presentation endocrine Dysfunction.pptx

Pptx

1. Paediatric Health Nursing Endocrine Dysfunction G-BSN Year III, Semester V Male College Of nursing lyari Ms.Fauzia Rafiq Date 20 / 10 / 2025

2. Group Members: SHAHZAIB MAQSOOD ALAM NAVEED KHAN ASAD REHMAN MUHAMMAD YASEEN NOMAN DURAJ SHAH SAWAR KHAN SARFARAZ

3. Objectives : Ath the end of this unit the learner will be able to: Insulin Dependent diabetes mellitus (IDDM) and
Diabetic insipidus
Cushing syndrome.
Hyperthyroidism
Hypothyroidism
Hypopituitarism Hyperpituitarism Nursing Care approaches for dealing with above health problems
Pharmacological, medical and surgical management for the above

4. Insulin Dependent Diabetes Mellitus (Type 1 Diabetes) Insulin Dependent Diabetes Mellitus (IDDM), also known as Type 1 Diabetes Mellitus, is a chronic metabolic disorder in which the pancreas fails to produce sufficient insulin due to the destruction of beta cells in the Islets of Langerhans. As a result, blood glucose levels rise, leading to hyperglycemia. It usually develops in childhood or adolescence and requires lifelong insulin therapy for survival.

5. Type 1 diabetes is more common in children because their immune system is more active and can easily make mistakes that destroy insulin-producing cells.
Adults mostly have Type 2 diabetes, which is caused by lifestyle and body weight problems.

6. Pathophysiology: The autoimmune system destroys insulin- producing beta cells in the pancreas. Without insulin, glucose cannot enter the cells for energy, leading to increased blood glucose (hyperglycemia). The body begins to break down fats and proteins for energy, producing ketones that can lead to diabetic ketoacidosis (DKA). This process results in dehydration, electrolyte imbalance, and cellular dysfunction.

7. Signs and Symptoms: Polyuria – frequent urination
Polydipsia – excessive thirst
Polyphagia – excessive hunger
Weight loss Fatigue
Blurred vision
Irritability

8. Causes: Autoimmune reaction: The immune system attacks and destroys insulin-producing beta cells in the pancreas. Viral infections: Infections such as mumps, rubella, or Coxsackie virus can trigger the immune attack. Environmental factors: Low vitamin D, early exposure to cow’s milk, or toxins may contribute.

9. Diagnosis Evaluation: Blood Glucose Levels:
Fasting blood glucose ≥ 126 mg/dL.
Random blood glucose ≥ 200 mg/dL with classic symptoms.
Hemoglobin A1C ≥ 6.5%.
Urine Ketones: Present during DKA.

10. Pharmacology Management: Pharmacology (Insulin Therapy):
Rapid-acting – Lispro , Aspart Short-acting – Regular insulin
Intermediate – NPH
Long-acting – Glargine , Detemir

11. SURGICAL MANAGEMENT: Pancreas transplant
Islet cell transplantation

12. Medical Management: Regular blood glucose monitoring –Balanced diet with low sugar intake
Physical exercise under supervision
Health education on insulin use and diet

13. Complications : Acute Complications: Hypoglycemia
Diabetic ketoacidosis (DKA) Chronic Complications: Neuropathy (nerve damage)
Retinopathy (eye damage)
Nephropathy (kidney damage) Cardiovascular diseases
Peripheral vascular disease (gangrene)

14. Nursing Interventions: Monitor blood glucose levels regularly.. Administer insulin as prescribed Educate patient on diet, insulin injection, and lifestyle change.
Assess for signs of hypo/hyperglycemia. Encourage regular exercise and fluid intake. Monitor for complications (eye, kidney, and foot care).
Provide psychological support and health education.

15. Diabetes insipidus : DEFINITION: Diabetic Insipidus (DI) in children is a rare endocrine disorder characterized by the excretion of large volumes of dilute urine and excessive thirst due to insufficient production of Antidiuretic Hormone (ADH) or renal resistance to its effects. Unlike Diabetes Mellitus, DI does not involve elevated blood sugar levels but affects fluid balance.

16. Pathophysiology : In pediatric patients, Diabetic Insipidus occurs when the hypothalamus or posterior pituitary gland fails to produce adequate Antidiuretic Hormone (Central DI), or when the kidneys do not respond to ADH (Nephrogenic DI). ADH normally acts on the renal tubules to promote water reabsorption. Its deficiency or insensitivity leads to the production of excessive amounts of dilute urine, resulting in dehydration, increased serum sodium levels, and excessive thirst. If fluid losses are not replaced, severe dehydration and circulatory collapse can occur.

17. Signs & Symptoms: Polyuria (frequent urination) Polydipsia (excessive thirst)
Dehydration and dry mouth Failure to thrive or poor weight gain (in infants) rritability relieved by water but not milk Nocturia (frequent urination at night) Lethargy and fatigue
Constipation
Fever (in case of dehydration)

18. Causes: Genetic disorders, damage to the hypothalamus or pituitary gland from head injuries, surgery, tumors, or infections, and certain medications or medical conditions like kidney disease.

19. Diagnostic EVALUATION: Water Deprivation Test: Helps to differentiate DI from other causes of polyuria. ADH (Vasopressin) Test: Determines if the condition is central or nephrogenic. Urine Specific Gravity: Very dilute urine with a low specific gravity (<1.005). Serum Osmolality : Elevated, indicating increased blood concentration. Serum Sodium: Hypernatremia (serum sodium >145 mEq /L).

20. Pharmacology Management : Desmopressin (DDAVP): Synthetic ADH replacement via nasal spray, oral, or injection. Vasopressin: Short-acting hormone replacement. Thiazide diuretics: Reduce urine output in nephrogenic DI. NSAIDS (e.g., Indomethacin): Enhance renal response to ADH.

21. SURGICAL MANAGEMENT: Treatment of pituitary or hypothalamic tumors causing DI.
Repair of head trauma affecting ADH production.

22. MEDICAL MANAGEMENT: Ensure adequate hydration (oral or IV fluids). Monitor intake, output, and urine specific gravity. Regular assessment of electrolyte balance. Educate parents about signs of dehydration and medication use.

23. COMPLICATIONS : Severe dehydration.
Hypernatremia (elevated sodium levels). Hypovolemic shock.
Seizures (due to electrolyte imbalance). Brain damage (from prolonged dehydration).
Growth retardation (in chronic untreated cases).

24. NURSING INTERVENTIONS: Monitor child’s fluid intake and urine output carefully. Administer prescribed medications ( Desmopressin , Vasopressin).
Assess for dehydration signs: dry lips, sunken eyes, poor skin turgor.
Encourage oral fluids or IV therapy as ordered. Monitor weight daily and vital signs. Educate parents on medication adherence and emergency signs.
Maintain safe environment in case of weakness or confusion.
Provide emotional support to the family and child.

25. Cushing syndrome: DEFINITION: Cushing Syndrome in children is a hormonal disorder caused by prolonged exposure to high levels of cortisol. It results from either excessive cortisol secretion by the adrenal glands, a pituitary tumor producing ACTH, or long-term corticosteroid therapy. Cortisol plays a key role in metabolism and stress response, but in exXcess , it leads to serious metabolic and growth disturbances.

26. Pathophysiology : Cushing Syndrome develops when cortisol levels in the body remain abnormally high for an extended period. This can occur due to pituitary overproduction of ACTH (Cushing disease), adrènal tumors, ectopic ÀCTH secretion, or chronic steroid medication use. Elevated cortisol increases glucose levels, promotes fat deposition on the trunk and face, and leads to protein breakdown causing muscle wasting and thin skin. In children, it also suppresses growth hormone, leading to growth retardation.

27. SING & SYMPTOMS: Truncal obesity with thin limbs
Moon face (rounded face)
Buffalo hump (fat pad on upper back) Growth retardation or delayed puberty Muscle weakness and fatigue
Purple striae on abdomen and thighs
Hypertension
Increased risk of infection
Mood changes, iritability , or depression Easy bruising and slow wound healing.

28. Causes: Endogenous Causes: Pituitary adenoma (Cushing disease), adrenal tumors, or ectopic ACTH secretion. Exogenous Causes: Prolonged use of corticosteroid medications, commonly used in conditions like asthma, autoimmune disorders, or after organ transplantation.

29. Diagnosis Evaluation: 24-Hour Urine Free Cortisol Test: Measures the amount of cortisol excreted in the urine over 24 hours. Low-Dose Dexamethasone Suppression Test: Administers a small dose of dexamethasone (a synthetic glucocorticoid) to check if cortisol production is suppressed. Failure to suppress cortisol levels suggests Cushing Syndrome. Blood Tests: Cortisol levels (elevated).
ACTH levels (helps differentiate between pituitary and adrenal causes). Imaging: CT or MRI scans may be done to identify adrenal tumors or pituitary adenomas.

30. Pharmacology Management : Ketoconazole, Metyrapone , Mitotane : Inhibit cortisol synthesis. Gradual tapering of corticosteroids if drug-induced. Hormone repla cement after adrenal surgery.

31. MEDICAL MANAGEMENT : Monitor blood pressure, glucose, and electrolytes.
Dietary management: high-protein, low-sodium, moderate carbohydrate diet.
Regular physical activity and stress reduction.
Emotional support and family counseling.

32. Surgical management: Removal of adrenal or pituitary tumor (if present). Bilateral adrenalectomy in severe unresponsive cases. Radiation therapy for pituitary tumors if surgery not possible.

33. COMPLICATIONS : Hypertension
Diabetes mellitus
Osteoporosis
Growth retardation in children Delayed wound healing Increased infection risk
Emotional and psychological disturbances Adrenal insufficiency after treatment

34. Nursing intervention: Monitor vital signs, especially blood pressure and blood glucose.
Assess for infection and delayed wound healing. Administer medications and monitor effects. Educate parents on gradual withdrawal of steroids. Provide high-protein, low-sodium diet. Offer psychological and emotional support to child and family.
Encourage rest and limit stressors. Observe for signs of adrenal crisis post-surgery. Promote growth monitoring and follow-up care.

35. Hyperthyroidism : DEFINITION: Hyperthyroidism in children is a disorder in which the thyroid gland produces excessive amounts of thyroid hormones (T3 and T4). This leads to an increased metabolic rate and overstimulation of body systems. The most common cause is Graves’ disease, an autoimmune condition where antibodies stimulate the thyroid gland to produce excess hormones.

36. Pathophysiology : In pediatric hyperthyroidism, thyroid-stimulating imimunoglobulins ( Tsls ) bind to TSH receptors on the thyroid gland, mimicking TSH activity. This causes the gland to release excessive thyroid hormones (T3 and T4), which increase cellular metabolişm , oxygen consumption, and sympathetic nervous activity. The elevated hormones accelerate body processes, leading to symptoms like tachycardia, tremors, heat intolerance, and weight loss. Chronic hyperthyroidism can impair growth and cardiac function in children.

37. SINGS AND SYMPTOMS: Tremors and hyperactivity Tachycardia and palpitations Nervousness, irritability, anxiety Heat intolerance and sweating Enlarged thyroid gland (goiter)
Bulging eyes (exophthalmos)
Poor sleep, fatigue
Increased bowel movements
Difficulty concentrating – Emotional instability
Growth delay

38. Causes: Grave’s disease
Thyroiditis
Excessive iodine intake
Congenital hyperthyroidism

39. Diagnosis Evaluation: Thyroid Function Tests: Elevated T3 and T4 levels. Low TSH (thyroid-stimulating hormone), indicating the overproduction of thyroid hormones. Thyroid-Stimulating Immunoglobulin (TSI): Often elevated in Graves’ disease and helps confirm the diagnosis.

40. PHARMACOLOGY MANAGEMENT: Methimazole or Propylthioura dil (PTU): Suppress thyroid hormone production. Beta-blockers (Propranolol): Control symptoms like tremors and tachycardia. lodine preparations: Temporarily block hormone release.

41. Surgical management: Subtotal or total thyroidectomy for large goiter or drug-resistant cases. Monitor for postoperative complications like hypocalcemia and thyroid storm.

42. MEDICAL MANAGEMENT: Monitor thyroid function (T3, T4, TSH). High-calorie, high-protein diet. Encourage rest and stress reduction. Provide education for medication adherence.

43. Complications : Thyroid storm (life-threatening hyperthyroid crisis) Heart failure
Osteoporosis
Hypocalcemia (post-surgery) Hypothyroidism (after treatment) Eye complications ( exoph thalmos ) Growth and developmental issues – Emotional and behavioral disturbances.

44. Nursing Interventions: Monitor vital signs (especially temperature and pulse).
Observe for thyroid storm symptoms (fever, tachycardia, agítation ).
Administer prescribed medications on time. Providea quiet, cool environment –Encourage adequate nutrition and hydration. Educate parents about lifelong follow-up and medication use. Monitor for post- thyroideçtomy complications (airway obstruction, tetany). Provide emotional support to child and family.

45. Hypothyroidism : DEFINITION: Hypothyroidism is a disorder where the thyroid gland produces insufficient thyroid hormones (T3 and T4), leading to a slowdown in metabolism. In children, it may be congenital or acquired and can affect growth and brain development.

46. Pathophysiology: Decreased secretion of thyroid hormones (T3, T4) causes an increase in thyroid- stimulating hormone (TSH) from the pituitary gland. This hormonal imbalance slows metabolism, affects protein synthesis, and impairs brain and organ development. Congenital hypothyroidism occurs when the thyroid gland is absent, underdeveloped, or unable to function properly.

47. Sings and symptoms: Lethargy or fatigue
Poor feeding and weight gain Constipation
Dry, coarse skin and hair
Cold intolerance
Delayed growth and milestones Hoarse cry, enlarged tongue (in infants) Bradycardia (slow heart rate)

48. Causes: Primary hypothyroidi sm may be caused by a number of defects. A congenital hypoplastic thyroid gland. A partial or complete thyroidectomy. Radiotherapy for Hodgkin disease or other malignancies. Infectious processes may cause hypothyroidism.
When dietary iodine is deficient.

49. Diagnosis Evaluation: TSH Levels: Elevated TSH is indicative of primary hypothyroidism, as the pituitary tries to stimulate the underactive thyroid. Free T4 and T3: Low levels of these hormones confirm the diagnosis. Anti-Thyroid Antibodies: In Hashimoto’s thyroiditis, high levels of anti- thyroid peroxidase (anti-TPO) antibodies are often present.

50. Pharmacological Management: Lifelong thyroid hormone replacement (Levothyroxine). SURGICAL MANAGEMENT: Rarely indicated only for thyroid tumors or structural issues.

51. MEDICAL MANAGEMENT: Regular thyroid function (TSH, T3, T4).
Parental education on adherence.
Balanced diet with adequate iodine.

52. COMPLICATIONS : Growth retardation.
Intellectual disability (if untreated).
Myxedema (severe hypothyroidism). Delayed puberty.
Cardiovascular issues (bradycardia, low cardiac output).

53. NURSING MANAGEMENT: Monitor vital signs and thyroid levels. Administer hormone replacement as prescribed.
Educate parents about lifelong therapy.
Monitor growth and developmental milestones.
Encourage a balanced diet.
Provide emotional and family support.

54. Hypopituitarism : Definition: Hypopituitarism is a disorder characterized by decreased secretion of one or more of the pituitary hormones. It may result from congenital defects, pituitary tumors, trauma, or infection, leading to impairment of growth and other endocrine functions in children.

55. Pathophysiology: In hypopituitarism, there is a deficiency of one or more hormones produced by the anterior pituitary gland, such as growth hormone (GH), thyroid-stimulating hormone (TSH), or adrenocorticotropic hormone (ACTH). The reduced hormone secretion disrupts the normal regulation of target glands (thyroid, adrenal, gonads), resulting in slowed imétabolism , growth retardation, and delayed puberty. In children, GH deficiency is the most common cause leading to short stature.

56. SINGS AND SYMPTOMS: Short stature and growth failure
Delayed bone age
Delayed puberty or absence of secondary sexual characteristics Fatigue and weakness Hypoglycemia in infants
Pale skin and dry hair
Cold intolerance
Decreased muscle mass

57. Causes: Intracranial tumors, bleeding, infarction Neurosurgery, head trauma, infection Idiopathic

58. Diagnosis Evaluation : X-ray, CT scan, MRI
Intracranial, ectopic tumors; bleeding. Infarction LAB RESULTS
Altered levels of pit OTHER DIAGNOSTICSs
History, physical examinationuitary , target tissue hormones

59. Pharmacological Management: Growth hormone replacement therapy ( Somatro pin). Thyroid hormone replacement (Levothyroxine). Corticosteroid replacement if ACTH deficiency present. Sex hormone replacement during puberty.

60. SURGICAL MANAGEMENT: Surgical removal of pituitary tumors if present.
Management of tumor-related complications.

61. MEDICAL MANAGEMET: Regular monitoring of hormone levels and growth. MRI to identify pituitary abnormalities. Endocrinology follow-up for lifelong therapy.

62. COMPLICATIONS: Growth retardation and dwarfism. Delayed puberty or infertility.
Hypoglycemia.
Hypothyroidism or adrenal insufficiency. Osteoporosis.
Psychological issues due to body image Concerns.

63. Nursing management : Monitor growth, weight, and developmental milestones.
Administer prescribed hormone therapy and monitor side effects.
Educate parents about medication adherence and follow-up visits.
Encourage balanced diet and physical activity. Provide emotional support for child and family.
Observe for signs of hormone imbalance or therapy complications.

64. HYPERPITUITARISM: Definition: Hyperpituitarism is a condition caused by excessive secretion of one or more hormones from the pituitary gland, often due to a pituitary adenoma (tumor). In children, it can lead to abnormal growth and development, especially gigantism or precocious puberty.

65. Pathophysiology: In hyperpituitarism , the anterior pituitary gland produces excessive amounts of growth hormone (GH) or other pituitary hormones. When GH is overproduced before epiphyseal closure in children, it leads to gigantism characterized by abnormal linear growth. The excess hormone secretion is commonly due to benign pituitary tumors (adenomas) that disrupt normal hormonal feedback regulation.

66. Sings and symptoms: Abnormally rapid growth in height and. Enlarged hands, feet, and facial features to tumor pressure).
Early puberty or menstrual irregularities. Fatigue and weakness. Joint pain and muscle weakness. Increased sweating
Coarse facial features

67. Causes: Genetic inheritance. Secreting tumors (intracranial, ectopic).

68. Diagnosis Evaluation: X-ray, CT scan, MRI
Intracranial, ectopic tumors; bleeding. Infarction
LAB RESULTS
Altered levels of pit
OTHER DIAGNOSTICSs
History, physical examinationuitary , target tissue hormones

69. Pharmacological Management: Dopamine agonists (e.g., Bromocriptine ) to suppress hormone secretion. Somatostatin analogs (e.g., Octreotide ) to inhibit GH release.

70. MEDICAL MANAGEMET: Regular monitoring of hormone levels.
MRI or CT scan to assess pituitary tumor
Hormone therapy adjustment as needed

71. Surgical management: Transsphenoidal surgery to remove pituitary tumor. Radiotherapy for residual or recurrent tumor.

72. Complications: Gigantism or acromegaly.
Vision impairment due to optic chiasm pressure.
Hypopituitarism (after treatment). Diabetes mellitus or glucose intolerance. Joint deformities.
Emotional and psychological problems.

73. Nursing intervention : Monitor growth patterns and vital signs. Observe for symptoms of hormone imbalance. Educate family about disease and treatment plan. Provide pre- and postoperative care if surgery indicated.
Support emotional well-being and body image Concerns.
Ensure regular follow-up for hormone level monitoring.
Administer prescribed medications and monitor effects.

74. REFERENCES: 1. Ball, J. W., Bindler , R. C., & Cowen, K. J. (2021). Principles of Pediatric Nursing: Caring for Children (8 th ed.). Pearson Education.
2. Hockenberry , M. J., & Wilson, D. (2019). Wong’s Nursing Care of Infants and Children (11 th ed.). Elsevier.
3. McKinney, E. S., James, S. R., Murray, S. S., Nelson, K., & Ashwill , J. W. (2018). Maternal-Child Nursing (5 th ed.). Elsevier Health Sciences.
4. American Thyroid Association (ATA). (2022). Hypothyroidism in Children and Adolescents. Retrieved from https://www.thyroid.org
5. World Health Organization (WHO). (2021). Thyroid Disorders and Iodine Deficiency. Geneva: WHO.
6. Mayo Clinic. (2023). Hypothyroidism (Underactive Thyroid) – Symptoms and Causes. Retrieved from https://www.mayoclinic.org