The power of change


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The power of change

  1. 1. A Clinical Case Presentation The Power of Change: A Case of a Adolescent with Multiple Medical Condition Alejandro E. Legarda III MD First Year Resident DFCM
  2. 2. Objectives • To present an adolescent with hypertension and obesity and its correlation to Metabolic syndrome and PCOS • To discuss the differential diagnosis for high BP in the young • To discuss the approach to management of adolescent with hypertension, obesity and the diagnose syndromes • To present short-term and long-term wellness plan appropriate for the patient's condition
  3. 3. Patient Profile EJ 13 years old Single Roman Catholic Incoming 3rd year high school student Chief Complaint ELEVATED BLOOD PRESSURE
  4. 4. Clinical History Five years prior to consult (2007) • The patient was then eight years old and sought a consult due to her re- occurring erythematous vesicular lesions. • Upon consultation, she was diagnosed with Post-streptococcal glomerulonephritis. The patients was admitted in the hospital for a week due to this condition. • Patient was documented to suffer from hypertension. Nifedipine was prescribed to control and manage her hypertension. After hospitalization, patient felt well again. No follow-up consult was recommended to the patient.
  5. 5. Three years prior to consult (2009) • The patient started gaining weight as food intake severely increased. • Patient’s BP was taken annually in school and showed elevated blood pressure. • The increased blood pressure readings was simply ignored by the patient and her parents, thus resulting in progressive, uncontrolled weight gain. Clinical History
  6. 6. Two weeks prior to consult • Patient sought consultation at the UP-PGH Dermatological Department for her vesicular lesions. • Patient featured an incidental finding of 160-90 blood pressure reading. • Assessment reveals: Acne vulgaris with etiology related to PCOS Hypertension secondary to (1) PCOS (2) Cushing’s Syndrome (3) Insect bite hyper sensitivity reaction Patient was given: • Amlodipine (5mg./tab) OD • Benzoyl Peroxide gel OD • Tretinoin cream for the face • Cloxacilin (500mg./tab) for 7 days • Mupirocin Bethamethasone ointment ITD • Sunscreen • mild soap Clinical History Patient was referred to Pedia adolescent, hence the consult.
  7. 7. Clinical History  At Consult (March 26, 2012)  Patient was seen at the Pedia Adolescent Clinic
  8. 8. Review of Systems (+) polyuria (+) polydipsia (-) rashes (-) epistaxis (-) gum bleeding (-) neck pain (-) dysphagia (-) chest pain (-) orthopnea (-) dyspnea on exertion (-) orthopnea (-) edema (-) neck pain (-) abdominal pain (-) constipation (-) diarrhea (-) urgency (-) frequency (-) dysuria (-) nocturia (-) hematuria (-) heat intolerance (-) jaundice
  9. 9. Past Medical History (-) Asthma (-) Allergy (-) Pulmonary Tuberculosis (-) Bronchial asthma No Accident and injury Hospitalizations: Admitted for (+) PSGN (2007) and Dengue Fever (2009) Surgeries: There was no previous surgery Medications: Co-amoxiclav for her recurrent skin infections
  10. 10. OB/GYNE History Menarche: January 2011 Irregular flow occurring only 3x since her menarche Lasting 4-5 days, Pads 2-4 a day No dysmenorrhea No sexual contact
  11. 11. Birth and Maternal History Patient was born full-term via spontaneous vaginal delivery at a local hospital delivered by an obstetrician with no known feto-maternal complications.
  12. 12. NUTRITIONAL HISTORY Patient was breastfed for 3 months and then shifted to bottle feeding of Bona milk every 3 to 4 hours starting at 4 months old up to 12 months old. Complementary feeding was started at 6 months old. Patient would skip breakfast but would have 2 snacks before a heavy lunch. She would have 2 heavy meriendas, e.g.,2 hamburgers/hotdogs or cups of ice cream .Most of the food she eats are either fried or salty and plenty of desserts. She loves to drink cola.
  13. 13. Immunization History Childhood Vaccinations Bacillus Calmette-Guerin (BCG), one dose Hepatitis B vaccine, three doses Diptheria Pertussis Tetatnus (DPT), three doses Oral Polio Vaccine, thress doses Measles, one dose
  14. 14. FAMILY GENOGRAM I II III Jorgo Family March 26, 2012 Hypertension Accident Overweight Diabetes 76 80 68 75 56 54 32 50 46 52 48 19 18 15 13 Elaisa JJMJ EJ
  15. 15. Personal and Social History Home: - lives with parents and four siblings in Imus, Cavite -good relationship with parents and siblings Education: -Incoming third-year high school student -With above-average grades - has close set of friends in school Activities: -Favorite past time– eating -Loves eating street foods and junk foods -Spends most of her free time in front of the TV or computer -Not involved in any outdoor activities such as sports
  16. 16. Personal and Social History Drugs: -No history of cigarette or alcohol use -Denies use or history of use of illicit drugs Sexual: -Does not showcase any consciousness with body weight and shape -Patient has not attempted to change her appearance -Currently no relationship with the opposite sex Suicidal Tendencies: -Patient exhibits no signs or episodes of depression or suicidal ideation Safety: -Patient together with her family lives in a peaceful and orderly community with minimum crime rate - uses public transportation to commute -Not a member of a gang or sorority
  17. 17. Physical Examination General Survey: Awake, alert, coherent, in pain, not in cardio-respiratory distress (-) muscle wasting (-) moon face (-) proximal muscle weakness (-) buffalo hump Vital Signs: Blood Pressure: 150/90(>99th percentile) Heart Rate: 75 beats/minute Respiratory Rate: 18 breaths/minute Temperature: 36.8 C
  18. 18. Physical Examination Anthropometrics: Height: 157 cm Weight: 96.5 kg Body Mass Index: 40.7 kg/m2 (Z score: 2.58) Abdominal Circumference 102cm
  19. 19. Physical Examination Head and Neck: Anicteric sclerae, pink conjunctivae, pupils 2-3mm OU reactive to light, (+) Short leg length (+) Acanthosis nigricans, (-) masses, (-) cervical lymphadenopathy, (-) anterior neck mass (-) tonsillopharyngealcongestion, (-) neck vein engorgement, (-)ear discharge
  20. 20. Physical Examination Chest and Lungs: Equal chest expansion, no deformities, no lesions, clear breath sounds, (-) crackles/rales/wheezes Heart: Adynamic precordium, distinct heart sounds, apex beat at 5th intercostal space left midclavicular line, regular rate and rhythm, no murmurs
  21. 21. Physical Examination Abdomen: flabby (+) Striae lower abodomen no deformities no lesions Soft normoactive bowel sounds (-)masses or tenderness liver span 8 cm right midclavicular line intact Traube’s space no costo-vertebral angle tenderness
  22. 22. Physical Examination Extremities pink nailbeds full and equal pulses no cyanosis/clubbing/ edema no crepitations no limitation of passive and active motion on both upper extremities (-) shooting pain on straight leg raise of both lower extremities (-) limitation of motion due to pain no crepitations on hips, knees or ankles no joint swelling or deformities (-) Pain on active leg raise of both lower extremities
  23. 23. Physical Examination Neuro Exam Cranial Nerve (CN) Examination CN I –intact gross olfaction CN II –pupils 2-3 mm OU briskly reactive to light CN III,IV,VI –full range of extraocular muscle movement CN V –brisk corneals, good masseter tone, CN VII –no facial asymmetry, no altered taste CN VIII –intact gross hearing, no lateralization on Weber Test CN IX –no altered taste, can swallow CN X –can swallow CN XI –good symmetrical shrug CN XII –can protrude tongue, no deviation
  24. 24. Physical Examination Sensory Pain: Intact on all dermatomes Light Touch: Intact on all dermatomes Vibratory: Intact on all dermatomes Motor Normal Gait Good muscle tone, no atrophy, no limb size discrepancy Full motor strength on both upper extremities Tanner Stage 3 External genitalia with dark, coarse curly hair spreads over mons pubis Elevation of Breast contour; areolae enlarged
  25. 25. Salient Features of the Case SALIENT FEATURES OF THE CASE A 13-year old female Chief complaint of elevated blood pressure History of hypertension ,DM and Obesity Previous history of renal disease (+) poluyuria, (+) polyphaga. Amenorrhea Obesity Anthropometrics: Height: 157 cm, Weight: 96.5 kg, Body Mass Index: 40.7 kg/m2 (Z score: 2.58), (+) Short neck length (+) Acanthosis nigricans nape area, Flabby abdomen with (+) Striae
  26. 26. Initial Impression Hypertension, Stage II-- etiology to be determined Acne Vulgaris probably secondary to PCOS DM suspect Obese, Type 2 Amenorrhea secondary to PCOS
  27. 27. Management Diagnostics: Complete Blood Count (CBC) Plasma sodium, potassium and calcium BUN, Creatinine Fasting plasma glucose Lipid profile Urinalysis Whole AB ultrasound Chest X--ray ECG TSH, FT4
  28. 28. Therapeutics Continue the following medications: Cloxacillin 500 for 7 days Tretnoin Cream for the face Mupirocine Betamethasone ointment, TID Sun screen use Mild soap use Start Amlodipine 5mg once a day
  29. 29. Approach to Hypertension
  30. 30. European Society of Hypertension The study mentioned childhood BP has been shown to track into adulthood Unlike adults, the diagnostic criteria for elevated BP in children are based on the concept that BP in children increases with age and body size, making it impossible to utilize a single BP level to define hypertension.
  31. 31. The recommended method is auscultatory. Use K1 for systolic BP and K5 for diastolic B. If the oscillometric method is used, the monitor needs to be validated and if hypertension is detected by the oscillometric method, it needs to be confirmed using the auscultatory method. The Use the appropriate cuff size according to arm width (40% of the arm circumference) and length (4_8 cm, 6_12 cm, 9_18 cm, 10_24 cm, to cover 80–100% of the individual’s arm circumference). Specific recommendations for office BP measurement in children and adolescents
  32. 32. Blood Pressure for Girls by Age and Height Percentiles
  33. 33. Systolic and diastolic ambulatory blood pressure (systolic/diastolic) values for clinical use
  34. 34. Task Force for Blood Pressure in Children, the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents The normal BP in children is defined as SBP and DBP less than 90th percentile for age, sex and height. Hypertension is defined as SBP and/or DBP persistently 95th percentile or more, measured on at least three separate occasions with the auscultatory method. Rule out White-coat (or isolated office) and masked (or isolated ambulatory) hypertensions
  35. 35. Definition and Classification of Hypertension in Children and Adolescents
  36. 36. Diagnostic Algorithm of Hypertension
  37. 37. FAMILY HISTORY Hypertension Cardiovascular and cerebrovascular disease Diabetes mellitus Dyslipidemia Obesity Hereditary renal disease (Policystic kidney disease) Hereditary endocrine disease (pheochromocytoma glucocorticoid-remediable aldosteronism, multiple endocrine neoplasia type 2, von Hippel–Lindau) Syndromes associated with hypertension (neurofibromatosis) Clinical Data To Note
  38. 38. Clinical Data To Note PERINATAL HISTORY Birth weight, gestational age, oligohydramnios, anoxia, umbilical artery catheterization PREVIOUS HISTORY Hypertension Urinary tract infection, renal or urological disease Cardiac, endocrine (including diabetes) or neurological disease Growth retardation Symptoms suggestive of secondary hypertension Dysuria, thirst/polyuria, nocturia, hematuria Edema, weight loss, failure to thrive Palpitations, sweating, fever, pallor, flushing Cold extremities, intermittent claudication Virilization, primary amenorrhea and male pseudohermaphroditism Symptoms suggestive of target organ damage Headache, epistaxis, vertigo, visual impairment Facial palsy, fits, strokes Dyspnea
  39. 39. Clinical Data To Note Sleep history: Snoring apnea, daytime somnolence Risk factor history: Physical exercise, dietary habits Smoking, alcohol Drug intake: Anti-hypertensives Steroids, cyclosporine tacrolimus or otherTri-cyclic anti-depressants atypical antipsychotics decongestants Oral contraceptives illegal drugs Pregnancy
  40. 40. Physical Examination To Note Height Weight Body mass index External features of syndromes/conditions associated with hypertension Neurofibromatosis Klippel–Trenaunay–Weber Feuerstein–Mims Von Hippel–Lindau Multiple endocrine neoplasia Pseudoxanthoma elasticum Turner, William Marfan Cushing Hyperthyroidism, Lupus Vasculitis Congenital adrenal hyperplasia Data to record:
  41. 41. Physical Examination Data to Record Cardiovascular examination Pulse and BP measurement in both arms and legs Bruits/murmurs – heart, abdomen, flanks, back, neck, head Signs of left ventricular hypertrophy or cardiac failure Abdomen Masses – Wilms, neuroblastoma, pheochromocytoma, autosomal dominant and recessive polycystic kidney disease, multicystic kidney displasia, obstructive uropathy Hepatosplenomegaly – autosomal recessive polycystic kidney disease Neurological examination Fundoscopy for hypertensive changes and retinal amartoma (von Hippel–Lindau) Evidence of VIII nerve palsy Other neurological defects including stroke
  42. 42. Indicators on Physical Exam of Etiology of Hypertension in a Child Thyromegaly Hyperthyroidism Acne, hirsutism, striae Cushing syndrome, anabolic steroid abuse Cafe´-au-lait spots Neurofibromatosis Adenoma sebaceum Tuberous sclerosis Malar rash Systemic lupus erythematosus Acanthrosis nigricans Type 2 diabetes Chest widely spaced nipples Turner syndrome Heart murmur Coarctation of the aorta Friction rub Systemic lupus erythematosus (pericarditis), Abdomen Mass Wilms tumor, neuroblastoma, pheochromocytoma Epigastric/flank bruit Renal artery stenosis Palpable kidneys Polycystic kidney disease, hydronephrosis, multicysticdysplastic kidney Genitalia Ambiguous/virilization Adrenal hyperplasia Extremities Joint swelling Systemic lupus erythematosus, collagen vascular ds Muscle weakness Hyperaldosteronism, Liddle syndrome
  43. 43. Patient PE Presentation Significant Anthropometrics: Height: 157 cm Weight: 96.5 kg, Body Mass Index: 40.7 kg/m2 (Z score: 2.58) (+) Short neck length (+) Acanthosis nigricans nape area Flabby abdomen with (+) Striae (+) Acne Other details were none pertinent
  44. 44. Target Organ Damage To Note Heart Blood Vessels Kidney Neuro Fundoscopy
  45. 45. Heart Left Ventricular Hyperthrophy (LVH) remains to date the most thoroughly documented form of end-organ damage caused by hypertension in children and adolescents.
  46. 46. Blood Vessels Morphological changes of the arterial wall, thickening of the intima-media complex. Children with familial hypercholesterolemia have higher IMT Overweight and obesity are associated with increased IMT in children with or without essential hypertension.
  47. 47. Kidney Hypertension-related renal damage is based on a reduced renal function or an elevated UAE. Proteinuria is a marker of glomerular damage in primary and secondary glomerulopathies. An indication for BP- lowering interventions. Microalbuminuria (20–300mg/g creatinine, 2–30 mg/mmol creatinine, 30–300 mg/day, 20–200mg/min) has been shown to predict the development of diabetic nephropathy . Overt proteinuria (>300 mg/day) indicates the existence of established renal parenchymal damage.
  48. 48. Neuro and Fundoscopy Cerebral seizures, stroke, visual impairment and retinal vascular changes are complications associated with severe hypertension. Fundoscopy was also done in because in a study of 97 children and adolescents with essential hypertension, found that 51% displayed retinal abnormalities, as detected from direct ophthalmoscopy.
  49. 49. Obesity and Hypertension Using the 2000 CDC growth charts, at risk of overweight for ages 2 to 20 years overweight is defined as a Body Mass Index (BMI)-for-age between the 85th and the 95th percentiles. Overweight in children is defined as a BMI-for-age at or above the 95th percentile on the charts. BMI is weight in kilograms divided by height in meters squared (kg/m2). BMI is used differently to define overweight in children and adolescents than it is in adults. In children and adolescents, BMI changes with age and gender.
  50. 50. Obesity and Hypertension Overweight children and adolescents are at increased risk for various chronic diseases in later life. The psychosocial consequences of overweight are significant. Overweight in children has been linked to social discrimination, a negative self-image in adolescence that often persists into adulthood, parental neglect, and behavioral and learning problems.
  51. 51. Obesity and Hypertension Being overweight is probably the most important of the conditions associated with elevated BP in childhood and accounts for more than half the risk for developing hypertension. Adiposity is the most powerful risk factor for higher BP. Waist circumference (abdominal obesity) has been shown to play a role. Dietary habits like high salt intake, have been implicated as factors favoring higher BP values.
  52. 52. Obesity and Hypertension The CDC mentions the Common Medical Consequences of Overweight (Dietz, 1998) hyperlipidemia glucose intolerance hepatic steatosis cholelithiasis sleep apnea Obesity hypoventilation syndrome hypertension a variety of orthopedic complications
  53. 53. Laboratory Investigations Full blood count Plasma sodium, potassium and calcium, urea, creatinine Fasting plasma glucose Serum lipids (cholesterol, LDL cholesterol, HDL cholesterol) Fasting serum triglycerides Urinalysis plus quantitative measurement of microalbuminuria and proteinuria Renal ultrasound Chest Xray, ECG and 2-D echocardiography Routine tests that have to be performed in all hypertensive children
  54. 54.  Recommended additional screening tests  Plasma renin activity, plasma aldosterone concentration  Urine and plasma catecholamines or metanephrines  Tc99 dimercaptosuccı´nic acid scan  Urinary free cortisol  More sophisticated tests that should await results of  above screening  Color Doppler ultrasonography  Captopril primed isotope studies  Renal vein renin measurements  Renal angiography  I123 metaiodobenzylguanidine scanning  Computed tomography/ Magnetic resonance imaging  Urine steroid analyses and more complex endocrine  investigations  Molecular genetic studies (Apparent mineralocorticoid  excess, Liddle’s syndrome, etc)
  55. 55. SECONDARY HYPERTENSION Sustained hypertension can be classified as secondary when a specific cause can be found, then it can be corrected with specific intervention. There should be work-up should be done if hypertension .
  56. 56. Diagnosis of Secondary Causes of Hypertension
  57. 57. MY MANAGEMENT Diagnostic Examinations Laboratory Plan: Complete blood count Plasma sodium, potassium and calcium, BUN, Crea Fasting plasma glucose Lipid Profile Urinalysis Whole AB ultrasound Chest Xray, ECG TSH, FT4
  58. 58. APPROACH TO MANAGEMENT Non pharmacologic Strategy Recommendations: GOALS: BMI<85th percentile: Maintain BMI to prevent becoming overweight BMI 85–95th percentile: Weight maintenance (younger children) or gradual weight loss in adolescents To reduce BMI to <85th percentile BMI>95th percentile: Gradual weight loss (1–2 kg/ month) to achieve value <85th percentile
  59. 59. GENERAL RECOMMENDATIONS Moderate to vigorous physical aerobic activity--40 min, 3–5 days/week and avoid more than 2 hours daily of sedentary activities Avoid intake of excess sugar, excess soft drinks, saturated fat and salt and recommend fruits, vegetables and grain products Implement the behavioural changes (physical activity and diet) tailored to individual and family characteristics Involve the parents/family as partners in the behavioural change process Provide educational support and materials Establish realistic goals Develop a health-promoting reward system Competitive sports participation should be limited only in the presence of uncontrolled stage 2 hypertension
  60. 60. For my patient… A. Counseling and Implement Behavioural Change 1.CEA(Catharsis Education Action): Patient 2.Motivational Interviewing- Pre Contemplation stage 3. CEA(Catharsis Education Action): : Parents
  61. 61. Counseling and Implement Behavior Change: CEA Patient Patient was not so much concerned of her weight. She doesn’t know the risk and the health issues regarding hypertension. She was not aware why she came to PGH for consult and really wanted to go home. She was also not aware her that being overweight has some health risks as well.
  62. 62. Use of Motivational Intervierwing Transtheoretical Model, "process involving progress through a series of stages:"  Precontemplation (Not Ready)-"People are not intending to take action in the foreseeable future, and can be unaware that their behaviour is problematic.”  Contemplation (Getting Ready)-"People are beginning to recognize that their behaviour is problematic, and start to look at the pros and cons of their continued actions.“  Preparation (Ready)-"People are intending to take action in the immediate future, and may begin taking small steps toward behaviour change.“  Action – "People have made specific overt modifications in modifying their problem behaviour or in acquiring new healthy behaviours.“  Maintenance – "People have been able to sustain action for awhile and are working to prevent relapse."
  63. 63. Use of Motivational Intervierwing Motivational Interviewing- Pre Contemplation stage Patient was on pre -contemplation stage at that time and I was hoping to make her aware and give her insight to bring her to the stage where she can contemplate. When I asked about her hypertension, she said she knew had it for years but no one told her about the dangers.
  64. 64. B. Counseling and Implement Behavior Change 3. CEA: Parents The parents are also unaware of the risk of hypertension and the eating habits and lifestyle that increase her obesity. They couldn’t believe that this would happen at her age. The whole family is at risk since everyone except the wife is obese.
  65. 65. My Management Plan for the Patient… Non-pharmacologic strategies A. Counseling and Behavior Change- Done B. I advised the patient to have Regular BP monitoring at home C. Physical Activity: I mentioned to the patient to start to lessen sedentary activities and start to walk more around the subdivision and play with pets. A Exercise program was not done yet as I want for the patient to reach the preparation/action D. Eating Habits: Change of eating was advised. The Patient love to skip breakfast and lessen snack intake. E. A Diet Program: I was planning to put the patient into a low Energy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet on the next follow up
  66. 66. Approach to Medical Management on Hypertension Pharmacologic/Therapeutic Strategies Aside from the non-pharamacologic strategies, I had a dilemma on how will I use therapeutic strategies for my patient EVIDENCE FOR THERAPEUTIC MANAGEMENT Reduce mortality and sequelea in life-threateningconditions Reduce left ventricular hypertrophy Reduce urinary albumin excretion Reduce rate of progression to end-stage renal disease
  67. 67. Approach to Medical Management on Hypertension Therapeutic management of hypertension Indications for Antihypertensive Drug Therapy in Children Symptomatic Hypertension Secondary hypertension Hypertensive target-organ damage Diabetes (types 1 and 2) Persistent hypertension despite non-pharmacologic measures >99 percentile BMI
  68. 68. Approach to Medical Management on Hypertension Therapeutic Management Treating Hypertension with drugs are most indicated in end organ damage of the Heart and Kidney/Renal Effect to Organ Damage: In the Heart, Regression of LVH was reported in three children with essential hypertension receiving enalapril, in 19 children with primary and secondary hypertension treated with ramipril for 6 months, and in 65 children with chronic kidney disease (CKD) stage 2–4 receiving ramipril for up to 2 years. In Renal: the Effect of Strict Blood Pressure Control and ACE Inhibition on Progression of Chronic Renal Failure in Pediatric Patients (ESCAPE) trial, which has shown efficient BP and proteinuria reduction for the ACE inhibitor ramipril in 352 children with CKD
  69. 69. Approach to Medical Management on Hypertension Monotherapy Choice of anti-hypertensive agents ACEIs Angiotensin receptor antagonists (ARBs) Calcium antagonists Beta-blockers Diuretics Combination therapy In children with renal disease, monotherapy is often not sufficient to achieve adequate BP control. Therefore, early combination therapy is required. The best choices of antihypertensive drug combinations are those recommended in the ESH/ESC 2007 Guidelines .
  70. 70. Clinical conditions for which specific antihypertensive drug classes are recommended or contraindicated
  71. 71. My Therapeutic Management For our patient, she was given a monotherapy of Amlopidine, 5mg./tab once daily.
  72. 72. Initial Management summary  Diagnostic Examinations  Laboratory Plan:  Complete blood count  Plasma sodium, potassium and calcium,  BUN, Crea  Fasting plasma glucose  Lipid Profile  Urinalysis  Whole AB ultrasound  Chest Xray, ECG  TSH, FT4
  73. 73. Initial Management summary  Non-pharmacologic strategies  Counseling and Behavior Change- Done  B. I advised the patient to have Regular BP monitoring at home  C. Physical Activity: I mentioned to the patient to start to lessen sedentary activities and start to walk more around the subdivision and play with pets. A Exercise program was not done yet as I want for the patient to reach the preparation/action  D. Eating Habits: Change of eating was advised. The Patient love to skip breakfast and lessen snack intake.  E. A Diet Program: I was planning to put the patient into a low Energy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet on the next follow up
  74. 74. Initial Management summary Medical Theraphy  For our patient, she was given a monotherapy of Amlopidine, 5mg./tab once daily.
  75. 75. 1st Follow-up April 2012 Maintained BP 150/90…no decrease in BP despite of Amlodipine 5mg tablet. Started to jog for several minutes around the house and roam around the area with her dog. Lessened her calorie intake thanks to the parents modifying the food menu at home. Parents started to prepare healthier food with less salt content. Parents have been very supportive. Siblings stopped eating with the patient for snacks and joined the patient in jogging as well. One of her sibling, who still was a bad influence to her was transferred to their grandmother’s house.
  76. 76. 1st Follow-up April 2012  1st Follow-up April 2012 Results  Hgb:139, Hct 0.432, Plt 356 WBC 8.7  Urinalysis : Dark yellow, 1.030, RBC 0-2, WBC 3-4 EC 3+ Sugar (-) Albumin (-)  CXR: Normal Chest Findings  Thyriod FT4- 20.6, Free T3- 5.5, TSH IRM 6.1  Glucose 6.4, BUN 3.30, Crea 45.5, Chole 5.0, Trigly 5.01 HDL 0.98, LDL 1.74, AST 38, ALT 46, Albumin 42 Calcium 2.44, Na- 138, K 4.8  ECG- Sinus Rhythm, Within Normal Limits  Whole Ab Ultrasound: normal  With the current labs results, I was able to rule out many etiology of hypertension including the secondary ones however there was elevation in Triglyceride and there was Impaired Fasting Glucose
  77. 77. 1st Follow-up April 2012  Previous Salient Features… SALIENT FEATURES OF THE CASE 13-year old female Chief complaint of elevated blood pressure History of hypertension ,DM and Obesity Previous history of renal disease (+) poluyuria, (+) polyphaga. Amenorrhea Obesity (+) Short neck length (+) Acanthosis nigricans nape area, (+) Striae New Finding from the Diagnostics Impaired Fasting Glucose Elevated Triglyceride Ruled out Cardiovascular, Renal and some secondary etiology
  78. 78. 1st Follow-up April 2012  Hypertension stage II secondary to 1) Obesity 2) Metabolic Syndrome  T/c PCOS sedondary to Metabolic Syndrome  Hyperlipidemia  Impaired Fasting Glucose
  79. 79. METABOLIC SYNDROME  Group of characteristics:  Most expert groups define metabolic syndrome as the presence of three or more of the following characteristics in a person:  Obesity, especially in the abdominal area  (defined by some groups as a waist size greater than 94 to 102 cm (38 to 41 in) in men or greater than 80 cm (32 in) in women)  Impaired fasting glucose  (fasting blood sugar of 100 to 125 mg/dL or 5.6 to 7 mmol/L)  Increased blood pressure  (130/85 or higher) or if you take medicine for high blood pressure  Increased fasting levels of triglycerides  (greater than 150 to 180 mg/dL or 1.7 mmol/L) or decreased fasting HDL cholesterol (less than 40 mg/dL or 1 mmol/L for men or 50 mg/dL or 1.3 mmol/L for women)
  80. 80. METABOLIC SYNDROME IN CHILDREN AND ADOLESCENTS  Definition Metabolic syndrome also occurs in children and adolescents but there is no consensus on the definition  The International Diabetes Federation (IDF) definition of metabolic syndrome in children 10 to 16 years old is similar to that used by the IDF for adults, except that the definition for adolescents uses ethnic-specific waist circumference percentiles and one cutoff level for HDL rather than a sex-specific cutoff.  For children 16 years and older, the adult criteria can be used.  For children younger than 10 years of age, metabolic syndrome cannot be diagnosed, but vigilance is recommended if the waist circumference is ≥90 percentile.
  81. 81. METABOLIC SYNDROME IN CHILDREN AND ADOLESCENTS Risk factors  Among obese children, the prevalence of the metabolic syndrome is high and increases with worsening obesity.  The prevalence of metabolic syndrome is high among obese children and adolescents and increases with the severity of the obesity, and with central adiposity in particular.
  82. 82. Clinical Implications of Metabolic Syndrome The definition of metabolic syndrome may be clinically useful for risk stratification and therapeutic intervention in pediatrics. However, lifestyle modification that emphasizes reduction of established risk factors, such as promotion of exercise, weight loss, and smoking cessation, is the main therapeutic goal in obese children and adolescents, regardless of a metabolic syndrome diagnosis.
  83. 83. METABOLIC SYNDROME TREATMENT  Reduce or eliminate underlying problems (eg, obesity, lack of activity) by losing weight and becoming more active.  Treat cardiovascular risk factors, such as high blood pressure and cholesterol, if these problems persist despite losing weight and exercising.  Weight loss  The Mediterranean diet is high in fruits, vegetables, nuts, whole grains, and olive oil  The DASH (Dietary Approaches to Stop Hypertension) The DASH diet requires you to eat no more than 2400 mg of sodium per day, four to five servings of fruit, four to five servings of vegetables, two to three servings of low-fat dairy products, and all foods must contain less than 25 percent total fat per serving.  Lifestyle modification — Prevention or reduction of obesity, particularly abdominal obesity, is the main therapeutic goal in patients with the metabolic syndrome  Exercise — . The standard exercise recommendation is a daily minimum of 30 minutes of moderate-intensity (such as brisk walking) physical activity. Increasing the level of physical activity appears to further enhance the beneficial effect
  84. 84. METABOLIC SYNDROME and Polycystic Ovary Syndrome (PCOS)  PCOS and Metabolic Sydnrome originally was described by Stein and Leventhal as the association of amenorrhea with polycystic ovaries, and variably, hirsutism and obesity  It is now recognized that PCOS represents a spectrum of disease characterized primarily by the following features:  Cutaneous hyperandrogenism (eg, hirsutism, treatment- resistant acne, and/or pattern balding [androgenetic alopecia]  Menstrual irregularity (eg, oligo- or amenorrhea, or irregular bleeding)  Polycystic ovary  Obesity and insulin resistance
  85. 85. Clinical Manifestations of The Insulin Resistance Syndrome in Children
  86. 86. Polycystic ovary syndrome (PCOS) Three sets of diagnostic criteria have been proposed for the diagnosis of PCOS in adults. In adolescents, using the NIH diagnostic criteria in most cases.  PCOS risk criterion proposed by the Androgen Excess and PCOS Society (AES), alternatively defined as hyperandrogenism and a polycystic ovary, be considered as indicative of risk for PCOS rather than as diagnostic.
  87. 87. PCOS Prevalence The prevalence of PCOS in the adolescent population is unknown.
  88. 88. PCOS DIFFERENTIAL DIAGNOSIS  Congenital adrenal hyperplasia Nonclassic  Classic CAH due to 21- hydroxylase deficiency  Classic CAH, and to a lesser extent nonclassic CAH,  Ovarian steroidogenic blocks  Other adrenal disorders  Cushing's syndrome include central obesity, dorsal fat pad, hypertension, easy bruising, striae, and proximal muscle weakness.  Hyperprolactinemia  Acromegaly  Virilizing tumors  Thyroid dysfunction  Drugs  Disorders of sex development  Idiopathic
  89. 89. DIAGNOSTIC CRITERIA Cutaneous signs of hyperandrogenism (eg, hirsutism, persistent acne, and/or pattern alopecia) Menstrual irregularity (eg, oligo- or amenorrhea, or irregular bleeding)  Polycystic ovary syndrome  Obesity and insulin resistance
  90. 90. DIAGNOSTIC APPROACH. Evidence of hyperandrogenism — The criterion of clinical hyperandrogenism is satisfied by hirsutism or other cutaneous signs of hyperandrogenism. Evidence of ovarian dysfunction Exclusion of non-PCOS causes of hyperandrogenemia Additional evaluation after the diagnosis of PCOS
  91. 91. TESTING FOR ANDROGEN EXCESS  Total testosterone  Free testosterone  Dehydroepiandrosterone sulfate (DHEAS)  Ultrasonography  Endocrine Test  Prolactin  Thyroid function  Insulin-like growth factor-I  Serum cortisol  Early-morning 17-hydroxyprogesterone
  92. 92. Manifestations of Polycystic Ovary Syndrome in Approximate Proportion to their Relative Incidence and Coincidence ANOVULATORY SYMPTOMS OBESITY HIRSUTISM,ACNE, ALOPECIA
  93. 93. Pathogenesis  Intraovarian androgen excess appears to be responsible for both anovulation and the formation of multiple ovarian "cysts" because of stimulated excessive growth of small follicles and hindrance of the maturation of the dominant follicle.  There is vigorous debate about whether this pathologic process is primarily a disorder of pituitary gonadotropin secretion or a disorder of ovarian and/or adrenal steroidogenesis.  PCOS may result from a metabolic disorder that includes insulin resistance.  Abnormal pituitary function  Abnormal steroidogenesis  Extrinsic factors contributing to dysregulated steroidogenesis
  94. 94. Abnormal Pituitary Function  Increased LH relative to FSH was the first laboratory abnormality identified in classic PCOS. Elevated LH levels occur in about half of PCOS patients. Elevated LH is thought to play a role in the pathogenesis of PCOS by increasing androgen production and secretion by ovarian theca cells.  Patients with PCOS have an increased LH pulse frequency and amplitude.  Obesity seems to attenuate the increase in LH pulse amplitude, in part because the pituitary gonadotropes of obese women with PCOS produce LH isoforms that are rapidly metabolized.
  95. 95. Abnormal Steroidogenesis  Alternative hypothesis that PCOS is due to intrinsic ovarian dysfunction. This hypothesis considers that primary functional ovarian hyperandrogenism (FOH) is the essence of PCOS.  The intraovarian level of androgens in FOH is higher than in most adrenal causes of androgen excess and results in excessive growth of small ovarian follicles while inhibiting follicular maturation and development of the dominant follicle.  These result in the polycystic appearance of the ovary and the anovulatory symptoms.
  96. 96. Extrinsic factors Contributing to Dysregulated Steroidogenesis  The insulin/insulin-like growth factors (IGF) system is capable of acting in synergy with trophic hormones, contributing to ovarian or adrenal excess androgen production.  In the ovary, insulin acts in conjunction with LH to enhance androgen production and reverse the LH- induced down-regulation of LH binding sites. Insulin and IGFs increase the activities of multiple steroidogenic enzymes in both the ovaries and adrenal glands.  This suggests that the hyperandrogenemia and obesity of PCOS are mechanistically linked.
  97. 97. Treatment for PCOS in adolescents is directed at the following clinical manifestations: Menstrual irregularity Cutaneous hyperandrogenism, primarily hirsutism and acne Obesity and insulin resistance
  98. 98. TREATMENT FOR PCOS Menstrual irregularity should be treated in adolescents with PCOS because chronic anovulation increases the risk of developing endometrial hyperplasia, which is associated with endometrial carcinoma. In addition, anemia can result from dysfunctional uterine bleeding or menorrhagia.
  99. 99. TREATMENT FOR PCOS  The combination oral contraceptive pill (OCP), which contains estrogen and progestin, usually is the first-line treatment for adolescents with PCOS and menstrual irregularity, especially in patients with cutaneous signs of androgen excess.  OCPs induce regular menstrual periods with a higher degree of reliability than other forms of treatment.  Progestin inhibits endometrial proliferation, preventing hyperplasia. Estrogen inhibits the activity of the hypothalamic-pituitary-gonadal axis, reducing ovarian androgen production as well as increasing serum sex hormone binding globulin (SHBG) levels.  OCP therapy also will normalize androgen levels within 18 to 21 days.  After three months, the efficacy of treatment is assessed by evaluating clinical symptoms and androgen levels. If the treatment is effective, as a general rule, OCPs should be continued until the patient is gynecologically mature (five years postmenarcheal). 
  100. 100. TREATMENT FOR PCOS Limitations — The role of OCPs in the management of PCOS in adolescents may be limited for several reasons:  OCP therapy may make weight loss more difficult to attain because it promotes salt and water retention.  The patient may believe the treatment is curative and defer a definitive diagnostic work-up.  OCPs do not permit conception if and when it is desired.  In perimenarcheal girls with short stature who have open epiphyses, OCPs are contraindicated because OCPs contain growth-inhibitory amounts of estrogen.
  101. 101. TREATMENT FOR PCOS Progestin Glucocorticoid GnRH agonists
  102. 102. OBESITY AND INSULIN RESISTANCE  The treatment of obesity improves ovulation, acanthosis nigricans, androgen excess, and cardiovascular risk in patients with PCOS.  Weight reduction is indicated in obese patients with PCOS as part of a program to reduce cardiovascular risk factors.  Diet and exercise are the first-line treatment for obese adolescents with PCOS as for obese individuals without PCOS.
  103. 103. Insulin Resistance  Obesity is of major importance in the insulin resistance of PCOS, although insulin resistance is disproportionate to the degree of adiposity. Insulin resistance is commonly manifested as acanthosis nigricans  The biguanides, of which metformin is the only one available in the US are thus a potential adjunct in the treatment of PCOS; thiazolidinediones also are effective in reducing insulin levels, but have raised safety concerns, as discussed below.  Although their mechanisms of action differ, both metformin and thiazolidinediones reduce insulin concentrations, promote ovulation, and lower androgen levels  Metformin is the only one of these agents that we currently use in adolescents with PCOS because of concerns of weight gain and rare hepatic and possible cardiac toxicity with thiazolidinediones.  Randomized, placebo-controlled trials in adolescents and adults have shown that metformin significantly increases the frequency of menses and ovulation (by about 50 percent), and lowers testosterone levels (by about 20 percent).
  104. 104. Pharmacologic Management Changed Amlodipine 5mg to Losartan 50mg/tab as there was no change for one month. Prevent target organ damage and decreased fluid retention 1st Follow-up April 2012
  105. 105. MY USE COUNSELING/MOTIVATIONAL INTERVIEW  I once again asked the patient how she was doing. How did she feel about the diet change? I asked if she was fully aware and really understood her condition.  “ok lang” “Ginagawa ko rin dahil sa mama ko.”  I asked her if she still remembers what I told her about the health risks involved with hypertension and obesity.  She said “Opo doc, naala ko naman.”  I asked her if her overweight condition made her conscious with her appearance, she said NO during the 1st consult, but she did admitted that it started to beome a concern especially when some of her classmates teases her. She also wanted to be noticed by her crush.
  106. 106. BEHAVIOR CHANGE TOOL AND DECISIONAL BALANCE TECHNIQUE  I asked her what are her goals in life.  She said she wants to work as an engineer and have a family for own. She wants to travel and meet lots of new friends.  I asked her what does eating to much and having a sedentary lifestyle has to do with her dream...  “Magkakasakit ako palagi at baka palagi nasa hospital”.
  107. 107. BEHAVIOR CHANGE TOOL AND DECISIONAL BALANCE TECHNIQUE  I used the Decisional Balance technique for my patient….
  108. 108. Decisional Balance  "reflects the individual's relative weighing of the pros and cons of changing.“  Decision making was conceptualized by Janis and Mann as a "decisional balance sheet" of comparative potential gains and losses.“  Decisional balance measures, the pros and the cons, have become critical constructs in the Transtheoretical Model  Sound decision making requires the consideration of the potential benefits (pros) and costs (cons) associated with a behavior's consequences.
  109. 109. Decisional Balance  Decisional balance is one of the best predictors of future change. TTM research has found the following relationships between the pros, cons, and the stage of change across 48 behaviors and over 100 populations studied.  The cons of changing outweigh the pros in the Pre- contemplation stage.  The pros surpass the cons in the middle stages.  The pros outweigh the cons in the Action stage
  110. 110. Decisional Balance Maintaining Current Use Changing Use Pattern Benefits Benefits Costs Costs “Masarap” “Hindi Magkakasakit” “Gaganda Ako “ “Mas Okay ang suot” “Magkakasakit ako” “Mas lalo tumaba” “Hindi na masarap”
  111. 111. BEHAVIOR CHANGE TOOL AND DECISIONAL BALANCE TECHNIQUE She then realized that she would have to change. The patient is now willing to change hence I made a treatment plan to target obesity hence decreased incidence of hypertension.
  112. 112. Hypertension, Metabolic Syndrome, PCOS Obesity Lifestyle modification Behavioral Change and Motivation
  113. 113. Treat Obesity Improve symptoms and minimize health risks
  114. 114. APPROACH ON TREATMENT TO OBESITY According the AAP’s Recommendations for Treatment of Child and Adolescent Overweight and Obesity— Comprehensive interventions that include behavioral therapy along with changes in nutrition and physical activity are the most closely studied and seem to be the most successful approaches to improving long-term weight and health status.
  115. 115. APPROACH ON TREATMENT TO OBESITY  In the study…showed a guideline on how to treat and manage adolescent obesity based on 1. Nutritional Treatment 2. Macronutrient Therapy 3. Food Behaviors 4. Dietary Interventions 5. Physical Activity and Reducing Sedentary Activities 6. Behavioral Approaches 7. Other Interventions 8. Recommendations of Stages of Treatment
  116. 116. APPROACH ON TREATMENT TO OBESITY Nutritional Treatment In the guideline, it reviewed nutritional treatment for our patient to decrease obesity which included:  Fruits and Vegetables  Fruit Juice  Sweetened Beverage  Dairy Food  Calcium  Dietary fiber Eight studies evaluating the relationship between fruit and/or vegetable intake and body weight were reviewed. All had mixed results but two studies found an inverse association with adiposity.
  117. 117. APPROACH ON TREATMENT TO OBESITY Macronutrient Therapy Carbohydrate Fat Protein
  118. 118. Glycemic index  Glycemic index (GI) has been proposed to affect body weight regulation and risk for obesity- associated complications.80 The GI is defined as the area under the glucose dose-response curve after consumption of 50 g of available carbohydrate from a test food, divided by the area under the curve after consumption of 50 g of available carbohydrate from a control food (either white bread or glucose).  Short-term feeding studies indicated that hunger and cumulative food intake were greater 3 to 5 hours after a high-GI versus low-GI meal, controlled for macronutrient and energy contents.
  119. 119. FOOD BEHAVIORS In terms of the FOOD BEHAVIORS of our patient  Breakfast Skipping  Snacking  Eating Out
  120. 120. DIETARY INTERVENTIONS Balanced-Macronutrient/Low-Energy Diet Salt reduced-energy diet The traffic light diet The Food Guide Pyramid
  121. 121. PHYSICAL ACTIVITY It used these measurements to calculate physical activity levels, as follows: physical activity level-total energy and expenditure/basal metabolic rate.
  122. 122. Amount of Physical Activity  The American Academy of Pediatrics recommends that 30 minutes of this activity occur during the school day. Very obese children may need to start with shorter periods of activity and gradually increase the time spent being active.  Reducing Sedentary Activities  Television Viewing and Obesity
  123. 123. Weight Recommendations According to Age and BMI Percentile
  124. 124. The AAP guideline provided a systematic approach which to manage obesity patients. The staged-care process is divided into 4 stages, that is: (1) Prevention Plus (healthy lifestyle changes) (2) Structured weight management (3) Comprehensive multidisciplinary intervention (4) tertiary care intervention.
  125. 125. Weight Recommendations According to Age and BMI Percentile
  126. 126. NONPHARMACOLOGIC PLAN  A. Use Prevention Plus Stage 1 Intervention  Using the algorithm, our patient is at the >99 percentile hence a Prevention Plus Stage 1 interventions should be based on the family’s readiness to change and include the following: 1. Consumption of 5 servings of fruits and vegetables per day 2. Minimization or elimination of sugar-sweetened beverages 3. Limits of 2 hours of screen time per day, no television in the room where the child sleeps, and no television viewing 4. 1 hour of physical activity per day  Physical activity can be increased gradually for sedentary children. Children may be unable to achieve 1 hour of activity per day initially but can gradually increase activity to reach 1 hour/day.
  127. 127. B. Stricter implementation on the Diet Low Energy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet and a strict decrease of salt content. C. Establishing an exercise plan Jogging at their area for 40 min starting from moderate to vigorous aerobic-based physical activity 3–5 days/week. NONPHARMACOLOGIC PLAN
  128. 128. My plan for Metabolic Syndrome
  129. 129. My Plan for PCOS
  130. 130. 2nd follow-up May 2012  S> Weight loss of 8 pounds for 2 monthS. Lessen of BP from 150/90 to 130/80… No OB consult yet.Patient was advised to take OB consult in the near future.Patient still has no menstruation. Management  Maintain medicines and continued diet and exercise plan.  Stop Losartan I also advised that their family; the parents and her brothers and sisters to seek consult for the obesity problem as well.
  131. 131. 3rd Follow-up August 2012  Patient had weight loss of 2 pounds but having trouble to maintain diet and exercise during the school year due to the availability of food and temptations. BP lowered to 120/80. Patient started to play badminton with family and still continue to jog if she has free time. Plan:  Advise to have a more structured diet and exercise to adapt to school by having a list of food to eart in day. Patient was advised to have cooked food from home
  132. 132. September 2012 S> Plan
  133. 133. Long Term Plan
  134. 134. PSYCHOSOCIAL ISSUES - ADOLESCENT ISSUES Self-Image Addiction to TV and Facebook Role of parents in adolescence
  135. 135. WELLNESS PLAN FOR THE PATIENT Lifestyle  Continue the Prevention Plus Plan for our patient with a advice increase Physical and outdoor activities. Screening  Patient was advised an annual screening to detect organ damage and risk of other disease like Type II Diabetes  Immunizations- Influenza vaccine yearly, Varicella vaccine.
  136. 136. GOING BACK TO THE PATIENT  The good news is that the patient’s BP is at 120-130/80-90.  Patient hasn’t made substantial weight loss, but the good thing is that during the past three months her lifestyle changed dramatically when compared alongside the years that she was excessively eating. She started to gain self-confidence since the change of eating habits. The family changed their eating habits and have modified their lifestyle accordingly too.
  137. 137. Insight Holistic care Interrelationship of Diseases The Importance of Lifestyle for being Healthy Counseling and Motivation Behavior change as part of being a Doctor The power of change Caring for patient is not a shot deal, have to do lots of follow-up and evaluation Importance of education and value formation in children and adults ( School and Government)
  138. 138. Insight Suggestions:  Comprehensive Government Plan to Educate and Change the Lifestyle of our Youth  Insight (slide) My message to everyone…  As doctors, we are privileged to have the power to change lives. Let us go forth and use this opportunity to be an instrument towards positive change.