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Diabetes mellitus
Definition
Diabetes mellitus (DM) - a group of
metabolic (metabolic)
diseases characterized by hyperglycemia,
which is
result of a lack of insulin secretion and / or
violation of the
insulin, which leads to a violation of all
kinds of metabolic
primarily of carbohydrate, the defeat of
vessels (angiopathy), nervous
system (neuropathy) and other organs and
systems.
Epidemiology
The prevalence of diabetes among people of
different stran
is 2-6%. In recent years, the prevalence of
the disease
increases rapidly.
Classification
1 Diabetes mellitus type I (insulindependent).
2. Diabetes mellitus Type II (insulinindependent).
Etiology
The reason for diabetes to date is not known.
Possible etiofactors for diabetes type I:
1) viral infection (rubella virus,Coxsackie B,
hepatitis B, mumps, infectious
mononucleosis, Phippen, etc.), and
2) a genetic predisposition, autoimmune
disorders, structural disease of the pancreas
(Pancreatic necrosis, sclerosing pancreatitis,
pancreatic resection cancer), toxic
substances that damage the E-cells
(nitrozaminy. cyanide compounds).
Possible etiofactors for diabetes type II:
genetic factors (nature of the dominant mode
of inheritance) overeating, excessive
carbohydrates, obesity, prolongeduse of
drugs diabetogenic action (corticosteroids
and etc.).
Pathogenesis
Pathogenesis of DM I type. The main
pathogenetic mechanism of diabetic

I type is the destruction of the (3-cells of


islets of Langerhans
pancreas, which leads to an absolute
deficiency of
insulin. The pathogenesis of diabetes
subtype IA (virus) is associated with
shortage of antiviral immunity. Under the
influence of some
viruses (rubella virus, Coxsackie, variola) is
selective
jJ-damaged cells of islets of Langerhans,
which are
genetic predisposition to this lesion.
Pathogenesis
diabetes subtype IB (autoimsch / st)
associated with genetically
caused by the immune system defect that
leads to
appearance of autoantibodies to B-cells of
islets of Langerhans from the
subsequent destruction of the (3-cells and,
reduction of synthesis
insulin. In both subtypes of type I diabetes
develops absolute
insulin deficiency.
The pathogenesis of type II diabetes. Is
associated with dysregulation of appetite,
overeating and obesity, which leads to
hyperinsulinemia and, in
Ultimately, (the feedback principle) lead to a
reduction
koliches of insulin receptors in tissues. In
addition, in these
patients are found in violation of the 19th
chromosome on the short
shoulder which is localized the gene
responsible for synthesis of receptors for
insulin. All this leads to disruption of tissue
glucose utilization,
which is denoted as the "relative insulin
failure. "
The clinical picture
The main clinical manifestations of
uncomplicated diabetes
are dry mouth, thirst, or polydipsia (patients
can

Drink 3-5 liters or more of fluid per day),


polyuria, increased
a. Petit, and expressed general muscle
weakness, weight loss, dry
in the mouth, itching of the skin and genitals
(in women). Other clinical signs
associated with complications of diabetes.
Laboratory data
1. Hyperglycemia (fasting blood glucose
capillary blood
greater than 6.1 mmol / l).
2. Blood glucose levels greater than> 11.1
mmol / l in the
during glucose tolerance test (TSH)
3. Glkzhozuriya (in this case
Glycosuria occurs after exceeding the renal
threshold, namely
at the level of blood glucose 9.9 mmol / l
and above).
4. Increase However, glycated (sugarcontaining substances) to 9-10% of
total hemoglobin (normal 4-6%).
5. The content of C-peptide in type I
diabetes
reduced, while type II diabetes are normal or
elevated.
6. Increasethe relative density of urine (due
to glycosuria).
7. Reduction of immunoreactive insulin in
type I diabetes and its increase in diabetes! a
types. *
Criteria for diagnosis
The criteria for diagnosis of diabetes are:
1) Glycemia Capillary blood glucose 6.1
mmol g
2) Glycemia 2 h afterglucose load (TSH), or
within a day or 2 hours after eating a 11.1
mmol / l. .
Feature of type I diabetes is a reduction in
the incidence (10-15%
of DM), the young age of patients (very
often starts in childhood
age), acute onset of the disease, pronounced
clinical
manifestations, underweight patients, for
labile,

pronounced tendency to ketoacidosis,


microvascular complications, a sharp
reduction of insulin in the blood and used in
the treatment of
insulin. A feature of type II diabetes is the
high
ubiquitous (85-90% of DM), older age of
patients
(Older than 40 years), gradual onset, is not
expressed in the clinical
manifestations (sometimes asymptomatic
symptoms), increased weight
the patient's body, steady flow, the absence
of ketoacidosis,
macroangiopathy, normal levels of insulin in
the blood and
the use of tablets in the treatment of
sahorosnizhayuschih drugs.
Stages of development of diabetes
There are three stages of development of
diabetes.
1. Compensation (for a
SD, when under the influence of treatment
achieved normal levels of
glucose and the absence of glucose in the
urine).
2. Subcompensation (for SD,
characterized by hyperglycemia <14.0
mmol, glucosuria <50 g
day and the absence of acetone in the urine).
3. Decompensation (for SD,
accompanied by hyperglycemia> 14 mmol /
L, glycosuria> 50 g
day and the appearance of acetone in the
urine).
Severity of diabetes
SD has three (3) the degree of severity.
1. mild (I) degree compensation of carbohydrate metabolism is
achieved by diet alone, no
complications, ability to work is preserved,
there is more frequent in patients
II'tipa with diabetes, blood glucose 7 mmol /
l, expressed little clinic.
2. The average (II) degree - blood glucose
to 12 mmol / l, the symptoms are, there are

complications, reduced work capacity, the


compensation of carbohydrate
exchange is achieved by the tablets
hypoglycemic diet +
drugs.
3. Severe (III) degree - a stable
hyperglycemia
(Blood glucose 12 mmol / L or more) for a
labile, vascular
eyes, kidneys, gangrene, the compensation
of carbohydrate metabolism is achieved
diet + insulin, lost work capacity.
Treatment
1. Diet therapy. Basic requirements for the
diet in diabetes. "Should
be a physiologic composition of products,
izokaloriynoy with diabetes <type
and subkaloriynoy with diabetes type II, the
food should be taken 4-5 times a
within days, elimination pegkousvaivaemyh
uglevodoz enough
amount of fiber in the diet of the total fat of
40-50%
must be of vegetable origin. The number of
carbohydrates in
diet should be considered permanent and
daily basis. In this case,
convenient to use a term such as grain unit
(XU). One
XE is 50 kcal. One XE contains 10-12 g of
carbohydrates and is equal to one
a piece of bread, cut off from the middle of a
standard loaf or
half a loaf, of a thickness of 1 cm Weight of
the piece of bread - '25
The number of carbohydrates taken during
the day can be expressed as
XE and spread throughout the day, based on
the fact that carbohydrates
should constitute 60% of the energy value of
the diet.
Two. Mode of physical activity. Physical
Activity
helps reduce blood glucose levels stable,
partially
absorption of glucose without insulin in the

working muscles, a decrease


insulin requirements, weight reduction (if
obese)
reduction of cholesterol and triglycerides in
the blood,
increased utilization of fatty acids and
ketone bodies in the working
muscles. Types of physical activity for
diabetes: a) fast walking: b)
Running c) swimming d) riding a bicycle, e)
light aerobics.
Z.Bazisnaya therapy of type I diabetes. The
main type of treatment of diabetes type I
is the use of insulin (insulin).
The daily insulin dose is adjusted
individually at the rate of 0.5-1.0
IU per 1 kg of patient weight, as well as the
levels of glucose and
glycosuria and limitations of the disease.
There are three types of insulin: a short,
expectancy and long-acting. Insulin is a
short
action (Actrapid, entrapid, Humulin R,
insulrap etc). We introduce
sc, in / m / in 4-5 times a day. The duration
of 5.8
hours. Intermediate-acting insulin (insulin B
semilong, protofan NM monotard, Depot-HInsulin, etc.).
Duration of action 12-16 hours.
Subcutaneously 2 times
Day. Insulin is prolonged (longer) action
(ultratard
NM, ultralente, Humulin, ultralong).
Duration of action
24-36 hours. We introduce a once-daily n / k
4. Basic therapy of type II diabetes. The
main type of treatment of diabetes II
type is the use of glucose-lowering tablets
(Hypoglycemic) drugs. Known types of
tablet antidiabetic drugs: 1) derivatives
sulfonylurea (or sulfa drugs), 2) biguanides;
3) meglitinidy 4) glitazones, 5) aglucosidase inhibitors. All these
groups of drugs stimulate (3-cells of the
pancreas,

increase insulin secretion and promote


glucose utilization
peripheral tissues. At present, mainly
used sulfa drugs II generation: a)
glyburide (Manin). Start with 0.0025 g in
the morning before breakfast,
then every 5-7 days, the dose was increased
to 0.0025 The maximum
daily dose of 0,015 g, and b), gliclazide
(diabeton, Predian). Start with 0.04 g
and gradually increased to 0.24 g per day, c)
glyurenorm (glikvidon).
The initial dose of 0,015 g, the maximum
dose was 0.06
B.Immunodelressivnaya therapy for type I
diabetes (150 mg azathioprine
orally daily for 8 weeks, then 50 mg orally
daily
for a long time) and the p-cell
transplantation (with type I diabetes).
1.2. Acute complications of diabetes
(diabetic
coma)
The speed of onset distinguish two (2) types
of diabetes complications:
Acute and late. For acute complications
(diabetic or komam)
are hyperglycemic and hypoglycemic coma.
1.2.1. Hyperglycemic ketoatsidoticheskaya
(hyperacidotic) coma
Definition
This is a medical emergency that develops
due to severe
insulin deficiency and reduced glucose
utilization by tissues,
characterized by severe ketoacidosis, a
violation of all kinds
metabolic disorder of the functions of all
organs and systems and
loss of consciousness. .
Etiology
The main reason - the absolute deficiency of
insulin in type I diabetes.
Factors that directly lead to coma
ketoatsidoticheskoy a)

complete cessation of insulin (3-cells of


pancreatic
gland, b) insulin error: insufficient dose, the
use of
expired or improperly stored insulin, the
termination
insulin, and c) urinary tract infections,
osteomyelitis,
dermatitis, pneumonia, diabetic foot
syndrome, myocardial
infarction, stroke, and e) Pregnancy e)
stress, shock, sepsis, trauma,
operations; g) prior dehydration, and h) late
diagnosis
SD.
The clinical picture
Coma develops gradually from 12-24 hours
to several days.
In the development of coma are 4 stages.
Easily one ketoatsidoticheskoe
state. Characterized by severe weakness,
lethargy, drowsiness, loss of
of appetite, nausea, vomiting, and
headaches. At this stage, dramatically
increasing polydipsia and polyuria, glycemia
more than 15 mmol / l,
Glycosuria, acetonuria, the smell of acetone
breath. Two. The marked
ketoatsidoticheskoe state. Marked lethargy
and torpor.
Three. Heavy ketoatsidoticheskoe state. It is
characterized by
soporous state (deep sleep pathology). 4.
Properly
coma. There is complete loss of
consciousness, the loud, deep breathing
Kussmaul, pungent smell of acetone in
exhaled air, the skin is dry,
Cold does not stretch, tone of the eyeballs is
reduced, muscles flabby,
tendon reflexes were decreased, t the body
is reduced, blood pressure is low.
Laboratory diagnosis of
Marked gilerglikemiya (18-30 mmol / l), a
sharp increase in
the level of ketones in the blood

(giperketonemiya) and urine


(giperketonuriya)
marked glycosuria, increase of acetone in
the urine (acetonuria)
hyponatremia, gilokaliemiya bicarbonate,
serum is less than 10
mEq / L, decreased blood pH (acidosis),
increased levels of urea and
creatinine in the blood.
Emergency
A. Removal of insulin deficiency. 1.1
Insulin Short deystviyav
regime of "small doses". Originally
introduced in 8.10 units of insulin / and
6.10 units / hour 8 / m, then it is prescribed,
6-10 IU / m under the control of
glycemia, if after 2 hours from the start of
insulin therapy
blood sugar does not decrease, then increase
the dose of insulin
up to 12 units / hour. By reducing blood
glucose levels up to 10.15 mmol / l, the dose
insulin was reduced to 4.2 U / h, while in /
injected
glucose, insulin, which is added to the rate
of 1 to 5 g units
glucose. 1 2. Currently, the method has
found wide application
constant in / infuzmi kortkogo insulin
action. At the same time in 400 ml
saline added to 40 units of insulin a simple.
Ynfuziya comes from
rate of 100 mL / h (33 drops / min.),
regardless of the level of glycemia.
Simultaneously introduce 10 units of insulin
/ in struimo and 10 IU / m, then
each hour is entered from 5-10 IU,
depending on the patient's weight
(For example, if the patient weighs 50 kg - 5
units) and so as ENT, while
blood glucose reaches 11-14 mmol / l. When
the consciousness
patient / introduction stop and switch to s /
m or s / c administration
to 6 units every 4 hours and 4 units after
each meal to

disappearance of acetone in the urine. Then


the patient is transferred to
intermediate-acting insulin. In order to avoid
hypoglycemia when blood glucose 11-14
mmol / l introduced in / drop 5%
glucose. Two. Deficiency of potassium ions.
Introduced in / 2% p-p COP!
rate of 75 ml / h for 4-5 hours before the
blood level to 6 mmol / l.
After that translate into tablets drugs for 3-7
s
days. Three. Reinforced rehydration. To fill
the water and control
dehydration with the onset of insulin / drip
introduce the p-p, or Ringer's saline to 5-6
liters per day. At the same time 50%
fluid injected into the first 6 hours and 50%
of the liquid - in the remaining 18
hours. 4. Normalization KSHR. Enter / v
2.5% p-p hydrogen
sodium (to combat acidosis). Five.
Eliminating (or treatment)
Immediate ketoatsidoticheskoy coma.
1.2.2. Hyperglycemic hyperosmolar
(Neketoatsidoticheskaya) coma
Definition
This is a medical emergency that occurs on
the background of pronounced
insulin deficiency, characterized by a sharp
increase in
plasma osmolality (hyperosmolarity)
without increasing
content of ketone bodies, pronounced
dehydration, severe
disorders of the organs and systems, and loss
of consciousness.
Hyperglycemic hyperosmolar coma
develops in patients
Type II diabetes, with hyperglycemia
develops at the expense of
filtration of glucose by the kidneys.
Etiology
a) the lack of compensation for diabetes type
II, and b) undiagnosed diabetes
I! type c) intercurrent disease, accompanied
by

dehydration, and d) the cerebral circulation,


and e) a long
diuretics and glucocorticoids e)
hemodialysis.
The clinical picture
The clinical picture is determined by
dehydration. Clinical
manifestations of hyperosmolar coma
develop gradually over
5-14 days. The features are: 1) dehydration
expressed as
the result of significant hyperglycemia and
polyuria, and 2) and focal
generalized seizures, and 3) a stiff neck in
the
result of irritation of the meninges, and 4)
the full range of features
and complications of dehydration and
giperfuzii: thirst, dry skin and
mucous membranes, tachycardia,
hypotension, nausea,
weakness, shock, 5), thrombosis of arteries
and veins, and b) DIC, 7) renal
failure.
Laboratory diagnosis of
Significant hyperglycemia (44-55 mmol / l
or more)
hyperosmolarity above 350 mOsm / l,
glkzhozuriya, hypernatremia,
increase in blood urea, an increase in
hemoglobin (from
blood clots), leukocytosis, the absence of
acetone in the urine, the normal
the level of ketones in the blood.
Emergency
A. Removal of dehydration, lack of insulin
and correction
electrolyte imbalance. 1.1. During the first
two hours: a) 0.45%
rr 2 l NaCl in / with the addition (with a
decrease in serum potassium levels)
8-15 ml of 10% solution of potassium
chloride pa, b) 20 units of insulin a simple I
/ O, then
8.5 units every hour in / or / m If you fall in
blood glucose levels up to

11-12mmol / l to prevent hypoglycaemia


spend infusion of 5%
Valium glucose 1.2. Follow-up therapy: a)
continuation of the introduction of
0.45% p-ra NaCl at a rate of 1 l / h up to the
normalization of venous
blood pressure, or osmolarity, and b) the
continuation of the infusion of potassium
chloride with severe hypokalemia, and c) the
continuation of the introduction of
insulin dose of 5.8 IU / h / m or / to
normalize glucose
blood. 1.3. The daily amount of fluid
administered during the first day did not
exceed 6.10 liters 2. Removal of
hypercoagulability (heparin
5000 units s / c 2 times a day). Three.
Symptomatic treatment.
1.2.3. Hyperglycemic
giperlaktatsidemicheskaya
(Lactic acid), coma
Definition
This is a medical emergency that develops
due to the sharp
deficiency of insulin in the blood and the
accumulation of a large number of
lactic acid, characterized by severe acidosis
and loss of
consciousness.
Giperlaktatsidemicheskaya (lactic acid)
occurs in a coma
elderly patients with type II diabetes against
a background of renal failure and
hypoxia.
Etiology
A. Chronic renal failure on a background of
diabetic nephropathy or chronic
kidney disease. Two. Hypoxemia in the
background of respiratory and cardiac
failure. Three. Chronic liver disease with
hepatic
failure. 4. Massive bleeding. Five.
Myocardial infarction. 6.
Chronic alcoholism. A. Treatment
biguanidami against diseases
kidney and liver.

The clinical picture


Develops rapidly. First - dyspepsia,
myalgia, angina, severe weakness, decrease
in
diuresis, and then Kussmaul breathing,
tachycardia, arterial
hypotension up to collapse, loss of
consciousness.
Laboratory data
Moderate hyperglycemia (12-16 mmol / l),
increased
lactic acid in the blood (more than 2 mmol /
L), a decrease bikarbonatov
blood (less than 2 mmol / L), decreased
blood pH, glucosuria, absence
acetone in the urine.
Emergency
A. Correction of acidosis. 1.1. Sodium
bicarbonate 2.5% of 1-2 liters per day
I / O cap. under the control of blood pH. 1.2.
Trisamin 3.66% 0.5 l / h / in the cap.
1.3. Methylene blue 1% of 50-100 ml / in.
1.4. Inhalation of humidified
02. 1.5. Cocarboxylase in large doses - 100
mg two times a day. 1.6.
Hemodialysis. Two. Insulin therapy: shortacting insulin 8 units per
500 ml 5% glucose / drip. Three.
Symptomatic treatment (including
correction of cardiovascular disease).
C 1.2.4.
Hypoglycemic coma
* The definition of T
This is a lump that develops due to a sharp
reduction of
blood glucose and express the energy deficit
in the brain
the brain.
Etiology
The main reasons: a) inadequate food intake,
and b) large
physical activity, and c) an overdose of
insulin or tablets
glucose-lowering drugs (GSP), d) autonomic
neuropathy;
d) To accelerate the resorption of insulin; e)

use of alcohol; g) the development of


associated endocrinopathies.
The clinical picture
Coma preceded by light and heavy
hypoglycemic state.
Hypoglycemic condition occurs attacks.
Suddenly, the patient
feels hunger, weakness, slight chilliness,
sweating,
blanching or redness of the face. In severe
cases,
the above symptoms are increasing. Patients
are excited,
sometimes aggressive. Consciousness is
confused, increased muscle tone, often
are tonic or clonic convulsions. Tendon and
periosteal reflexes were raised, eyes wide.
The pulse can be
be speeded up. In the absence of appropriate
treatment is developed
hypoglycemic coma, the absence of
consciousness, areflexia, lower
body temperature, weakness, sweating, and
termination of seizures
tachycardia.
Laboratory diagnosis of
Hypoglycemia less than 3.0 mmol / l, the
absence of glucose and acetone
urine.
Emergency
A. With the development of the first signs of
hypoglycemia, oral
Reception digestible carbohydrates (2-3
tbsp. tablespoons sugar in a glass
water or fruit juice, 1-2 cups of milk,
cookies, crackers). Two.
If the patient is in a coma: 40% solution of
glucose in / up to 100 ml, 1.0%
glucagon, n / k Three. If the patient regained
consciousness, and in / a drip of 5% p-p
glucose to raise blood glucose to 10 mmol /
L (the maximum
introduction of glucose to 2 liters), but then
an injection of insulin
Short-acting, 2 units p / c, with a gradual
increase in dose

insulin based on blood glucose levels,


prednisolone 30 mg / v and 30
mg / m
1.3. Late complications of diabetes
By the late complications of diabetes include
damage organs and tissues and
diabetic angiopathy, developing in patients
with diabetes on average
10-15 years from the onset of the disease.
The defeat of the organs and tissues in
diabetes and their diverse
symptoms depends on the destruction of an
organ. Consider
the most common symptoms of organ and
tissue lesions in DM.
The defeat of the skin and muscles of dry
skin, decreased turgor, and
elasticities are often abrasions, and other
pustular lesions
skin and fungal skin lesions. Xanthomatosis
of the skin (due to
hyperlipidemia), with localization in the
buttocks, legs, knees and
elbows, forearms. Xanthelasma in the
eyelids. Rubeoz
(Extension of skin capillaries and arterioles)
and flushing of the skin
(Diabetic blush) in the zygomatic bone,
forehead and cheeks. Nails
brittle and dull. Muscle atrophy, muscle
weakness. Poor
wound healing in the skin and in severe
cases, purulent skin lesions,
common until the gangrene of the limbs.
Defeat
the digestive system. Progressive caries,
periodontal,
loosening and tooth loss, alveolar pyorrhea,
gingivitis,
stomatitis. Chronic gastritis A (low
secretion)
decrease in gastric motor function. The
syndrome of exocrine
pancreatic insufficiency (diarrhea,
steatorrhea, kreatoreya,
amylorrhea). Diabetic gepatolatiya

(hepatomegaly, tenderness
liver). The defeat of the cardiovascular
system .. Arterial
hypertension, diabetes or heart disease,
"diabetes
the heart. " (Manifested apnea, various types
of arrhythmias and
heart block, ECG changes, cardiomegaly,
heart
failure), CHD (see. diabetic
macroangiopathy)
metabolic syndrome X (a combination of
features such as CD 11,
obesity, hyperlipidemia, and arterial
giperteizii). Defeat
respiratory system. Most pulmonary
tuberculosis. It is also often develop
lobular pneumonia, acute exacerbation of
chronic bronchitis and
bronchitis. The defeat of urine. Often,
cystitis,
exacerbation of chronic pyelonephritis,
sometimes acute renal abscess
(Carbuncle, abscess). Almost all patients
have an asymptomatic
urinary infection in the form of bacteriuria,
leukocyturia.
It should be noted that the classic types of
long-term complications
Diabetes are diabetic angiopathy, which are
generalized vascular lesions. Diabetic
angiopathy
divided into two categories:
macroangiopathy and microangiopathy.
1.3.1. Diabetic macroangiopathy
Definition
This defeat of the arteries of large and
medium-sized patients
diabetes is characterized by rapid
development
atherosclerotic narrowing of the arteries.
Classification
There are diabetic macroangiopathy
associated with the development of
atherosclerosis-1) of the aorta and coronary
arteries, 2) cerebral

arteries, and 3) peripheral arteries, including


the arteries of the lower
extremities (diabetic macroangiopathy of the
lower limbs).
The clinical picture
Clinical manifestations of diabetic
macroangiopathy depend on
forms, as well as the localization of the
atherosclerotic process.
Diabetic macroangiopathy associated with
atherosclerosis of the aorta
and coronary arteries. Manifested by
different forms of CHD in
First of all, myocardial infarction and angina
pectoris.
Symptomatology of these forms of CHD is
the same as for CHD without diabetes
diabetes. The features of myocardial
infarction in diabetic
macroangiopathy is-a) of the same
frequency in men and
Women, and b) high frequency of painless
forms of CHD, entailing
high risk of sudden death, and c) high
frequency of postinfarction
complications, and d) mortality in the acute
and subacute stage of myocardial infarction
in 2 times
higher than in patients without diabetes. The
features of angina
Diabetic macroangiopathy is rapid
progression,
is often asymptomatic (no pain). Treatment
of this
complication lies in the timely treatment of
diabetes, atherosclerosis,
myocardial infarction and angina pectoris.
Diabetic macroangiopathy,
associated with atherosclerosis of cerebral
arteries. Appears
encephalopathy, and in severe cases - acute
ischemic
circulation (ADCC). Symptoms of
encephalopathy and stroke have
diabetes is the same as without diabetes.
Treatment "These events include the

correction of diabetes
diabetes, the treatment of atherosclerosis and
emergency treatment of stroke.
Diabetic macroangiopathy of the lower
extremities is manifested
symptoms such as sensitivity to cold feet,
weakness in the legs during walking and
prolonged standing, the syndrome of
intermittent claudication (pain - in the
gastrocnemius muscle, emerging or
aggravated by walking and
decreasing at rest), dry skin of feet and legs,
cold
foot, muscle atrophy legs, loss of hair on the
legs, cyanosis
fingers, the weakening or absence of pulse
in large arteries
legs and feet, trophic changes (up to the
trophic ulcers)
skin of feet and legs, in severe cases it may
be the development of gangrene
the toes of this form of treatment
complications of diabetes include
timely treatment of atherosclerosis and
diabetes, the use of
vasodilators, and thrombolytic drugs,
surgical
treatment (see treatment of diabetic foot).
1.3.2. Diabetic microangiopathy
Definition
"This is generalized loss of small vessels
(capillaries,
precapillaries, arterioles, venules) in patients
with diabetes, characterized by
the development of thickening of the
basement membrane of blood vessels,
proliferation of endothelial mikrotrombozov
and microaneurysms, which in
Ultimately, accompanied by impaired
patency of the
vessels.
Diabetic microangiopathy is a classic view
complications of diabetes and occurs in 5090% of patients with diabetes.
Classification
Depending on the vascular bed

microcircular
of a body distinguished the following types
of
Diabetic microangiopathy: 1. Retinopathy,
2. Nephropathy 3.
Microangiopathy of the lower extremities. 4.
Neuropathy. Five. Syndrome
diabetic foot.
1.3.2.1. Diabetic retinopathy
Definition
This defeat of the retina in diabetes,
characterized by
narrowing of the capillaries, increasing the
aggregation of formed elements
blood, swelling of the retina, progressive
obliteration of the retinal
capillaries.
Diabetic retinopathy is the leading cause of
Blindness and visual impairment. When
diabetes develops blindness is 25 times more
likely
than the general population.
The clinical picture
Flickering before the eyes of flies and
patches of fog and a sense of
odd items, a progressive decrease of visual
acuity
including blindness. But the more specific
signs of diabetic
retinopathy, detected during the
ophthalmologic examination. These
signs depend on the stage of retinopathy,
and so we list these
signs depending on the stage of diabetic
retinopathy. /.
Nonproliferative retinopathy,
microaneurysms (hemorrhage,
edema, exudative lesions in the retina.
Hemorrhages are of the form
small dots, lines or dark spots rounded,
localized in the center of the fundus or along
the large veins in the
deep layers of the retina. Hard and soft
exudates, as a rule,
located in the central part of the fundus and
have yellow or

white. An important element of this stage is


the swelling of the retina,
which is localized in the macular area and
along major
vessels. / /. Preproliferative retinopathy.
Venous anomalies:
beaded, tortuous, looped, doubled and
expressed
fluctuations in the caliber of blood vessels.
A large number of solid and "cotton"
exudates. Intraretinalnye microvascular
abnormalities, many
large retinal hemorrhages. HI. Proliferative
retinopathy.
Neovascularization of the optic nerve and
other parts of the retina,
bleeding into the vitreous, the formation of
fibrous tissue in
of newly-formed blood vessels hemorrhage
preretinalnyh
very thin and fragile, resulting in frequent
re-emerge
hemorrhage. Vitreoretinal traction leads to
detachment
the retina. Newly formed blood vessels of
the iris (rubeoz) often
cause of secondary glaucoma.
i. \ i i
Treatment
A. Laser photocoagulation of the retina. This
is the most effective
treatment of diabetic retinopathy and the
prevention of blindness.
Two. Cryotherapy of retina. In some cases,
can be used
instead of photocoagulation and combined
treatment of proliferative
form reduces the neovascularization of the
retina. Three. Vitrzktomiya.
It is recommended for patients with severe
proliferative form
traktsionnoi retinal detachment and vitreous
hemorrhage in the
body. 4. Drug therapy. 4.1. Treatment of
diabetes mellitus. 4.2. Angioprotectors
(0.25-0.5 g anginin 3 times a day for 3-6

months). 4.3.
Antiplatelet agents and anticoagulants
(aspirin 375 mg per day, five thousand
heparin
IU 2 times n / a in the abdomen).
1.3.2.2. Diabetic nephropathy
Definition
This particular kidney disease in diabetic
patients,
morphological basis of which is
nefroangioskleroz
renal glomeruli, clinically manifested by
proteinuria and
progressive renal insufficiency.
The incidence of diabetic nephropathy is 4050%
with type I diabetes and 15-30% for type II
diabetes. Diabetic nephropathy
is the leading cause of disability and
disability in patients
SD.
Clinical and laboratory data
The earliest sign of diabetic nephropathy is
moderate proteinuria (albuminuria exact)
from 50 to 300 mg per day.
Over time, as the disease progresses,
proteinuria
increases and can reach up to 1.0-3.5 grams
per day or more. In 30% of patients
developed nephrotic syndrome. In later
stages
appears. hypertension with a sharp increase
diastolic blood pressure. In the final, has
been steadily growing
progressive chronic renal failure.
Treatment
A. Treatment of diabetes mellitus. Two.
Angioprotectors, antiplatelet agents, and
anticoagulants (see the treatment of diabetic
retinopathy). Three. Diuretics
(With the appearance of edema and
hypertension): furosemide 40-120 mg or
more in the morning
an empty stomach. 4. ACE inhibitors (for
hypertension): znalapril 5-20 mg per day.
Five.

Treatment of chronic renal failure. Vir.


1.3.2.3. Diabetic microangiopathy of the
lower extremities
The clinical picture
When this complication diabetes are the
following signs
disease: pain in the feet, fatigue when
walking, "marbling"
foot skin, decreased skin temperature and
velocity of the lower extremities
blood vessels in the feet, coldness and
weakness in the legs, throbbing in the
major arteries of the foot remains,
hypotrophy of leg muscles, dry
skin, trophic nail changes, further develops
trophic ulcer of lower leg and foot.
Treatment
A. Treatment of diabetes mellitus. Two.
Angioprotectors, antiplatelet agents, and
anticoagulants (see the treatment of diabetic
retinopathy). Three.
Nicotinic acid 1% to 2 ml / m April 20
Andekalin 0.005 g of 2 tab
3 times a day a month.
1.3.2.4. Diabetic neuropathy
This is one of the most frequent
complications of diabetes detected at
prolonged duration of almost 100%.
Classification
I. Sensorimotor peripheral neuropathy. II.
Autonomous
(Visceral) neuropathy.
The clinical picture
Sensorimotor peripheral neuropathy
(polyneuropathy)
shows a complex motor and sensory
disorders
tactile, pain, temperature, vibration, and
jointmuscular sense. This change in the bilateral
distal
sensitivity, less fatigue and loss of the upper
extremities.
Paresthesias and pain in the feet, the
weakening of reflexes, loss of
vibration and pain sensitivity, Charcot foot.

Autonomous
(Visceral) neuropathy. Clinical
manifestations depend on the
destruction of an organ or system. Heart
disease:
tachycardia rest, orthostatic hypotension and
syncope
status, respiratory arrhythmia. The defeat of
the gastrointestinal tract: with gastroparesis
delayed or, conversely, a very rapid gastric
emptying,
atony of the esophagus, reflux esophagitis,
dysphagia, change in the aqueous
diarrhea, constipation, excessive salivation,
diskinezyi biliary tract with
propensity to stone formation, reactive
pancreatitis. Defeat
urinary system: atony of the ureters and
bladder,
violation of the separation of urine and a
tendency to develop urinary infections
Erectile dysfunction (about 50% of diabetic
patients), retrograde
ejaculation and testicular innervation
violation of pain, impaired
moistening the vagina. Violation of the pupil
function: violation
adaptation to darkness. Violation of the
function of sweat glands: the skin
becomes doughy, atrophic and dry
(anhidrosis).
Treatment
A. Treatment of type 2 diabetes.
Angioprotectors, antiplatelet agents and
anticoagulants
(See treatment "for diabetic retinopathy). 3.
Symptomatic
treatment.
1.3.2.5. Diabetic foot syndrome (SDS)
Definition
This is a pathological condition in the
diabetic foot that occurs in the
background lesions of peripheral nerves,
skin, soft tissues, bones and
joints, manifested by acute and chronic
ulcers, osteo-

articular lesions and purulent-necrotic


processes.
Occurs in 30-80% of patients with diabetes.
Amputation of lower limbs
diabetic patients with diabetic foot
syndrome produced by 15 times
more likely than the general population.
Classification
Depending on the release of the
pathogenesis of two (2) the basic forms
CDC: 1. Neuropathic form of: a) without
osteoarthropathy, and b)
diabetic osteoarthropathy. Two. Coronary
heart shape.
The clinical picture
Neuropathic form appears at least three
kinds of
lesions: 1. Neuropathic ulcers. Localized in
the foot
and interdigital spacing, ie in the areas of
maximum pressure. Two.
Osteoarthropathy (Charcot's joint with the
development). Is the result of
marked degenerative changes in the
osteoarticular apparatus
foot (osteoporosis, osteolysis, hyperostosis).
Severe bone
deformity of the foot (Charcot foot). Three.
Neyropatichesshy edema. Is
consequence of vasomotor disturbances, in
particular arterial
bypass surgery, increasing the
hydrodynamic pressure
Coronary microvasculature is the SDS Form
consequence of atherosclerosis of arteries of
lower extremities, leading to
disruption of the main flow, ie is one of the
options
diabetic microangiopathy. The skin on the
feet may be pale
or cyanotic: rarely has a pinkish-red hue due
to the
expansion of the surface of the capillaries in
response to ischemia.
The affected foot are cold. Lesions are the
type of akralnyh

necrosis (the fingertips, the boundary


surface of the heel). Pulse on
arteries of the foot, popliteal and femoral
arteries is weakened or not
palpated.
Treatment of '*
Neuropathic forms: a) optimization of the
diabet, 'b)
systemic antibiotic therapy, c) complete rest
and unloading of the joint, d)
Local wound treatment, and e) removing
parts of hyperkeratosis, e)
correct selection and wearing of special
shoes. Coronary
forms: 1) optimization of the compensation
of diabetes, and 2) revascularization
operations (trombendarterektomiya, the
formation of roundabout
anastomosis), and 3) occupational therapy
(in the absence of necrotizing
lesions) - is a 2-hour walking a day,
promoting the
collateral blood flow, and 4) the impact on
hemostasis (aspirin 100
mg / day, heparin 10 thousand units p / day),
5) local thrombolysis, 6)
-298 amputation of the leg (with the development
of extensive purulent necrotic
lesions).