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Diabetes Mellitus (DM)
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الطب الباطنيEndocrinologyDiabetes Mellitus (DM)
Red Flags

Must-Not-Miss / Red Flags

  • Diabetic ketoacidosis (DKA): Nausea, vomiting, fruity breath, Kussmaul respirations, confusion
  • Hyperosmolar hyperglycemic state (HHS): Severe dehydration, mental status changes, glucose >600 mg/dL
  • Severe hypoglycemia (Level 2): Glucose <54 mg/dL requiring assistance
  • Foot ulcer: Can lead to amputation if not addressed urgently
  • Cardiovascular symptoms: Silent ischemia common in diabetes
Patient Explanation
Your body either doesn't make enough insulin or can't use the insulin it makes properly, causing sugar to build up in your blood instead of going into your cells for energy.
Board Fact
Hemoglobin A1C ≥6.5%, SGLT2 inhibitors, GLP-1 receptor agonists, Time in Range (TIR) >70%, Ambulatory Glucose Profile (AGP)
Definition & Core Concept

Definition & Core Concept

Diabetes Mellitus (DM) encompasses a group of heterogeneous metabolic disorders sharing the common phenotype of chronic hyperglycemia. The pathophysiology diverges heavily based on etiology. Type 1 Diabetes (T1D) is defined by a T-cell-mediated autoimmune destruction of pancreatic beta cells, culminating in absolute insulin deficiency. Conversely, Type 2 Diabetes (T2D) represents a complex, progressive interplay of peripheral insulin resistance—highly associated with central adiposity—and subsequent beta-cell secretory failure.

The 2026 American Diabetes Association (ADA) Standards of Care firmly mandate the use of inclusive, person-first language across all clinical documentation (e.g., ‘people with diabetes’ rather than ‘diabetics,’ or ‘person with obesity’ rather than ‘obese’), emphasizing patient autonomy, psychosocial well-being, and shared decision-making regarding complex pharmacological choices.

Pathophysiology (Rule of 3)

Pathophysiology

Type 1 Diabetes (T1D):

  • Autoimmune destruction: T-cell-mediated destruction of pancreatic beta cells
  • Autoantibodies: GAD, IA-2, ZnT8, insulin autoantibodies
  • Absolute insulin deficiency: Requires exogenous insulin therapy
  • Genetic predisposition: HLA-DR3/DR4, non-HLA genes
  • Staging: Stage 1 (2+ autoantibodies, normoglycemia), Stage 2 (2+ autoantibodies, dysglycemia), Stage 3 (clinical diagnosis)

Type 2 Diabetes (T2D):

  • Insulin resistance: Impaired peripheral glucose uptake (muscle, adipose tissue, liver)
  • Beta-cell dysfunction: Progressive loss of insulin secretion
  • Hepatic glucose production: Increased gluconeogenesis
  • Adipose tissue: Lipolysis → increased free fatty acids → worsens insulin resistance
  • Incretin effect: Reduced GLP-1 and GIP secretion from gut
Clinical Presentation

Clinical Presentation

Classic Symptoms:

  • Polyuria: Increased urination from osmotic diuresis
  • Polydipsia: Increased thirst due to hyperosmolarity
  • Polyphagia: Increased hunger from cellular starvation
  • Unintentional weight loss: Catabolic state
  • Blurred vision: Lens osmotic changes
  • Fatigue: Cellular glucose deprivation
  • Recurrent infections: Bacterial (skin, UTIs) and fungal (vulvovaginal candidiasis)

Physical Examination Findings:

  • Acanthosis nigricans: Velvety, hyperpigmented skin in flexural areas (T2D)
  • Obesity: Central adiposity (T2D)
  • Diabetic dermopathy: Shiny atrophic patches on shins
  • Retinopathy: Microaneurysms, hemorrhages on fundoscopy
  • Neuropathy: Sensory loss, decreased vibration, distal stocking-glove pattern
  • Foot examination: Ulcers, calluses, absent pulses, diminished reflexes
Diagnostic Workup

Diagnostic Workup

Diagnostic Criteria (ADA 2026):

AssayPrediabetesDiabetes
Hemoglobin A1C5.7% – 6.4%≥6.5%
Fasting Plasma Glucose (FPG)100-125 mg/dL≥126 mg/dL (8-hour fast)
2-hour PG during OGTT140-199 mg/dL≥200 mg/dL
Random Plasma GlucoseN/A≥200 mg/dL with symptoms

Additional Laboratory:

  • Lipid panel: Assess cardiovascular risk
  • Comprehensive metabolic panel: Renal function, electrolytes
  • Urine albumin/creatinine ratio: Microalbuminuria screening
  • Autoantibody testing: GAD, IA-2, ZnT8 if T1D suspected
  • Thyroid function: TSH (T1D association with autoimmune thyroid disease)
  • Vitamin B12: If on metformin long-term

Screening:

  • Overweight/obese adults with ≥1 risk factor: Screen at any age
  • Without risk factors: Start at age 35
  • Repeat every 3 years if normal, more frequently if prediabetes
Management Protocol

Management Protocol (Blue Box)

Type 1 Diabetes (T1D):

  • Multiple daily injections (MDI): Basal (long-acting) + bolus (rapid-acting)
  • Continuous subcutaneous insulin infusion (CSII): Insulin pump
  • Ambulatory Glucose Profile (AGP): Continuous Glucose Monitoring (CGM) recommended
  • Targets: A1C 70%, TBR (<70 mg/dL) <4%

Type 2 Diabetes (T2D) – Atherosclerotic Cardiovascular Disease (ASCVD):

  • GLP-1 RA or SGLT2i with proven cardiovascular benefit are recommended to reduce MACE
  • Heart Failure:
    • HFrEF/HFmrEF: SGLT2i is foundational therapy
    • HFpEF and obesity: GIP/GLP-1 RA (tirzepatide) or high-efficacy GLP-1 RA (semaglutide) recommended

Type 2 Diabetes (T2D) – Chronic Kidney Disease (CKD):

  • eGFR 20-60 mL/min/1.73 m² or significant albuminuria → SGLT2i indicated
  • If SGLT2i contraindicated → GLP-1 RA with proven renal benefit

Glycemic Targets (Nonpregnant Adults):

  • A1C <7% (general goal)
  • A1C <8% (older adults with limited life expectancy or polypharmacy)
  • TIR >70% (70-180 mg/dL)
  • TBR <4% (<70 mg/dL), <1% (<54 mg/dL)

Hypoglycemia Treatment:

  • Conscious (Level 1, <70 mg/dL): 15-20g fast-acting glucose, recheck in 15 minutes
  • Unconscious: Glucagon 1 mg IM/SC or IV glucose 50% 25-50 mL
Complications & Prognosis

Complications & Prognosis

Microvascular Complications:

  • Retinopathy: Leading cause of blindness in working-age adults
  • Neuropathy: Peripheral (sensory loss, pain), autonomic (gastroparesis, erectile dysfunction, orthostatic hypotension)
  • Nephropathy: Leading cause of end-stage renal disease

Macrovascular Complications:

  • Coronary artery disease (CAD): Silent ischemia, MI
  • Cerebrovascular disease: Stroke
  • Peripheral arterial disease (PAD): Claudication, amputation

Other Complications:

  • Diabetic ketoacidosis (T1D, can occur in T2D with severe stress)
  • Hyperosmolar hyperglycemic state (T2D)
  • Periodontal disease
  • Hearing impairment
  • Alzheimer’s disease (increased risk)
  • Depression

Prognosis:

  • Diabetes reduces life expectancy by ~5-10 years
  • Cardiovascular disease is the leading cause of death
  • Early detection and treatment of complications improves outcomes
  • Glycemic control delays microvascular complications
  • Comprehensive management (glycemic, BP, lipid, lifestyle) reduces cardiovascular events
ICU Criteria

Admission vs. ICU Criteria

Indications for Admission:

  • DKA or HHS requiring intravenous therapy and close monitoring
  • Uncontrolled diabetes with acute illness (pneumonia, UTI, MI, etc.)
  • Severe hyperglycemia with significant electrolyte abnormalities
  • New-onset T1D requiring insulin initiation and education
  • Severe hypoglycemia requiring continuous monitoring

ICU Admission Criteria:

  • DKA with pH <7.1, bicarbonate 20
  • HHS with severe dehydration, altered mental status, or serum osmolality >340 mOsm/kg
  • Hypoglycemia requiring ICU-level monitoring (e.g., recurrent severe episodes)
  • Diabetic emergencies complicated by:
    • Hemodynamic instability
    • Respiratory failure
    • Acute kidney injury requiring RRT
    • Cerebral edema (DKA, especially in children)

Inpatient Glycemic Targets (ADA 2026):

  • Non-critically ill: Target 100-180 mg/dL
  • Critically ill: Target 140-180 mg/dL (tighter targets not recommended)
  • Initiate insulin when glucose ≥180 mg/dL on two successive occasions
Clinical Vignette
A 55-year-old female with a BMI of 38 presents for routine follow-up. She has a family history of T2D (mother and sister) and was diagnosed with hypertension 2 years ago. She reports mild fatigue and increased thirst over the past few months. Laboratory: FPG 138 mg/dL, A1C 7.2%, LDL 150 mg/dL, eGFR 72. She has no known cardiovascular disease or albuminuria.
Discharge & Follow-Up

Discharge & Outpatient Follow-up

  • Glycemic control: Review A1C, AGP report, and adjust therapy
  • Blood pressure: Target <130/80 mmHg
  • Lipid management: Statin therapy per ASCVD risk
  • Microalbuminuria: Annual urine albumin/creatinine ratio
  • Eye exam: Comprehensive dilated eye exam annually
  • Foot exam: Comprehensive foot exam annually; inspect at every visit
  • Vaccinations: Influenza, COVID-19, hepatitis B, pneumococcal
  • Lifestyle: Medical nutrition therapy, physical activity (≥150 min/week)
  • Follow-up: Every 3-6 months depending on control and comorbidities
Literature & Guidelines

Literature & Guidelines

American Diabetes Association Professional Practice Committee. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2026. Diabetes Care. 2025;49(Supplement_1):S183-S215. doi:10.2337/dc26-S009.

American Diabetes Association Professional Practice Committee. Standards of Care in Diabetes—2026. Diabetes Care. 2025;48(Supplement_1):S1-S360.

Cosentino F, Grant PJ, Aboyans V, et al. 2019 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases. Eur Heart J. 2020;41(2):255-323.

Pearls & Pitfalls

Pearls & Pitfalls

  • Pearl: SGLT2 inhibitors reduce HF hospitalizations regardless of baseline A1C or diabetes duration – start early in patients with HF risk factors.
  • Pearl: For HFpEF with obesity, tirzepatide or high-dose semaglutide improves symptoms and reduces HF events.
  • Pearl: CGM is now recommended for all patients on insulin therapy, not just T1D.
  • Pitfall: Do NOT use strict glucose control (80-130 mg/dL) in ICU patients – increases severe hypoglycemia risk without benefit.
  • Pitfall: SGLT2 inhibitors should be held in patients with DKA or severe volume depletion.
  • Pitfall: Metformin should be adjusted or held in patients with eGFR <30 mL/min/1.73 m².

Personal Clinical Notes