Note on "Archith Boolor" book: This specific textbook is not available in the medical library database. The answer below is compiled from Harrison's Principles of Internal Medicine, 22nd Edition (2025) - the gold-standard internal medicine reference used in most medical universities for exam preparation. The content is comprehensive and exam-theory oriented.

TYPE 1 DIABETES MELLITUS

1. DEFINITION

• Absolute requirement for exogenous insulin for survival
• Susceptibility to diabetic ketoacidosis (DKA)
• Presence of islet-directed autoantibodies in most patients

2. ETIOLOGY

A. Genetic Factors

• HLA genes (chromosome 6p21) account for ~40-50% of genetic susceptibility
• HLA-DR3, HLA-DR4, HLA-DQ8 alleles confer highest risk
• HLA-DR2 (DQB1*0602) is protective
• Non-HLA genes: insulin gene (INS), PTPN22, CTLA4, IL2RA (CD25) contribute to risk
• Concordance in identical twins is ~50%, confirming that environmental triggers are also necessary

B. Immunologic Factors (Pathogenic mechanism - see Section 3)

• Cell-mediated (T-lymphocyte) and humoral (autoantibody) immune destruction of beta cells

C. Environmental Factors (Triggers)

• Viral infections: Coxsackievirus B, enteroviruses, rubella, CMV, EBV - suspected triggers
• Early dietary antigens: cow's milk proteins (bovine serum albumin), early introduction of cereals
• Gut microbiome alterations ("hygiene hypothesis")
• Vitamin D deficiency
• Definitive proof of a specific trigger is lacking; the mechanism likely involves molecular mimicry - viral antigens resemble beta cell antigens, causing immune cross-reactivity

3. PATHOGENESIS

Step 1: Genetic Predisposition

• Susceptibility HLA alleles alter T-cell education in the thymus, reducing tolerance to beta cell antigens (insulin, GAD65, IA-2)

Step 2: Environmental Trigger

• An infectious or environmental stimulus (e.g., enterovirus infection) initiates the autoimmune cascade in genetically susceptible individuals

Step 3: Autoantibody Formation

• Islet cell antibodies (ICA) - against cytoplasmic antigens
• Insulin autoantibodies (IAA) - most common in young children
• Anti-GAD65 (glutamic acid decarboxylase) - most sensitive, persists longest
• Anti-IA-2 / anti-IA-2β (tyrosine phosphatase-like molecules)
• Anti-ZnT8 (zinc transporter 8)

Step 4: Progressive Beta Cell Destruction

• CD4+ T helper cells activate macrophages and CD8+ cytotoxic T lymphocytes
• CD8+ CTLs directly kill beta cells
• Insulitis: mononuclear infiltrate in islets (lymphocytes, macrophages)
• Pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β) amplify beta cell destruction
• Beta cell mass declines gradually over months to years

Step 5: Loss of First-Phase Insulin Response

• Earliest detectable functional abnormality - precedes overt diabetes by years

Step 6: Clinical Onset (Stage 3)

• When ~80-90% of beta cell mass is destroyed, insufficient insulin production leads to frank hyperglycemia
• Absolute insulin deficiency → unchecked glycogenolysis, gluconeogenesis, lipolysis → DKA risk

"Honeymoon Phase"

• After initial clinical presentation, residual beta cells temporarily recover → reduced insulin requirements
• This phase is transient (months); eventually all residual beta cells are destroyed

4. CLINICAL FEATURES

Classic Triad ("3 Ps")

• Polyuria - osmotic diuresis from glucosuria
• Polydipsia - compensatory thirst from dehydration
• Polyphagia - cellular starvation despite hyperglycemia (controversial in type 1)

Additional Symptoms

• Weight loss - from caloric loss (glucosuria), muscle breakdown (protein catabolism), lipolysis
• Fatigue and weakness - cellular glucose starvation
• Blurred vision - osmotic changes in lens water content (resolves with glucose control)
• Recurrent infections - fungal (vulvovaginitis, balanitis), skin (furunculosis), UTI
• Slow wound healing
• Nocturia - from nocturnal polyuria

Acute Presentation

• 25-50% of children with new-onset type 1 DM present with Diabetic Ketoacidosis (DKA)
• Features of DKA: nausea, vomiting, abdominal pain, Kussmaul respiration, fruity breath (acetone), altered consciousness, dehydration

Age of Onset

• Can occur at any age (not restricted to childhood)
• Classic onset: prepuberty/adolescence
• ~40% of type 1 DM onset occurs after age 30 (often misdiagnosed as type 2 DM)
• Adult-onset slowly progressive type 1 = LADA (Latent Autoimmune Diabetes in Adults)

Physical Examination

• Low BMI / weight loss (contrast with type 2)
• Signs of dehydration in acute presentation
• No acanthosis nigricans (which is a feature of insulin resistance/type 2)
• Lipodystrophy or lipohypertrophy at injection sites in treated patients

5. INVESTIGATIONS / DIAGNOSIS

A. Diagnostic Criteria for Diabetes (ADA/WHO)

Abnormal values should be repeated for confirmation (unless acute metabolic derangement or markedly elevated glucose is present)

B. Specific Investigations for Type 1 DM

• Fasting plasma glucose, random glucose
• Point-of-care capillary blood glucose

• Reflects average blood glucose over 2-3 months
• Diagnostic and monitoring tool
• Target: typically <7.0% (individualized)

• Anti-GAD65 (most sensitive, persists longest)
• Anti-IA-2 / Anti-IA-2β
• Insulin autoantibodies (IAA)
• Anti-ZnT8
• Islet cell antibodies (ICA)
• Presence of ≥2 antibodies = Stage 1 type 1 DM

• Marker of endogenous insulin secretion
• Low/undetectable in type 1 DM (supports absolute insulin deficiency)
• Used to distinguish type 1 from type 2 and LADA

• Glucosuria (positive urine glucose)
• Ketonuria - present in DKA or prolonged fasting
• Microalbuminuria (screening for nephropathy after 5 years of type 1 DM)

• Real-time interstitial glucose measurement
• Preferred over repeated fingerstick in type 1 DM management

• Urine ketones (acetoacetate) or blood beta-hydroxybutyrate
• Elevated in DKA

• Serum electrolytes (Na, K, Cl, HCO3) - critical in DKA
• BUN/creatinine (renal function)
• Lipid profile (dyslipidemia common)
• Thyroid function tests (autoimmune thyroid disease co-exists in type 1 DM)
• Liver function tests

• Research/screening tool; not routine clinical test
• HLA-DR3/DR4 increases risk

• Not routinely needed for diagnosis
• Chest X-ray if infection suspected

6. MANAGEMENT

1. Eliminate symptoms of hyperglycemia
2. Reduce/eliminate long-term microvascular and macrovascular complications
3. Allow the patient to achieve as normal a lifestyle as possible
4. Avoid hypoglycemia

A. Insulin Therapy - The Cornerstone

Insulin Preparations

Insulin Regimens for Type 1 DM

• Basal insulin (long-acting): 1-2 injections/day (e.g., Glargine at bedtime)
• Bolus/prandial insulin (rapid-acting): given before each meal
• Dose adjusted based on carbohydrate content and pre-meal glucose level
• Correction doses for hyperglycemia

• Delivers basal insulin continuously + bolus at meals
• Requires manual entry for bolus doses
• Better glycemic control and flexibility

• Pump + Continuous Glucose Monitor (CGM)
• Algorithm suspends insulin when glucose is low or predicted to drop

• Pump + CGM + algorithm
• Automatically increases/decreases basal insulin in real-time based on CGM data
• Some systems deliver automatic correction boluses
• Most advanced current technology

B. Glycemic Goals

C. Glucose Monitoring

• CGM preferred over fingerstick capillary monitoring in type 1 DM
• Reduces hypoglycemia, reduces HbA1c, improves time-in-range

D. Medical Nutrition Therapy (MNT)

• Carbohydrate counting is essential for accurate prandial insulin dosing
• Consistent meal timing to match insulin action
• Dietitian consultation essential
• No absolute restriction of carbohydrates - matching insulin to intake is key

E. Physical Activity

• Regular aerobic exercise improves insulin sensitivity
• Glucose monitoring before/during/after exercise
• Adjust insulin dose and/or carbohydrate intake for exercise
• Risk of hypoglycemia during and after exercise (especially prolonged exercise)

F. Psychosocial Care

• Screening for depression, anxiety, diabetes distress (common in type 1 DM)
• Behavioral health professional involvement
• Diabetes self-management education and support (DSMES)

G. Multidisciplinary Team

7. TREATMENT OF ACUTE COMPLICATION - DKA

8. PREVENTION OF COMPLICATIONS

Microvascular

• Retinopathy: Annual dilated fundus exam starting 5 years after diagnosis
• Nephropathy: Annual urine microalbumin/creatinine ratio; ACE inhibitor/ARB if microalbuminuria present
• Neuropathy: Annual foot exam; 10-g monofilament test

Macrovascular

• Blood pressure control (<130/80 mmHg)
• Statin therapy for dyslipidemia
• Antiplatelet therapy in high-risk patients
• Smoking cessation

Summary Table

Regarding "Archith Boolor" textbook: This book is not available in the medical library database. However, the content above is drawn from Harrison's 22E (2025) - the standard reference for MBBS/MD examinations globally. The structure, staging, autoantibody panel, AID systems, and diagnostic criteria reflect the most current (2024-2025) evidence and ADA Standards of Care. If you have access to the Archith Boolor book, the core concepts will be very similar; cross-reference the insulin preparations table and DKA management protocol with that specific book for your exam.

TYPE 2 DIABETES MELLITUS

1. DEFINITION

• Variable degrees of insulin resistance (decreased ability of insulin to act on target tissues)
• Impaired insulin secretion (progressive beta cell dysfunction)
• Increased hepatic glucose production

• Impaired Fasting Glucose (IFG): FPG 5.6-6.9 mmol/L (100-125 mg/dL)
• Impaired Glucose Tolerance (IGT): 2-h OGTT glucose 7.8-11.0 mmol/L (140-199 mg/dL)
• HbA1c 5.7-6.4% (39-47 mmol/mol)

2. ETIOLOGY

A. Genetic Factors

• Type 2 DM is strongly polygenic
• Concordance in identical twins is ~90% (much higher than type 1 DM, reflecting dominant genetic influence)
• Risk in first-degree relatives: 15-40%
• Key susceptibility loci: TCF7L2 (strongest known genetic risk factor), KCNJ11, PPARG, HHEX, SLC30A8, CDKAL1, CDKN2A/B, and >100 other loci (genome-wide association studies)
• These genes primarily affect beta cell function, insulin secretion, and glucose sensing
• No strong HLA association (unlike type 1 DM)

B. Environmental/Modifiable Risk Factors

• Obesity (especially central/visceral adiposity) - most important modifiable risk
• Physical inactivity
• Unhealthy diet (high caloric density, refined carbohydrates, saturated fat)
• Aging - prevalence rises sharply after age 45
• Intrauterine environment (low birth weight followed by excess weight gain)
• Ethnicity: South Asians, African Americans, Hispanics, Pacific Islanders have higher risk
• Gestational diabetes history
• Polycystic ovary syndrome (PCOS)
• Drugs: glucocorticoids, second-generation antipsychotics, HIV medications, thiazide diuretics

C. Metabolic Risk Factors

• The metabolic syndrome (central obesity + hypertension + dyslipidemia + insulin resistance) is a major risk cluster
• Dyslipidemia with elevated triglycerides, low HDL, increased small dense LDL

3. PATHOGENESIS

Defect 1: Insulin Resistance

• Skeletal muscle (major site of postprandial glucose uptake)
• Liver (site of fasting glucose production)
• Adipose tissue (site of lipolysis regulation)

• Insulin receptor signaling is impaired at the post-receptor level (tyrosine kinase activity is reduced)
• Lipid intermediates (ceramides, diacylglycerol) accumulate within skeletal myocytes, impairing mitochondrial oxidative phosphorylation and insulin-stimulated ATP production
• Reduced insulin-stimulated glucose utilization - 30-60% lower than in non-diabetic individuals
• Adipokine dysregulation: Obesity-driven adipocyte hypertrophy causes:
  • Increased TNF-α, IL-6, resistin, free fatty acids (pro-inflammatory, worsen insulin resistance)
  • Decreased adiponectin (insulin-sensitizing hormone)
  • Adipose-resident macrophage activation → low-grade metabolic inflammation
• Reactive oxygen species from impaired fatty acid oxidation amplify insulin resistance

• Skeletal muscle: decreased postprandial glucose uptake → postprandial hyperglycemia
• Liver: failure of hyperinsulinemia to suppress gluconeogenesis → fasting hyperglycemia
• Adipose: increased lipolysis → raised free fatty acids → hepatic VLDL synthesis → dyslipidemia

Defect 2: Progressive Beta Cell Dysfunction

1. Insulin resistance develops → beta cells compensate by increasing insulin output
2. Impaired first-phase insulin response is the earliest detectable defect
3. IGT/IFG develops as postprandial glucose rises
4. Increased glucagon secretion (alpha cell dysfunction) worsens hyperglycemia
5. Progressive beta cell exhaustion and failure → frank type 2 DM

• Glucotoxicity: Chronic hyperglycemia is directly toxic to beta cells
• Lipotoxicity: Elevated free fatty acids impair beta cell function and promote apoptosis
• Islet amyloid polypeptide (IAPP/amylin): Deposits in islets of type 2 DM - amyloid fibrils displace and destroy beta cells
• Mitochondrial dysfunction in beta cells
• Reduced beta cell mass (though far less than in type 1 DM)
• Endoplasmic reticulum stress from increased demand for insulin production

Defect 3: Increased Hepatic Glucose Production

• Insulin resistance in the liver + elevated glucagon → failure to suppress gluconeogenesis
• Fasting hyperglycemia is predominantly driven by increased hepatic glucose output
• Postprandial hyperglycemia driven by impaired peripheral glucose disposal (muscle)
• Excess hepatic lipid retention → MASLD (metabolic dysfunction-associated steatotic liver disease)

Additional Defects - "Ominous Octet" (DeFronzo)

1. Impaired beta cell insulin secretion
2. Skeletal muscle insulin resistance
3. Hepatic insulin resistance
4. Increased glucagon secretion (alpha cells)
5. Decreased incretin effect (GLP-1/GIP)
6. Increased renal glucose reabsorption (SGLT-2 upregulation)
7. Adipose tissue lipolysis (increased FFA flux)
8. Brain: insulin resistance in appetite centers → increased caloric intake

4. CLINICAL FEATURES

A. Classic Symptoms ("3 Ps" + weight gain)

B. Key Differences from Type 1 DM Presentation

C. Signs on Physical Examination

• Obesity - especially central/abdominal (waist circumference elevated)
• Acanthosis nigricans - velvety hyperpigmented plaques in skin folds (axilla, neck, groin) - hallmark of insulin resistance
• Skin tags (acrochordons) - associated with insulin resistance
• Lipodystrophy/lipohypertrophy at insulin injection sites (in treated patients)
• Hypertension - commonly co-existing
• Peripheral neuropathy signs: reduced vibration sense, monofilament loss, absent ankle reflexes
• Peripheral vascular disease: reduced pedal pulses, cool peripheries
• Fundoscopy: diabetic retinopathy (may already be present at diagnosis in type 2 DM)
• Foot pathology: calluses, ulcers, Charcot foot

D. Complications Already Present at Diagnosis

• Retinopathy (~20-30%)
• Microalbuminuria/nephropathy
• Peripheral neuropathy

E. Associated Conditions (Metabolic Syndrome)

• Hypertension (very common)
• Dyslipidemia (elevated triglycerides, low HDL, elevated small dense LDL)
• Non-alcoholic/metabolic steatotic liver disease (MASLD)
• Obstructive sleep apnea
• PCOS (in women)
• Hyperuricemia/gout

5. INVESTIGATIONS / DIAGNOSIS

A. Diagnostic Criteria (Same as Type 1 - ADA Standards 2024)

All tests should be repeated for confirmation unless symptoms + markedly elevated glucose are present.

B. Screening for Type 2 DM (ADA 2024)

• Test all adults ≥35 years every 3 years
• Test earlier (any age) if overweight/obese (BMI ≥25, or ≥23 in Asians) + any one of:
  • Family history of DM
  • High-risk ethnicity
  • Hypertension (≥130/80 mmHg)
  • HDL <35 mg/dL and/or triglycerides >250 mg/dL
  • PCOS or acanthosis nigricans
  • History of cardiovascular disease, physical inactivity
• History of gestational DM: screen every 3 years
• Previous IFG/IGT or HbA1c 5.7-6.4%: screen annually

C. Laboratory Investigations

• HbA1c - 2-4 times/year for monitoring; reflects 2-3 month average glucose
• Fasting plasma glucose - routine monitoring
• CGM (Continuous Glucose Monitoring) - preferred in patients on insulin; measures time-in-range (TIR)
• Post-prandial glucose (2-h after meals)

• C-peptide: Measurable/normal or elevated in type 2 DM (endogenous insulin present); low/absent in type 1 DM
• Autoantibodies (GAD65, IA-2, ZnT8): Negative in type 2 DM; positive in type 1/LADA

• Urine albumin-to-creatinine ratio (ACR): Annual screening for diabetic nephropathy (microalbuminuria = 30-300 mg/g)
• Serum creatinine + eGFR: Renal function assessment
• Lipid profile: Total cholesterol, LDL, HDL, triglycerides
• Liver function tests (MASLD co-exists)
• Thyroid function tests (autoimmune thyroid disease co-exists)
• Urine ketones / serum beta-hydroxybutyrate: Only if hyperglycemic crisis is suspected
• ECG: Cardiovascular risk assessment
• Annual dilated fundus examination: For retinopathy (from time of diagnosis in type 2 DM)
• Annual foot examination: 10-g monofilament, vibration (128 Hz tuning fork), pedal pulses

• Blood pressure measurement
• Waist circumference
• Serum uric acid

6. MANAGEMENT - OVERALL GOALS

1. Eliminate symptoms of hyperglycemia
2. Reduce/eliminate long-term micro- and macrovascular complications
3. Allow as normal a lifestyle as possible
4. Reduce cardiovascular risk - this is the leading cause of mortality in type 2 DM

Individualized Glycemic Targets

7. TREATMENT

A. Lifestyle Modification (First and Ongoing Foundation)

• Reduce total caloric intake for weight loss
• Carbohydrate quality: favor whole grains, legumes, vegetables; limit refined carbohydrates and sugars
• Reduce saturated fats and trans fats
• Mediterranean or DASH diet patterns - evidence of benefit
• Sodium restriction for hypertension management
• Dietitian consultation essential

• 150 minutes/week of moderate-intensity aerobic exercise (e.g., brisk walking)
• Resistance training 2-3 times/week
• Reduces insulin resistance and promotes weight loss
• Even modest activity (30 min/day, 5 days/week) reduced type 2 DM incidence by 58% in the Diabetes Prevention Program (DPP)

• Even 5-10% body weight loss significantly improves glycemic control
• Weight loss of ≥15% may produce remission of type 2 DM in some patients
• GLP-1 receptor agonists, bariatric surgery, and lifestyle changes are the most effective approaches

• Laparoscopic sleeve gastrectomy, Roux-en-Y gastric bypass, biliopancreatic diversion
• 28-33% average total body weight loss at 12-18 months
• 68.2% of patients experienced initial complete remission of type 2 DM at 5 years
• Indicated for BMI ≥40, or BMI ≥35 with diabetes/metabolic comorbidities

B. Pharmacologic Therapy

Step 1: Metformin (First-line for most patients)

• Mechanism: Reduces hepatic glucose production (gluconeogenesis) + improves peripheral insulin sensitivity; activates AMPK; reduces hepatic lipid accumulation
• Dose: Start low (500 mg), increase every 1-2 weeks to max 2000 mg/day
• Benefits: Mild weight loss, lowers FPG and insulin levels, improves lipid profile, low cost
• Side effects: GI (diarrhea, nausea, metallic taste) - minimized by dose escalation and extended-release formulation; Vitamin B12 deficiency (monitor)
• Major toxicity: Lactic acidosis (rare but serious)
• Contraindications: eGFR <30 mL/min, hepatic failure, severe hypoxemia (CHF, respiratory failure), acidosis, contrast media administration, hospitalized patients

Step 2: Add a Second Agent Based on Patient Profile

• Patient with ASCVD (established cardiovascular disease): Prefer GLP-1 RA (Semaglutide, Liraglutide) or SGLT-2 inhibitor (Empagliflozin, Canagliflozin) - proven cardiovascular outcome benefit (EMPA-REG, LEADER, SUSTAIN-6 trials)
• Patient with Heart Failure: Prefer SGLT-2 inhibitor (most benefit in HFrEF and HFpEF)
• Patient with CKD: Prefer SGLT-2 inhibitor (slows progression); avoid metformin if eGFR <30
• Patient with obesity: Prefer GLP-1 RA (Semaglutide - most weight loss ~15-20% body weight) or SGLT-2 inhibitor
• Patient where cost is a concern: Metformin + sulfonylurea

GLP-1 Receptor Agonists - Detailed

• Stimulate insulin secretion in a glucose-dependent manner (low hypoglycemia risk)
• Suppress glucagon
• Slow gastric emptying (reduce post-prandial glucose)
• Act on hypothalamus to reduce appetite and food intake → significant weight loss
• Reduce hepatic fat accumulation

SGLT-2 Inhibitors - Detailed

• Glucose-independent mechanism → low hypoglycemia risk
• Osmotic diuresis → mild BP reduction
• Natriuresis → reduce preload/afterload → cardiac benefit
• Reduce uric acid
• Promote weight loss

Insulin in Type 2 DM

• Severe hyperglycemia (FPG >13.9-16.7 mmol/L / >250-300 mg/dL) at diagnosis
• Failure to achieve glycemic targets with oral agents
• Catabolism (weight loss, ketonuria)
• Pregnancy
• Acute illness, surgery, hospitalization
• Renal/hepatic failure precluding oral agents

• Start with single dose of long-acting (basal) insulin at bedtime (NPH, Glargine, Degludec)
• Starting dose: 0.1-0.4 U/kg/day OR fixed 10-15 units
• Adjust in 10-20% increments based on CGM/fasting glucose
• Add prandial (rapid-acting) insulin as diabetes progresses → basal-bolus regimen

Step-Up Algorithm (ADA/EASD Approach)

Lifestyle modification (MNT + exercise + weight loss)
         ↓ (if HbA1c not at target after 3 months)
Metformin (unless contraindicated)
         ↓ (if HbA1c not at target after 3 months)
Add 2nd agent based on comorbidities:
  - ASCVD/HF/CKD → GLP-1 RA or SGLT-2 inhibitor
  - Weight a concern → GLP-1 RA or SGLT-2 inhibitor
  - Hypoglycemia a concern → DPP-4 inhibitor / GLP-1 RA / SGLT-2 inhibitor
  - Cost a concern → Sulfonylurea / TZD
         ↓ (if HbA1c still not at target)
Add 3rd agent / Insulin therapy
         ↓
Basal-bolus insulin ± oral agents

C. Management of Associated Conditions

• Target: <130/80 mmHg
• ACE inhibitors or ARBs preferred (additional renoprotective benefit in diabetic nephropathy)
• Add amlodipine, thiazide as needed

• Statin therapy for all patients with type 2 DM >40 years or with cardiovascular risk factors
• Target LDL: <70 mg/dL (<1.8 mmol/L) in high/very-high CV risk
• Add ezetimibe or PCSK9 inhibitor if LDL not at target on maximum statin
• Fibrates for severe hypertriglyceridemia (>500 mg/dL)

• Aspirin 75-100 mg/day in patients with established ASCVD (secondary prevention)
• Smoking cessation
• GLP-1 RA and SGLT-2 inhibitor with proven cardiovascular outcome benefit

• ACE inhibitor or ARB (reduce proteinuria, slow progression)
• SGLT-2 inhibitor (slow CKD progression - CREDENCE, DAPA-CKD trials)
• GLP-1 RA (FLOW trial: Semaglutide reduced kidney disease progression)
• Finerenone (non-steroidal MRA) in CKD with type 2 DM

8. ACUTE COMPLICATION - HYPEROSMOLAR HYPERGLYCAEMIC STATE (HHS)

1. Aggressive IV fluid resuscitation (0.9% NaCl initially, then 0.45% NaCl)
2. Insulin infusion (0.1 units/kg/h IV) - lower doses than DKA often sufficient
3. Potassium replacement (total body depleted despite serum levels)
4. Thromboprophylaxis (high DVT/PE risk due to hyperviscosity)
5. Treat precipitating cause (e.g., antibiotics for infection)
6. Monitor glucose, electrolytes, osmolality hourly

9. PREVENTION OF TYPE 2 DM

• Intensive lifestyle changes (diet + 150 min/week exercise + weight loss) → reduced incidence by 58% (Diabetes Prevention Program)
• Metformin → reduced incidence by 31% (DPP trial)
• GLP-1 RA (Semaglutide) → 3mg oral dose reduces progression in prediabetes
• Bariatric surgery in severely obese patients

Summary Comparison: Type 1 vs Type 2 DM

The "Archith Boolor" textbook is not in the library database, but this content from Harrison's 22E is fully aligned with the standard MBBS/MD exam syllabus. The core concepts - pathogenesis, pharmacology (especially GLP-1 RA and SGLT-2 inhibitors), and management algorithms - are current to the 2024 ADA Standards of Care and will be comprehensive for your exam theory paper.