This document discusses diabetes mellitus, a common endocrine disorder in childhood characterized by glucose intolerance and insulin deficiency. Type 1 diabetes results from autoimmune destruction of beta cells and requires lifelong insulin treatment. Type 2 diabetes is rare in children and not associated with autoimmunity. The pathophysiology involves insulin deficiency leading to high blood glucose and metabolic abnormalities. Clinical manifestations include hyperglycemia and related symptoms. Diagnosis involves history, exam, lab tests and management focuses on insulin therapy, diet, exercise and education.

1. PAEDIATRICS

2. ENDOCRINE
DISORDER
DIABETES
MELLITUS

3. INTRODUCTION
DIABETES IS A DISORDER OF
GLUCOSE INTOLERANCE DUE TO
DEFICIENCY IN INSULIN
PRODUCTION AND ITS ACTION
LEADING TO HYPERGLYCEMIA AND
ABNORMALITIES IN
CARBOHYDRATE , PROTEIN AND
FAT METABOLISM.
IT IS A COMMONEST ENDOCRINE
METABOLIC DISORDER OF
CHILDHOOD AND ADOLSCECNCE
WITH LONG TERM EFFECT ON
CHILD’S PHYSICAL AND
PSYCHOLOGICAL GROWTH AND
DEVELOPMENT .

4. INCIDENCE
APPROXIMATELY 5% OF ALL
DIABETICS ARE CHILDREN.
PEAK INCIDENCE IN
CHILDREN IS FOUND
AROUND 5YRS. AND ABOUT
10 TO 12 YRS.
ETIOLOGY

5. 1) GENETIC
PREDISPOSITON
2) AUTO- IMMUNE PROCESS
MECHANISMS
OF BETA CELL DAMAGE IS
BELIEVED TO BE AN AUTO-
IMMUNE PROCESS.
3) ENVIRONMENTAL
FACTORS
a) STERSS ( EMOTIONAL
AND PHYSICAL
FACTORS)

6. CLASSIFICATION
1. TYPE- 1 INSULIN
DEPENDENT DIABETES
MELLITUS.
2. TYPE-2 NON- INSULIN
DIABETES MELLITUS.

7. TYPE-1 INSULIN
DEPENDENT
DIABETES MELLITUS
IT RESULTS FROM AUTO-
IMMUNE DESTRUCTION OF BETA
CELLS. IT IS CHARACTERISED
BY GROSS DEFICIENCY OF
INSULIN AND DEPENDENCE ON
EXOGENOUS INSULIN FOR
PREVENTION OF KETO-ACIDOSIS
. IT OCCURS MAINLY IN
CHILDHOOD THOUGH THERE IS

8. NO AGE BAR . MAJORITY OF
TYPE-1 CASES AS IDIOPATHIC.
TYPE-2 NON- INBSULIN
DEPENDENT DIABETES
MELLITUS
IT IS RARE IN CHILDHOOD
AND IS NOT ASSOSCIATED
WITH AUTO- IMMUNE
PROCESS. IT IS USUALLY
NOT COMPLICATED BY
KETO- ACIDOSIS.
PREVIOUSLY IT WAS ALSO
KNOWN AS ADULT-ONSET
DIABETES OR MATURITY
ONSET DIABETES.

9. PATHOPHYSIOLOGY
DUE TO ETIOLOGICAL
FACTOR
↓
DEFICIENCY OF INSULIN
↓
GLUCOSE IS UNABLE TO
ENTER THE CELL AND ITS
CONCENTRATION INCREASES
IN BLOOD STREAM.
↓
MOVEMENT OF BODY
FLUIDS FROM
INTRACELLULAR SPACES TO
EXTRACELLULAR SPACE.

10. ↓
PROTEIN AND FAT IS
BREAKDOWN AND
CONVERTED TO GLUCOSE
FOR ENERGY.
↓
AS THE BODY ATTEMPTS TO
MEET ITS ENERGY NEEDS,
HUNGER MECHANISMS IS
TRIGGERED.

11. CLINICAL
MANIFESTATION
a)
 HYPERGLYCEMIA
 GLYCOSURIA
 POLYURIA
 POLYDEPSIA
 POLYPHAGIA
 WEIGHT LOSS
 IRRITABILITY

12.  OVERLY TIRED
 DRY SKIN
 BLURRED VISION
 SLOW- HEALING PROCESS
 FREQUENT INFECTION
 FAINTING ATTACKS
 NAUSEA , VOMITTING

13. DIAGNOSTIC
EVALUATION
a) HI
ST
OR
Y
CO
LL
EC
TI
O
N
b) PH
YS
IC
AL
EX
A

14. M
NT
N.
c) LA
B
IN
VE
ST
IG
AT
IO
N
d) U
RI
NE
EX
A
MI
N
AT

15. IO
N
MANAGEMENT
a) INSULIN THERAPY
b) EXERCISE AND PHYSICAL
ACTIVITY
c) DIET THERAPY
d) FOLLOW- UP

16. e) EMOTIONAL SUPPORT
AND DIABETIC EDUCATION
NURSING DIAGNOSIS
 ALTERED NUTRITION
INTKE DUE TO INSULIN
DEFICIENCY AND
ALTERATION OF
METABOLISM.
 FLUID VOLUME DEFICIT
r/t DIABETIC
KETOACIDOSIS

17.  RISK FOR INFECTION r/t
HYPERGLYCEMIA
 RISK FOR INJURY r/t
HYPOGLYCEMIA
 KNOWLEDGE DEFICIT r/t
INSULIN THERAPY
 FEAR AND ANXIETY r/t
LONG- TERM ILLNESS