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DIABETES MELLITUS

Harrison's Principles of Internal Medicine 22E (2025)

MNEMONIC OVERVIEW: "DICE CAMP"

D - Definition & Diagnosis I - Incidence & Epidemiology C - Classification E - Etiology & Pathophysiology C - Clinical Features A - Acute Complications M - Management P - Prevention & Prognosis (Chronic Complications)

1. DEFINITION

Diabetes Mellitus (DM) is a group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Chronic hyperglycemia is associated with long-term damage, dysfunction, and failure of various organs - especially the eyes, kidneys, nerves, heart, and blood vessels.

2. INCIDENCE / EPIDEMIOLOGY

Affects ~537 million people worldwide (IDF 2021); projected 783 million by 2045
Type 2 DM accounts for ~90-95% of all cases
Type 1 DM accounts for ~5-10%
Prevalence in India: ~10% of adults (one of the highest globally)
50% of type 2 DM cases remain undiagnosed
Type 2 DM may be present up to a decade before clinical diagnosis

3. CLASSIFICATION

Mnemonic: "OGT"

O - Other specific types G - Gestational DM T - Type 1 & Type 2

Type	Key Feature
Type 1 DM	Autoimmune beta cell destruction → absolute insulin deficiency
Type 2 DM	Insulin resistance + relative insulin deficiency
Other types	MODY, pancreatic disease, drugs, endocrinopathies
Gestational DM (GDM)	Diagnosed during pregnancy

Type 1 DM - 3 Stages:

Stage 1: Multiple autoantibodies, normoglycemia, asymptomatic
Stage 2: Multiple autoantibodies + dysglycemia, asymptomatic
Stage 3: Clinical hyperglycemia, symptomatic

Other Specific Types (Mnemonic: "GAMED"):

Genetic defects of beta cell (MODY 1-6)
Acquired pancreatic disease (pancreatitis, cystic fibrosis, hemochromatosis)
Medications/Chemicals (glucocorticoids, thiazides, antipsychotics)
Endocrinopathies (Cushing's, Acromegaly, Pheochromocytoma, Glucagonoma)
Disease - genetic insulin receptor defects (type A insulin resistance, leprechaunism)

4. ETIOLOGY & PATHOPHYSIOLOGY

Type 1 DM - Mnemonic: "GAVIN"

G - Genetic susceptibility (HLA-DR3, HLA-DR4) A - Autoimmune destruction (anti-GAD, anti-islet cell antibodies) V - Viral triggers (Coxsackie B, Rubella, Enteroviruses) I - Insulitis (lymphocytic infiltration of islets) N - No insulin (absolute deficiency → ketoacidosis prone)

HLA association: HLA-DR3 and HLA-DR4 alleles confer risk; HLA-DR2/DQ6 is protective
Autoantibodies present: Anti-GAD65, anti-insulin antibodies (IAA), islet cell antibodies (ICA), anti-IA-2, anti-ZnT8
Concordance in identical twins: ~50% (environmental factor plays role)

Type 2 DM - Mnemonic: "TIROH"

T - Tissue insulin resistance (skeletal muscle, liver, adipose) I - Impaired insulin secretion (progressive beta cell failure) R - Raised hepatic glucose production (gluconeogenesis) O - Obesity (visceral/central; >80% of T2DM patients) H - Hyperglucagonemia (excess alpha cell activity)

Pathophysiology sequence: Insulin resistance → compensatory hyperinsulinemia → beta cell exhaustion → frank DM
"Ominous Octet" (DeFronzo): Decreased insulin secretion, decreased incretin effect, increased lipolysis, increased glucagon, increased glucose reabsorption by kidney, neurotransmitter dysfunction, decreased glucose uptake in muscle, increased hepatic glucose output
Genetic risk: >600 susceptibility loci; concordance in identical twins 70-90%
Strong environmental factors: obesity, sedentary lifestyle, poor diet, aging

5. DIAGNOSIS

Mnemonic: "FAR2" (Four criteria, ANY ONE is sufficient)

Criterion	Value
Fasting Plasma Glucose (FPG)	≥ 126 mg/dL (7.0 mmol/L) - 8h fast
Any time (Random) Plasma Glucose + symptoms	≥ 200 mg/dL (11.1 mmol/L)
2-hour PG during 75g OGTT	≥ 200 mg/dL (11.1 mmol/L)
2-HbA1c	≥ 6.5% (48 mmol/mol)

In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing.

Pre-Diabetes:

State	FPG	2h OGTT	HbA1c
IFG	100-125 mg/dL	Normal	5.7-6.4%
IGT	Normal	140-199 mg/dL	5.7-6.4%

6. CLINICAL FEATURES

Classical Symptoms - Mnemonic: "3 Ps + W"

Polyuria, Polydipsia, Polyphagia + Weight loss

Additional features:

Type 1 DM:

Sudden onset, young age, lean body
Prone to DKA (may be first presentation)
Acanthosis nigricans absent

Type 2 DM:

Insidious onset, middle-aged/elderly
Often obese, asymptomatic initially
Acanthosis nigricans, skin tags
Diagnosed incidentally on routine screening

7. ACUTE COMPLICATIONS

Mnemonic: "DKA - HHS - H"

A. Diabetic Ketoacidosis (DKA) - Mainly Type 1

Triad: Hyperglycemia (>250 mg/dL) + Metabolic acidosis (pH <7.3, HCO₃ <15) + Ketonemia
Precipitants: Mnemonic "5 Is" - Infection, Infarction, Insulin omission, Intoxication, Iatrogenic
Clinical: Kussmaul breathing, fruity breath, N/V, abdominal pain, dehydration
Treatment: IV fluids (0.9% NaCl) → Insulin infusion (0.1 u/kg/hr) → Potassium replacement → Treat precipitant

B. Hyperosmolar Hyperglycemic State (HHS) - Mainly Type 2

Glucose >600 mg/dL, Osmolality >320 mOsm/kg
No significant ketosis
Extreme dehydration, altered sensorium
High mortality (15-20%)

C. Hypoglycemia (most common acute complication)

Glucose <70 mg/dL
Whipple's triad: Symptoms + low glucose + relief with glucose
Causes: Excess insulin/OHAs, missed meals, exercise, alcohol
Treatment: 15-15 rule (15g glucose, recheck in 15 min); if unconscious → IV 25% dextrose or glucagon IM

8. CHRONIC COMPLICATIONS

Mnemonic: "MiMa" (Microvascular + Macrovascular)

A. MICROVASCULAR - Mnemonic: "RRN"

1. Retinopathy (Leading cause of new blindness in 20-74 yr age group)

Non-proliferative: Microaneurysms, dot-blot hemorrhages, hard exudates, cotton-wool spots
Proliferative: Neovascularization → vitreous hemorrhage → retinal detachment
Macular edema can occur at any stage
Screening: Annual dilated eye exam from diagnosis (T2DM); 5 years after onset (T1DM)
Treatment: Laser photocoagulation, intravitreal anti-VEGF (bevacizumab/ranibizumab)

2. Renal Disease (Diabetic Nephropathy)

Leading cause of End-Stage Renal Disease (ESRD)
Stages (Mogensen): Microalbuminuria (30-300 mg/day) → Macroalbuminuria (>300 mg/day) → Progressive GFR decline → ESRD
Kimmelstiel-Wilson nodules on histology (pathognomonic)
Treatment: ACE inhibitors/ARBs (renoprotective), SGLT-2 inhibitors

3. Neuropathy (Most common complication overall)

Peripheral polyneuropathy: Symmetric, distal, "stocking-glove" pattern; burning/tingling feet (worse at night)
Autonomic neuropathy: Gastroparesis, orthostatic hypotension, bladder dysfunction, ED, silent MI
Mononeuropathy: Cranial nerve III palsy (pupil-sparing), carpal tunnel
Charcot joint: Neuropathic arthropathy; painless joint destruction

B. MACROVASCULAR - Mnemonic: "CAP"

Coronary artery disease (2-4x increased risk; may be silent)
Atherosclerotic peripheral arterial disease (→ diabetic foot, gangrene)
Peripheral cerebrovascular disease (stroke, TIA)

Diabetic Foot - Mnemonic: "WINDS"

Wound (neuropathic ulcer) Infection (polymicrobial) Neuropathy (loss of sensation → trauma unnoticed) Dysvascularity (ischemia) Sepsis risk

9. MANAGEMENT

Treatment Goals (Mnemonic: "ABC" of DM management)

A - A1c <7% (individualised; <6.5% if newly diagnosed, no CVD) B - Blood pressure <130/80 mmHg C - Cholesterol (LDL <100 mg/dL, or <70 if CVD)

Stepwise Treatment for Type 2 DM:

Step 1 - Lifestyle modification (ALWAYS first)

MNT (Medical Nutrition Therapy): Reduce calories, low glycemic index, high fiber
Exercise: 150 min/week moderate aerobic activity
Weight loss: Even 5-7% weight loss improves glycemia significantly

Step 2 - Oral Hypoglycemic Agents (OHAs)

Drug Class	Mechanism	Mnemonic
Biguanides (Metformin - 1st line)	↓ Hepatic glucose output, ↑ insulin sensitivity	"Metformin Moves glucose out of liver"
Sulfonylureas (Glipizide, Gliclazide)	↑ Insulin secretion (close K-ATP channel)	"Sulfonylureas Stimulate secretion"
SGLT-2 inhibitors (Empagliflozin, Dapagliflozin)	Block renal glucose reabsorption → glycosuria	"SGLT-2 Spills sugar in urine"
GLP-1 RAs (Semaglutide, Liraglutide)	↑ Insulin, ↓ glucagon, slow gastric emptying	"GLP-1 gives weight loss bonus"
DPP-4 inhibitors (Sitagliptin)	Prolong endogenous GLP-1	"DPP-4 Delays GLP-1 degradation"
Thiazolidinediones (Pioglitazone)	↑ Insulin sensitivity (PPAR-γ agonist)	"TZD Tackles insulin resistance"
Alpha-glucosidase inhibitors (Acarbose)	Delay carbohydrate absorption	"Acarbose Allows slow sugar"

Key 2024 ADA Update: In patients with T2DM + ASCVD/HF/CKD, GLP-1 RA or SGLT-2 inhibitor should be prioritized regardless of HbA1c.

Step 3 - Insulin Therapy

Preparation	Onset	Peak	Duration
Rapid-acting (Aspart, Lispro)	<15 min	0.5-1.5h	3-5h
Short-acting (Regular)	30-60 min	2-4h	5-8h
Intermediate (NPH)	2-4h	4-10h	10-18h
Long-acting (Glargine, Detemir)	1-2h	Peakless	20-24h
Ultra-long (Degludec)	1h	Peakless	>42h

Management of Type 1 DM:

Insulin is mandatory - Basal-bolus regimen (multiple daily injections)
Target HbA1c <7% (individualized)
Continuous Glucose Monitoring (CGM) preferred
Automated Insulin Delivery (AID) systems - latest standard of care

Monitoring:

Self-monitoring blood glucose (SMBG): Before meals and bedtime
HbA1c: Every 3 months until stable, then every 6 months
Annual screening: Urine microalbumin, lipids, serum creatinine, eye exam, foot exam
BP: Every visit

10. PREVENTION

Type 1 DM: No proven prevention currently

Type 2 DM - Mnemonic: "WEDS"

Weight reduction (5-7% body weight) Exercise (150 min/week) Diet modification (low calorie, low fat, high fiber) Screening high-risk individuals + Metformin in prediabetes (ADA recommended)

Diabetes Prevention Program (DPP): Intensive lifestyle modification reduced T2DM incidence by 58%; Metformin reduced it by 31%

QUICK REVISION MNEMONICS SUMMARY

Topic	Mnemonic
Overall structure	DICE CAMP
Symptoms	3 Ps + W (Polyuria, Polydipsia, Polyphagia + Weight loss)
Classification	OGT
Other specific types	GAMED
Type 1 pathogenesis	GAVIN
Type 2 pathogenesis	TIROH
Diagnosis criteria	FAR2
DKA precipitants	5 Is
Complications	MiMa → RRN + CAP
Treatment goals	ABC
T2DM drugs	Each drug class mnemonic above
Prevention	WEDS

EXAM TIPS FOR FINAL YEAR MBBS

Always know the diagnostic criteria by heart (FPG ≥126, HbA1c ≥6.5%, Random ≥200 + symptoms, OGTT 2h ≥200)
DKA vs HHS - know the key differences (ketosis, pH, glucose levels)
Kimmelstiel-Wilson nodules = pathognomonic of diabetic nephropathy
Whipple's triad for hypoglycemia
Metformin is contraindicated in eGFR <30, contrast media use, heart failure (decompensated)
SGLT-2 inhibitors and GLP-1 RAs have cardioprotective and renoprotective benefits - most tested in recent exams
Diabetic autonomic neuropathy causes pupil-sparing 3rd nerve palsy - classic exam question
The Diabetes Prevention Program (DPP) figures (58% lifestyle, 31% metformin)

Source: Harrison's Principles of Internal Medicine, 22nd Edition (2025) - Chapters 415, 416, 417, 418

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