DEFINITION
CLASSIFICATION AND ETIOLOGY
PATIENT PROFILE
METABOLIC SYNDROME
CLINICAL FEATURES
DIAGNOSIS AND INVESTIGATIONS
DAWN AND SOMOGYI PHENOMENON
MANAGEMENT
COMPLICATIONS AND METABOLIC MEMORY
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Update on DIABETES MELLITUS (2020) By Dr Rahul Jain , Dr Sharda Jain
1. Topic :- Update on DIABETES MELLITUS (2020)
Dr Rahul JainDr Sharda Jain
for Gynaecologist & Surgery Specialist
2. Over 400 ppts are available on
slideshare.net ***for use of public/Doctors
www.slideshare.net / Lifecarecentre
3. LEARNING POINTS-
• DEFINITION
• CLASSIFICATION AND ETIOLOGY
• PATIENT PROFILE
• METABOLIC SYNDROME
• CLINICAL FEATURES
• DIAGNOSIS AND INVESTIGATIONS
• DAWN AND SOMOGYI PHENOMENON
• MANAGEMENT
• COMPLICATIONS AND METABOLIC MEMORY
4. DEFINITION-
• DIABETES MELLITUS IS A METABOLIC
SYNDROME CHARACTERIZED BY
HYPERGLYCEMIA DUE TO ABSOLUTE/RELATIVE
INSULIN DEFICIENCY OR BOTH.
• NORMAL PHYSIOLOGY
• REFERENCE
5.
6.
7. CLASSIFICATION-
• TYPE 1 DIABETES MELLITUS
• TYPE 2 DIABETES MELLITUS
• GDM
• OTHERS-
1) MATURITY ONSET DIABETES OF YOUNG
2) ENDOCRINOPATHIES
3) INFECTIONS-VIRAL
4) DRUGS-STERIODS,DIAZOXIDE,PENTAMIDINE
5) LATENT AUTOIMMUNE DIABETES IN ADULTS(LADA)
8. PATHOGENESIS-
• TYPE 1 DM-AUTOIMMUNE DESTRUCTION OF
BETA CELLS
• GDM-PRESENCE OF HPL AND INSULINASE
• TYPE 2 DM-INSULIN RESISTANCE
Adipose cell
big
Adipose
cell
9. PATIENT PROFILE-
• TYPE 1 DM-young
child,thin,undernourished,presents with DM
symptoms,family h/o+
• Type 2 DM-middle aged to
elderly,obese,metabolic syndrome patient
with DM Symptoms,fat distribution,family
history +/-
• Gdm-pregnant patient usually in 6-7 months
of pregnancy
13. INVESTIGATIONS-
• ROUTINE INVESTIGATIONS TO LOOK FOR ANY
SIGN OF INFECTIONS
• CBC,FASTING LIPID PROFILE,LFT,KFT,SERUM
ELECTROLYTES,U/R
• FUNDOSCOPY(GUIDELINES-5YR AFTER DX
AND IMMEDIATELY AFTER DX)
• ECG AND 2D ECHO
16. DAWN AND SOMOGYI PHENOMENON-
• DAWN
• FASTING GLUCOSE MORE
• NIGHT INSULIN
INADEQUATE
• MEASURE 12 AND 3 AM
GLUCOSE LEVELS
• RX-INCREASE INSULIN
DOSE
• SOMOGYI
• FASTING GLUCOSE MORE
• EXCESS NIGHT INSULIN
CAUSING MIDNIGHT
HYPOGLYCEMIA
TRIGGERING EXCESS
COUNTER REGULATORY
HORMONE SECRETION
• RX-DECREASE INSULIN IN
NIGHT
17. MANAGEMENT-
• TARGETS-
1) HbA1c Target-≤7.0%
2) Pre prandial glucose<130mg/dl
3) Post prandial glucose<180mg/dl
4) BP<140/80mmhg
18. LIFESTYLE CHANGES-
• DIABETIC DIET-SHORT,FREQUENT,LOW GLYCEMIC
INDEX FOODS
• TOTAL CALORIE CONTENT OF FOOD(36KCAL/KG-
MALES,34KCAL/KG-FEMALES)
• DISTRIBUTION-C:F:P-50:30:20%
• FIBER CONTENT IN DIET
• CUT DOWN ALCOHOL CONSUMPTION AND
SMOKING
• EXERCISE AND STRESS FREE LIFE
• MEDICATIONS
23. S/E AND C/I-
• WEIGHT GAIN-SULFONYLUREAS,INSULIN
• HYPOGLYCEMIA-SULFONYLUREAS,INSULIN
• PANCREATITIS-GLP-1 ANALOUGES
• HEART FAILURE-THAIZOLINEDINEDIONES
• CKD-METFORMIN NOT TO BE GIVEN
27. TREATMENT GUIDELINES-
• HbA1C>10.0%-INSULIN THERAPY
• HbA1C=9-10%-DUAL THERAPY
• FIRST DRUG TO BE ALWAYS STARTED
METFORMIN UNLESS C/I
• ADD INCRETIN OR SU OR SGLT-2 INH. AFTER
EVERY 3 MONTHS IF TARGETS NOT ACHIEVED.
• INCRETINS ARE COSTLY BUT PREFERABLE
• TYPE 1 DM,PREGNANCY-INSULIN ONLY
29. CASE STUDIES-
• A 45YR OLD MALE,K/C/O HTN SINCE 10 YRS
WELL CONTROLLED ON TELMA-H OD AND
NOW COMES WITH ELEVATED HbA1C OF
8%,FBG-110 AND PPBG-190MG/DL DETECTED
ON ROUTINE INVESTIGATIONS,WHAT
TREATMENT PATIENT SHOULD BE STARTED
ON?
30. CASE 2-
• A 68YR OLD FEMALE K/C/O HTN,T2DM SINCE
10 YRS WITH H/O ISCHEMIC STROKE
INVOLVING RT SIDED BODY 5 YRS BACK,ON
METFORMIN 500MG BD,LOSART-H
BD,ECOSPRIN,ATORVASTATIN,MULTIVITAMINS
AND NOW COMES WITH HbA1C OF
7.8%,IDEAL TREATMENT?
31. CASE 3-
• DR RAMESH SURGEON BY PROFESSION 65 YRS
OLD MALE K/C/O T2DM SINCE 3 YRS,ON
METFORMIN 1000MG BD AND NOW
DETECTED TO HAVE HIGH HbA1C WHICH
ANTIDIABETIC DRUG CAN BE IDEALLY ADDED
IN HIS REGIME?
33. ACUTE COMPLICATION-
• DIABETIC KETOACIDOSIS
1) BLOOD SUGARS>250MG/DL
2) URINARY KETONES++
3) BLOOD pH- <7.35
4) ALWAYS LOOK FOR PRECIPITATING FACTORS
AND WATCH FOR HYPOKALEMIA
• HYPEROSMOLAR HYPERGLYCEMIC STATE
• LACTIC ACIDOSIS
• HYPOGLYCEMIA
34. COMPLICATIONS MECHANISM-
• Pericyte necrosis and neoangiogenesis(VEFG
AND TGF-beta) which causes production of
leaky and incompetent blood vessels.
• AGE’s formation due to high intracellular
glucose leads to crosslinking extracellular
matrix proteins which causes basement
membrane thickening,LDL trapping in
intima,endothelial dysfunction.
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Editor's Notes
DIABETES COMPLICATION CONTROL TRIAL,UK PROSPECTIVE STUDY
L CELLS IN JEJUNUM
Pericytes stabilize and monitor the maturation of endothelial cells by means of direct communication between the cell membrane as well as through paracrine signaling.