STEPTRACKERENDOCRINE | PATHOLOGY + BIOCHEMISTRY + PHARMACOLOGY | HIGH-YIELD REVIEW

Diabetes Mellitus

Two very different paths to high glucose, the acute crises, and the slow damage to small and large vessels.

FOCUS ON
Type 1: autoimmune β-cell destruction (HLA-DR3/DR4, anti-GAD), young, ↓ C-peptide, DKA. Type 2: insulin resistance + β-cell failure, obesity, islet amyloid, HHS. Chronic damage: glycation (AGEs, hyaline arteriolosclerosis) and sorbitol (lens, nerves, retina, kidney). Macrovascular disease (MI) is the leading cause of death.
TOPIC
MECHANISM
FEATURES
CLUE · TREATMENT
Type 1 diabetes
T-cell (type IV) destruction of β cells; HLA-DR3/DR4; anti-GAD65, anti-insulin, IA-2, ZnT8 antibodies
Children/young adults; abrupt polyuria, polydipsia, polyphagia, weight loss; insulitis
↓ C-peptide · insulin required
Type 2 diabetes
Insulin resistance (visceral obesity, inactivity) + progressive β-cell dysfunction; strong family link
Adults; gradual or asymptomatic; acanthosis nigricans; islet amyloid (amylin) deposits
Metformin first · normal/↑ C-peptide early
Diagnosis
Thresholds for hyperglycemia
Fasting glucose ≥ 126 mg/dL, HbA1c ≥ 6.5%, 2-h OGTT ≥ 200, or random ≥ 200 with symptoms
HbA1c reflects ~3 months
Diabetic ketoacidosis
No insulin + ↑ glucagon, cortisol, catecholamines → lipolysis → FFAs → hepatic ketones (acetoacetate, β-hydroxybutyrate)
High anion gap acidosis, Kussmaul breathing, fruity breath, vomiting, abdominal pain, dehydration; trigger: infection, missed insulin
Fluids + IV insulin + K⁺; add dextrose as glucose falls
DKA — potassium
Insulin lack and acidosis shift K⁺ out of cells; osmotic diuresis wastes it
Serum K⁺ normal or ↑ but total body K⁺ depleted
Insulin drives K⁺ in → hypokalemia; check K⁺ before insulin
Hyperosmolar hyperglycemic state
Enough insulin to block ketogenesis, not hyperglycemia; type 2, older
Glucose > 600, osmolality > 320, severe dehydration, confusion/coma; little or no acidosis
Aggressive fluids · higher mortality than DKA
Microvascular — mechanisms
Nonenzymatic glycation (AGEs) of proteins → hyaline arteriolosclerosis, thick BM · aldose reductase → sorbitol accumulates in cells lacking sorbitol dehydrogenase
Lens (cataracts), Schwann cells, retina, kidney
Glycemic control prevents
Retinopathy
Pericyte loss, microaneurysms, ischemia → VEGF
Nonproliferative: microaneurysms, dot-blot hemorrhages, hard exudates, cotton wool spots · proliferative: neovascularization → vitreous hemorrhage, detachment
Anti-VEGF, laser photocoagulation
Neuropathy
Sorbitol + microvascular injury to nerves
Symmetric stocking-glove sensory loss → ulcers, Charcot joints; autonomic (gastroparesis, ED, orthostasis); CN III palsy with pupil sparing
Nephropathy: see 12.05
Macrovascular disease
Accelerated atherosclerosis
Coronary artery disease (often silent MI), stroke, peripheral artery disease → gangrene, amputation
Leading cause of death · statins, BP control
Infections
Neutrophil dysfunction, poor perfusion, high glucose
Mucormycosis (DKA), malignant otitis externa (Pseudomonas), emphysematous pyelonephritis, foot infections, candidiasis
Black necrotic nasal eschar → Mucor
Other forms
Monogenic or secondary
MODY (GCK, HNF1A — AD, young, lean) · pancreatitis, CF, hemochromatosis, Cushing, acromegaly, glucagonoma, steroids
HNF1A MODY: very sulfonylurea-sensitive

Mechanism — DKA

No insulin+ ↑ glucagon
→
↑ Gluconeogenesis, glycogenolysisHyperglycemia
→
Osmotic diuresisDehydration, K⁺/PO₄³⁻ loss
Hormone-sensitive lipaseLipolysis
→
FFA → liverβ-oxidation
→
Ketone bodiesAnion gap acidosis
→
Kussmaul respirationsCompensation

Urine dipstick detects acetoacetate, not β-hydroxybutyrate (the main ketone in DKA).

Type 1 vs type 2

FEATURE
TYPE 1
TYPE 2
Cause
Autoimmune β-cell loss
Resistance + β-cell failure
Genetics
HLA-DR3/DR4; weaker family link
Polygenic; strong family link
Body habitus
Thin
Obese
Islet histology
Insulitis, β cells lost
Amyloid deposits
Acute crisis
DKA
HHS
Treatment
Insulin
Lifestyle, metformin, others

How it's tested

COMMON CONFUSIONDKA = ketoacidosis with moderately high glucose; HHS = extreme glucose and osmolality with no meaningful acidosis. Mental status tracks osmolality.
THE TRAPA DKA patient's normal potassium hides a total-body deficit. Starting insulin without checking and replacing K⁺ can cause fatal hypokalemia.
YOUR APPROACHType (age, habitus, antibodies, C-peptide) → acute state (anion gap, ketones, osmolality) → chronic complication (glycation vs sorbitol, micro vs macro) → treatment.

If you see… think…

Thin 12-year-old with weight loss, polyuria, anti-GAD⁺ → type 1 diabetes
Vomiting, deep rapid breathing, fruity breath, anion gap 24 → DKA
Confused nursing-home patient, glucose 1100, no ketoacidosis → HHS
Islet amyloid on autopsy → type 2 diabetes
Cataracts and neuropathy from intracellular sugar alcohol → sorbitol (aldose reductase)
Diabetic with new retinal blood vessels and vitreous bleed → proliferative retinopathy (VEGF)
Diabetic with ptosis and "down and out" eye, normal pupil → ischemic CN III palsy
Diabetic in DKA with black necrotic nasal tissue → mucormycosis
Lean 20-year-old with mild diabetes and three affected generations → MODY
Leading cause of death in diabetes → coronary artery disease