight, the visceral fat

produces a cytokine hormone (tumor necrosis factor), that desensitizes the insulin receptor within cells to insulin.

In response, production of insulin is increased & a state of hyperinsulimia occur. That continue until the increased insulin resistance & high level of insulin leads to dysfunction of the Beta cells. & no longer produce insulin.

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Clinical manifestations

Little or no weight loss, polyuria, polydipsia, glycosuria, Ketoacidosis, lipid disorder, hypertension.

Acanthosis nigricans, hyperpigmentation & thickening of the skin of axilla, neck, elbows, knees, & abdomen. Associated with chronic hyperinsulinemia.

The diagnosis is made for blood glucose level of 200 mg/dl without fasting, or fasting glucose more than 126 mg/dl.

Fasting sugar is high as well as C-peptide in children with type 2 diabetes.

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Clinical therapy The treatment is directed into decreasing weight,

blood sugar, lipid profile, blood pressure, & prevent complications.

If the child has sever Ketoacidosis, insulin is needed, once balance is gained, oral medication (metformin) is initiated.

This medication improve receptor sensitivity to insulin, reduce hepatic & renal glucose production.