Presentation Explanation Guide: Type 2 Diabetes

Slide 1 - Title: TYPE 2 DIABETES

"Good morning/afternoon everyone. Today our group will be presenting on Type 2 Diabetes Mellitus - one of the most prevalent chronic diseases worldwide. We will cover its epidemiology, risk factors, clinical features, complications, diagnosis, investigations, screening, management, and pharmacological treatment."

Slide 2 - Epidemiology

"Type 2 Diabetes Mellitus, or T2DM, is a chronic metabolic disorder defined by two core problems: insulin resistance - where the body's cells stop responding properly to insulin - and relative insulin deficiency, meaning the pancreas cannot produce enough insulin to compensate.

It accounts for more than 90% of all diabetes cases globally. Currently, over 800 million adults worldwide live with the condition - making it a true global epidemic. A concerning fact is that more than 40% of cases remain undiagnosed, meaning millions of people are living with the disease without knowing. We are also seeing a rise in T2DM among children and adolescents, largely driven by increasing obesity rates."

Slide 3 - Risk Factors

"Risk factors are divided into three categories:

Modifiable - things we can change. The biggest one is obesity, especially central or abdominal obesity, because visceral fat drives insulin resistance. Physical inactivity, an unhealthy diet high in refined sugars and processed foods, and smoking are all modifiable.

Non-modifiable - things we cannot change. Age 45 and above, family history of diabetes, genetic predisposition, and belonging to a high-risk ethnic group such as South Asian, African, or Hispanic populations.

Other clinical risk factors include history of gestational diabetes - women who had diabetes during pregnancy are at much higher lifetime risk - Polycystic Ovary Syndrome (PCOS), and Metabolic Syndrome, which is a cluster of conditions including high blood pressure, high blood sugar, and abnormal cholesterol."

Slide 4 - Clinical Features

"T2DM often develops slowly and silently, but the classic triad of symptoms is:

• Polyuria - frequent urination, because high blood glucose spills into urine and pulls water with it
• Polydipsia - excessive thirst, as a result of fluid loss
• Unexplained weight loss - because cells cannot use glucose for energy and start breaking down fat and muscle

General symptoms include fatigue, blurred vision, mood changes, dry mouth, and itching.

Because high glucose impairs immune function, patients also get recurrent infections - slow wound healing, skin infections, UTIs, and fungal (yeast) infections.

Neurological signs include numbness or tingling in the hands and feet, which is diabetic neuropathy. A skin sign called Acanthosis Nigricans - dark, velvety patches in skin folds like the neck or armpits - is a marker of insulin resistance."

Slide 5 - Complications & Secondary Causes

"Complications are divided into microvascular and macrovascular.

Microvascular (small blood vessel damage):

• Diabetic Retinopathy - damage to retinal blood vessels, leading to vision loss
• Diabetic Nephropathy - kidney damage, a leading cause of chronic kidney disease
• Diabetic Neuropathy - nerve damage

Macrovascular (large blood vessel damage):

• Coronary Artery Disease - heart attacks
• Peripheral Arterial Disease - reduced blood flow to the legs

Secondary causes of T2DM are important to recognize. Pancreatic disorders like chronic pancreatitis, cystic fibrosis, or pancreatic tumors can destroy insulin-producing cells. Certain drugs also cause diabetes - especially glucocorticoids (steroids), some HIV antiretroviral medications, and immunosuppressive drugs given after organ transplants."

Slide 6 & 7 - ADA 2026 Diagnostic Criteria

"According to the American Diabetes Association 2026 guidelines, diabetes can be diagnosed using four criteria - any ONE of these is sufficient:

1. HbA1c ≥ 6.5% - reflects average blood sugar over the past 2-3 months
2. Fasting Plasma Glucose ≥ 126 mg/dL (fasting means no caloric intake for at least 8 hours)
3. 2-hour Plasma Glucose ≥ 200 mg/dL during an Oral Glucose Tolerance Test (OGTT)
4. Random Plasma Glucose ≥ 200 mg/dL in a patient with classic symptoms

Prediabetes is defined as HbA1c 5.7-6.4%, fasting glucose 100-125 mg/dL, or 2-hr OGTT 140-199 mg/dL - this is the window for prevention.

Note: For criteria 1, 2, and 3 without symptoms, a repeat confirmatory test is required."

Slide 8 - Baseline Laboratory Investigations

"Once a diagnosis is made, we run baseline labs to assess glycemic control, organ function, and cardiovascular risk.

• HbA1c and fasting blood glucose tell us current glycemic status
• UACR (Urine Albumin-to-Creatinine Ratio), serum creatinine, and eGFR screen for diabetic nephropathy
• Lipid profile (LDL, HDL, total cholesterol, triglycerides) assesses cardiovascular risk since T2DM patients have very high CVD risk
• Liver function tests because fatty liver is common in T2DM
• TSH because thyroid disease and diabetes commonly co-exist
• Vitamin B12 is checked in anyone on long-term Metformin, which depletes B12
• Islet autoantibodies are checked if LADA (Latent Autoimmune Diabetes in Adults) is suspected to distinguish T2DM from a slowly progressing type 1"

Slide 9 & 10 - Screening Criteria

"Screening means testing people who have NO symptoms to catch diabetes early.

Screen any adult at any age if they are overweight (BMI ≥25, or ≥23 in Asian populations) AND have even one additional risk factor - such as family history, hypertension, abnormal lipids, PCOS, or history of cardiovascular disease.

For everyone else, routine screening starts at age 35 and is repeated every 3 years if results are normal.

Special high-risk groups need more frequent or earlier screening:

• Prediabetes patients: screen ANNUALLY
• Women with previous gestational diabetes: every 3 years
• Patients on steroids, antipsychotics, or HIV medications: regular monitoring
• Cystic fibrosis patients: begin screening at age 10 using OGTT
• Post-transplant patients: OGTT recommended"

Slide 12 & 13 - Nutritional Recommendations

"Lifestyle modification is the foundation of T2DM management - before or alongside medications.

Diet should emphasize vegetables, fruits, whole grains, legumes, and low-fat dairy. High-fiber, low glycemic index foods are preferred because they cause a slower, lower rise in blood sugar.

A Mediterranean-style diet is specifically recommended - rich in healthy fats like olive oil, fish, and nuts.

Carbohydrate management is key: monitor total carb intake, spread meals evenly through the day, avoid refined carbs and sugar-sweetened beverages.

Protein: choose lean sources - fish, poultry, legumes.

Additional advice: limit sodium to under 2300 mg/day, ensure adequate Vitamin D and Calcium, maintain regular meal timing, and adjust eating schedules during fasting periods to avoid hypoglycemia."

Slide 14 - Ongoing Comprehensive Care

"Diabetes management is lifelong and multi-dimensional.

Glycemic monitoring: HbA1c should be checked 2-4 times per year. Continuous Glucose Monitoring (CGM) is increasingly used as it gives real-time data and reduces hypoglycemia risk. Targets are individualized based on age, comorbidities, and patient preference.

Lifestyle: Diabetes self-management education, medical nutrition therapy, regular physical activity (at least 150 minutes of moderate activity per week), and psychosocial support.

Mental health screening is important - depression and anxiety are significantly more common in people with diabetes, and diabetes distress is a recognized condition that affects self-care."

Slide 15-19 - Pharmacological Approach

"Pharmacological treatment follows a stepwise approach guided by ADA 2026:

Step 1 - First-line: Metformin (unless contraindicated) - reduces hepatic glucose production, improves insulin sensitivity, weight-neutral, cheap, well-tolerated. Check B12 levels with long-term use.

Step 2 - Add-on agents based on patient profile:

Drug Class	Examples	Key Benefit
GLP-1 Receptor Agonists	Semaglutide, Liraglutide	Weight loss, CV benefit
SGLT-2 Inhibitors	Empagliflozin, Dapagliflozin	CV & renal protection
DPP-4 Inhibitors	Sitagliptin	Weight-neutral, safe in elderly
Sulfonylureas	Glipizide, Glibenclamide	Low cost, risk of hypoglycemia
Insulin	Basal/bolus regimens	When oral agents fail

For patients with established cardiovascular disease or chronic kidney disease, GLP-1 agonists or SGLT-2 inhibitors are preferred regardless of glycemic control because they have proven organ-protective effects."

Possible Questions to Expect After Your Presentation

Basic/Conceptual Questions

1. What is the difference between Type 1 and Type 2 diabetes?
   • T1DM is autoimmune destruction of beta cells, absolute insulin deficiency, usually in young patients. T2DM is insulin resistance + relative deficiency, usually in adults, strongly linked to obesity.
2. Why does insulin resistance happen?
   • Visceral fat releases inflammatory cytokines that impair insulin receptor signaling. Over time the pancreatic beta cells cannot compensate and fail.
3. What is HbA1c and why is it useful?
   • Glycated hemoglobin reflects average blood glucose over 2-3 months. It is not affected by short-term fluctuations and is used for both diagnosis and monitoring.
4. What is the difference between prediabetes and diabetes?
   • Prediabetes: HbA1c 5.7-6.4%, FPG 100-125 mg/dL. Diabetes: HbA1c ≥6.5%, FPG ≥126 mg/dL.

Clinical Questions

1. Why do diabetic patients get recurrent infections?
   • Hyperglycemia impairs neutrophil function, chemotaxis, and phagocytosis. It also creates a high-glucose environment where fungi and bacteria thrive.
2. What is Acanthosis Nigricans and what does it indicate?
   • Dark, velvety skin patches in body folds. It is a cutaneous marker of insulin resistance and hyperinsulinemia.
3. What is LADA and how is it different from T2DM?
   • LADA (Latent Autoimmune Diabetes in Adults) is a slow-onset autoimmune diabetes in adults that is initially misclassified as T2DM. Distinguished by positive islet autoantibodies (GAD antibodies) and a lean phenotype.

Pharmacology Questions

1. Why is Metformin the first-line drug for T2DM?
   • Proven efficacy, weight-neutral or causes slight weight loss, low cost, low hypoglycemia risk, cardiovascular safety data, reduces hepatic glucose output.
2. When would you choose an SGLT-2 inhibitor over other drugs?
   • In patients with established heart failure, chronic kidney disease (eGFR ≥20), or atherosclerotic cardiovascular disease - SGLT-2 inhibitors have proven outcomes in these settings.
3. Why do we check Vitamin B12 in patients on long-term Metformin?
   • Metformin reduces intestinal absorption of Vitamin B12 by competing with intrinsic factor-B12 complex. Deficiency can cause peripheral neuropathy, which is already a complication of diabetes, making diagnosis confusing.
4. What is the main side effect of Sulfonylureas?
   • Hypoglycemia, because they stimulate insulin secretion regardless of blood glucose levels.

Complications Questions

1. What is the most common cause of blindness in working-age adults?
   • Diabetic retinopathy.
2. How does diabetes cause kidney damage (nephropathy)?
   • Hyperglycemia causes glomerular hyperfiltration, thickening of the glomerular basement membrane, and mesangial expansion. The earliest sign is microalbuminuria (raised UACR).
3. What cardiovascular risk do T2DM patients carry?
   • T2DM is considered a cardiovascular risk equivalent - patients have a 2-4x higher risk of heart attack and stroke. Dyslipidemia, hypertension, and obesity often co-exist.

Prevention/Lifestyle Questions

1. Can Type 2 Diabetes be prevented?
   • Yes. The Diabetes Prevention Program showed that lifestyle modification (5-7% weight loss + 150 min/week physical activity) reduced progression from prediabetes to diabetes by 58%.
2. Why is a Mediterranean diet recommended?
   • It improves insulin sensitivity, reduces cardiovascular risk, lowers LDL, and is high in anti-inflammatory foods (olive oil, fish, nuts, vegetables).

Flowchart & Image Explanations

Slide 6 - Prediabetes Criteria Table (ADA 2026)

"This table shows that prediabetes sits just below the diabetes threshold. It is a warning zone - the patient's glucose is abnormally high but not yet diabetic. It is reversible with lifestyle changes. IFG means Impaired Fasting Glucose, and IGT means Impaired Glucose Tolerance. The important point the table notes is that risk is continuous - it doesn't suddenly jump at the cut-off, it gradually increases."

Slide 7 - Diabetes Diagnostic Criteria Table (ADA 2026)

"This is the official ADA diagnostic table. There are 4 ways to diagnose diabetes. For HbA1c, FPG, and OGTT - if the patient has no clear symptoms - you must confirm with a repeat test because a single result can be a lab error. Only a random glucose with classic symptoms like polyuria and polydipsia does not need confirmation."

Slide 11 - THE MAIN FLOWCHART: 2026 Diagnostic Algorithm for T2DM

People with symptoms of hyperglycemia, OR people with risk factors, OR routine screening candidates.

Choose one of four: HbA1c, Fasting Plasma Glucose (FPG), 75g OGTT (2-hour glucose), or Random Plasma Glucose (RPG).

• HbA1c ≥ 6.5%, OR
• FPG ≥ 126 mg/dL, OR
• 2-hr OGTT ≥ 200 mg/dL, OR
• RPG with symptoms ≥ 200 mg/dL

If NO - classify as Normal (HbA1c <5.7%, FPG <100) or Prediabetes, and reassess/rescreen later.

Symptoms = polyuria, polydipsia, weight loss, blurred vision, DKA, HHS.

• If YES with symptoms - no confirmation needed - DIABETES DIAGNOSED immediately.
• If NO symptoms - proceed to Step 5.

Repeat the same test on another day, OR get a second abnormal test (same day, different test).

• Two abnormal results? - DIABETES DIAGNOSED
• Still unclear? - Repeat testing later.

If uncertain - measure C-peptide and check autoantibodies to distinguish T1DM from T2DM.

"This is the complete diagnostic algorithm. It tells you who to test, which test to use, how to interpret the result, whether you need confirmation, and finally how to classify the type of diabetes. The most important branch is Step 4 - if the patient has symptoms, one positive test is enough. If there are no symptoms, you always need two abnormal results before labeling someone as diabetic."

Slide 16 - SGLT-2 Inhibitors Flowchart (ADA 2026)

1. Start with a T2DM patient who has a potential indication for SGLT-2 inhibitor.
2. Check contraindications - do NOT use if: Type 1 DM, dialysis/ESKD, active DKA, pregnancy, serious hypersensitivity, or history of SGLT-2-related DKA.
3. If no contraindication - prescribe with individual dosing:

• T2DM glycemic control
• ASCVD/high CV risk (canagliflozin, empagliflozin - proven MACE benefit)
• Heart failure (HFrEF and HFpEF)
• CKD with albuminuria

"The SGLT-2 inhibitor flowchart tells us when to use and when to avoid this class. These drugs work by blocking glucose reabsorption in the kidney, causing glucose to be excreted in urine. Their biggest advantage beyond glucose lowering is organ protection - they reduce heart failure hospitalizations and slow kidney disease progression. The key contraindication is active DKA, and we hold them before surgery."

Slide 17 - Sulfonylureas Flowchart (ADA 2026)

1. Consider sulfonylurea in T2DM patient.
2. Check contraindications: T1DM, DKA, sulfa allergy, pregnancy, severe liver disease, elderly/frail patients (high hypoglycemia risk), avoid if elevated fracture risk (ADA 2026).
3. Prescribe:

"Sulfonylureas are one of the oldest and most cost-effective diabetes drugs. They stimulate the pancreas to release insulin regardless of blood glucose level, which is why their main risk is hypoglycemia. Glipizide is preferred in kidney disease. Glyburide should be avoided in CKD because its active metabolite accumulates and causes prolonged hypoglycemia. ADA 2026 advises reducing sulfonylureas when you add a GLP-1 or SGLT-2 drug."

Slide 18 - DPP-4 Inhibitors & Pioglitazone Flowchart (ADA 2026)

1. Consider in T2DM patient.
2. Do NOT use: hypersensitivity, saxagliptin in heart failure, do not combine with GLP-1 RA (redundant mechanism), caution with pancreatitis history.
3. Dose adjustments by kidney function (eGFR):

• Do NOT use in: Active heart failure (worsens fluid retention), active or prior bladder cancer, osteoporosis/high fracture risk.
• Indications: T2DM with MASLD/MASH (fatty liver), high cardiovascular risk.

"DPP-4 inhibitors work by blocking the enzyme that breaks down incretin hormones - so more GLP-1 stays active after eating, stimulating glucose-dependent insulin release. They are weight neutral and have no hypoglycemia risk as monotherapy, making them excellent for older or frail patients. Linagliptin is the safest in kidney disease as it requires no dose adjustment. Avoid saxagliptin in heart failure."

Slide 19 - GLP-1 Receptor Agonists & Tirzepatide Flowchart (ADA 2026)

1. Consider GLP-1 RA in T2DM or a patient with comorbidities.
2. Contraindications: Personal/family history of Medullary Thyroid Cancer (MTC) or MEN2 syndrome, active pancreatitis, hypersensitivity, pregnancy, severe gastroparesis, BMI <18.5 kg/m².
3. Individual agent dosing:

• T2DM glycemic control (very high efficacy)
• Established ASCVD / high CV risk
• Heart failure (HFpEF) with semaglutide preferred
• MASLD/MASH (fatty liver)
• Obesity (BMI ≥30, or ≥27 with comorbidity) - Tirzepatide specifically indicated

"GLP-1 receptor agonists mimic the incretin hormone GLP-1 which is released after eating. They stimulate glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying, and reduce appetite - which is why they cause significant weight loss. Semaglutide and tirzepatide are the most potent agents in this class. Tirzepatide is a dual agonist acting on both GIP and GLP-1 receptors, giving even greater HbA1c reduction and weight loss. The most important contraindication is a personal or family history of medullary thyroid cancer."

• Slide 6 - Prediabetes criteria table
• Slide 7 - Diabetes diagnostic criteria table
• Slide 11 - Main diagnostic algorithm flowchart (7 steps)
• Slide 16 - SGLT-2 inhibitor prescribing flowchart
• Slide 17 - Sulfonylurea prescribing flowchart
• Slide 18 - DPP-4 inhibitor + Pioglitazone flowchart
• Slide 19 - GLP-1 RA + Tirzepatide flowchart

DKA - Key Points (BMJ Best Practice 2025)

1. What is DKA?

• Most common acute complication of Type 1 DM
• Can also occur in Type 2 DM (especially with infection, illness, or SGLT-2 inhibitor use)

2. Common Causes (Precipitants)

1. Missed or insufficient insulin - #1 cause
2. Infection - UTI and pneumonia are most common
3. New diagnosis of diabetes - up to 25% present this way
4. Drugs - steroids, SGLT-2 inhibitors, antipsychotics, thiazides
5. Acute illness - MI, stroke, pancreatitis

3. Symptoms & Signs

• Nausea, vomiting, abdominal pain (>50% of cases)
• Kussmaul breathing - deep, rapid, laboured breaths (body trying to blow off CO₂ to compensate for acidosis)
• Acetone (fruity) breath
• Dehydration - dry mouth, poor skin turgor, tachycardia, hypotension
• Drowsiness or confusion in severe cases

4. Diagnosis

• Blood glucose, arterial/venous blood gas (pH, bicarbonate)
• Beta-hydroxybutyrate (BOHB) - best ketone marker (>90% sensitivity and specificity if ≥3 mmol/L)
• Electrolytes (Na, K, Cl) - anion gap >12 suggests DKA
• Urine ketones and glucose
• FBC, creatinine, ECG (rule out MI), cultures if infection suspected
• Potassium - check before starting insulin. May be normal or HIGH on admission (false reassurance) but total body K is depleted

5. Treatment - The 5 Pillars

Pillar 1: FLUIDS (start immediately)

• Average fluid deficit = 6 litres
• 0.9% Normal saline - 500-1000 mL/hour for first 2-4 hours
• Correct deficit gradually over 24-48 hours (rapid correction causes cerebral oedema)
• When glucose drops below 13.9 mmol/L (250 mg/dL) - add 5-10% dextrose to prevent hypoglycaemia

Pillar 2: INSULIN

• Do NOT start insulin if potassium <3.5 mmol/L (causes fatal hypokalaemia)
• 0.1 units/kg/hour IV continuous infusion of short-acting insulin
• When glucose <250 mg/dL, reduce to 0.05 units/kg/hour
• Target glucose: 8.3-11 mmol/L (150-200 mg/dL) while treating ketoacidosis
• Continue IV insulin until DKA resolved, then overlap with subcutaneous insulin by 1-2 hours before stopping the drip

Pillar 3: POTASSIUM

• This is the most dangerous electrolyte issue in DKA
• Insulin drives K into cells - potassium crashes during treatment
• K <3.5 - give potassium first, delay insulin
• K 3.5-5.0 - start insulin + replace 20-40 mmol K per litre of fluid
• K >5.0 - start insulin, hold K replacement, recheck every 2 hours
• Target K: 4-5 mmol/L
• Severe hypokalaemia (≤2.5 mmol/L) is associated with 3x increased mortality

Pillar 4: BICARBONATE (only if needed)

• NOT routinely recommended
• Only give if pH <7.0 (severe acidosis)
• Dose: 100 mmol sodium bicarbonate over 2 hours until pH >7.0
• Add potassium chloride to bicarbonate infusion (bicarbonate also drops K)

Pillar 5: TREAT THE CAUSE

• Give antibiotics if infection
• Treat MI, pancreatitis, etc.
• Stop SGLT-2 inhibitors on admission

6. Monitoring During Treatment

7. DKA Resolution Criteria

• BOHB <0.6 mmol/L AND
• Venous pH ≥7.3 OR bicarbonate ≥18 mmol/L
• Glucose ideally <11.1 mmol/L

8. Complications of Treatment

9. Special Situations

• SGLT-2 inhibitors can cause euglycaemic DKA - glucose may be normal (<11.1 mmol/L) but patient still has ketoacidosis. Always check ketones, not just glucose.
• Pregnancy - DKA can occur at lower glucose levels. Requires immediate specialist input.
• Elderly/frail - more likely to have HHS or mixed DKA/HHS. Be cautious with fluid rates.

10. After Recovery

• Transition to subcutaneous insulin with 1-2 hour overlap with IV insulin
• Investigate WHY DKA occurred and address the cause
• Diabetes education before discharge to prevent recurrence
• If newly diagnosed with diabetes - start basal + bolus insulin regimen