Effects of Hyperglycaemia and Blood Glucose Ranges

Study Notes

The lecture covered the effects of acute and chronic hyperglycaemia.
Learning outcomes included describing the normal blood glucose range, recollecting diagnostic criteria for hyperglycaemia and diabetes, describing causes, symptoms, diagnosis and treatment of acute hyperglycaemia (particularly diabetic ketoacidosis), and describing causes and symptoms of chronic hyperglycaemia and illustrating its molecular physiology and consequences.

NICE recommended target ranges for blood glucose levels vary based on type.
Non-diabetic ranges: fasting blood glucose 4.0-5.4 mmol/L, before meals 4.0-5.9 mmol/L, 2h after meal <7.8 mmol/L.
Type 2 diabetes (T2DM): fasting 5.0-7.0 mmol/L, before meals 4.0-7.0 mmol/L, 2h after meal <8.5 mmol/L
Type 1 diabetes (T1DM): fasting 5.0-7.0 mmol/L, before meals 4.0-7.0 mmol/L, 2h after meal 5.0-9.0 mmol/L
Children with type 1 diabetes: fasting 4.0-7.0 mmol/L, before meals 4.0-7.0 mmol/L, 2h after meal 5.0-9.0 mmol/L

Fasting plasma glucose ≥ 7.0 mmol/L (126 mg/dL)
Random plasma glucose ≥ 11.1 mmol/L (200 mg/dL)
Specific indications for oral glucose tolerance tests (OGTT) are discussed
HbA1c levels are mentioned as a diagnostic criterion, as well as symptoms
Additional diagnostic criteria, including ketone levels in urine (≥ 2+) and blood glucose levels (≥ 11 mmol/L) are also included for diagnosing diabetic ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS).

Causes: T1DM, stress, Cushing's syndrome, infections, medication side effects including corticosteroids, beta-blockers, thiazides and checkpoint inhibitors. Lifestyle factors and other endocrine disorders are also cited.
Symptoms: Fasting glucose ≥ 7.0 mmol/L and 2 h blood glucose (OGTT) ≥ 11.1 mmol/L, which can also be symptomatic if ≥15-20 mmol/L. Glycosuria is also a key symptom (>8-10 mmol/L).
Further details on the acute metabolic effects on carbohydrate metabolism, and metabolism of fat and protein demonstrating the mechanisms leading to acidosis, are provided. This includes the breakdown of triglycerides and glucose into ketones.

Effects on the body, including non-enzymatic glycosylation (NEG), and osmotic cellular damage are explained. The process of sorbitol accumulation in tissues that lack sorbitol dehydrogenase is detailed, explaining how this causes damage to the lens (leading to cataracts), nerves (diabetic neuropathy), and other organs.
Factors contributing, symptoms, and management of Diabetic ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS) and their distinguishing features are included. Distinguishing features include ketosis, presence of acidosis in DKA but not HHS.
Chronic complications of hyperglycaemia include microvascular complications (diabetic nephropathy, retinopathy, neuropathy) and macrovascular complications (heart disease, stroke, peripheral vascular disease).
NEG occurs when glucose attaches itself to cell proteins and lipids without the help of an enzyme (AGE). Increased production of ketone bodies is a further detail.
The lecture also covered specific diagnostic criteria, including blood glucose and ketone levels to distinguish between DKA and HHS.
Further details were given about typical initial presentation of patients with these conditions.

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