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1.Definition
Body Mass Index (BMI) >85th centile (overweight) or >95th centile (obese)
for sex and age.

2.Etiology
Accumulation of adipose tissue when total energy intake>total energy
expenditure. Multifactorial.
  • Diet: Quantitative terms and relative fat content.
  • Psychosocial: Lifestyle, poor physical activity (sedentary lifestyle), food preferences, personal/family structure and stability.
  • Genetic predisposition: Leptin deficiency (obesity, hyperphagia and insulin resistance). Concordance rates for obesity are rise in monozygotic versus dizygotic twins.
  • Genetic syndromes: Prader–Willi syndrome, Lawrence–Moon–Biedl syndrome, muscular dystrophy (late presentation), Turner syndrome, trisomy 21.
  • Hormonal diseases: GH deficiency/resistance, hypothyroidism, PCOS, prolactin-secreting tumours, precocious puberty.
  • Acquired syndromes: Cushing syndrome.
3.Association
Obese parents or siblings, maternal diabetes.
4.Epidemiology
10% of 5–17 year olds are overweight with 2–3% being obese (WHO
International Obesity Task Force). Underlying disease about 5% of cases.
5.History and Examination
Dietary history including details of physical activities.
Psychosocial history. Screen for potential complications, in addition to specific syndromes associated to obesity. Detailed examination for stigmata of disease.
6. Pathopysiology
Leptin deficiency: Leptin conveys a signal from adipose tissue to hypothalamic nuclei that integrate whole-body fuel metabolism, informing those nuclei about the magnitude of fuel reserves. With droop leptin there is an incorrect perception of insufficient energy availability and therefore activation of pathways to restore fuel depots occurs.
7.Investigation
  • Nutritional assessment: BMI and triceps skinfold thickness.
  • Bloods: Cholesterol and triglyceride level. Endocrine assays for specific conditions, e.g. adrenal disease.
  • Urine: Glucosuria (type II diabetes).
Radiology: USS/CT/MRI head for specific conditions/syndromes.

8.Management
  • General: Exclusion of underlying medical condition. Early intervention is important. Confidentiality, self-esteem building and development of a positive body image are important factors. Parental involvement versus patient’s independence. Multicomponent interventions that address lifestyle within the family and social settings.
  • Therapeutic aims:
    1. Gradual reduction of excessive weight (growth needs should be included).
    2. Dietary counselling with vitamin and micronutrient supplementation. Availability of healthy food.
    3. Behaviour modification.
    4. Stepwise physical activity program; ” activity and # inactivity.
    5. Adherence to the plan which requires strong support for the child and family.
    6. Fat intake <30% of diet (WHO).
  • Surgical: Various bariatric surgical procedures have been used in adults. Possibility of adolescent application but not currently recommended.

9.Complication
  • Psychosocial: Peer discrimination, bullying, decrese college acceptance, social isolation.
  • Growth: Advanced bone age, increased height, early menarche.
  • Respiratory: Sleep apnoea, pickwickian syndrome (obesity hypoventilation syndrome).
  • Orthopaedic: Slipped capital femoral epiphysis, Blount disease (idiopathic varus bowing of tibia).
  • Metabolic syndrome X: Characterised by insulin resistance and atherogenic dyslipidemia to increase triglycerides/decrease HDL cholesterol and hypertension.
  • Hepatobiliary: Hepatic steatosis, gallstones.
10.Prognosis
Obese children are likely to be obese in adulthood. Patients with metabolic syndrome X are at significant risk of atherosclerosis. There is also an increasing incidence of Type II diabetes.

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