One hyperglycaemia, two mechanisms. Drive the beta-cell output and tissue-resistance dials and watch which exit the patient takes — ketoacidosis when insulin is truly absent, hyperosmolarity when a little insulin is still holding lipolysis down. Then switch to Diagnose the panel and decide whether four lab values actually make the diagnosis.
Set the pancreas
100%
0% is a destroyed islet. Above 100% is the hyperinsulinaemic compensation of early type 2 — the pancreas shouting to be heard.
10%
How deaf muscle, liver and fat are to the insulin that arrives. Driven by visceral adiposity, inactivity, genetics — and by steroids.
Cut-points are the chapter’s: A1C 5.7–6.4% and 6.5%; fasting 100–125 and 126; 2-hour 140–199 and 200; random 200 with symptoms.
Normal fed-fasted balanceGlucose held near 70–140 mg/dL all day
Glucose into muscle (GLUT4)0
Hepatic glucose output0
Lipolysis → ketogenesis0
Osmotic diuresis / volume loss0
Balanced
The bars are an illustrative teaching model of the chapter’s physiology, not a clinical calculator. Lipolysis is suppressed by far less insulin than glucose disposal needs — that single fact is why type 2 usually decompensates without ketones.
Enter a panelAny one test can diagnose — but confirmation has rules
Waiting for values
Type in at least one value and select Interpret the panel.