DIABETES MELLITUS (DM)

ICD-10 code E10–E14.

MD, Djusupbekov Samat
RELEVANCE
DM refers to a group of common metabolic disorders that share the phenotype of
hyperglycemia.
Several distinct types of DM exist and are caused by a complex interaction of
genetics and environmental factors. Depending on the etiology of the DM, factors
contributing to hyperglycemia include reduced insulin secretion, decreased glucose
utilization, and increased glucose production. The metabolic dysregulation
associated with DM causes secondary pathophysiologic changes in multiple organ
systems that impose a tremendous burden on the individual with diabetes and on
the health care system. In the United States, DM is the leading cause of end-stage
renal disease (ESRD), nontraumatic lower extremity amputations, and adult
blindness. It also predisposes to cardiovascular diseases. With an increasing
incidence worldwide, DM will be a leading cause of morbidity and mortality for
the foreseeable future.
DEFINITION
A group of metabolic (metabolic) diseases characterized by
hyperglycemia resulting from a defect in the secretion of
insulin, its action or the combined effect of factors.
Several pathogenetic processes are involved in the
development of DM: from autoimmune damage to pancreatic
β-cells with the subsequent development of absolute insulin
deficiency to disorders that cause the development of
resistance of the receptors of peripheral target organs to the
action of insulin.
CLASSIFICATION
DM is classified on the basis of the pathogenic process that
leads to hyperglycemia, as opposed to earlier criteria such as
age of onset or type of therapy. The two broad categories of
DM are designated type 1 and type 2. Both types of diabetes
are preceded by a phase of abnormal glucose homeostasis as
the pathogenic process progresses. Type 1 diabetes is the
result of complete or near-total insulin deficiency. Type 2 DM
is a heterogeneous group of disorders characterized by
variable degrees of insulin resistance, impaired insulin
secretion, and increased glucose production.
Distinct genetic and metabolic defects in insulin action
and/or secretion give rise to the common phenotype of
hyperglycemia in type 2 DM and have important
potential therapeutic implications now that
pharmacologic agents are available to target specific
metabolic derangements. Type 2 DM is preceded by a
period of abnormal glucose homeostasis classified as
impaired fasting glucose (IFG) or impaired glucose
tolerance (IGT).
Two features of the current classification of DM diverge from previous
classifications. First, the terms insulin-dependent diabetes mellitus
(IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) are
obsolete. Since many individuals with type 2 DM eventually require
insulin treatment for control of glycemia, the use of the term NIDDM
generated considerable confusion. A second difference is that age is not
a criterion in the classification system. Although type 1 DM most
commonly develops before the age of 30, an autoimmune beta cell
destructive process can develop at any age. It is estimated that between
5 and 10% of individuals who develop DM after age 30 have type 1
DM. Likewise, type 2 DM more typically develops with increasing age
but is now being diagnosed more frequently in children and young
adults, particularly in obese adolescents.
 Symptoms of chronic hyperglycemia
• Polyuria.
• Polydipsia.
• Weight loss, sometimes with polyphagia.
• Reduced visual acuity.
• Poor growth in children.
• Increased susceptibility to infections.
 Acute, life-threatening complications of
diabetes
• Hyperglycemia with ketoacidosis.
• Hyperosmolar syndrome without ketosis.
• Hypoglycemic conditions.
Chronic complications of diabetes
• Retinopathy with the possible development of blindness.
• Nephropathy leading to kidney failure.
• Peripheral neuropathy and angiopathy with the risk of lower
limb ulcers.
• Autonomic neuropathy that causes gastrointestinal,
urogenital, cardiovascular symptoms and sexual
dysfunction.
Among patients with DM, the frequency of atherosclerotic lesions of
the heart vessels, peripheral and cerebral vessels, hypertension,
disorders of lipoprotein metabolism and periodontal disease is high.
Training of patients
The results of treatment of diabetes strongly depend on
the behavior of the patient, his active and competent
participation in the therapeutic process, since it is he
who day by day implements the plan of control and
therapeutic measures prescribed by the doctor. To
master such skills, special training of the patient with
the participation of medical professionals is necessary,
which should be carried out at each contact of the
patient with the specialists serving him.
Criteria for compensation of carbohydrate metabolism

Recommended levels of carbohydrate metabolism compensation at DM are shown in the

table

Just remember this.

 TYPE 1 DIABETES MELLITUS
Type 1 diabetes mellitus is caused by the
destruction of the pancreatic β-cells, which
leads to an absolute insulin deficiency.

ICD-10 code E10. Insulin-dependent diabetes mellitus.

Prevention
The only way is primary prevention of disease in individuals
at high genetic risk:
• prevention of intrauterine viral infections, and viral
infections in children and adolescents (rubella, measles,
mumps, chickenpox, etc.);
• exclusion from the diet of infants formula made with cow's
milk or gluten (it is shown that these components may cause
an autoimmune response against β-cells);
• exclusion from the diet of products with nitroso-containing
preservatives and dyes.
Identification of individuals in the preclinical period of
type 1 diabetes is based on the determination of
immunological (autoantibodies to various structures of
the β-cell) and hormonal-metabolic (C-peptide level,
absence of early phase of insulin secretion, increase in
glycohemoglobin HbA1c) markers and certain HLA-
antigens.
Classification
There are two forms of type 1 diabetes: autoimmune
and idiopathic.
Etiology and pathogenesis
In most cases of type 1 diabetes, autoantibodies to various
structures of the β-cell are detected: to the surface antigens of
β-cells (ICA), insulin (IAA), glutamate decarboxylase (GAD),
tyrosine phosphatase of islet cells (IA2a and IA2β); a typical
combination of alleles is HLA-DQA1-DQB1. Autoimmune
diabetes usually begins in childhood and adolescence, but can
develop at any age, including in old age. This form of diabetes
(formerly known as insulin-dependent diabetes, type 1
diabetes, and juvenile onset diabetes) is the result of cell-
mediated autoimmune destruction of pancreatic beta cells.
In childhood, the loss of β-cells occurs rapidly and by
the end of the first year of the disease, the residual
secretory function of the islets of Langerhans of the
pancreas fades. In adults, the residual function of beta
cells persists for a long time. At the same time, the
level of insulin secretion is sufficient to prevent
ketoacidosis for many years. In the future, insulin
secretion gradually decreases and absolute insulin
deficiency develops, confirmed by a low or
undetectable level of C-peptide in the blood plasma.
In a small number of patients, there are no signs of an
autoimmune process (there are no immunological and
genetic markers of type 1 diabetes), but there are
symptoms of absolute insulin deficiency. These cases
are classified as idiopathic type 1 diabetes.
Type 1 diabetes has a long latent period that can last for a
number of years.
Stage I – a genetic predisposition that is realized in less than
half of identical twins and in 2-5% of Siblings. Great
importance is attached to the presence of HLA antigens,
especially class II (DR3, DR4, DQ). At the same time, the risk
of developing type 1 diabetes increases many times.
Stage II – hypothetical trigger factor (viral infection, stress,
diet, chemical factors).
Stage III – immune disorders while maintaining the
amount of insulin in the blood. Immunological markers
of type 1 diabetes are determined: autoantibodies to
beta-cell surface antigens (ICA), insulin (IAA),
glutamate decarboxylase (GAD), and islet cell tyrosine
phosphatase (IA2a and IA2ß). There is a violation of
the function of beta-cells (due to a decrease in their
number), the absence of the first phase of insulin
secretion (diagnosed with an intravenous glucose
tolerance test).
Stage IV – severe immune disorders: progressive decrease in
insulin secretion due to developing insulitis, impaired glucose
tolerance in the absence of clinical signs of DM (normal
blood glucose level). With an oral glucose tolerance test, an
increase in the level of glucose in the blood plasma on an
empty stomach and/or 2 hours after it is performed is
detected.
Stage V is a clinical manifestation that develops after
the death of 80-90% of the mass of beta cells. At the
same time, the residual secretion of C-peptide is
preserved.
Stage VI – complete destruction of β-cells. Not even
the basal level of C-peptide is detected. Antibody titers
can be reduced. At this stage, the course of DM usually
becomes less controlled.
Triggers can be both infectious and non-infectious agents.
• Infectious: enteric viruses; retroviruses; the togaviridae
(congenital rubella).
• Non-infectious:
✧ Dietary ingredients: gluten; soy, other plants; cow's milk,
tea, coffee; unsaturated fats; antioxidants;
✧ introduction of insulin, glucose;
✧ exposure to heavy metals, nitrites/nitrates;
✧ psychosocial factors (stress);
✧ultraviolet radiation, radiation, ambient temperature, time of
year.
Insulin deficiency stimulates glycogenolysis and
gluconeogenesis in the liver. This leads to hyperlipidemia
(increased cholesterol, non-esterified fatty acids, triglycerides,
lipoproteins) and ketoacidosis. The increased intake of lipids to
the liver, where they are strongly oxidized, leads to an increase
in the production of ketone bodies and hyperketonemia
(accumulation of acetone, β-hydroxybutyric and acetoacetic
acids), which leads to the development of tissue hypoxia,
increases tissue dehydration, hypovolemia, hemoconcentration
with a tendency to develop disseminated intravascular
coagulation syndrome, hypoxia, edema of the cerebral cortex
and eventually the development of diabetic coma.
CLINICAL PICTURE
Type 1 diabetes is usually characterized by an acute onset and
rapid development of pronounced metabolic disorders. Often,
the disease first manifests itself as a diabetic coma or severe
acidosis.
In children and adolescents, the manifestation of the disease
occurs, as a rule, with the phenomena of ketoacidosis. With
the development of the disease at the age of over 25 years,
moderate fasting hyperglycemia is noted, which often with the
addition of infection or stress can quickly be replaced by
severe hyperglycemia or ketoacidosis.
Main symptoms:
• dry mouth, thirst (dehydration of the body due to
excessive fluid release through the kidneys, as well
as increased blood glucose, urea, sodium), polyuria
(due to osmotic diuresis);
• increased appetite, weight loss (increased lipolysis
and glucose excretion in the urine);
• weakness;
• skin itching, increased susceptibility to infectious diseases
(characterized by the development of furunculosis,
ostiofolliculitis, panaritia, paronychia, fungal lesions of the
skin, mucous membranes and nails, tuberculosis, acute
respiratory diseases and pneumonia with a prolongedcourse
and chronization);
• decreased libido and potency;
• changes in visual acuity (swelling of the lens and weakness
of accommodation caused by hyperglycemia);
• progressive caries, periodontal disease, alveolar pyorrhea,
gingivitis.
The examination reveals hyperglycemia and
glucosuria.
In severe decompensation skin, lips, tongue dry; turgor
subcutaneous fat tissue is reduced; as a result paretic
expansion of the capillaries of the skin are watching
diabetic robes (flushing of the cheeks, chin, forehead).
With prolonged and poorly compensated DM, they develop:
• trophic ulcers of the shins and feet
• osteoporosis and diabetic osteoarthropathy;
• decreased external secretory function of the stomach,
intestines, and pancreas;
• diabetic peripheral and autonomic neuropathy;
• diabetic retinopathy;
• diabetic nephropathy;
• decreased fertility in young women;
• impaired growth and physical development in children
(Moriac syndrome).
Acute complications of DM — diabetic ketoacidotic,
hyperosmolar (non-ketonemic) and lactate-acidotic
coma.
In DM, ischemic heart disease and arterial
hypertension are more often diagnosed.
Myocardial infarction (often pain-free) is the cause of
death of almost half of patients with DM.
Diagnostics
The clinical picture of the disease and an increase in the level
of glucose in the blood plasma at any time of the day more
than 11.1 mmol/l allow the diagnosis of DM. The criteria for
the diagnosis of diabetes, proposed by WHO experts in 1999,
are generally accepted worldwide.
Fasting glucose — the level of glucose in the blood
plasma after a night of fasting for 8-14 hours.
Random determination of glucose — the level of
glucose in the blood plasma at any time of the day
without taking into account the time of the last meal.
For epidemiological or screening purposes, a single
measurement of fasting blood glucose levels or 2 hours
after an oral glucose tolerance test is sufficient.
Mandatory laboratory tests to assess the degree of DM compensation:
• determination of glycosylated hemoglobin (HbA1c) to assess the
state of carbohydrate metabolism in the previous 3 months;
• determination of the concentration of glucose in the blood plasma on
an empty stomach and 2 hours after eating;
• general clinical blood and urine tests (if indicated);
• the content of ketone bodies and glucose in the daily urine;
• a biochemical study that includes the determination of bilirubin,
cholesterol, LDL-C, HDL-C, triglycerides, total protein, ketone
bodies, ALT, AST, potassium, calcium, phosphorus, sodium, urea,
and creatinine;
• determination of microalbuminuria (if indicated — Rehberg tests or
urine analysis according to Nechiporenko, glomerular filtration rate).
In difficult cases, the content of immunological and
genetic markers of type 1 diabetes and the level of C-
peptide are determined to establish a diagnosis.
Mandatory instrumental research:
• ECG;
• chest X-ray;
• direct ophthalmoscopy (with dilated pupils).
Indications for hospitalization
• The debut of DM (for the selection of insulin therapy and
teaching the patient the rules of self-control of blood
glucose levels, diet, work, etc.).
• Diabetic ketoacidosis.
• Precoma or coma (ketoacidotic, hypoglycemic).
• Progression of vascular complications.
• Urgent conditions (infections, intoxication, surgical
intervention).
Treatment
Goals: to preserve life, eliminate the symptoms of the
disease, prevent acute and chronic complications,
reduce mortality, treat concomitant diseases and
improve the quality of life.
Complex treatment of type 1 diabetes includes:
• insulin therapy;
• diet;
• metered-dose physical activity;
• patient training, self-monitoring of plasma glucose;
• prevention and treatment of late complications.
Non-drug treatment as monotherapy for type 1 diabetes is not
used. However, in combination with insulin therapy, it is
necessary to observe a special diet and exercise regime.
Insulin therapy
This is the only lifelong treatment for type 1 diabetes inconditions of
absolute insulin deficiency.
In our country, only genetically engineered insulins or human insulin
analogues are used.
Rational nutrition
Goals: to normalize body weight and promote the maintenance of
normal blood glucose levels in the blood plasma. This can be achieved
by reducing the caloric content of the diet, excluding refined
carbohydrates and observing regular meals.
The ratio of the main ingredients in the daily diet of a patient with type
1 diabetes should not differ from the physiological one.
THANK YOU FOR YOU ATTENTION!