This document presents information on Insulin Dependent Diabetes Mellitus (IDDM) and Diabetes Insipidus (DI). It defines the conditions, discusses their incidence, etiology, pathophysiology, clinical manifestations, diagnosis, and management. IDDM is characterized by a lack of insulin production resulting in high blood sugar levels, while DI is a disorder of water regulation due to a deficiency of antidiuretic hormone leading to excessive urine production. The document provides details on treating and caring for patients with each condition.

1. 9/22/2016 1

2. Insulin dependent diabetes
mellitus & Diabetes Insipidus
Presenter
Irfan Ali Chandio
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3. Objectives
• At the end of this presentation, the learners will be able
to;
• Define IDDM & DI
• Discuss incidence and etiology of IDDM & DI
• Describe pathophysiology of IDDM
• Explain clinical manifestations of IDDM & DI
• Describe diagnostic findings of IDDM & DI
• Discuss management of IDDM & DI
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4. INSULIN DEPENDENT DIABETES MELLITUS
(IDDM)
Juvenile diabetes mellitus (type-1 or Insulin dependent
diabetes mellitus) is a chronic metabolic disorder
resulting from absolute lack of insulin and resulting in
carbohydrate and lipid metabolism is impaired, and
characterized by hyperglycemia, glycosuria.
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5. INCIDENCE & ETIOLOGY
• IDDM is the most common endocrine disorder in children,
peak age of onset is 11 years in girls 13 in boys the average
age of the onset of puberty.
• Siblings and offspring of a diabetic patient have 5% and twins
50% risks.
• Diabetes Mellitus is due to lack of insulin, type 1
characterized by pancreatic islet beta cell destruction
mediated by immune mechanism.
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6. Cont.…
• An autoimmune disease that occurs genetically susceptible
individuals.
• Several environmental factors such as Viruses (Cytomegalo
Virus, mumps, rubella virus)
• Chemicals (child exposed cow’s milk before 2 years of age).
• Or idiopathic
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7. PATHOPHYSIOLOGY
• The autoimmune destruction, mediated by T-lymphocytes of
the beta cells results in inadequate insulin secretion and
eventually insulin deficiency.
• Deficiency of insulin results in non-utilization of glucose by
the peripheral tissues and hence hyperglycemia.
• The excess glucose causes polyuria and body tries to
compensate that increase thirst and large intake of fluids
(polydipsia).
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8. Cont.…
• Lack of glucose utilization by body leads to increased
appetite (polyphagia).
• Now body utilize alternate source of energy fat from adipose
tissues, when rate of free fatty acids exceeds rate of
utilization, excess fatty acids are converted to ketone bodies
and ketonuria occur.
• Protein synthesis is impaired resulting in loss of weight,
muscle wasting and growth retardation.
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9. CLINICAL MANIFESTATIONS
• The individual with type 1 DM most commonly with a history
of polyuria, polydipsia, polyphagia, weight loss and
dehydration.
• In some individuals abdominal pain and vomiting will be
presents.
• Lethargy, hypotension and recurrent infection may occur.
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10. DIAGNOSIS
• Blood sugar (fasting serum glucose above 126mg/dl) &
(random above 200mg/dl).
• Urine examination ( reveals glycosuria & ketonuria).
• Serum electrolytes (low chlorides).
• Blood examination (Hemoglobin and hematocrit elevated
due to dehydration).
• The measurement of HbA1c levels is also helpful in diabetic
monitoring.
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11. NURSING MANAGEMENT
• Insulin management
• The patients and their parents should be knowledgeable
about the action of the various types of insulin that are
available.
• Insulin can be given subcutaneously into the thighs and
lower abdominal wall by fine needle syringes.
• Prepubertal diabetic children will require 0.7–1 unit of
insulin/kg per day.
• Children during puberty will require 30–50% more insulin.
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12. Cont.…
• Nutritional management
• The diet should provide adequate nutrition and calories for
optimal growth and development.
• The total energy intake should comprise 55% complex
unrefined carbohydrates, 15% protein and 30% fat.
• Avoid refined sugars and give more food with high fiber
content.
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13. Cont.…
• Exercise
• Children with IDDM should be encouraged to exercise
regularly at least 25mints.
• With exercise, insulin requirements lowered, and metabolic
control is improved.
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14. DIABETES INSIPIDUS (DI)
• DI or neurogenic DI is a disorder of water regulation.
• The function of ADH is to concentrate urine by stimulating
reabsorption of water in the renal collecting tubules.
• A deficiency of ADH results in excretion of large amount of
dilute urine (more than 2 L/ per day).
• Affected children could be admitted in a severe dehydrated
state.
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15. INCIDENCE AND ETIOLOGY
• DI is most often seen in children as a complication following
head trauma or cranial surgery to remove tumors of
hypothalamic-pituitary regions.
• Other causes vascular anomalies, infections (meningitis), and
genetic factor.
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16. CLINICAL MANIFESTATION
• In infants, failure to thrive, fever, vomiting, constipation,
dehydration and poor growth.
• In older child polyuria, polydipsia, nocturnal enuresis which
interrupts sleep and increased thirst.
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17. DIAGNOSIS
• An outpatient screening includes obtaining first morning
urine sample for osmolarity and specific gravity.
• Further investigation a Water deprivation test is commonly
performed. The object of the water deprivation test is to
measure the vasopressin release from pituitary in response
to depriving the child’s of water.
• Further I & O fluid intake, weight measure, Vital sign,
hydration assessment and urine and blood samples most
frequently by nurse.
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18. NURSING MANAGEMENT
• Encourage and support patient.
• Instruct patient and family members about following care &
everyday measure.
• Provide skin and mouth care.
• Keep accurate records of hourly fluid intake and urine
output, vital signs, and daily weight.
• Monitor urine specific gravity and serum electrolyte and
blood urea nitrogen levels.
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19. Cont.…
• During dehydration testing, watch for signs of hypovolemic
shock.
• Check laboratory values for hyponatremia and hypoglycemia.
• Encourage the patient to maintain adequate fluid intake
during the day to prevent severe dehydration.
• Inform the patient and his family about long-term hormone
replacement therapy.
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20. Reference:
1. L.Barbara L. mandleco & L.Nicke Potts. Pediatric Nursing ed:2002 by
Delmar Thomon Learning
2. E. Mary Muscari. Paediatric Nursing. Third Edition..Copy right 2001
by Lippincott Williams Wilkins.
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21. Thank you
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