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NEET SS Endocrinology (DM) Syllabus

The Endocrinology (DM) syllabus for NEET SS in full: 4 chapters, 13 topics and 18 sub-topics, every one listed below, plus 51 Endocrinology (DM) flashcards with answers.

4Chapters
13Topics
18Sub-topics
51Flashcards

Endocrinology (DM) syllabus: all 4 chapters

Expand any chapter to see its topics and sub-topics.

  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. 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. 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. 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

NEET SS Endocrinology (DM) flashcards — 51 questions with 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.

  20. What is the mechanism of statins and their primary adverse effects?

    Inhibit HMG-CoA reductase, reducing hepatic cholesterol synthesis and upregulating LDL receptors → lower LDL. Adverse effects: myalgia/myopathy/rhabdomyolysis, transaminitis, slight increase in diabetes risk.

Show the other 31 Endocrinology (DM) flashcards

  1. What is the most common cause of hyperthyroidism, and its pathophysiology?

    Graves disease: TSH receptor-stimulating autoantibodies (TRAb/TSI) cause diffuse goiter, hyperthyroidism, ophthalmopathy, and pretibial myxedema.

  2. Differentiate Graves disease, toxic multinodular goiter, and subacute thyroiditis by radioactive iodine uptake.

    Graves: diffusely increased RAIU. Toxic multinodular goiter/toxic adenoma: focal/patchy increased uptake. Subacute (de Quervain) thyroiditis: low/absent RAIU (preformed hormone release, painful gland).

  3. What is thyroid storm and how is it managed?

    Life-threatening thyrotoxicosis: fever, tachyarrhythmia, agitation, GI dysfunction. Management: beta-blocker (propranolol), thionamide (PTU preferred), iodine (given ≥1 hr after thionamide—Wolff-Chaikoff), hydrocortisone, supportive care.

  4. Compare methimazole and propylthiouracil (PTU).

    Both inhibit thyroid peroxidase. PTU also blocks peripheral T4→T3 conversion; preferred in first trimester pregnancy and thyroid storm. Methimazole: once-daily, more potent, first-line otherwise but teratogenic (aplasia cutis) in first trimester. PTU risk: hepatotoxicity; both: agranulocytosis.

  5. What is the most common cause of hypothyroidism in iodine-sufficient areas?

    Hashimoto (chronic autoimmune lymphocytic) thyroiditis: anti-TPO and anti-thyroglobulin antibodies; gland infiltrated by lymphocytes with germinal centers and Hürthle cells.

  6. Define subclinical hypothyroidism and when to treat.

    Elevated TSH with normal free T4. Treat if TSH >10 mIU/L, or with symptoms, positive anti-TPO, pregnancy/infertility, or goiter. Otherwise monitor.

  7. What are the phases of subacute (de Quervain) thyroiditis?

    Triphasic: initial thyrotoxic phase (release of preformed hormone, low RAIU, painful tender gland, post-viral) → hypothyroid phase → recovery to euthyroid. Treat with NSAIDs/steroids and beta-blockers.

  8. What is the management of thyrotoxicosis in pregnancy?

    PTU in first trimester (methimazole teratogenicity), switch to methimazole in second/third trimester; use lowest effective dose to keep free T4 high-normal; avoid radioiodine; beta-blockers short-term.

  9. How are thyroid nodules evaluated?

    Measure TSH; if low, do radioiodine scan (hot nodule rarely malignant). If normal/high TSH, do ultrasound; FNA based on TI-RADS/sonographic risk and size. Report cytology by Bethesda system.

  10. Name the major types of thyroid cancer and their key features.

    Papillary (most common, lymphatic spread, Orphan-Annie nuclei/psammoma bodies, excellent prognosis); Follicular (hematogenous spread, capsular/vascular invasion); Medullary (parafollicular C-cells, calcitonin, MEN2); Anaplastic (aggressive, elderly, poor prognosis).

  11. Which thyroid cancer is associated with MEN2 and what tumor marker is used?

    Medullary thyroid carcinoma (parafollicular C cells); tumor marker calcitonin (and CEA). Associated with RET proto-oncogene mutation. In MEN2A/2B prophylactic thyroidectomy is indicated.

  12. What are the sonographic features suggesting thyroid malignancy?

    Marked hypoechogenicity, microcalcifications, irregular margins, taller-than-wide shape, extrathyroidal extension, and suspicious cervical lymphadenopathy.

  13. What is the most common functional pituitary adenoma and its presentation?

    Prolactinoma: hyperprolactinemia causing galactorrhea, amenorrhea/oligomenorrhea, infertility (women), and decreased libido/erectile dysfunction (men); mass effect causes bitemporal hemianopia. First-line treatment: dopamine agonists (cabergoline).

  14. How do you diagnose acromegaly?

    Elevated IGF-1 for age, and failure to suppress GH (<1 ng/mL) after oral glucose load (OGTT). MRI localizes the GH-secreting pituitary adenoma. Treatment: transsphenoidal surgery, somatostatin analogs, pegvisomant.

  15. What is Sheehan syndrome?

    Postpartum pituitary necrosis from hypotension/hemorrhage causing hypopituitarism; failure of lactation (low prolactin), amenorrhea, and other anterior pituitary hormone deficiencies.

  16. Differentiate central from nephrogenic diabetes insipidus using the water deprivation/desmopressin test.

    Both: dilute urine despite high serum osmolality. After desmopressin (DDAVP): central DI urine osmolality rises >50% (ADH deficient); nephrogenic DI shows little/no response (renal ADH resistance).

  17. What distinguishes Cushing disease from Cushing syndrome?

    Cushing syndrome = any cause of chronic glucocorticoid excess. Cushing disease = Cushing syndrome specifically due to an ACTH-secreting pituitary adenoma (the most common endogenous cause).

  18. Outline the diagnostic workup for Cushing syndrome.

    Screen: 24-hr urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression test. Then measure ACTH (low = adrenal; normal/high = ACTH-dependent). High-dose dexamethasone and inferior petrosal sinus sampling differentiate pituitary from ectopic ACTH.

  19. What is the most common cause of primary hyperaldosteronism (Conn syndrome) and its biochemical profile?

    Bilateral adrenal hyperplasia or aldosterone-producing adenoma. Profile: hypertension, hypokalemia, metabolic alkalosis, high aldosterone with suppressed renin (high aldosterone-to-renin ratio).

  20. What is Addison disease and its biochemical hallmarks?

    Primary adrenal insufficiency (commonly autoimmune): deficiency of cortisol and aldosterone → hyponatremia, hyperkalemia, hypoglycemia, hypotension, hyperpigmentation (high ACTH/MSH). High ACTH; low cortisol failing to rise on ACTH stimulation test.

  21. How is congenital adrenal hyperplasia from 21-hydroxylase deficiency characterized?

    Most common CAH: low cortisol and aldosterone, elevated 17-hydroxyprogesterone, and androgen excess → virilization, ambiguous genitalia in females, salt-wasting (hyponatremia/hyperkalemia) in severe forms.

  22. What is the classic triad of pheochromocytoma and the best screening test?

    Episodic headache, palpitations, and diaphoresis with paroxysmal hypertension. Best screening: plasma free metanephrines or 24-hr urinary fractionated metanephrines. Tumor of adrenal medulla chromaffin cells.

  23. What is the rule of 10s for pheochromocytoma, and preoperative management?

    ~10% extra-adrenal, bilateral, malignant, familial, in children. Preop: alpha-blockade first (phenoxybenzamine) THEN beta-blockade to avoid unopposed alpha-mediated hypertensive crisis; volume expansion.

  24. How is an adrenal incidentaloma evaluated?

    Assess for hormone hypersecretion (1-mg dexamethasone suppression test for cortisol, plasma metanephrines for pheo, aldosterone/renin ratio if hypertensive) and for malignancy (imaging: size >4 cm, irregular margins, high unenhanced HU >10, slow washout suggest malignancy).

  25. What is the function of PTH and its effects on calcium and phosphate?

    PTH raises serum calcium: increases bone resorption, increases renal calcium reabsorption, decreases phosphate reabsorption (phosphaturia), and stimulates renal 1-alpha-hydroxylase → more calcitriol (gut Ca absorption). Net: high Ca, low phosphate.

  26. Differentiate primary, secondary, and tertiary hyperparathyroidism.

    Primary: autonomous PTH (usually adenoma) → high Ca, low phosphate, high PTH. Secondary: compensatory PTH rise (e.g., CKD/vitamin D deficiency) → low/normal Ca, high PTH. Tertiary: autonomous hyperplasia after prolonged secondary → high Ca, very high PTH.

  27. What are the causes and management priorities of hypercalcemia?

    Most common: primary hyperparathyroidism (outpatient) and malignancy (inpatient, PTHrP/osteolytic). Acute management: IV normal saline hydration, then bisphosphonates/calcitonin; treat underlying cause. Severe: consider denosumab/dialysis.

  28. How is osteoporosis diagnosed by DEXA and what is the WHO T-score classification?

    DEXA T-score: normal ≥−1.0; osteopenia −1.0 to −2.5; osteoporosis ≤−2.5; severe osteoporosis ≤−2.5 with fragility fracture. T-score compares to young adult peak bone mass.

  29. What are the components of the MEN syndromes?

    MEN1 (MEN1/menin gene): parathyroid hyperplasia, pancreatic islet tumors (gastrinoma/insulinoma), pituitary adenoma (3 Ps). MEN2A (RET): medullary thyroid cancer, pheochromocytoma, parathyroid hyperplasia. MEN2B (RET): medullary thyroid cancer, pheochromocytoma, mucosal neuromas/marfanoid habitus.

  30. What are the diagnostic criteria for PCOS (Rotterdam) and its endocrine features?

    Rotterdam: ≥2 of—oligo/anovulation, clinical/biochemical hyperandrogenism, polycystic ovaries on ultrasound (after excluding other causes). Features: elevated LH:FSH ratio, insulin resistance, hyperandrogenism; managed with lifestyle, OCPs, metformin.

  31. How is the cause of male hypogonadism localized using LH/FSH levels?

    Primary (hypergonadotropic) hypogonadism: low testosterone with HIGH LH/FSH (testicular failure, e.g., Klinefelter). Secondary (hypogonadotropic): low testosterone with LOW/normal LH/FSH (hypothalamic-pituitary cause, e.g., Kallmann syndrome with anosmia).

NEET SS Endocrinology (DM) FAQ

What is in the NEET SS Endocrinology (DM) syllabus?

NEET SS Endocrinology (DM) is split into 4 chapters: Diabetes Mellitus and Metabolic Disorders, Thyroid Disorders, Pituitary and Adrenal Disorders and Calcium, Bone, Gonadal and Genetic Endocrine Disorders. Together they contain 13 topics and 18 sub-topics.

How many chapters are in NEET SS Endocrinology (DM)?

4 chapters, containing 13 topics and 18 sub-topics. The largest chapter is Diabetes Mellitus and Metabolic Disorders, with 4 topics.

Are there flashcards for NEET SS Endocrinology (DM)?

Yes — a 51-card Endocrinology (DM) deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.