APPROACH TO AN ADOLESCENT WITH OBESITY By: Camille-Marie A. Go.
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Transcript of APPROACH TO AN ADOLESCENT WITH OBESITY By: Camille-Marie A. Go.
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APPROACH TO AN ADOLESCENT WITH OBESITY
By: Camille-Marie A. Go
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ObjectivesObjectives
To present a case of a child with obesity
To discuss the burden of disease, pathophysiology, management and possible complications of obesity
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Our Patient
P.N. 14 year old Male Filipino Roman Catholic San Mateo, Rizal
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Chief complaint
Rapid weight gain
and hyperglyce
mia
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General: (-) weight loss, (+) voracious appetite Cutaneous: (-) rashes, (-) discoloration, (-) jaundice HEENT: (-) blurring of vision, (-) nasoaural discharge,
(-) epistaxis, (-) gum bleeding Cardiovascular: (-) cyanosis, (-) chest pain, (-) orthopnea, (-) easy fatigability (-) palpitation Respiratory: (-) cough, (-) colds, (-) difficulty of breathing,
(-) sneezing Gastrointestinal: (-) vomiting (-) abdominal pain, (-)
diarrhea, (-) constipation, bowel movement once a day
Review of Systems
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GUT: yellow urine, (-) edema of the hands and feet, (-) frothy urine
Metabolic: (-) polydipsia, (-) polyuria Extremities: (-) swelling, (-) joint swelling, (-)
limitation in movement Nervous/Behavioural: (-) headache, (-) dizziness, (-)
nausea, (-) tremors, (-) convulsions , (-) change in sensorium (-) behavioral change
Hematopoietic: (-) pallor, (-) easy bruisability (-) prolonged bleeding
Review of Systems
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Family History
(+) DM – both parents; maternal GM
(+) HPN - maternal GM
(+) obesity - father (-) PTB (-) Heart disease (-) Thyroid disorders (-) Blood dyscrasia (-) Mental retardation, (-) Seizure
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BCG 3 doses of Hepatitis B DPT x 3 OPV x 3 Measles MMR Boosters: of BCG and MMR No untoward reactions
Immunization History
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Born to a 30 year old G2P1 (1001) nonsmoker nonalcoholic mother
Prenatal check up since 1 month AOG; (+) MVS, Feso4 (+) GDM at 6 months AOG, advised diet
modification; repeat exam after 1 month normal Delivered Full term via NSD assisted by OB; (+) good
cry and activity (+) small for gestational age Newborn Screening and Hearing Screening not done;
Birth and Maternal History
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Breastfed until two months old Milk formula thereafter Complementary feeding at 6 months High carbohydrate and high fat diet prepared by
the mother Fastfood 2x – 3x weekly Fond of junk foods and chocolates
Nutritional History
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Food Food CHO (g) CHON (g) Fats (g) KcalBreakfast 3 pcs
hotdog4 cups of riceWater
184g
24g16g
18g 258 kcal800 kcal
Snacks 6 pcs BiscuitsOrange juice
23g10g
2g 100kcal40 kcal
Lunch 2 cups Pork Sinigangvegetables3 cups of rice
6g138g
32g2g12g
24g 344kcal32 kcal600 kcal
Snacks 6 pcs BiscuitsOrange juice
23g10g
2g 100kcal40 kcal
Dinner 3 cups Chicken Adobo4 cups of ricewater
184g
32 g16g
24 g 344 kcal800 kcal
Total ACIRENI
% intake
3,458 kcal2,800 kcal 123.5%
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Home: Concrete house with 6 household members Nuclear patriarchal clan
Education: Second year high school at school in San Mateo, Rizal Favorite subject: Math Average grade - 89%. Aspires to be a successful accountant when he grows
up
Psychosocial History
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Activity: Fond of computer games Spends 4 to 6 hours per day Most of activities are sedentary
Drugs: No intake of alcoholic beverage or cigarette use Does not know anyone using prohibited drugs
Sexual: Has female crushes among his schoolmates No girlfriend. He has not courted any girl.
Psychosocial History
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Suicide: No personal history of attempted suicide Sees himself as overweight, not happy or proud of it
Safety: Walks on the sidewalk to school Does not ride in cars with drivers who are intoxicated
Spirituality: Hears mass every Sunday together with his whole
family Actively participates in church activities
Psychosocial History
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No previous history of hospitalization, or transfusions, or allergies
No history of communicable diseases (measles, varicella)
Underwent Circumcision at 10 years of age
Past Medical History
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Conscious, coherent, oriented to 3 spheres, not in cardiorespiratory distress, ambulatory, over-nourished, well-hydrated, well-looking
Wt: 75kg (z> 3) ; Ht: 163cm (z<0); BMI: 28.2 (z>3) CR 110 beats/min; RR 30 breaths/min; T 36.5 C; BP
110/60 mmHg (p 25) Warm and moist skin, dark pigmentation of skin
creases and flexural areas, most prominent along the nape
Pink palpebral conjunctivae, anicteric sclerae
Physical Examination:
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No alar flaring, no nasoaural discharge, intact tympanic membrane, AU
Moist buccal mucosa, no dental carries, non-hyperemic posterior pharyngeal walls, tonsils not enlarged
Supple neck, no cervical lymphadenopathies, no thyroid enlargement
No retractions, symmetrical chest expansion, clear breath sounds
Adynamic precordium, PMI at 5th left intercostal space midclavicular line, regular rate and rhythm no heaves, thrills, lifts or murmurs
Physical Examination:
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Globularly enlarged abdomen, no striae, normoactive bowel sounds, no organomegaly, no tenderness, no masses
Grossly male, bilaterally descended testes, Tanner St. II
Full and equal peripheral pulses, capillary refill time less than 2 seconds, no cyanosis, no edema
No limitation in range of motion of all joints
Physical Examination:
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Cerebrum: conscious, coherent, oriented to 3 spheres Cranial nerves: pupils isocoric, 2-3mm equally reactive
to liht, (+) direct and consensual light reflex, extraocular movements full and intact, can clench teeth, (-) gross facial asymmetry, gross hearing intact, (+) gag reflex, can turn head from side to side against resistance, tongue midline
Cerebellum: (-) no involuntary movements, able to do tandem gait
Neurological Exam:
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Reflexes: ++ on all extremities Motor: (-) rigidity, (-) spasticity, (-) flaccidity,
(-) deficits Sensory: (-) deficits Meningeal Signs: (-) nuchal rigidity, (-)
Brudzinski’s, (-) Kernig’s, (-) tonic neck reflex
Neurologic Examination
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Obesity Hyperglycemia probably
secondary to Diabetes Mellitus Type II
Middle Adolescent with Psychosocial Issues (Body
Image)
Diagnosis:
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Obesity
“Excessive storage of energy as FAT relative to lean body mass”
Energy intake exceeds expenditure
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Pediatrics Obese - BMI> 95% for gender and age At risk/overweight - BMI=85-95%
Adults Obese – BMI> 30 Overweight – BMI=25-30
Definition based on BMI
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Measurement
Weight Weight:Height BMI
kg÷m2
Skin Thickness Waist:Hip Ratio Growth Charts
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Patient
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Variable definitions Increasing incidence in developed and
developing nations Similar prevalence to US: Latin America,
Caribbean, Middle East, Northern Africa, Central-Eastern Europe
Asia and Africa: no increase in incidence
Incidence: Worldwide
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Worldwide
Gayya et. al (2008) FNRI – DOST digest January 2014
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Thailand – 23% Taipei – 28% Vietnam – 14 – 16%
Asian Prevalence
Gayya et. al (2008) FNRI – DOST digest January 2014
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0%
5%
10%
15%
20%
1963- 1965 1966- 1970 1971- 1974 1976- 1980 1988- 1994 1999- 2002
2 -5 yrs
6 - 11 yrs
12 - 19 yrs
Trends in children and adolescents
Gayya et. al (2008) FNRI – DOST digest January 2014
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Etiology
Heterogeneous and Multifactorial Environmental Psychosocial Genetic
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Males – Increased visceral fat Females – Increased hip fat At all ages females have more adipose tissue
than males
Sex Difference
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Weights of adopted children correlate better with biological parents
BMIs of identical twins reared apart= together
Monozygotic twins more similar in fat deposition and weight than dizygotic twins
Genetics vs. Environment
Reference
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ObesityDifferential Diagnosis
Idiopathic Endocrine:
Hypothyroidism Hypercortisolism Growth hormone
deficiency
Genetic Prader-Willi Turner
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CNS conditions: hypothalamic damage Medications
Glucocorticoids Phenothiazines Lithium Amytryptiline Estrogen/progesterone
Differential Diagnosis
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Polypeptide Y From L cells of small intestine Reduce food intake
Ghrelin Stimulates food intake Elevated in Prader Willi
Physiology of Regulation Of Energy Expenditure
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Pathogenesis
LEPTIN - Adipostatic signal (1994)
produced by adipose tissue
Acts on Hypothalamus Decreases food intake Increases energy
expenditure
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Low neuropeptide Y stimulates appetite High MSH inhibits appetite Fasting decreases Leptin Eating increases Leptin
Leptin
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Common obesity due to multiple allelic variations in hundreds of genes
Monogenic obesity Leptin deficiency Leptin insensitivity
Leptin and Obesity
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Central role of energy intake Lesions cause hyperphagia and obesity
Hypothalamus
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Environmental Factors:Increased Energy Input
High caloric-density food
Supersized portions Eating out Working parents Advertising
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Environmental Factors:Decreased Energy
Expenditure
TV Computers Transportation Inadequate safe
areas for physical activity
Sedentary Lifestyle
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Diabetes (Type 2) Hypertension and Heart Disease Neurologic Complications Respiratory Disease Orthopedic Condition Psychosocial Disorders Hyperlipidemia GI Manifestations Menstrual Disorders
Complications
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Clustering of CV risk factors related to insulin resistance
Not well defined in Pediatrics Insulin resistance Dyslipidemia Hypertension Obesity
DOES OUR PATIENT HAVE MS?
Metabolic Syndrome
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Course in the Clinics
First consult Laboratories:
Type 2 Diabetes Mellitus with Obesity
Metformin (20 mkday) Referred to Nutrition Clinic
for dietary modification Increase physical activity
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Universal Assessment of Obesity Risk: Steps to Prevention and Treatment
American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart. Elk Grove Village, IL: American Academy of Pediatrics; 2008.
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Steps to Prevention and Treatment of Pediatric
Obesity
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Steps to Prevention and Treatment of Pediatric
Obesity
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Prevention Plus BMI >85%Diet Modification
Build on prevention Eating behaviors
Family meals at least 5 to 6 times per week Allow child to self-regulate his or her meals Avoid overly restrictive behaviors—“Parents
provide, child decides.” Structured activity
American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008
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Prevention Plus BMI >85%Diet Modification
Goal: weight maintenance with growth a decreasing BMI as age increases
Monthly follow-up for 3 to 6 months If no improvement go to Stage 2
American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008
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Prevention Plus BMI >85%Physical Activity/Inactivity
60 minutes of moderate physical activity per day or 20 minutes of vigorous activity 3 times a week Community activity programs Family activities Pedometer use
Limit screen time to <2 hours per day No TV/computer in bedroom
American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008
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American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008
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Global IDF/ ISPAD Guideline
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Approved for Type 2 diabetes and hyperinsulinemiaDecreases hepatic glucose productionEnhances insulin sensitivityResults in modest weight lossSide effects: nausea, flatulance, bloating, diarrhea, lactic acidosis
Pharmacotherapy: Metformin
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Not approved for pediatrics Drug options
Appetite suppressants Serotonin agonists Inhibitors of fat absorption Antihyperglycemic agents
Pharmacotherapy
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Second consult Gradual weight loss of 1.8%
75 kilograms to 73.6 kilograms BMI from 28.2 to 27.7 (z > 2) TABLE OF LABS
Course in the Clinics
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Steps to Prevention and Treatment of Pediatric
Obesity
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Structured Weight Management
Dietary and physical activity behaviors Balanced macronutrient diet with low
amounts of energy-dense foods Increased structured daily meals and
snacks Supervised active play: 60 minutes a day Screen time: 1 hour or less a day
Increased monitoring
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Structured Weight Management
Weight maintenance Decreases BMI as age and height increases
Weight loss 1 lb/month: 2–11 years oldor 2 lb/week: older overweight/obese children and
adolescents If no improvement in BMI/weight after 3 to 6
months Stage III
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Counseling
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Steps to Prevention and Treatment of Pediatric
Obesity
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ObesityTreatment: Surgery
Gastric bypass Gastic plication Gastric banding Jejuno-ileal bypass
no longer performed
Not routine for children
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Course in the Clinics
Sustained weight loss 73.6 kilograms to 72.7
kilograms BMI
27.7 to 27.3 (z >2)
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Course in the Clinics
Regular follow up at the Endocrinology clinic every three months
Continuation of weight loss 70kg, with a BMI of
25.9 (z > 1) Disappearance of the
skin hyperpigmentation around the nape area
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OverweightDiabetes Mellitus Type II,
controlledADOLESCENT?
Final Diagnosis:
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Childhood ObesityConclusion
Heterogeneous disorder
Multifactorial causes
Global epidemic Genetics Sedentary lifestyle Too much in Too little out
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