Etiology and pathophysiology of the process
The development of type 1 diabetes mellitus is caused by irreversible damage to the islets of Langerhans in the pancreas. Most often, this process is autoimmune in nature, which is confirmed by the presence of specific autoantibodies in the patient's blood in the early stages (at the onset of the disease).
As a result of $\beta$-cell destruction, absolute insulin deficiency occurs. Insulin acts as a kind of "key" that opens cells to glucose. In its absence, insulin-mediated transport of glucose from the bloodstream into target tissues is blocked. This leads to a dual situation: on the one hand, blood sugar levels rise rapidly (pronounced hyperglycemia), while on the other hand, the body's cells experience acute energy starvation because they cannot utilize the glucose circulating nearby.
Pathogenetic symptom cascade
The clinical presentation of type 1 diabetes mellitus does not form chaotically, but represents a strict logical cascade of the body's reactions to insulin deficiency. The disease manifests acutely, with pronounced symptoms passing through the following stages:
- Hyperglycemia. Due to the lack of hormonal control, blood glucose levels steadily rise.
- Polydipsia (severe thirst). High sugar concentration makes the blood thick. To dilute it and reduce osmotic pressure, the body "draws" fluid from the cells, leading to their dehydration and causing unbearable thirst.
- Glucosuria. Normally, the kidneys do not let sugar pass into the urine. However, when glycemia reaches a critical mark of 10–12 mmol/L, this "renal threshold" is overcome. Glucose begins to be massively excreted by the kidneys, making the urine characteristically sticky.
- Polyuria and osmotic diuresis. Glucose in the urine draws a huge amount of water along with it according to the laws of osmosis. The volume of urine excreted increases manifold, and enuresis may develop in children.
- Lethargy and weakness. Tissues deprived of glucose intake experience severe energy deficiency, which clinically manifests as constant fatigue in the patient.
- Catabolism and weight loss. To compensate for the lack of cellular energy, the body triggers the destruction (catabolism) of its own fat and protein stores. The patient rapidly loses body weight against the background of a normal or even increased appetite.
- Ketogenesis. Massive fat breakdown has a dangerous side effect: the formation of ketone bodies (acetone). They accumulate in the blood (ketonemia) and are excreted in the urine (ketonuria), which without treatment leads to a life-threatening condition—diabetic ketoacidosis.
Differential diagnosis with type 2 diabetes
To understand the specifics of the disease, it is important to distinguish it from type 2 diabetes mellitus (historical name: non-insulin-dependent), which has a fundamentally different mechanism of development.
In type 2 diabetes, the pancreas continues to produce insulin, but peripheral tissues lose sensitivity to it (insulin resistance develops). The hormone simply cannot adequately bind to cellular receptors.
Key differences:
- Nature of the course: Type 1 manifests acutely, whereas type 2 develops slowly and gradually.
- Risk of complications: The development of ketoacidosis is extremely typical for type 1, while in type 2 this condition is rare.
- Association with body weight: Type 1 is accompanied by weight loss, while type 2 is traditionally associated with obesity. It is important to note that due to the modern childhood obesity epidemic, pediatric practice is now seeing a steady increase in cases of type 2 diabetes.
- Approach to therapy: Treatment for type 1 is always immediate and lifelong insulin replacement therapy. Type 2 diabetes in the initial stages is compensated by oral medications (which increase receptor sensitivity or stimulate secretion) and requires switching to insulin only upon prolonged $\beta$-cell exhaustion.
The rule of three "Ps" for the classic triad of manifestation symptoms: Polyuria (excessive urination), Polydipsia (severe thirst), Polydipsia/Weight loss (catabolism due to cellular starvation).
Class and exam questions
Why does severe thirst occur in type 1 diabetes mellitus?
Polydipsia (excessive thirst) occurs due to cellular dehydration. The body attempts to dilute the high glucose concentration in the bloodstream by drawing fluid from cells and tissues.
At what blood sugar level does glucose appear in the urine?
Glucose begins to be excreted in the urine (glucosuria) when the glycemia level exceeds the "renal threshold," which is 10–12 mmol/L.
Can type 1 diabetes be treated with pills, like older people do?
No. In type 1, $\beta$-cells are destroyed and absolute insulin deficiency occurs. The only treatment method vital for the patient is continuous insulin replacement therapy.
Where does acetone in the blood and urine come from during diabetes decompensation?
Due to the fact that glucose does not enter the cells, the body begins emergency breakdown of its own fats to obtain energy. The byproduct of this massive breakdown is ketone bodies (acetone).
What else to study on this topic
- Detailed mechanisms of autoimmune destruction of $\beta$-cells in the islets of Langerhans.
- Specific autoantibodies as markers for predicting and diagnosing the onset of the disease.
- Biochemical bases of ketogenesis: how fat breakdown leads to the formation of ketone bodies.
- Pathophysiology of the development of diabetic ketoacidosis and life-threatening conditions.
- Impact of the childhood and adolescent obesity epidemic on the rising incidence of type 2 diabetes in pediatrics.
- Modern regimens and principles of continuous insulin replacement therapy in children.
Master the entire topic in the Pediatrics course
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Other topics in the section «Chapter 11. Endocrine Diseases in Children»
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