Obesity: assessment, complications and treatment — branching viva

Stem

The examiner will test whether you can reason through childhood obesity classification under pressure, integrate systematic comorbidity screening and selective secondary-cause exclusion, and defend a staged, weight-neutral management plan that escalates appropriately for severe disease. [1] [2]

Branch 1 — Classification and comorbidity screening

Examiner: A 10-year-old plots above the 97th percentile on his growth chart. Is he obese, and what does that definition rest on? [1]

Strong answer: Yes. Obesity in the two-to-nineteen age group is defined as a BMI at or above the 95th percentile for age and sex on a CDC or WHO growth reference. His BMI above the 97th percentile clearly meets that. I would also calculate his percentage of the 95th percentile, because severe obesity is defined as at least 120 percent of the 95th percentile or an absolute BMI of at least 35, and that threshold drives escalation. [1] [5]

Examiner: What baseline investigations do you order? [2]

Strong answer: The four core baseline screens are fasting glucose or HbA1c for pre-diabetes and type 2 diabetes, a fasting lipid panel for dyslipidaemia, ALT for metabolic dysfunction-associated steatotic liver disease, and blood pressure with an appropriately sized cuff. I add an oral glucose tolerance test if fasting glucose sits in the pre-diabetes range. I would also screen his mental health and eating behaviour, because these are investigations in their own right that change the plan. [1] [2]

Branch 2 — Secondary-cause exclusion

Examiner: How do you decide whether to look for a secondary or syndromic cause? [2]

Strong answer: Secondary-cause testing is selective rather than universal. In a thriving child of normal height with a straightforward family history, a blanket endocrine screen has a low yield. I investigate when red-flag features are present — short stature relative to the family, decelerating growth, developmental delay, dysmorphism, hyperphagia, Cushingoid features, or a clear temporal link to a medication such as a glucocorticoid or antipsychotic. Those fingerprints trigger targeted testing such as TSH, a morning cortisol or dexamethasone suppression test, IGF-1, and genetic testing for syndromes such as Prader-Willi or the MC4R pathway. [2]

Examiner: Give an example of a syndromic cause and why it matters. [2]

Strong answer: Prader-Willi syndrome presents with infantile hypotonia, short stature, hyperphagia, developmental delay and obesity. It matters because some monogenic and syndromic obesities have targeted therapy — recombinant leptin for leptin deficiency, or setmelanotide for certain MC4R-pathway defects — so accurate genetic sub-typing changes management rather than leaving these children labelled as lifestyle failure. [2]

Branch 3 — Staged treatment

Examiner: Outline your staged management. [1]

Strong answer: Stage 1 is lifestyle for every patient: at least 60 minutes of moderate-to-vigorous activity daily, a sustainable healthy eating pattern, sleep optimisation, reduced recreational screen time, delivered with motivational interviewing and framed around health behaviours. Stage 2 is structured multidisciplinary weight management. Stage 3 is anti-obesity pharmacotherapy, escalated to for moderate-to-severe obesity or when earlier stages have not worked after three to six months. Stage 4 is metabolic and bariatric surgery at a specialist centre. Comorbidity treatment runs in parallel at every stage. [1]

Examiner: What pharmacotherapy options exist and what is the evidence? [12]

Strong answer: Orlistat inhibits pancreatic lipase and is given as 120 mg three times daily with meals, with fat-soluble-vitamin monitoring. GLP-1 receptor agonists are now first-line Stage 3 therapy: the liraglutide trial by Kelly and colleagues demonstrated BMI reduction in adolescents with obesity, and the once-weekly semaglutide trial by Weghuber and colleagues extended this benefit. Metformin is used for insulin resistance or type 2 diabetes alongside these agents. [12] [13]

Branch 4 — Surgery and comorbidity-directed care

Examiner: When do you consider surgery, and what does the evidence show? [6]

Strong answer: Surgery is considered for severe obesity, with a common threshold of a BMI at least 35 with a comorbidity or at least 40 without, at an accredited specialist centre with lifelong follow-up and full family consent. The Teen-LABS data by Inge and colleagues showed bariatric surgery achieved far better type 2 diabetes remission than medical therapy in severely obese adolescents. I would not leave severe obesity with diabetes risk on lifestyle and metformin alone when surgery is evidence-based. [6] [5]

Examiner: How do you manage a persistently elevated ALT found on screening? [7]

Strong answer: Per the NASPGHAN guideline, persistently elevated ALT warrants a liver ultrasound and gastroenterology referral. A normal ultrasound does not exclude early steatosis because the scan is insensitive for it. I treat the comorbidity in parallel with the weight intervention, and measure success through liver-enzyme normalisation and comorbidity resolution alongside health behaviours, not the scale alone. [7] [1]

Branch 5 — Prognosis and pitfalls

Examiner: What is the long-term prognosis, and what is the most damaging pitfall? [4]

Strong answer: Childhood obesity tracks strongly into adult obesity and morbidity, with the risk scaling with severity and persistence; the Simmonds meta-analysis found a child with obesity is roughly five times more likely to become an adult with obesity. Treating comorbidities early and well is among the most consequential things I can do. The most damaging pitfall is weight stigma in clinical settings, which reduces engagement, worsens mental health, and paradoxically worsens the obesity — so I use weight-neutral, person-first language and measure success beyond BMI. [4] [1]

Examiner extras

• State the BMI percentile definition and the severe-obesity threshold precisely in your opening classification answer. [1] [5]
• Name all four baseline comorbidity screens — glucose, lipids, ALT, blood pressure — before moving on. [1]
• Always present lifestyle as the foundation, then justify escalation for severe disease. [1]
• Frame secondary-cause testing as selective, triggered by red-flag features. [2]
• Name GLP-1 receptor agonists as evidence-based Stage 3 therapy and cite the trials. [12] [13]