APM Welcome, APM North West Network Conference, Synergies Across Sectors
Diabetes mellitus part 2
1. DIABETES MELLITES : PART 2
PRESENTED BY: DR.SOMESH HARIDAS
NAGRE(R2MU6)
UNDER GUIDANCE OF
DR.AMIT L.GAMIT (HOU MU6)
DR.PRIYANKA MODY(AP MU4)
DR.KUNJAN CHAUDHARY(APMU6)
2. 1) Classification and dignosis of diabetes
2)Glycemic targets
3)Pharmacological approach to glycemic
treatments.
3. # CLASSIFICATION
• 1) Type 1 DM : due to autoimmune beta cell
destruction, usually leading to absolute
insulin deficiency.
• Screening for type 1 diabetes with an
antibody panel is recommended only in the
setting of a clinical research study or in a
first-degree family members of a proband
with type 1 diabetes.
• Type 1 DM can be differentiated from Type 2
DM and MODY by testing for C-Peptide.
4. Staging of Type 1 Diabetes
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2017; 40 (Suppl. 1): S11-S24
5. • 2)Type 2 DM : due to progressive loss of
insulin secretion on the background of insulin
resistance.
• Old age
• Obesity
• Insulin resistance
6. • 3) Gestational DM: diabetes diagnosed in
2nd or 3rd trimester of pregnancy that was
not clearly overt diabetes prior to
gestation
-Test for undiagnosed T2DM at the 1st prenatal visit
in those with risk factors.
-Test for GDM at 24–28 weeks of gestation in
women not previously known to have diabetes.
-Screen women with GDM for persistent diabetes at
4–12 weeks postpartum, using the OGTT.
7. • 4)specific type of diabetes:
a)monogenic diabetes syndromes
b)disease of exocrine pancreas
c) drug or chemical induced diabetes
8. MATURITY ONSET DIABETES OF
YOUNG (MODY)
• Onset at early age , classically before age of 25.
• Impaired insulin secretion with no defect in
insulin action.
• Autosomal dominant
• Six subtypes are identified ,of which mody 2 is
most common.
• Mild, asymptomatic increase in blood glucose
• Prominent family history of diabetes in 2-3 generation.
• Usually not associated with obesity.
• Slowly progressive hypoglycemia.
9. TYPE 1 DM AND MODY
SIMILARITIES:
1)Young age
2)Insulin deficiency, no insulin
resistance
3)May run in families.
4)Not associated with obesity.
DIFFERENCES:
1)Type 1 DM is autoimmune
whereas MODY is inherited.
2)Type 1 DM pts are prone to
other autoimmune
disorders , not so in MODY.
3)Multiple autoantibosies
found in type 1 DM.
4)Genetic testing is only
definitive way to confirm
MODY.
10. LATENT AUTOIMMUNE DIABETES IN
ADULTS(LADA):TYPE 1.5
-Autoimmune diabetes which is diagnosed in individuals
who are older than usual age of onset of type 1 DM.
-Progress to insulin requirement.
-Age of onset <50 years.
-Acute symptoms.
-Nonobese.
-Personal or family history of autoimmune disease.
-Low C-peptide level.
-Anti-GAD (glutamic acid decarboxylase) Ab and Islet cell
ab are common.
-No insulin resistance.
11. FIBROCALCULOUS PANCREATIC
DIABETES(FCPD)
• Diabetes secondary to non-alcoholic chronic
calcific pancreatitis, in absence of alcohol
abuse, predominantly seen in tropical
developing countries.
• Usually non ketotic.
• Classical triad : Diabetes + abdominal pain +
pancreatic calculi
• Usually requires insulin for tratment.
12. #CRITERIA FOR DIAGNOSIS OF
DIABETES
• FPG >126 mg/dl(7.0 mmol/L).
OR
2Hr PG>200 mg/dl(11.1 mmol/L) during OGTT
OR
HbA1C>6.5%(48mmol/mol)
OR
In pts with classic symptoms of hyperglycemia or
hyperglycemic crisis, RBS>200 mg/dl(11.1
mmol/L)
13. PREDIABETES??
• PREDIABETES:
• FPG between 100 to 125mg/dl
OR
• 2-hr plasma glucose during 75gm OGTT between
140 to 200mg/dl
OR
• HbA1C 5.7-6.4%.
#RSSDI REC: use of HbA1C as sole diagnostic test for
screening is not reccomanded.
14. CRITERIA FOR TESTING DIABETES OR
PREDIABETES IN ASYMPTOMATIC ADULTS
-Overweight or obese with one or more of the following risk factors:
1.First degree relative with Dm
2.High risk race or ethnicity
3.H/O CVD or HTN
4.HDL chole. <35mg /dl and or triglyceride>250mg/dl
5.Physical inactivity
6.Conditions associted with insulin resistance
-Patients with prediabetes should be tested yearly
-womens with GDM should be tested lifelong every 3 years.
-for all patients testing should begin at age of 45 and every 3 yearly.
#RSSDI rec: individual presenting to healthcare setting for unrelated
illness, ANC pts, people over age of 30 should be encouraged for
voluntary testing.
16. SCREENING AND DIAGNOSIS OF GDM
One-Step Strategy
• At 24-28 weeks gestation in women not
previously dx’d with overt diabetes
• 75-g OGTT; Measure plasma glucose at fasting
and at 1 and 2 hours.
• GDM dx’d when plasma glucose exceeds:
– Fasting: 92 mg/dL (5.1 mmol/L)
– 1 h: 180 mg/dL (10.0 mmol/L)
– 2 h: 153 mg/dL (8.5 mmol/L)
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2017; 40 (Suppl. 1): S11-S24
17. Two-Step Strategy
Step 1:
• In women not previously dx’d with overt
diabetes,
perform 50-g GLT (nonfasting); Measure
plasma
glucose at 1 hour.
• If 1 hour plasma glucose level is ≥140 mg/dL*
(7.8 mmol/L), proceed to step 2.
*ACOG recommends either 135 mg/dL or 140 mg/dL in high-risk
ethnic minorities with higher prevalence of GDM.
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2017; 40 (Suppl. 1): S11-S24
18. Two-Step Strategy (2)
Carpenter/Coustan or NDDG
Fastin
g
95 mg/dL (5.3 mmol/L) 105 mg/dL (5.8
mmol/L)
1h 180 md/dL (10.0
mmol/L)
190 mg/dL (10.6
mmol/L)
2h 155 mg/dL (8.6
mmol/L)
165 mg/dL (9.2
mmol/L)
Step 2:
100-g OGTT is performed while
patient is fasting.
The diagnosis of GDM is made if 2 or
more of the
following plasma glucose levels are
met or exceeded:
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2017; 40 (Suppl. 1): S11-S24
19. #GLYCEMIC TARGETS
• Glycemic recommandations for MOST* non
pregnant adults with DM:
• HbA1C <7.0 %(53mmol/mol)
• Preprandial capillary plasma glucose:80-
130mg/dl
• Peak postprandial capillary plasma
glucose:<180mg/dl
*glycemic targets should be individualised based on
duration,age/life expectancy, comorbid conditions,
hypoglycemia awareness and individual patient consideration.
21. HbA1C
• Is indirect measure of average glycemia over
aprox. 3months and has strong predictive
value for diabetic complications
• Conditions that affects RBC turnover
(hemolytic and other anemias, recent blood
transfusion, pregnancy, hemodialysis,
erythropoitein therepy) plasma glucose
criteria should be used.
22. #PHARMACOLOGICAL APPROACH
• TYPE 1 DM:
-Insulin is mainstay therapy in type 1 DM. Starting insulin
dose is based o weight, with starting dose ranging from 0.4-
1.0 units/kg/day of total insulin.
-Pramlintide: amylin analogue, agent that delays gastric
emptying , blunts pancreatic secretion of glucagon, and
enhances satiety.It is FDA approved for use in type 1 DM
adults.
Starting dose: 15mcg SC injections
Max dose :30-60 mcg SC injections
S/E: GI intolerence
-Surgery.
23. • Type 2 DM:
• Lifestyle modification
- Metformin is preferred initial pharmacological
drug.
- Consider initiating insulin therapy in pts with
newly diagnosed type 2 DM who are
symptomatic or A1C >10.0% and or blood glucose
>300mg/dl.
- Consider initiating dual therapy in pts with newly
diagnosed type 2 DM who have A1C>9.0%.
- Patient centered approach.
- DM with atherosclerotic cardiovascular disease
- Continuous reevaluation.
24.
25. Individualized treatment
• For a patients who has been diagnosed with diabetes consider a combination of
metformin and one of these treatment options based on Patients
• Drug choice should be based on patient preferences as well as presence of
various comorbidities and complications, and drug characteristics, with the goal
of reducing blood glucose levels while minimizing side effects, especially
hypoglycemia and weight gain
Age
BMI
CKD
Duration of Diabetes
Established CVD
Financial concern
Glycemic status
Hypoglycemia concern
28. BIGUANIDES
Metformin
- It is primary drug of choice for type 2 diabetes.
-Act by inhibiting liver gluconeogenesis & increasing insulin
sensitivity in other tissues.
- It reduces fasting plasma glucose, improves lipid profile, weight
neutral. Causes little or no hypoglycemia. Prevents
macrovascular and microvascular complications of diabetes’
-Contraindicated in: Organ Failure:renal failure, Liver failure, CHF,
Hypotension/Sepsis, Active Vitamin B12 Deficiency, alcoholism
-Adverse effects : GI disturbance, lactic acidosis, Vitamin B12
Deficiency (0.5%)
Starting dose:500 mg OD or BD, Max dose:2500 mg,
A1C reduction:1-2%
29. SULFONIYLUREAS: Insulin secretogogues
• Stimulate insulin secretion by interacting with ATP sensitive K
channel on beta cells.
• Most effective in recent onset type 2 DM, who have residual
endogenous insulin production.
• Reduces both fasting and postprandial glucose.
• First G:chlorpropamide,tolazamide, tolbutamide . have longer half
life, greater incidence of hypoglycemia and drug interactions. Rarely
used.
• Second G:glimeperide, glipizide, gliburide, gliclazide.
• S/E:Causes profound and persistent hypoglycemia and weight gain.
• Secreted in milk.
• C/I: renal and hepatic impairement.
• Dose: Glimepiride (1-8mg), Glipizide (5-40mg),Gliburide(1.25-20mg)
• HbA1c reduction: 1-2%
30. GLP-1 RECEPTOR AGONISTS
• GLP-1 induces insulin release from pancreatic
beta cells, inhibit glucagon release from alpha
cells, suppresses appetite.
• Exenatide and Liraglutide
• Lowers postprandial and fasting blood
glucose, HbA1C, and body weight.
• Liraglutide is C/I in pts with medullary ca of
thyroid and multiple endocrine neoplasia.
31. DPP-4 INHIBITORS
• Inhibits Dipeptidyl peptidase-4 enzyme and
prolonges endogenous GLP-1 action.
• Saxagliptan, vildagliptan and sitagliptan
• Do not cause hypoglycemia.
• Reduce dose in renal impairement.
• HbA1C reduction:0.5-0.8%
32. THIAZOLIDINEDIONE (PPAR-gamma
agonist)
• Pioglitazone: selective agonist for nuclear
peroxisome proliferator-activated receptor. It
enhances transcription of several insulin
responsive genes.
• Reduces insulin resistance.
• C/I:CHF ,liver ds
• HbA1C reduction:0.5-1.4%
33. ALPHA GLUCOSIDASE INHIBITOR
• Acarbose, voglibose, migitol
• Slows down and decreases digestion and
absorption of polysaccharide and sucrose.
• Use in prediabetes, reduces occurance of type
2 diabetes, HTN and cardiac ds.
• C/I:renal and liver failure, inflammatory bowel
ds, gastroparesis.
• HbA1C reduction:0.5-0.8%
34. SGLT-2 INHIBITORS
• SGLT-2 inhibition induces glycosuria and
lowers blood glucose level.
• Canagliflazone, empagliflazone ,
dapagliflazone
• Causes weight loss, reduces major
cardiovascular events and cardiovascular
mortality.
• S/E:urinary and genital tract infection,
electrolyte imbalance, increased frequency.