MBBS Year
1st Year
Subject
What Is Usually Asked
Insulin actions, glucose metabolism, ketone bodies, HbA1c, OGTT
Resource HubAll Years (1st-Final)Medical Topic AuthorityDiabetes Mellitus
Diabetes Mellitus: Notes, PPT and PYQs for MBBS
Diabetes mellitus is a chronic metabolic disorder characterised by hyperglycaemia resulting from defects in insulin secretion, insulin action, or both. It is taught across MBBS: Biochemistry and Physiology in 1st Year, Pathology and Pharmacology in 2nd Year, Community Medicine in 3rd Year, and General Medicine, Obstetrics and Paediatrics in Final Year.
SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and notesQuick Summary: What You Need to Know for University Exams
- Diabetes is classified into Type 1, Type 2, gestational diabetes and specific types due to other causes.
- Type 1 results from autoimmune destruction of pancreatic beta cells, causing absolute insulin deficiency.
- Type 2 results from insulin resistance combined with progressive beta-cell dysfunction.
- Diagnosis uses fasting plasma glucose, the 75 g oral glucose tolerance test (OGTT), HbA1c or random plasma glucose with symptoms.
- Metformin is usually the first-line oral drug in Type 2 diabetes; insulin is essential in Type 1.
- Acute complications: diabetic ketoacidosis (DKA), hyperosmolar hyperglycaemic state (HHS) and hypoglycaemia.
- Chronic complications: retinopathy, nephropathy and neuropathy (microvascular), and coronary, cerebrovascular and peripheral arterial disease (macrovascular).
Diabetes Mellitus Across MBBS Subjects
| MBBS Year | Subject | What Is Usually Asked |
|---|---|---|
| 1st Year | Biochemistry | Insulin actions, glucose metabolism, ketone bodies, HbA1c, OGTT |
| 1st Year | Physiology | Endocrine pancreas, actions and regulation of insulin |
| 2nd Year | Pathology | Classification, pathogenesis, morphology of complications |
| 2nd Year | Pharmacology | Insulin preparations, oral antidiabetic drugs |
| 3rd Year | Community Medicine | Epidemiology, risk factors, prevention, national programme |
| Final Year | General Medicine | Diagnosis, management, DKA, chronic complications |
| Final Year | Obstetrics and Gynaecology | Gestational diabetes |
| Final Year | Paediatrics | Type 1 diabetes in children, DKA |
MBBS Year
1st Year
Subject
What Is Usually Asked
Endocrine pancreas, actions and regulation of insulin
MBBS Year
2nd Year
Subject
What Is Usually Asked
Classification, pathogenesis, morphology of complications
MBBS Year
2nd Year
Subject
What Is Usually Asked
Insulin preparations, oral antidiabetic drugs
MBBS Year
3rd Year
Subject
What Is Usually Asked
Epidemiology, risk factors, prevention, national programme
MBBS Year
Final Year
Subject
What Is Usually Asked
Diagnosis, management, DKA, chronic complications
MBBS Year
Final Year
Subject
What Is Usually Asked
Gestational diabetes
MBBS Year
Final Year
Subject
What Is Usually Asked
Type 1 diabetes in children, DKA
Definition and Classification
Definition: Diabetes mellitus is a group of metabolic disorders characterised by chronic hyperglycaemia due to defects in insulin secretion, insulin action, or both, with disturbances of carbohydrate, fat and protein metabolism.
Classification (American Diabetes Association):
- Type 1 diabetes: Autoimmune beta-cell destruction, usually leading to absolute insulin deficiency.
- Type 2 diabetes: Progressive loss of adequate beta-cell insulin secretion, frequently on a background of insulin resistance.
- Gestational diabetes mellitus (GDM): Diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt before pregnancy.
- Specific types due to other causes:
- Monogenic diabetes, such as maturity-onset diabetes of the young (MODY) and neonatal diabetes
- Diseases of the exocrine pancreas, such as chronic pancreatitis and cystic fibrosis
- Drug- or chemical-induced diabetes, such as with glucocorticoids
- Endocrinopathies, such as Cushing's syndrome and acromegaly
Type 1 Versus Type 2 Diabetes
| Feature | Type 1 | Type 2 |
|---|---|---|
| Usual age of onset | Childhood or young adulthood | Adulthood, increasingly seen in younger people |
| Body build | Usually lean | Often overweight or obese |
| Basic defect | Absolute insulin deficiency | Insulin resistance with relative insulin deficiency |
| Islet autoantibodies | Usually present | Absent |
| HLA association | HLA-DR3, HLA-DR4 | No HLA association |
| Ketosis | Prone to ketosis | Usually resistant to ketosis |
| Islet pathology | Insulitis, beta-cell loss | Amyloid deposition in islets |
| Treatment | Insulin essential | Lifestyle measures and oral drugs; insulin may be needed later |
| Typical acute complication | DKA | HHS |
Feature
Usual age of onset
Type 1
Childhood or young adulthood
Type 2
Adulthood, increasingly seen in younger people
Feature
Body build
Type 1
Usually lean
Type 2
Often overweight or obese
Feature
Basic defect
Type 1
Absolute insulin deficiency
Type 2
Insulin resistance with relative insulin deficiency
Feature
Islet autoantibodies
Type 1
Usually present
Type 2
Absent
Feature
HLA association
Type 1
HLA-DR3, HLA-DR4
Type 2
No HLA association
Feature
Ketosis
Type 1
Prone to ketosis
Type 2
Usually resistant to ketosis
Feature
Islet pathology
Type 1
Insulitis, beta-cell loss
Type 2
Amyloid deposition in islets
Feature
Treatment
Type 1
Insulin essential
Type 2
Lifestyle measures and oral drugs; insulin may be needed later
Feature
Typical acute complication
Type 1
DKA
Type 2
HHS
Aetiology (Causes and Risk Factors)
Type 1 Diabetes
- Genetic susceptibility: HLA-DR3 and HLA-DR4 on chromosome 6
- Environmental triggers: Viral infections and other factors have been proposed as triggers of autoimmunity
- Autoimmunity: Autoantibodies against glutamic acid decarboxylase (GAD65), insulin, islet antigen 2 (IA-2) and zinc transporter 8 (ZnT8)
Type 2 Diabetes
- Family history and genetic predisposition
- Obesity, especially central (abdominal) obesity
- Physical inactivity and unhealthy diet
- Increasing age
- South Asian ethnicity, with risk appearing at lower body weight than in many other populations
- Previous gestational diabetes
- Polycystic ovary syndrome
Pathophysiology
Type 1 Diabetes: Flowchart
- Genetic susceptibility plus an environmental trigger
- T-cell mediated autoimmune attack on beta cells (insulitis)
- Progressive beta-cell destruction
- Absolute insulin deficiency
- Hyperglycaemia plus uncontrolled lipolysis and ketogenesis
- Risk of diabetic ketoacidosis
Type 2 Diabetes: Flowchart
- Genetic predisposition plus obesity and inactivity
- Insulin resistance in muscle, liver and adipose tissue
- Beta cells compensate by secreting more insulin
- Progressive beta-cell dysfunction
- Relative insulin deficiency
- Hyperglycaemia
The ominous octet (DeFronzo): Eight contributors to hyperglycaemia in Type 2 diabetes: reduced insulin secretion (beta cells), increased glucagon (alpha cells), increased hepatic glucose production, reduced muscle glucose uptake, increased lipolysis (adipose tissue), increased renal glucose reabsorption, reduced incretin effect (gut) and neurotransmitter dysfunction (brain).
Metabolic Effects of Insulin Deficiency
| Process | Change | Result |
|---|---|---|
| Glucose uptake by muscle and fat | Decreased | Hyperglycaemia |
| Glycogenolysis and gluconeogenesis | Increased | Hyperglycaemia |
| Lipolysis | Increased | Raised free fatty acids |
| Ketogenesis | Increased | Ketosis and acidosis |
| Protein breakdown | Increased | Weight loss, muscle wasting |
| Glycosuria | Present when renal threshold is exceeded | Osmotic diuresis, polyuria, polydipsia |
Process
Glucose uptake by muscle and fat
Change
Decreased
Result
Hyperglycaemia
Process
Glycogenolysis and gluconeogenesis
Change
Increased
Result
Hyperglycaemia
Process
Lipolysis
Change
Increased
Result
Raised free fatty acids
Process
Ketogenesis
Change
Increased
Result
Ketosis and acidosis
Process
Protein breakdown
Change
Increased
Result
Weight loss, muscle wasting
Process
Glycosuria
Change
Present when renal threshold is exceeded
Result
Osmotic diuresis, polyuria, polydipsia
(Examiner may ask you to draw the pathophysiology flowchart.)
Clinical Features
Classic symptoms:
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss (more marked in Type 1)
Other features:
- Fatigue and weakness
- Blurred vision
- Recurrent infections such as candidiasis, urinary tract infections and skin infections
- Delayed wound healing
- Acanthosis nigricans, a marker of insulin resistance
- Many people with Type 2 diabetes have no symptoms and are detected on screening
Diagnosis
Diagnostic Criteria (American Diabetes Association)
| Test | Diabetes | Prediabetes |
|---|---|---|
| Fasting plasma glucose (no calorie intake for at least 8 hours) | 126 mg/dL or more | 100 to 125 mg/dL (impaired fasting glucose) |
| 2-hour plasma glucose during 75 g OGTT | 200 mg/dL or more | 140 to 199 mg/dL (impaired glucose tolerance) |
| HbA1c | 6.5% or more | 5.7% to 6.4% |
| Random plasma glucose with classic symptoms of hyperglycaemia | 200 mg/dL or more | Not applicable |
Test
Fasting plasma glucose (no calorie intake for at least 8 hours)
Diabetes
126 mg/dL or more
Prediabetes
100 to 125 mg/dL (impaired fasting glucose)
Test
2-hour plasma glucose during 75 g OGTT
Diabetes
200 mg/dL or more
Prediabetes
140 to 199 mg/dL (impaired glucose tolerance)
Test
HbA1c
Diabetes
6.5% or more
Prediabetes
5.7% to 6.4%
Test
Random plasma glucose with classic symptoms of hyperglycaemia
Diabetes
200 mg/dL or more
Prediabetes
Not applicable
In the absence of unequivocal hyperglycaemia, the diagnosis should be confirmed by repeat testing.
Gestational diabetes in India: National guidelines recommend a single-step 75 g OGTT for pregnant women regardless of fasting state, with a 2-hour value of 140 mg/dL or more diagnosed as GDM.
Other Investigations
| Investigation | Purpose |
|---|---|
| Urine glucose and ketones | Screening and detection of ketosis |
| HbA1c | Reflects average glycaemia over roughly the previous two to three months |
| C-peptide | Assesses endogenous insulin secretion; helps distinguish Type 1 from Type 2 |
| Islet autoantibodies | Support the diagnosis of Type 1 diabetes |
| Lipid profile | Cardiovascular risk assessment |
| Renal function and urine albumin | Screening for diabetic nephropathy |
| Fundus examination | Screening for diabetic retinopathy |
| ECG | Screening for coronary artery disease |
Investigation
Urine glucose and ketones
Purpose
Screening and detection of ketosis
Investigation
HbA1c
Purpose
Reflects average glycaemia over roughly the previous two to three months
Investigation
C-peptide
Purpose
Assesses endogenous insulin secretion; helps distinguish Type 1 from Type 2
Investigation
Islet autoantibodies
Purpose
Support the diagnosis of Type 1 diabetes
Investigation
Lipid profile
Purpose
Cardiovascular risk assessment
Investigation
Renal function and urine albumin
Purpose
Screening for diabetic nephropathy
Investigation
Fundus examination
Purpose
Screening for diabetic retinopathy
Investigation
ECG
Purpose
Screening for coronary artery disease
For reference ranges, see the normal lab values chart.
Management
Goals of Treatment
- Relieve symptoms of hyperglycaemia
- Achieve individualised glycaemic targets
- Prevent acute and chronic complications
- Manage associated risk factors such as hypertension, dyslipidaemia and smoking
Lifestyle Measures (All Patients)
- Medical nutrition therapy with a balanced, portion-controlled diet
- Regular physical activity
- Weight reduction in overweight patients
- Stopping smoking
- Patient education, including self-monitoring and foot care
Drug Treatment
Type 1 diabetes: Insulin is essential, commonly as a basal-bolus regimen.
Type 2 diabetes: Metformin is usually the first-line drug unless contraindicated. Other drugs are added according to the patient's needs and comorbidities.
| Drug Class | Examples | Mechanism | Key Adverse Effects |
|---|---|---|---|
| Biguanides | Metformin | Reduces hepatic glucose production, improves insulin sensitivity | Gastrointestinal upset, vitamin B12 deficiency, rare lactic acidosis |
| Sulfonylureas | Glimepiride, gliclazide | Close ATP-sensitive potassium channels in beta cells, increasing insulin release | Hypoglycaemia, weight gain |
| DPP-4 inhibitors | Sitagliptin, vildagliptin | Prevent breakdown of incretin hormones | Generally well tolerated, low risk of hypoglycaemia |
| SGLT2 inhibitors | Dapagliflozin, empagliflozin | Block glucose reabsorption in the proximal renal tubule | Genital fungal infections, euglycaemic ketoacidosis |
| GLP-1 receptor agonists | Liraglutide, semaglutide | Enhance glucose-dependent insulin secretion, slow gastric emptying | Nausea, vomiting |
| Thiazolidinediones | Pioglitazone | PPAR-gamma agonist, improves insulin sensitivity | Weight gain, fluid retention |
| Alpha-glucosidase inhibitors | Acarbose, voglibose | Delay intestinal carbohydrate absorption | Flatulence, abdominal discomfort |
Drug Class
Biguanides
Examples
Metformin
Mechanism
Reduces hepatic glucose production, improves insulin sensitivity
Key Adverse Effects
Gastrointestinal upset, vitamin B12 deficiency, rare lactic acidosis
Drug Class
Sulfonylureas
Examples
Glimepiride, gliclazide
Mechanism
Close ATP-sensitive potassium channels in beta cells, increasing insulin release
Key Adverse Effects
Hypoglycaemia, weight gain
Drug Class
DPP-4 inhibitors
Examples
Sitagliptin, vildagliptin
Mechanism
Prevent breakdown of incretin hormones
Key Adverse Effects
Generally well tolerated, low risk of hypoglycaemia
Drug Class
SGLT2 inhibitors
Examples
Dapagliflozin, empagliflozin
Mechanism
Block glucose reabsorption in the proximal renal tubule
Key Adverse Effects
Genital fungal infections, euglycaemic ketoacidosis
Drug Class
GLP-1 receptor agonists
Examples
Liraglutide, semaglutide
Mechanism
Enhance glucose-dependent insulin secretion, slow gastric emptying
Key Adverse Effects
Nausea, vomiting
Drug Class
Thiazolidinediones
Examples
Pioglitazone
Mechanism
PPAR-gamma agonist, improves insulin sensitivity
Key Adverse Effects
Weight gain, fluid retention
Drug Class
Alpha-glucosidase inhibitors
Examples
Acarbose, voglibose
Mechanism
Delay intestinal carbohydrate absorption
Key Adverse Effects
Flatulence, abdominal discomfort
Insulin preparations:
| Type | Examples |
|---|---|
| Rapid-acting | Insulin lispro, insulin aspart |
| Short-acting | Regular (soluble) insulin |
| Intermediate-acting | NPH (isophane) insulin |
| Long-acting | Insulin glargine, insulin detemir, insulin degludec |
Type
Rapid-acting
Examples
Insulin lispro, insulin aspart
Type
Short-acting
Examples
Regular (soluble) insulin
Type
Intermediate-acting
Examples
NPH (isophane) insulin
Type
Long-acting
Examples
Insulin glargine, insulin detemir, insulin degludec
For a revision-ready version, see the antidiabetic drugs classification chart.
Principles of Managing Acute Complications (MBBS Level)
- DKA: Intravenous fluids, intravenous insulin, potassium replacement with monitoring, and treatment of the precipitating cause such as infection.
- Hypoglycaemia: Oral glucose if the patient is conscious; intravenous dextrose or glucagon if the patient cannot take orally.
Monitoring
- Self-monitoring of blood glucose
- Regular HbA1c
- Periodic screening for complications: eye examination, urine albumin, renal function and foot examination
Complications
Acute Complications
| Complication | Key Features |
|---|---|
| Diabetic ketoacidosis (DKA) | Triad of hyperglycaemia, ketosis and metabolic acidosis; Kussmaul breathing, fruity odour of breath, dehydration; more common in Type 1 |
| Hyperosmolar hyperglycaemic state (HHS) | Severe hyperglycaemia, high plasma osmolality and dehydration without significant ketoacidosis; usually older patients with Type 2 |
| Hypoglycaemia | Usually treatment-related (insulin or sulfonylureas); sweating, tremor, confusion, seizures if severe |
Complication
Diabetic ketoacidosis (DKA)
Key Features
Triad of hyperglycaemia, ketosis and metabolic acidosis; Kussmaul breathing, fruity odour of breath, dehydration; more common in Type 1
Complication
Hyperosmolar hyperglycaemic state (HHS)
Key Features
Severe hyperglycaemia, high plasma osmolality and dehydration without significant ketoacidosis; usually older patients with Type 2
Complication
Hypoglycaemia
Key Features
Usually treatment-related (insulin or sulfonylureas); sweating, tremor, confusion, seizures if severe
Chronic Complications
Microvascular:
- Diabetic retinopathy: Non-proliferative (microaneurysms, dot and blot haemorrhages, hard exudates) and proliferative (new vessel formation)
- Diabetic nephropathy: Increasing albuminuria followed by declining kidney function; pathology includes nodular glomerulosclerosis (Kimmelstiel-Wilson lesions), diffuse glomerulosclerosis and hyaline arteriolosclerosis
- Diabetic neuropathy: Distal symmetric sensory neuropathy in a glove and stocking pattern, autonomic neuropathy and mononeuropathies
Macrovascular:
- Coronary artery disease
- Cerebrovascular disease (stroke)
- Peripheral arterial disease
Others:
- Diabetic foot (ulcers, infection, gangrene)
- Increased susceptibility to infections
- Cataract
Prevention (Community Medicine Angle)
| Level | Measures |
|---|---|
| Primordial | Promoting healthy diet and physical activity to prevent risk factors from emerging |
| Primary | Weight control, physical activity and diet in people at risk |
| Secondary | Screening and early diagnosis; in India, population-based screening for common non-communicable diseases is carried out for people aged 30 years and above under the national NCD programme |
| Tertiary | Preventing and managing complications, rehabilitation |
Level
Primordial
Measures
Promoting healthy diet and physical activity to prevent risk factors from emerging
Level
Primary
Measures
Weight control, physical activity and diet in people at risk
Level
Secondary
Measures
Screening and early diagnosis; in India, population-based screening for common non-communicable diseases is carried out for people aged 30 years and above under the national NCD programme
Level
Tertiary
Measures
Preventing and managing complications, rehabilitation
Prognosis
Prognosis depends largely on glycaemic control and on control of associated risk factors. Good long-term control of blood glucose, blood pressure and lipids reduces the risk of microvascular and macrovascular complications. Cardiovascular disease is a leading cause of death in people with diabetes.
How Diabetes Mellitus Appears in MBBS University Exams
Diabetes is asked in several subjects. Here are the typical question styles (not attributed to specific papers or years):
- "Classify diabetes mellitus. Discuss the aetiology, clinical features, diagnosis and management of Type 2 diabetes mellitus." (Long essay, General Medicine)
- "Write a short note on diabetic ketoacidosis." (Short note, General Medicine or Paediatrics)
- "Describe the pathogenesis of Type 1 and Type 2 diabetes mellitus. Add a note on diabetic nephropathy." (Long essay, Pathology)
- "Classify oral antidiabetic drugs. Write the mechanism of action and adverse effects of metformin." (Long essay or short note, Pharmacology)
- "Enumerate the chronic complications of diabetes mellitus." (Short answer)
- "Write a short note on gestational diabetes mellitus." (Short note, Obstetrics)
- "Describe the epidemiology and prevention of diabetes mellitus." (Community Medicine)
Frequently Asked Questions
What is the difference between Type 1 and Type 2 diabetes mellitus?
Type 1 is caused by autoimmune destruction of beta cells, leading to absolute insulin deficiency, and needs insulin from diagnosis. Type 2 is caused by insulin resistance with progressive beta-cell dysfunction and is initially managed with lifestyle measures and oral drugs.
What are the diagnostic criteria for diabetes mellitus?
Fasting plasma glucose of 126 mg/dL or more, 2-hour plasma glucose of 200 mg/dL or more during a 75 g OGTT, HbA1c of 6.5% or more, or random plasma glucose of 200 mg/dL or more with classic symptoms, as per American Diabetes Association criteria.
Can I download the diabetes mellitus PPT for my presentation?
Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.
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