Obesity: assessment, complications and treatment — formative SAQs

SAQ 1 — Classification, comorbidity screening and secondary-cause exclusion (10 marks)

A 10-year-old boy is referred because his BMI plots above the 97th percentile for age and sex. He has acanthosis nigricans and his father has type 2 diabetes. The father asks whether his son is "obese and sick," and wants to know what to do. [1] [5]

Questions

1. Classify his weight status using the correct BMI-for-age definitions, and state the severe-obesity threshold and the adult crossover. (3 marks) [1] [5]
2. Outline the baseline comorbidity investigations you would order and why, naming the four core screens. (4 marks) [1] [2]
3. Describe how you would decide whether to investigate for a secondary or syndromic cause, and which red-flag features would trigger testing. (3 marks) [2]

Model answer

Classification (3). Obesity is defined as a BMI at or above the 95th percentile for age and sex on a CDC or WHO growth reference; this boy plots above the 97th percentile, so he meets obesity. Severe obesity is defined as a BMI at least 120 percent of the 95th percentile, or an absolute BMI of at least 35. I would calculate his percentage of the 95th percentile to determine whether he has crossed into severe obesity, because that threshold drives escalation. At 18 years the classification switches to adult cut-offs (overweight at least 25, obesity at least 30). I would use person-first, weight-neutral language with the family rather than the word "obese" directed at the child. [1] [5]

Baseline comorbidity investigations (4). The four core screens are fasting glucose or HbA1c to detect pre-diabetes or type 2 diabetes (warranted by his acanthosis and family history), a fasting lipid panel for dyslipidaemia, ALT to screen for metabolic dysfunction-associated steatotic liver disease, and blood pressure with an appropriately sized cuff. I would add an oral glucose tolerance test if fasting glucose sits in the pre-diabetes range. Given his acanthosis, I am specifically alert to insulin resistance and glucose intolerance. [1] [2]

Secondary-cause work-up (3). Secondary-cause testing is selective, not universal, and is triggered by red-flag features. In a thriving child of normal height with a straightforward family history, a blanket endocrine screen has a low yield. I would investigate if he had short stature relative to the family, decelerating growth, developmental delay, dysmorphism, hyperphagia, Cushingoid features, or a temporal link to a medication. In this boy, the acanthosis and family history point to primary insulin resistance, so I would not order TSH, cortisol or genetic testing unless a red flag emerged. [2]

SAQ 2 — Staged management and comorbidity-directed treatment (10 marks)

A 15-year-old girl has a BMI of 38 kg/m² with newly diagnosed impaired glucose tolerance and a persistently elevated ALT. She reports years of weight-based bullying and low mood. Her mother asks whether anything beyond "diet and exercise" can help. [1] [5]

Questions

1. Outline the staged management plan, naming each stage and the escalation trigger. (4 marks) [1] [5]
2. Justify the role of pharmacotherapy and surgery for her severe obesity, citing the relevant evidence. (4 marks) [12] [13] [6]
3. Describe how you would treat her comorbidities in parallel with the weight intervention, including her elevated ALT. (2 marks) [7] [1]

Model answer

Staged management (4). Stage 1 is lifestyle for every patient: at least 60 minutes of moderate-to-vigorous activity daily, a sustainable healthy eating pattern, sleep optimisation, and reduced recreational screen time, delivered with motivational interviewing and framed around health behaviours rather than weight. Stage 2 is structured multidisciplinary paediatric weight management adding dietetics, psychology and exercise physiology. Stage 3 is anti-obesity pharmacotherapy, which she has reached immediately because she has severe obesity with a comorbidity. Stage 4 is metabolic and bariatric surgery at a specialist centre. The escalation trigger is failure to improve after three to six months at the current stage, combined with comorbidity burden and the family's readiness. [1] [5]

Pharmacotherapy and surgery rationale (4). Because severe obesity rarely responds to lifestyle alone, the evidence supports escalation. 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. Surgery is endorsed for carefully selected adolescents with severe obesity; a common threshold is a BMI at least 35 with a comorbidity. The Teen-LABS data by Inge and colleagues showed bariatric surgery achieved markedly better type 2 diabetes outcomes than medical therapy in severely obese adolescents, supporting surgery as evidence-based rather than extreme care. [12] [13] [6]

Parallel comorbidity treatment (2). I would treat the impaired glucose tolerance with metformin alongside lifestyle, and address the elevated ALT per the NASPGHAN guideline with a liver ultrasound and gastroenterology referral, recognising that ultrasound is insensitive for early steatosis so a normal scan does not exclude disease. Her low mood and weight-based bullying require screening and psychology input, and throughout I would use weight-neutral, person-first language because weight stigma itself worsens every outcome. [7] [1]