This document provides information on the diagnosis and management of type 2 diabetes mellitus. It discusses the different types of diabetes, risk factors for type 2 diabetes, acute and chronic complications, glucose monitoring techniques, lifestyle management including diet and exercise, oral and injectable drug therapies, and considerations for diabetes management in special populations and situations.

1. Diagnosis & Management Of
T2 Diabetes Mellitus

2.  Diabetes mellitus is a syndrome with disordered
metabolism & inappropriate hyperglycaemia due to
either deficiency of insulin secretion or combination of
insulin resistance & inadequate insulin secretion.

3. • Type 1 DM
• Type 2 DM
• Other specific types:
1. Genetic defects of Beta cells ( MODY)
2. Genetic defects in insulin action
3. diseases of exocrine pancreas(pancreatitis)
4.endocrine diseases like cushing synd, phaeochromocytoma,
hyperthyroidism
5. Drugs glucocorticoids, beta blockers
thiazides,antipsychotics
• Gestational DM (GDM)

4.  Type 1 A due to destruction of beta cells by auto
immune process
Type 1 B idiopathic
Younger age ,ketosis prone
Antibodies present ICA,GAD, IAA

5.  Occurs in adults
 Ketosis is not common
 Insulin resistance leads to hyperglycaemia
 Genetic factors
 Environmental factors
obesity ....visceral BMI>25
physical inactivity
h/o GDM
HT

6.  Due to insulin resistance related to metabolic changes
in late pregnancy
 Reverts to normal glucose tolerance after delivery
 35 to 50% will develop dm in next 10 yrs follow up

7. 1. Assessing glucose tolerace
Normal
FPG < 100mg
PPG < 140 mg
Glucose intolerance
FPG >100MG <126 MG
PPG >140 mg <200mg
Diabetes
FPG >126mg
PPG >200mg
2. HbA1c >6.5 %

8.  Acute Complications
DKA (diabetic ketoacidosis)
HHS (hyperglycemic hyperosmolar state)
• Chronic complications
microvascular
Eye ..retinopathy....macular oedema.....cataract
Neuropathy...sensory ..motor..autonomic
Nephropathy
Macrovascular
Coronary artery disease
Cerebrovascular disease
Peripheral arterial disease
Others
Gastro intestinal ( gastroparesis,diarrhea )
Genito urinary (sexual dysfunction ,uropathy)
Skin
infections
Periodontal disease
Hearing loss

9.  theories to explain
1)Increased glucose>>>>advanced glycosylation end
products (AGEs)>>>>combines with cellular
proteins>>>>accelerates atherosclerosis>>>>endothelial
dysfunction
2) increase glucose>>>metabolism by sorbitol
pathway>>>increase sorbitol>>>cellular dysfunction

11.  Diet
 Drugs (OAD)
secretogoges
sulfonylureas
1st generation Tolbutamide, chlorpropamide
2nd generation glipizide,glyclazide
3rd generation glimepiride
Meglitinides analog repaglinide Neteglinide
Insulin sensitisers
Metformin
glitazones pioglitazone
alpha glucosidase inhibitors
Acarbose,voglibose
Incretins
GLP1 agonist Exenatide , Liraglutide
DPP4 inhibitors (gliptins)
teneligliptins,vildagliptin,linagliptins,sitagliptin,sexagliptin
SGLT2 inhibitors (Gliflozines)
canagliflozines,dapa empagliflozines
Others
Bromocriptins, Hydroxychlroquine
 Insulins

12.  In general most patient is advised 45% of total calories
as carbohydrates,30% as fat,25% as proteins.
 Dietary fibres delay absorption of glucose & may have
beneficial effect on colonic function
 Low glycemic index foods are prefered

20.  Oral glucose leads to higher insulin response with
equivalent dose of i.v..This is because oral glucose
releases gut hormone GLP1 which stimulates insulin
secretion (incretin effect)
 GLP1 is proteolysed by enzyme DPP4 (dipeptidyl
peptidase 4 )
 GLP1 agonist are with longer half life e.g.Exenetide,
Liraglutide
 DPP4 inhibitors inhibit enzyme & prolongs action of
GLP1 e.g.Teneligliptin,vildagliptin,linagliptin,sitagliptin

21.  Glucose is filtered freely by glomeruli & is reabsorbed
by proximal convolated tubules by sodium-glucose co-
transporter 2(SGLT2)
 SGLT2 inhibitors leads to glycosuria & lowering plasma
glucose levels
 Canagliflozine,dapa &empagliflozines are commonly
used

22.  Bromocriptin is dopamin recepter agonist inhibites
sympathetic tone in CNS resulting decrease plasma
glucose
 Hydroxychlroquine (HCQS) acts by altering insulin
metabolism

23. Which patients require insulin?
1. type 1 dm
2. type 2 dm with OAD failure (sec. Failure)
3.during major surgery
4.pregnancy
5. FPG>250 or RPG >300 or HbA1c >10%

24.  Rapidly acting human insulin analogs
 insulin lispro (Humalog...lilly)
 insulin aspart (Novolog....novo nordisk)
 insulin glulisine (Apidra.....sonofi)
 Short acting regular insulin
 human Actrapid(novo....lily)
 Technosphere inhaled insulin(Afrezza)
 Intermediate insulin
 NPH insulin
 Long acting analogs
 insulin glargine (Lantus)
 insulin detemir (Levemir)
 insulin degludec (Tresiba)
 Premixed insulin
 NPH +regular 70/30
 NPL + lispro 75/25 (humalog mix)
 NPA+aspart 70/30 (novolog mix)
 degludec+aspart 70/30 (Ryzodeg)

25.  Insulin which resembles nomal secretery pattern of
insulin i.e. Basal insulin for 24 hrs control & additional
insulin to control prandial glucose increase
 Basal bolus regime

26.  Start with 0.1 to 0.2 units/kg
 Or 10 units at bed time
 Adujust the dose to achieve target FPG <100
 If FPG 100 -120 increase by 2units
 120-140 4
 140-160 6
 160-180 8

27.  Initial dose of prandial insulin is decided by fixed dose
of 4 units each meal
 Further titration is done acc to ppg value
 If ppg>140-180 4units & so on
 Total dose of insulin calculated as 0.3-0.5units/kg &
given as 50% bolus & 50% basal

28.  Hyperglycemia in hospital is defined as RBS>140mg/dl
 If not addressed leads to poor clinical outcome
 Hyperglysemia may be in ICU setting or may be in non
critical setting i.e. In wards

29.  Glycemic targets in icu
 140-180 mg/dl
 RBS <110 or >180 is not recommended
 Intensive glycemic control leads to increase mortality
 OADs should be avoided
 Continuous IV insulin infusion (CII)is prefered method
 Initial rate of insulin infusion is RBS/100 units/hr

30. Blood glucose With any increase in
BG from prior BG
BG decrease <30
from prior BG
BG decrease >30
from prior BG
>240 Increase rate
3unit/hr
Inrse 3units/hr No change
210-240 2units/hr 2 No change
180-210 1 1 no
140-180 no no no
110-140 decrease d d
90-110 hold h h

31.  Calculate insulin requirement for last 6 hrs for i. V.
Insulin * 4
 Give 80% of total dose as s.c.
 Give 50% basal 50% bolus
 Start s.c. Insulin 1-2 hrs before discontinuing i v insulin
infusion

32.  Administer basal insulin along with rapid acting analogs
 Test RBS before each feed

33.  Usually S.C. Insulin is given
 Basal –bolus is preferred
 Supplemental insulin (correctional) insulin is given for
dose adjustment

34.  Calculate total daily dose as below
 If BG 140-200 0.4 units/kg
 BG 200-400 0.5 units/kg
 50% basal 50% bolus
 Glycemic targets in non icu settings
 premeal glucose <140
 RBS <180
 Supplemental insulin is given to correct hypeaglycemia

35. BLOOD GLUCOSE Usual insulin
140-180 4
180-220 6
220-260 8
260-300 10
300-340 12
340-380 14
Insulin resistant may require more doses Insulin sensitive may require less dose

36.  All OAD should be stopped on morning of surgery
 Stop long acting insulin 1 day before surgery
 Omit morning dose of s.c.insulin
 Start 5% DNS with regular insulin at breakfast time 8
a.m. 100ml/hr
 Monitor BG 2hrly during surgery
 Target BG is <140-180

37.  Diabetes management involves targeting
FPG,PPG,HBA1C,Glycemic variability,quality of life
 Glycemic variability is swings in blood glucose levels
that occur throughout day
 BG swings is responsible for increase in cvs morbidiy
 Glycemic variability can be measured by CGM studies
(continuous glucose monitoring)

38.  Involves inserting subcutaneus sensor that measures
glucose concentration in interstitial fluid for 14 days
 Graphs are created & with the help of software
ambulatory glucose profile (AGP) is created for analysis
 Episodes of hypo or hyperglycemia can be identified
with glucose variability

39.  Is an estimation of health &effects of health care.
 Concept of disease specific QoL is a treatment goal
 Philosophy has changed from physician-centered to
patient centered

41.  THANK YOU

42. THANK YOU