DIABETES ASSESSMENT

DEFINITION
Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycemia, which is the result of:
- disorders of insulin secretion,
- action of insulin
- both of these factors
Chronic hyperglycemia is accompanied by damage, dysfunction and failure of various organs, especially the eyes, kidneys, nerves, heart and blood vessels.

DIAGNOSIS CRITERIA FOR DIABETES MELLITUS

Fasting capillary Up to 5.6 mmol/l >= 6.1 mmol/l Up to 6.1 mmol/l
blood glucose
Fasting venous blood Up to 6.1 mmol/l >= 7.0 mmol/l Up to 7.0 mmol/l
glucose
Venous blood glucose - >=11.1 mmol/l -
with random measure-
ment
Venous blood glucose Up to 7.8 mmol/l >= 11.1 mmol/l 7.8-11.1 mmol/l
with OGTT after 2
hours
HbA1c Up to 6.0% >=6.5% -
Indicators Norm DM Impaired glucose tolerance
Gestational diabetes mellitus:
OGTT after 1 hour - >10 mmol/l
OGTT after 2 hours 8.5-11.1 mmol/l
On an empty stomach 5.1-7.0 mmol / l
GDM: up to 24 weeks - fasting venous blood glucose, venous blood glucose regardless of food intake
24-26 weeks - OGTT with 75 g glucose
Treatment of GDM:
1) diet therapy
2) Aerobic exercise
 3) Self-monitoring (on an empty stomach, before and after 1 hour of main meals - a total of 7 measurements per day)
4) Insulin therapy: no effect on self-control within 1-2 weeks + signs of fetal fetopathy (large fetus, weight>=75 precentile , hepato-
splenomegaly, cardiomegaly, fetal head bypass , swelling and thickening of the pancreas, thickening of the cervical fold)
ORAL SUGAR-REDUCING DRUGS ARE CONTRAINDICATED

COMPLICATIONS OF DIABETES MELLITUS

Acute Late/Chronic
Ketoacidotic coma Microangiopathies Macroangiopathies Diabetic polyneuropathy
Hyperglycemic ( hyperosmolar ) coma Nephropathy ischemic heart disease
hypoglycemia retinopathy Cerebrovascular diseases
lactic acidosis Diseases of the arteries of the lower
extremities
diabetic foot syndrome

Complication Diagnostic criteria Treatment

Ketoacidosis Glucose >=13 mmol/l Pre-hospital stage: glucose + ketone bodies in urine using an indicator test strip + IV drip of
Ketonemia >5 mmol/l 0.9% NaCl 1l/h
Urinary ketone bodies >=++ Insulin therapy - 0.1-0.15 U / h
pH < 7.3 , HCO3 < 15 mmol/l Rehydration (with unstable hemodynamics, under the control of blood pressure)
In the presence of ketone bod- 1 hour - 1.5 l
ies, a high level of glucose, 2 hour - 1 l
but without changes in acid- 3 hours 500 ml
base balance - ketosis ! Choice: NaCl 0.9, with hypernatremia (>165 mmol / l) - hypotonic solution of 0.45% NaCl
Bicarbonate at pH < 6.9
hypoglycemia Light: 3.0-3.9 mmol/l Light:
Moderate: <3.0 mmol/l with- Glucose tablet, grape juice, do not give chocolates or rolls (there are fats)
out neurological symptoms Moderate or severe: Glucose 40% bolus 100 ml, then drip 5-10%
(no impairment of conscious-
ness)
 Severe: <3.0 mmol/l + im-
pairment of consciousness
Hyperosmolar >35 mmol/l Rehydration
/hyperglycemic coma Hyperosmolarity >350 mOsm Insulin only 0.5-2 U /h due to low insulin sensitivity
/L Correction of Na and K (potassium under ECG control)
lactic acidosis >4 mmol/l (with tissue hy- 2-5 U /h insulin
poxia and impaired perfusion Hemosorption or sorbents (activated carbon)
>2 mmol/l)

TACTICS OF CHOOSING HYPOGLYCEMIC THERAPY IN PATIENTS WITH DM

LEVEL HbA1c Treatment Control

Baseline HbA1c=6.5-7.5%
In debut Monotherapy: Metformin, DPP-4 iDPP, arGLP-1
Alternative: SM (except glibenclamide), glinides, acarbose
HbA1c reduction >=0.5% or individ- Initial monotherapy
ual goal achieved Control at least 1 time in 3 months
Decreased HbA1c <0.5% Combination of 2 drugs Decision to intensify therapy no later than 6
Rational combinations: months
Metformin + iDPP-4
Metformin + arGLP-1
Metformin + Glinide
Metformin + iNGlT-2
Baseline HbA1c=7.6%-9.0%
In debut Combination of 2 drugs
Rational combinations Control at least 1 time in 3 months
 Reserve: combination with insulin Decision to intensify therapy no later than 6
months
Decreased HbA1c by >=1% Initial 2-Drug Combination Therapy
Decreased HbA1c <1% Combination of 3 drugs
Baseline HbA1c>9.0%
In debut Insulin + - other drugs Control at least 1 time in 3 months
Decision to intensify therapy no later than 6
Decreased HbA1c by >=1.5% Combination of 3 drugs months
Decreased HbA1c <1.5% Intensification of insulin therapy

Stable combinations of hypoglycemic drugs

Galvus Met Vildagliptin + Metformin
Janumet Sitagliptin + Metformin
Sinjarji Empagliflozin + Metformin
Sigduo Long Dapagliflozin + Prolong Metformin
Sultophy Insulin degludec + Liraglutide
Soliqua Insulin glargine + Lixisenatide
gentadueto Linagliptin + Metformin

INSULIN THERAPY
Ultra-short action Effect in 5-10 minutesadministration during meals Lizpro, Aspart
short action Effect in 15-30 minutesadministration before each meal Actrapid,
Average duration of action There is a peak of actionneed to adjust the meal NPH
 Long duration of action No peak action, no connection with food intake Tujeo, Lantus,
Twice in the morning and evening introduction Levemir
Extra long duration of action No peak action, no connection with food intake Tresiba
1 time introduction in the eveningglycemic control in the morning

ORAL SUGAR-REDUCING DRUGS

GROUP REPRESENTATIV MECHANISM OF ACTION ADVANTAGES FLAWS RESTRICTIONS
ES
biguanides Metformin (Siofor, Inhibition of glucose absorption in Low risk of hypoglycemia Risk of B12 defi- CKD C3b up to
Glucoage, Gliformin, the small intestine Approved for use in prediabetes ciency (OAC, 1000 mg/day, with
Bagomet) Decreased production of glucose Reducing the risk of colorectal neurological con- C4-C5 - cancella-
by the liver and breast cancer sultation) tion
Increasing tissue sensitivity to in- Increased fibrinolysis and de- Discomfort of the Liver diseases
sulin creased platelet aggregation gastrointestinal (hepatitis, cirrho-
Reduced fatty acid oxidation Any combination except thiza- tractstart with sis, increased ALT,
lindinediones low doses and AST> 2.5VGN)
Does not affect body weight then gradually in- Pregnancy and
Low price crease over 1-2 lactation (RF)
Anti-age effect weeks
Risk of RG-in-
duced nephropa-
thy (cancellation 2
days before RG-
contrast studies)
The risk of lactic
acidosis in hy-
poxia of any ori-
gin!
Sulfonylureas I generation: tolbu- Blockade of ATP-dependent potas- Use in type 2 diabetes with in- Reception 30 min- In CKD of any
tamide, tolazamide sium channelsdepolarization of sufficient insulin secretion utes before meals stage, gliclazide
II generation: gliben- beta cellsopening of voltage- Starting therapy with minimal and no fasting MB, gliquidone,
 clamide (Maninil), gated calcium channelsexocyto- doses glimepiride are
gliclazide (Dia- sis of insulin granules Prescribing short-acting drugs to used.
beton), gliquidone the elderly
(Glurenorm) Glibenclamide - the gold stan-
III generation: dard from PSM
glimepiride (Amaryl) Gliclazide - a positive effect on
hemostasis and MCR
Glimepiride - decrease in IR,
preservation of the secretory re-
serve of beta cells
Gliquidone - 5% excreted by the
kidneys, 95% by the intestines
thizalindinediones Rosiglitazone (Avan- Muscles: increased glucose uptake Low risk of hypoglycemia weight gain CHF OF ANY
dia) – canceled by Adipose tissue: increased FFA up- Potential protective effect of Peripheral edema FUNCTIONAL
FDA take, increased lipogenesis, in- beta cells Increased risk of CLASS
Pioglitazone (Actos) creased glucose uptake Improvement of blood lipid tubular bone frac- Liver disease
Liver: decreased gluconeogenesis spectrum tures IHD (nitrate in-
Risk reduction Slow onset take)
OKS
insulin therapy
Pregnancy and
lactation
Ketoacidosis
Glinides Nateglinide (Starlix) Blockade of ATP-dependent potas- Before every meal Do not combine
Repaglinide sium channelsdepolarization of with ICD
(Novonorm) beta cellsopening of voltage- Do not combine
gated calcium channelsexocyto- with other secreta-
sis of insulin granules gogues (either
PSM or Glinides)
SGLT-2 inhibitors Dapagliflozin Decreased reabsorption of glucose Weight loss The risk of devel- CKD C4-C5
(Forxiga) and sodium in the proximal tubules Edema reduction oping urogenital
Canagliflozin of the kidneysinfluence on mac- Decreased blood pressure infections
(Invokana) ula densaRAAS inactivation Nephroprotection Risk of develop-
Cardioprotection ing ketoacidosis
Fracture risk
(canagliflozin)
High price
Risk of NK ampu-
tation
(canagliflozin)

DPP-4 inhibitors Linagliptin (trajenta) They actively bind to the DPP-4 Does not affect body weight High price
Sitagliptin (Januvia) enzyme (the relationship is re- Low risk of hypoglycemia The risk of devel-
versible), which causes a steady in- No CKD restrictions oping pancreatitis
crease in the concentration of in- (linagliptin)
cretins and a long-term preserva-
tion of their activity.
GLP-1 receptor Semaglutide (Ozem- They have an incretin-like effect: Weight loss High price CKD C4-C5
agonists pic) Reduce glucagon synthesis Decreased blood pressure Injectable forms
Dulaglutid (Trulic- Increase insulin synthesis Nephroprotection (liraglutide) (the only oral glu-
ity) Reduce glucose production by the tide is
Liraglutide (Vintoza) liver The risk of devel-
Slow down the evacuation of food oping pancreatitis
from the stomach
Alpha-glucosidase Acarbose Slow absorption of carbohydrates No effect on body weight Reception three For CKD of any
inhibitors in the intestine Low risk of hypoglycemia times a day stage (when pre-
Low efficiency scribing
linagliptin, the
dose does not need
to be adjusted)
 LATE COMPLICATIONS OF DIABETES MELLITUS
Diabetic microangiopathies: Diabetic macroangiopathies:
diabetic retinopathy ischemic heart disease
diabetic nephropathy Cerebrovascular diseases
Diseases of the arteries of the lower extremities

Definition
diabetic retinopathy-microvascular complication of DM, characterized by damage to the retina as a result of ischemia, increased permeability and vascular
endothelial dysfunction, leading to a significant decrease in vision up to its complete loss.
Classification of diabetic retinopathy

Complicated forms of proliferative DR:iris rubeosis, secondary neovascular glaucoma, hemophthalmos, traction syndrome and/or traction retinal detach-
ment
At any stage of DR, diabetic macular edema (DME) can develop -thickening of the retina associated with the accumulations of fluid in the intercellular space
due to a violation of the hematoretinal barrier and a mismatch between the release of fluid and the ability to reabsorb it by pigmented epithelial cells.
Screening for diabetic retinopathy
If preproliferative and proliferative DR and any stage of DME are detected, urgently refer the patient to specialized centers to an ophthalmologist
Indications and timing of a complete ophthalmological examination by a specialist ophthalmologist

Other indications for referral of patients to specialized centers to a specialist ophthalmologist

· Complaints about decreased visual acuity
· Visual acuity below 0.5
· If a visual acuity test or retinal examination cannot be done at the screening test
· Patients who have undergone LKS should be referred to for a second complete ophthalmological examination.
LKS - laser coagulation of the retina

Ophthalmological examination of patients with DR and DME

 The main methods of treatment of DR and DME
Laser coagulation of the retina Intravitreal administration of intravitreal steroid injection Vitrectomy
angiogenesis inhibitors
Stage of preproliferative DR - pan- First-line therapy for clinically Second-line therapy for clinically significant DME of traction origin
retinal LKS significant DME DME Proliferative DR complicated by hemophthal-
Proliferative DR - emergency pan- Anti-VEGF drugs mos, traction/traction hematogenous retinal
retinal LKS detachment involving the macula
DME – LKS + intravitreal injec-
tions of angiogenesis inhibitors or
administration of steroids

Diabetic Nephropathy-specific kidney damage in diabetes, accompanied by the formation of nodular glomerulosclerosis, leading to the development of ter-
minal renal failure, requiring renal replacement therapy (dialysis, transplantation).
chronic kidney disease (CKD)- a supra-nosological concept that generalizes kidney damage or a decrease in glomerular filtration rate (GFR) less than 60
ml / min / 1.73 m2, persisting for more than 3 months, regardless of the primary diagnosis
CKD by GFR
 CKD by albuminuria level

CKD A1 - even in the absence of signs of kidney damage with GFR <60 ml/min

DN screening
Annual assessment of albuminuria (ratio of albumin/creatinine in a single portion of urine) + calculation of GFR
Patients:
· Type 1 diabetes from 5 years
· All patients with type 2 diabetes
· In children over 11 years of age with DM for more than 2 years
· All patients with concomitant arterial hypertension

CKD diagnosis
· Based on the presence of elevated albuminuria and/or decreased GFR in the absence of symptoms and signs of primary renal disease
· The typical presentation includes: a long history of diabetes, the presence of diabetic retinopathy, albuminuria without hematuria, and a rapid decline in
GFR
· In patients with type 2 diabetes, DN can also be in the absence of diabetic retinopathy (moderately sensitive and specific marker), as well as a decrease in
GFR against the background of normoalbuminuria
· With rapidly increasing albuminuria, the sudden development of nephrotic syndrome, a rapid decrease in GFR, the absence of diabetic retinopathy (in the
case of type 1 diabetes), a change in urine sediment (hematuria, leukocyturia, cylindruria), an alternative or additional cause of renal pathology can be as-
sumed
· For GFR <60 ml/min/1.73 m2, assessment of CKD complications
Complications of CKD
 CKD treatment
CKD C1-C3a C3b C4 C5

For patients with type 2 diabetes and CKD C1-3a, con- + Dose adjustment of Cancellation of biguanides, cancellation of iSGLT-2, ar- Dialysis
sider iSGLT-2 or arGLP-1 biguanides (up to 1000 mg/ GLP-1, acarbose Linagliptin or insulin
day) Possible: linagliptin, gliclazide, gliquidone therapy

Sodium restriction to 2.3 g/day (salt to 5 g/day) Correction of anemia (drugs For non-pregnant patients, drugs of choice: ACE in-
that stimulate erythropoiesis, hibitors or ARBs require dose reduction. Combined anti-
Target BP <130/80 mmHg may be considered based on hypertensive therapy to achieve target BP.
iron preparations).
individual expected benefits and risks For non-pregnant
correction of hyperkalemia.
patients, drug of choice: ACE inhibitors or ARBs
Correction of anemia (drugs that stimulate erythro- Correction of mineral-bone
poiesis, iron preparations - with hemoglobin <100 g / l) disorders (in case of vitamin Correction of dyslipidemia.
D deficiency, compensated
in the same way as in the
Avoid the use of nephrotoxic drugs (aminoglycosides, Correction of anemia (drugs that stimulate erythropoiesis,
general population
non-steroidal anti-inflammatory drugs). iron preparations). Correction of mineral and bone disor-
ders (use active metabolites and vitamin D analogues)
DIABETIC FOOT SYNDROME
Diabetic Foot Syndrome (DFS)combines pathological changes in the peripheral nervous system, arterial and microvasculature, osteoarticular apparatus of
the foot, representing an immediate threat or the development of ulcerative necrotic processes and foot gangrene.
RISK GROUPS
1. Patients with distal polyneuropathy at the stage of clinical manifestations
2. Individuals with peripheral arterial disease of any origin
3. Patients with foot deformities of any origin
4. Blind and visually impaired
5. Patients with diabetic nephropathy and CKD C3-5
6. Lonely and elderly patients
7. alcohol abusers
8. smokers
classification:Neuropathic form of DFS: trophic foot ulcer / diabetic neuroosteoarthropathy (Charcot foot) / Ischemic form of DFS / Neuroischemic form of
DFS
Diagnostics
· Collection of anamnesis
· Examination of the lower extremities
· Assessment of neurological status
· Assessment of the arterial blood flow of the lower extremities
· X-ray of the feet and ankle joints in frontal and lateral projections
· Bacteriological examination of wound tissues
Collection of anamnesis

Physical Exam Results

Classification of wound defects in SDS according to Wagner

Principles of local treatment for SDS

 Criteria for the diagnosis of LAD (diseases of the arteries of the lower extremities)
· The presence of complaints: intermittent claudication, stopped by stopping or rest pains, stopped by taking analgesics;
· The presence of necrotic wound defects, ischemic gangrene of the fingers and feet;
· Decrease or absence of pulsation on TAS or ZBBA at the medial malleolus;
· Monophasic or biphasic form of the Doppler wave or its absence on one of the arteries of the foot;
· ABI less than 0.9 in at least one of the arteries of the foot.
Features of the clinical picture of LANK in DM
· Early onset and rapid progression of atherosclerotic changes;
· High prevalence of comorbid ASCVD; The low-symptomatic course of LAD due to concomitant diabetic neuropathy) is characterized by blurred,
atypical or absent pain syndrome/intermittent claudication (IC);
· Untimely seeking medical help, often at the stage of trophic changes in the soft tissues of the foot and/or gangrene;
· Pain symptoms can also be caused by neurogenic causes (spinal stenosis, etc.), including those without a clinically significant decrease in blood flow;
· Trophic disorders of the soft tissues of the lower extremities can develop at any stage of LAD;
· Approximately 50% of patients with DM and lower extremity wounds have LAD.
Criteria for critical arterial ischemia of the lower extremities
· Persistent rest pain requiring regular analgesics for two weeks or more (low risk) and/or
· Trophic ulcer or gangrene of the fingers or foot, which arose against the background of chronic arterial insufficiency (moderate and high risk)
+ in the absence of trophic disorders PAP <50 mm Hg or digital pressure <30 mm Hg, Transcutaneous oximetry <25 mm Hg, skin perfusion pressure <40 mm
Hg
In the presence of an ulcer or gangrene, PAP < 70 mm Hg or digital < 50 mm Hg, Transcutaneous oximetry < 25 mm Hg, skin perfusion pressure < 40 mm
Hg
Algorithm for managing a patient with LE arterial ischemia in DM