Nursing 250 Endocrine Disorder Assignment

Nursing care of a child with an endocrine disorder. Jalissa Twyman, 8 years old, was admitted to the pediatric intensive care unit with a closed head trauma after being involved in a bicycle/motor vehicle accident. Jalissa is unconscious. The nurses caring for Jalissa document a weight loss of 1.82 kg over a 24- hour period, decreased skin turgor, and dry mucous membranes. Urine output for the same 24-hour period is 3.5 L/m2. (a) What further assessments should the nurse perform on Jalissa? (b) What laboratory tests would the nurse expect to be performed on Jalissa? (c) What nursing interventions should be done for Jalissa?

a. What further assessments should the nurse perform on Jalissa?

b. What laboratory tests would the nurse expect to be performed on Jalissa?

c. What nursing interventions should be done for Jalissa?

Other Answers

(a) Further assessments

■ Tachycardia

■ Urine concentration

 ■ Increased respiratory rate

 (b) Lab Tests Nursing 250 Endocrine Disorder Assignment

■ UA

■ Fluid deprivation test

■ CT scan, MRI, or ultrasound of kidneys and the skull

■ Serum sodium

 ■ Serum osmolarity

 (c) Nursing Interventions

■ Promoting hydration

■ Administration of ordered medications

■ Maintenance of nasogastric feeding tube

■ Comfort measures

■ Frequent monitoring of vital signs

■ Emotional support for Jalissa and her family

Pain assessment

It’s 8 p.m. on Tina Jones’ first day as a patient here at Shadow General Hospital. Your role in this simulation is that of a healthcare provider who will perform a full abdominal exam on Ms. Jones. She’s spent the whole day in bed, so you will want to determine whether she has full abdominal function and if bed rest has impacted her gastrointestinal health.

In your interview with Ms. Jones, you will ask about her inputs and outputs (I’s and O’s) and the overall health of her abdominal system so that you can identify any issues and document findings accurately. If you discover any disease states, ask about the symptoms and the patient’s experiences of them.

 Multiple gland failure

This is caused by autoimmune disease as detailed. Commonest are the associations of primary hypothyroidism and type 1 diabetes, and either of these with Addison’s disease or pernicious anemia.

Multiple endocrine neoplasia

This is the name given to the simultaneous or metachronous recurrence of tumors involving a number of endocrine glands. They are inherited in an autosomal dominant manner and are thought to arise from the expression of a recessive oncogenic mutation, which has now been isolated.

Affected persons may pass on the mutation to their offspring in the germ cell, but for the disease to become evident a somatic mutation must also occur, e.g. deletion or loss of a normal homologous chromosome. The defect in MEN 1 is on the long arm of chromosome 11 near an area containing a number of oncogenes that encode for proteins with fibroblast growth factor activity. The gene for MEN 2a is on chromosome 10 close to the retinol binding gene.Screening unaffected members of a family shows that a significant number of affected individuals are unrecognized, especially with hypercalcaemia.



 Endocrine Disorder Assignment


 Treatment is surgical.

TYPE 1. All four parathyroid glands are removed (as all may be involved) followed by vitamin D (1,25- dihydroxycalciferol) replacement therapy. Pancreatic tumors are often multiple and recurrence after partial pancreatectomy is invariable. Other tumors are treated surgically if necessary.

 TYPE 2. Tumors may also be recurrent or bilateral and a careful follow-up is necessary.


 Anxiety or panic attacks Palpitations


 Sweating Headache Flushing

Nausea and/or vomiting Weight loss

Constipation or diarrhea Raynaud’s phenomenon Chest pain Polyuria/nocturia


 Hypertension-intermittent or constant Tachycardia plus arrhythmias Bradycardia Orthostatic hypotension Pallor or flushing Glycosuria


 (Signs of hypertensive damage)


A careful family history should first be taken. If negative, it does not exclude involvement and it may need repeating at regular (1-5 year) intervals.

1 Type 1. Fasting calcium estimation (if elevated, look for other manifestations of MEN 1). 2 Type 2

(a) Medullary carcinoma of thyroid (MCT). Pentagastrin and calcium infusion test with measurement of calcitonin to pick up ‘C’ cell hyperplasia: doubling of the calcitonin level is abnormal.

(b) Pheochromocytoma. VMA and metanephrine estimations.



This terminology refers to hormone synthesis, and normally secretion, from a neoplastic non-endocrine cell, most usually seen in tumors that have some degree of embryological resemblance to specialist endocrine cells. Multiple theories have been advanced to explain the occurrence. The clinical effects may be those of the hor- .mone produced, with or without manifestations of systemic malignancy.

The commonest situations seen are:

HYPERCALCAEMIA OF MALIGNANT DISEASE, often from squamous cell tumors of lung and breast, often with bone metastases. It is mediated by many different factors, but very rarely by PTH itself; a PTH-related protein (PTHrP) with considerable sequence homology has recently been isolated and appears to be the most frequent cause.

SIAD H. Again, this is commonest from a primary lung tumor. ECTOPIC ACTH

 SYNDROME. Small-cell carcinoma of the lung, carcinoid tumors and medullary thyroid carcinomas are the commonest causes.

PRODUCTION OF INSULIN-LIKE ACTIVITY may result in hypoglycemia.


Endocrine forms of treatment for malignancy have been used for many years, for example oophorectomy for breast cancer and orchiectomy for prostatic malignancy. Newer more acceptable therapies include the anti estrogen tamoxifen for breast carcinoma and the LHRH analogues, buserelin and goserelin, for prostatic cancer.