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Summary Table

Feature	Detail
Risk Factors	Family history of obesity/cardiometabolic disease, sedentary lifestyle, high-calorie diet, medications (insulin, sulfonylureas, TZDs, beta-blockers, glucocorticoids, atypical antipsychotics with -pine/-done suffix, TCAs, valproate, lithium, antihistamines), psychiatric disorders (depression, binge eating disorder, ADHD), poor sleep quality, low socioeconomic status
Etiology	Chronic metabolic disease with complex, multifactorial causation; the balance between dietary intake and energy expenditure is central. Visceral adipocyte accumulation drives systemic and vascular inflammation
Patient Presentation	Weight gain, increased waist circumference, fatigue, dyspnea on moderate exertion, joint pain (knees, low back), snoring/daytime somnolence, acanthosis nigricans
Classic Physical Exam	BMI $\geq 25\ \text{kg/m}^2$ (Asia-Pacific), waist circumference >90 cm (male) / >80 cm (female), acanthosis nigricans, moon facies (if secondary cause), goiter (if hypothyroid)
Key Diagnostic Results	BMI and waist circumference confirm diagnosis; lipid profile, fasting glucose/OGTT/HbA1c, liver enzymes, TSH screen for comorbidities; body composition analysis (BIA) identifies sarcopenic obesity (FFMI <17 male, <15 female); EOSS staging classifies severity
Management	Lifestyle modification (diet + exercise + behavioral therapy) is the foundation for all patients. Pharmacotherapy (orlistat, liraglutide, semaglutide, tirzepatide) as adjuvant for BMI $\geq 30$ or $\geq 25$ with comorbid. Bariatric surgery for BMI $\geq 35$ or $\geq 30$ with uncontrolled comorbidities failing medical therapy
Keywords	Acanthosis nigricans, central obesity, metabolic syndrome, Edmonton staging, weight cycling, binge eating, ketosis-induced appetite suppression, dumping syndrome (post-bypass)

1. Pathophysiology

Obesity is a chronic metabolic disease characterized by excessive fat mass accumulation that increases the risk of numerous non-communicable diseases and reduces life expectancy. The fundamental mechanism revolves around a sustained positive energy balance where caloric intake exceeds energy expenditure over prolonged periods.

The critical pathophysiological driver is visceral adipocyte hypertrophy and hyperplasia. As visceral fat depots expand, adipocytes become dysfunctional and shift toward a pro-inflammatory secretory profile. These cells release increased amounts of TNF-alpha, IL-6, and other adipokines while simultaneously reducing adiponectin output. This creates a state of chronic low-grade systemic inflammation that damages vascular endothelium, promotes insulin resistance, and accelerates atherogenesis. This is why obesity is tightly linked to hypertension, type 2 diabetes, dyslipidemia, and coronary artery disease as a cluster rather than isolated conditions.

Insulin resistance is another central mechanism. Excess free fatty acids from enlarged visceral adipocytes impair insulin signaling in skeletal muscle and liver. The pancreas compensates with hyperinsulinemia, which further promotes lipogenesis and sodium retention (contributing to hypertension). Over time, beta-cell exhaustion leads to overt type 2 diabetes. This explains why the metabolic syndrome criteria (waist circumference, triglycerides, HDL, blood pressure, fasting glucose) are all downstream consequences of visceral adiposity.

From a mechanical standpoint, excess body weight places disproportionate stress on weight-bearing joints (particularly the knees), the lumbar spine, and the plantar fascia. This is why osteoarthritis, low back pain, and plantar fasciitis are common musculoskeletal comorbidities. Excess pharyngeal and neck soft tissue contributes to upper airway collapse during sleep, producing obstructive sleep apnea (OSA).

In critically ill patients, obesity increases ICU mortality by 2.52-fold (95% CI 1.3-4.9), prolongs ventilator duration, and raises the risk of surgical site infection by 4.42-fold, ARDS by 1.8-fold, and acute kidney injury by 3.07-fold. These outcomes reflect impaired respiratory mechanics, heightened inflammatory responses, and increased technical difficulty of procedures.

2. Classification and Clinical Manifestation

BMI Classification (Asia-Pacific Criteria)

Classification	BMI (kg/m^2)	Comorbid Risk
Underweight	<18.5	Low (but increases risk of other illness)
Normal	18.5 - 22.9	Average
Overweight	23 - 24.9	Increased
Obesity I	25 - 29.9	Moderate
Obesity II	$\geq 30$	Severe

Waist Circumference Cutoffs (Asia-Pacific Consensus)

Sex	Cutoff
Male	>90 cm
Female	>80 cm

Body Fat Percentage (General Threshold for Obesity)

Sex	Upper Limit of Normal
Male	>25%
Female	>35%

Edmonton Obesity Staging System (EOSS)

This staging system is central to clinical decision-making because it goes beyond BMI alone and incorporates the presence and severity of comorbidities, psychological status, and functional limitations. A patient with BMI 27 but EOSS Stage 3 warrants more aggressive therapy than a patient with BMI 32 at EOSS Stage 0.

Stage	Criteria
Stage 0	No risk factors, no physical symptoms, no psychological symptoms, no functional limitation
Stage 1	Subclinical risk factors (impaired fasting glucose, borderline hypertension, elevated liver enzymes) OR mild physical symptoms not requiring medication (dyspnea on moderate exertion, easy fatigue) OR mild psychological symptoms (not affecting quality of life)
Stage 2	Established comorbidities requiring treatment (hypertension, type 2 DM, PCOS, OSA) OR moderate psychological symptoms (depression, anxiety, eating disorder) OR moderate functional limitation (quality of life affected)
Stage 3	End-organ damage related to obesity (myocardial infarction, heart failure, DM with complications, osteoarthritis) OR severe psychological disturbance (major depression, suicidal ideation) OR clear functional limitation and impaired quality of life
Stage 4	End-stage comorbidities OR severe psychological symptoms OR severe functional limitation (immobility)

Metabolic Syndrome Criteria

Diagnosed when 3 of 5 criteria are met:

Parameter	Male	Female
Waist circumference	>90 cm	>80 cm
Triglycerides	$\geq 150$ mg/dL or on lipid-lowering therapy	Same
HDL cholesterol	<40 mg/dL	<50 mg/dL
Blood pressure	Systolic $\geq 130$ or diastolic $\geq 85$ mmHg, or on antihypertensives	Same
Fasting glucose	$\geq 100$ mg/dL or previously diagnosed type 2 DM	Same

Sarcopenic Obesity Classification

Screened using the SARC-F questionnaire (score $\geq 4$ suggests possible sarcopenia), then confirmed by measuring muscle mass, strength, and function:

Stadium	Muscle Mass	Muscle Strength	Function
Pre-sarcopenia	Decreased	Normal	Normal
Sarcopenia	Decreased	Decreased	Normal
Severe sarcopenia	Decreased	Decreased	Decreased
Dynapenia	Normal	Decreased	Decreased

3. Diagnostic Workup

Test	Purpose	Frequency
BMI + Waist Circumference	Screening and diagnosis	Every visit
Lipid profile (TC, HDL, LDL, TG)	Screen metabolic syndrome, cardiovascular risk	Baseline, then every 3 months until controlled
Fasting glucose, 2h OGTT, HbA1c	Screen prediabetes/type 2 DM	Baseline, repeat in 1-2 years if normal
EKG	Detect cardiac abnormalities, pre-exercise clearance	Baseline, repeat as indicated
Liver function (SGOT, SGPT, Gamma-GT)	Screen for hepatic steatosis	If symptomatic, repeat per visit if abnormal
Renal function (Creatinine)	Screen renal impairment	Baseline, repeat if symptomatic
TSH	Screen hypothyroidism	Baseline
Leukocyte count, Neutrophil count, ESR	Screen for chronic inflammation	Baseline
BIA (body composition)	Measure fat mass, FFMI (sarcopenic obesity screening)	Baseline and follow-up
Abdominal USG	Detect hepatic steatosis, renal or reproductive abnormalities	If indicated
Chest X-ray	Cardiomegaly, aortic calcification	If indicated
Knee X-ray	Osteoarthritis screening	If indicated

The best initial step in diagnosis is anthropometry: calculating BMI and measuring waist circumference. For Asia-Pacific populations, obesity is defined as BMI $\geq 25\ \text{kg/m}^2$ with waist circumference >90 cm (male) or >80 cm (female). This is lower than the WHO global cutoff of $\geq 30\ \text{kg/m}^2$, a frequent source of confusion.

Once obesity is established, the priority shifts to screening for comorbidities rather than confirming the obesity itself. The routine workup includes a lipid profile, fasting glucose with OGTT and HbA1c, and an EKG. These are ordered to detect metabolic syndrome, prediabetes or type 2 DM, and baseline cardiac status. Liver enzymes are checked for hepatic steatosis. TSH is obtained to rule out hypothyroidism as a contributing or exacerbating factor.

Body composition analysis via bioimpedance analysis (BIA) provides additional value beyond BMI. It measures fat-free mass index (FFMI), which is essential for identifying sarcopenic obesity, a condition where fat mass replaces muscle mass. Normal FFMI cutoffs are $\geq 17\ \text{kg/m}^2$ for males and $\geq 15\ \text{kg/m}^2$ for females. BMI alone can miss sarcopenic obesity entirely because muscle loss is masked by fat gain.

For cardiovascular risk stratification in obese patients, stress echocardiography is the preferred noninvasive cardiac imaging modality because it has no weight limit, no radiation, and maintains diagnostic validity in obese patients. In contrast, standard EKG has low sensitivity and sensitivity for ischemia detection in this population, and CT/MRI-based methods face technical limitations from body habitus (image degradation, bore size, weight limits).

EOSS staging is then performed by integrating all clinical findings to classify the patient into Stage 0-4, which directly guides therapeutic intensity.

4. Management and Treatment

IMT Category	Therapy Approach
25-29.9 without comorbid	Lifestyle modification (diet, exercise, behavioral therapy) at primary care
25-29.9 with comorbid, or $\geq 30$	Lifestyle modification + pharmacotherapy. Refer to secondary/tertiary care if no >5% weight loss in 3 months
$\geq 30$ with uncontrolled comorbid failing medical therapy	All of the above + bariatric endoscopy or surgery
$\geq 35$ with or without comorbid	Eligible for bariatric surgery

Pharmacotherapy Summary

Drug	Mechanism	Dose	Key Side Effects	Contraindications	Success Criteria
Orlistat	Lipase inhibitor	3 x 120 mg PO	Steatorrhea, fecal urgency, flatus, oily spotting	Pregnancy, chronic malabsorption, cholestasis	>5% weight loss in 12 weeks
Liraglutide	GLP-1 agonist	Titrate 0.6 mg/day SC up to 3.0 mg/day	Nausea, vomiting, diarrhea, tachycardia	Pregnancy, medullary thyroid cancer/MEN2 history, pancreatitis, gastroparesis	>5% weight loss in 12 weeks; discontinue if <4% loss at 16 weeks
Semaglutide	Long-acting GLP-1 agonist	Titrate 0.25 mg/week SC up to 2.4 mg/week (q4 week dose escalation)	Nausea, vomiting, constipation	Same as liraglutide	>5% weight loss in 12 weeks
Tirzepatide	Dual GLP-1/GIP agonist	2.5 mg/week SC, escalate by 5 mg q4 weeks to max 15 mg/week	Nausea, vomiting, diarrhea, sinus tachycardia	Same as liraglutide	>5% weight loss in 12 weeks

Bariatric Surgery Summary

Procedure	Target Weight Loss	Key Advantage	Key Risk
Roux-en-Y gastric bypass	30-35%	Strong metabolic effect, effective for GERD	Marginal ulcer, internal hernia, long-term micronutrient deficiency
Sleeve gastrectomy	25-30%	Technically simpler, no anastomosis	Leak is difficult to manage, 20-30% develop GERD
Biliopancreatic diversion with duodenal switch	35-45%	Strongest metabolic effect, durable weight loss	Malabsorption risk, 3-5% protein-calorie malnutrition
Endoscopic sleeve gastroplasty	15-20%	Minimally invasive, repeatable, no incision	Risk of suture dehiscence
Intragastric balloon	10-12%	Via endoscopy, good safety profile	Temporary (6 months), 10-19% early removal rate

Phase 1: Lifestyle Modification (All Patients)

This is the foundation for every obesity patient regardless of BMI or comorbidity status.

Nutritional therapy centers on caloric restriction. The most evidence-supported approach is reducing total daily energy intake by 500 kcal with fat restriction (<30% of total calories). Very low-calorie diets (<800 kcal/day) and low-calorie diets (800-1000 kcal/day) require medical supervision and may only be sustained for a maximum of 12 weeks. These approaches can produce 15-25% relative weight loss but carry risk of yo-yo rebound if not managed by experienced practitioners. A high-protein, low-carbohydrate diet achieves more weight loss in the first 6 months due to fluid loss and ketosis-induced appetite suppression, but must be used cautiously in patients with osteoporosis, renal disease, or elevated LDL. The Mediterranean diet reduces risk of coronary artery disease, cancer, and chronic inflammatory disease and emphasizes plant-based foods, whole grains, olive oil, and fish.

Physical activity should combine aerobic exercise ($\geq 5$ times/week, progressing from 150 to 300 minutes/week at moderate intensity), resistance training (2-3 times/week, 2-4 sets of 8-12 reps at 60-70% of 1-RM), and flexibility training ($\geq 2-3$ times/week). Before starting, patients should undergo EKG and spirometry. A realistic target is approximately 4 hours/week of exercise or roughly 2000 kcal/week of energy expenditure. Aerobic exercise at moderate to high intensity reduces visceral and ectopic fat (Level 1a, Grade A evidence) even without weight loss on the scale.

Behavioral therapy requires 12-24 structured sessions. Techniques include goal-setting, self-monitoring of intake and activity, stimulus control (limiting cues to eat), cognitive restructuring (addressing maladaptive thoughts about body image and weight), and motivational interviewing for ambivalent patients. Patients with binge eating disorder or comorbid depression require cognitive behavioral therapy with psychiatric referral.

Phase 2: Pharmacotherapy (Adjuvant)

Indicated for BMI $\geq 30$ or $\geq 25$ with at least one comorbidity, in addition to lifestyle modification. Drug therapy is never standalone.

Orlistat (3 x 120 mg daily) inhibits gastrointestinal lipase, reducing fat absorption by roughly 30%. It produces approximately 2.9 kg weight loss after one year. Side effects (steatorrhea, fecal urgency, oily spotting) diminish when fat intake is restricted. Safe for up to 4 years of use. Contraindicated in cholestasis and chronic malabsorption syndrome.

GLP-1 receptor agonists (liraglutide, semaglutide) and the dual GLP-1/GIP agonist (tirzepatide) work by enhancing satiety signaling, slowing gastric emptying, and improving insulin sensitivity. Semaglutide 2.4 mg/week has demonstrated safety up to 68 weeks. All three share the same contraindication profile: personal/family history of medullary thyroid carcinoma or MEN2, pancreatitis, gastroparesis, and pregnancy. The critical response checkpoint is 3 months: if $\geq 5%$ weight loss is not achieved, the patient is classified as a non-responder and must be switched to a different agent or escalated to bariatric intervention.

For patients with comorbid conditions, the algorithm guides drug selection. In patients with tachycardia or uncontrolled hypertension, phentermine/topiramate and naltrexone/bupropion are avoided. In patients with history of medullary thyroid cancer or pancreatitis, all GLP-1 agonists are contraindicated; naltrexone/bupropion, orlistat, and phentermine/topiramate remain options. For patients on chronic opioid therapy or with seizure history, naltrexone/bupropion is contraindicated.

Psychiatric medication modification is an often-overlooked aspect of obesity management. When antipsychotics or antidepressants contribute to weight gain, switching to weight-neutral alternatives is recommended: olanzapine to aripiprazole or quetiapine, or amitriptyline/mirtazapine to fluoxetine or sertraline. This must be done carefully with monitoring for psychiatric symptom relapse.

Phase 3: Bariatric Intervention

Indications for bariatric surgery include BMI $\geq 35$ (with or without comorbid), BMI 30-34.9 failing medical therapy, or BMI $\geq 30$ with type 2 DM. Absolute contraindications are inability to undergo general anesthesia, uncontrolled psychiatric disorder, active substance abuse, pregnancy, and active malignancy. Even patients with extreme BMI (>70) can undergo surgery safely.

Post-bariatric nutrition follows a strict progression: clear liquids only for 24-48 hours, full liquids with high protein from day 3-14, pureed foods at week 3, soft foods at week 4, gradual reintroduction of solids by weeks 6-8, and full regular diet by 2 months. Protein requirements post-surgery are 1.1-1.5 g/kg/day (up to 2 g/kg/day after biliopancreatic diversion). Lifelong micronutrient supplementation is mandatory, particularly vitamin B1 ($\geq 12$ mg/day), vitamin B12 (350-500 mcg/day PO or 1000 mcg/month IM), folate (400-800 mcg/day), iron, vitamin D3 (3000 IU/day targeting serum level $\geq 30$ ng/mL), and calcium (1200-2400 mg/day depending on procedure type).

Target and Timeline

The realistic weight loss target is 0.5-1 kg per week (Recommendation A). The initial goal is 5-10% of baseline body weight within the first 6 months. If this is unattainable, the minimum acceptable outcome is preventing further weight gain. Long-term maintenance targets 10-20% total weight loss from baseline.

5. Differential Diagnosis and Distractors

Obesity itself has no differential diagnosis per the PNPK. However, the exam frequently tests whether the student can distinguish primary (exogenous) obesity from secondary causes and comorbid look-alikes.

Distractor	Why It Is Similar	Key Discriminator
Cushing syndrome	Central obesity, moon facies, weight gain, hypertension, hyperglycemia	Look for purple striae (not white), proximal muscle weakness, easy bruising, buffalo hump. Confirm with 24h urinary free cortisol or overnight dexamethasone suppression test
Hypothyroidism	Weight gain, fatigue, constipation	Hypothyroid patients gain modest weight (5-10 kg, mostly fluid), not the degree seen in primary obesity. TSH is elevated, free T4 is low
Polycystic ovarian syndrome (PCOS)	Obesity, insulin resistance, acanthosis nigricans in young women	PCOS presents with menstrual irregularity, hirsutism, and anovulatory infertility. Obesity is a feature of PCOS, not the other way around
Metabolic syndrome	Overlapping criteria with obesity (waist circumference, lipids, glucose, BP)	Metabolic syndrome is a comorbid cluster diagnosed by meeting 3 of 5 criteria. Obesity is one component, not the syndrome itself
Sarcopenic obesity	Patient may have a normal or only mildly elevated BMI but high body fat and low muscle mass	SARC-F score $\geq 4$, low FFMI on BIA, low handgrip strength, slow gait speed. BMI alone will miss this diagnosis
Medication-induced weight gain	Progressive weight gain temporally related to drug initiation	History of starting insulin, sulfonylureas, TZDs, olanzapine, clozapine, valproate, glucocorticoids, or mirtazapine. Weight gain resolves or stabilizes with drug substitution
Binge eating disorder	Recurrent episodes of excess intake leading to obesity	Unlike simple obesity, binge eating involves discrete episodes of loss-of-control eating without compensatory purging. Requires psychiatric evaluation and CBT

6. Traps and High-Yield Pearls

The most common mistake students make with obesity questions is treating BMI as the sole diagnostic and therapeutic criterion. The PNPK explicitly states that diagnosis is not limited to BMI cutoff values alone; the Edmonton Obesity Staging System must be applied to determine the presence and severity of complications (cardiometabolic, mechanical, and mental). A question may present a patient with BMI 26 but with uncontrolled type 2 DM, OSA, and depression, and the correct answer is that this patient warrants pharmacotherapy and possibly surgical referral, not just lifestyle counseling.

A second trap involves the Asia-Pacific BMI cutoffs. Students accustomed to WHO global criteria will miss the diagnosis entirely. For Asia-Pacific populations, overweight begins at BMI 23 and obesity at BMI 25, not 25 and 30 respectively.

Third, students often confuse the pharmacotherapy response checkpoint. After starting any anti-obesity medication, the patient must be reassessed at 3 months (12 weeks). A responder is someone who achieves $\geq 5%$ weight loss; for liraglutide, specifically, if <4% weight loss is achieved at 16 weeks, the drug must be discontinued. Continuing an ineffective drug is a wrong answer.

Fourth, the role of pharmacotherapy as adjuvant only is frequently tested. Medications are never first-line standalone therapy. Every patient must have a concurrent program of nutritional modification, structured physical activity, and behavioral intervention. A vignette that jumps straight to semaglutide without establishing lifestyle modification is testing whether you will choose the answer that includes the foundational therapy first.

Finally, bariatric surgery questions often hinge on the contraindication list. The absolute contraindications (inability to tolerate general anesthesia, uncontrolled psychiatric disorder, active substance abuse, pregnancy, active malignancy) must be memorized. A common distractor is offering surgery to a patient with uncontrolled schizophrenia or active IV drug use, both of which are absolute contraindications regardless of BMI.

The core competency being tested is the ability to stage obesity severity beyond BMI, select therapy intensity based on staging and comorbidity burden, and apply pharmacotherapy response thresholds to make evidence-based escalation decisions.

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