NEET SS Endocrinology (DM) Syllabus

Endocrinology (DM) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Endocrinology (DM) in NEET SS, not a summary of it.

1. 1

   Diabetes Mellitus and Metabolic Disorders

   4 topics

   • Classification and Pathophysiology of Diabetes
     • Type 1, type 2, MODY and secondary diabetes
   • Pharmacotherapy of Diabetes
     • Oral agents, GLP-1 RA and insulin regimens
   • Acute and Chronic Complications
     • DKA and hyperosmolar hyperglycemic state
     • Microvascular and macrovascular complications
   • Obesity and Dyslipidemia
     • Metabolic syndrome
2. 2

   Thyroid Disorders

   3 topics

   • Hyperthyroidism
     • Graves' disease and thyroid storm
   • Hypothyroidism and Thyroiditis
     • Hashimoto's and subacute thyroiditis
   • Thyroid Nodules and Cancer
     • FNAC and Bethesda system
3. 3

   Pituitary and Adrenal Disorders

   3 topics

   • Pituitary Adenomas
     • Acromegaly and prolactinoma
     • Hypopituitarism
   • Adrenal Cortical Disorders
     • Cushing's syndrome and Addison's disease
     • Primary aldosteronism
   • Adrenal Medulla and Incidentaloma
     • Pheochromocytoma
4. 4

   Calcium, Bone, Gonadal and Genetic Endocrine Disorders

   3 topics

   • Calcium and Bone Metabolism
     • Hyperparathyroidism and hypoparathyroidism
     • Osteoporosis and metabolic bone disease
   • Reproductive Endocrinology
     • PCOS and hypogonadism
     • Disorders of sexual differentiation
   • Multiple Endocrine Neoplasia and Genetic Syndromes
     • MEN 1 and MEN 2

Endocrinology (DM) flashcards for NEET SS

19 of 51 cards from the Endocrinology (DM) deck — real questions with worked answers.

1. What are the diagnostic glycemic criteria for diabetes mellitus (ADA)?

   FPG ≥126 mg/dL, 2-hr OGTT (75g) plasma glucose ≥200 mg/dL, HbA1c ≥6.5%, or random glucose ≥200 mg/dL with classic symptoms. Confirm with a repeat test unless unequivocal hyperglycemia.

2. What defines prediabetes by FPG, OGTT, and HbA1c?

   Impaired fasting glucose (IFG): FPG 100-125 mg/dL; Impaired glucose tolerance (IGT): 2-hr OGTT 140-199 mg/dL; HbA1c 5.7-6.4%.

3. Contrast the pathophysiology of Type 1 vs Type 2 diabetes.

   Type 1: autoimmune T-cell-mediated destruction of pancreatic beta cells causing absolute insulin deficiency (anti-GAD65, IA-2, ZnT8, islet-cell antibodies). Type 2: insulin resistance plus relative insulin secretory defect, associated with obesity; no autoimmunity.

4. What is MODY and how does it differ from type 1/2 diabetes?

   Maturity-Onset Diabetes of the Young: autosomal dominant monogenic diabetes, onset <25 yr, non-obese, non-ketotic, no autoantibodies. Common types: HNF1A (MODY3, sulfonylurea-responsive), GCK (MODY2, mild stable hyperglycemia), HNF4A (MODY1).

5. What are the key features of Latent Autoimmune Diabetes in Adults (LADA)?

   Adult-onset autoimmune diabetes with positive GAD antibodies, initially non-insulin-requiring (slow beta-cell failure), often misdiagnosed as type 2; progresses to insulin dependence faster than type 2.

6. List the classes of oral antidiabetic drugs and their primary mechanisms.

   Biguanides (metformin)—decrease hepatic gluconeogenesis; Sulfonylureas/meglitinides—stimulate insulin secretion; TZDs—PPAR-gamma agonists improve insulin sensitivity; DPP-4 inhibitors—increase incretins; SGLT2 inhibitors—increase renal glucose excretion; alpha-glucosidase inhibitors—delay carbohydrate absorption.

7. What are the cardiovascular and renal benefits of SGLT2 inhibitors?

   Reduce heart failure hospitalization, MACE, and progression of CKD; slow eGFR decline and reduce albuminuria independent of glucose lowering. Examples: empagliflozin, dapagliflozin, canagliflozin.

8. What is the mechanism and key benefit of GLP-1 receptor agonists?

   Mimic incretin GLP-1: glucose-dependent insulin secretion, suppress glucagon, delay gastric emptying, promote satiety/weight loss; semaglutide/liraglutide reduce cardiovascular events. Risk: nausea, pancreatitis, contraindicated in personal/family history of medullary thyroid cancer/MEN2.

9. Why is metformin the first-line agent in type 2 diabetes, and what is its main serious adverse effect?

   Weight-neutral, no hypoglycemia, low cost, cardiovascular benefit. Main serious adverse effect: lactic acidosis (risk in renal impairment/hypoxia); also B12 deficiency. Avoid if eGFR <30.

10. State the diagnostic criteria for diabetic ketoacidosis (DKA).

    Hyperglycemia (>250 mg/dL), high anion gap metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L), and ketonemia/ketonuria. Caused by absolute insulin deficiency with elevated counter-regulatory hormones.

11. How does hyperosmolar hyperglycemic state (HHS) differ from DKA?

    HHS: marked hyperglycemia (often >600 mg/dL), serum osmolality >320 mOsm/kg, minimal/no ketosis and acidosis (pH >7.3, bicarb >18), profound dehydration, altered mental status. Typically type 2 with residual insulin.

12. Outline the management priorities in DKA.

    1) IV fluids (normal saline) for volume; 2) IV insulin infusion; 3) Potassium replacement (insulin drives K into cells—start K when <5.2 and urine output adequate); 4) treat precipitant. Monitor glucose, electrolytes, anion gap closure.

13. What are the microvascular and macrovascular complications of diabetes?

    Microvascular: retinopathy, nephropathy, neuropathy. Macrovascular: coronary artery disease, cerebrovascular disease, peripheral arterial disease.

14. Describe the stages of diabetic nephropathy and first-line therapy.

    Hyperfiltration → microalbuminuria (30-300 mg/g) → macroalbuminuria (>300 mg/g) → declining GFR → ESRD. First-line: ACE inhibitor or ARB (reduce albuminuria/intraglomerular pressure); SGLT2 inhibitors add renoprotection; tight glucose and BP control.

15. Differentiate non-proliferative from proliferative diabetic retinopathy.

    Non-proliferative (NPDR): microaneurysms, dot/blot hemorrhages, hard exudates, cotton-wool spots, venous beading. Proliferative (PDR): neovascularization (retina/disc) with risk of vitreous hemorrhage and traction retinal detachment; treat with panretinal photocoagulation/anti-VEGF.

16. What is the most common form of diabetic neuropathy and its presentation?

    Distal symmetric sensorimotor polyneuropathy: 'stocking-glove' loss of sensation, paresthesias, burning pain, loss of ankle reflexes and vibration sense; predisposes to foot ulcers/Charcot joint.

17. What are the WHO/Asian BMI cut-offs for overweight and obesity?

    WHO: overweight BMI ≥25, obesity ≥30 kg/m². Asian-specific: overweight ≥23, obesity ≥25 kg/m² (lower thresholds due to higher metabolic risk at lower BMI).

18. List the criteria for metabolic syndrome.

    ≥3 of: central obesity (increased waist circumference), triglycerides ≥150 mg/dL, HDL <40 (men)/<50 (women) mg/dL, BP ≥130/85 mmHg, fasting glucose ≥100 mg/dL.

19. How is LDL cholesterol calculated (Friedewald formula) and when is it invalid?

    LDL = Total cholesterol − HDL − (Triglycerides/5) (mg/dL). Invalid when triglycerides >400 mg/dL or in chylomicronemia; use direct LDL measurement instead.

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