DIABETES
MELLITUS
Nhamier M. Jikiri, RN, MD, FPCP
Internal Medicine
INTRODUCTION – GLOBAL BURDEN
The International Diabetes Federation (IDF) has estimated
that 366 million individuals worldwide have diabetes in 2011;
and 552 million by the year 2030.
80% live in low- and middle-income countries.
The greatest number of patients are between 40 – 59 years
of age.
78,000 children develop type 1 diabetes every year.
IDF Atlas. The Global Burden5th Edition. 2012
INTRODUCTION – PHILIPPINES
The prevalence of type 2 diabetes mellitus is
7.2% and that of prediabetes (IFG or IGT) is
10.6%.
Total of 17.8% or 1 out of 5 Filipino adults
could potentially have diabetes or prediabetes
Limited data on type 1 diabetes mellitus
National Nutrion and Health Survey 2008
TOP 10 COUNTRIES WITH HIGHEST NUMBER
OF DM (20-79YR) 2011 AND 2030
IDF Atlas. The Global Burden5th Edition. 2012
WHAT IS DIABETES?
Diabetes is a life-long disease
marked by high levels of sugar
in the blood.
It
lasts a lifetime, but it can be
controlled.
DIABETES MELLITUS
Classification
classifiedon the basis of the pathogenic process
that leads to hyperglycemia
2 Broad types
Type 1 DM
complete or near-total insulin deficiency
Type 2 DM
heterogeneous group of disorders characterized by variable
degrees of insulin resistance, impaired insulin secretion, and
increased glucose production
INSULIN
Secretion
Glucose : key regulator
of insulin secretion
Plasma glucose >3.9
mmol/L or 70 mg/dL
stimulate insulin
synthesis
TYPE 1 DIABETES MELLITUS
The result of the interactions of genetic,
environmental, and immunologic factors that
lead to the destruction of pancreatic beta cells
and insulin deficiency
TYPE 1 DIABETES MELLITUS
Autoimmune destruction of beta cells
Most individuals with type 1 DM have evidence
of islet-directed immunity
Common environmental trigger: viral infection
TYPE 2 DIABETES MELLITUS
TRIUMVIRATE – MAJOR PATHOPHYSIOLOGY
DeFronzo R. Diabetes 1988
OMINOUS OCTATE
GLP-1 AND GIP: ROLE IN GLUCOSE
HOMEOSTASIS
Food ingestion
Glucose dependent
Release of Insulin Glucose
uptake by
active incretins (GLP-1 and GIP) peripheral tissue
Pancreas
GLP-1 and GIP
Beta cells Blood
GI tract
Alpha cells
glucose
DPP-4 Glucose
enzyme Glucose dependent production
by liver
Glucagon
Inactive Inactive (GLP-1)
GLP-1 GIP
Incretin hormones GLP-1 and GIP are released by the intestine throughout the day;
Incretin hormone levels increase in response to a meal
1. Kieffer TJ et al. Endocr Rev. 1999;20(6):876–913. 2. Drucker DJ. Diabetes Care. 2003;26(10):2929–2940. 3. Holst
JJ. Diabetes Metab Res Rev. 2002;18(6):430–441.
DIABETES MELLITUS
EXAMS AND TESTS:
Fasting Blood Glucose Level:
Higher than 126 mg/dL on two occasions.
Levels between 100 and 125 mg/dl are referred to as
impaired fasting glucose or pre-diabetes.
Random (non-fasting) Blood Glucose Level:
Higher than 200 mg/dL and accompanied by the classic
symptoms of increased thirst, urination, and fatigue.
Oral Glucose Tolerance Test:
Glucose level is higher than 200 mg/dL after 2 hours.
RISK FACTORS FOR DIABETES
A parent, brother, or sister with diabetes
Obesity
Age greater than 45 years
Some ethnic groups (African Americans, Native
Americans, Asians, Pacific Islanders, and Hispanic Americans)
Gestational Diabetes or Delivering a baby weighing
more than 9 pounds
High Blood Pressure
High Blood Levels of Triglycerides
High blood Cholesterol level
Not Getting Enough Exercise
AMERICAN DIABETES ASSOCIATION
Alladults over age 45 be screened
for diabetes at least every 3 years.
A person at high risk should be
screened more often.
SYMPTOMS OF DIABETES
Frequent urination
Excessive Thirst
Hunger
Fatigue
Weight Loss
Blurry Vision
Slow-healing
infections
Impotence in Men
Type 1 diabetes usually develop
symptoms over a short period of time,
and the condition is often diagnosed in
an emergency setting.
Type 2 diabetes develops slowly, some
people with high blood sugar
experience no symptoms at all.
COMPLICATIONS
Acute
Diabetic Ketoacidosis
Hyperglycemic hyperosmolar state
PRECIPITATING FACTORS
Most common for both DKA and HHS
Inadequate or inappropriate insulin therapy
Infections
Pancreatitis
MI
CVD
Drugs
COMPLICATIONS
Chronic
COMPLICATIONS
Chronic
TREATMENT
There is No Cure for Diabetes!
Treatment involves:
Medicines
Diet
Exercise
Maintaining an ideal body weight
and an active lifestyle may prevent
the onset of type 2 diabetes.
There is no way to prevent type 1
diabetes.
Medication Mechanism of Action Examples
Oral
Biguanides Decrease hepatic glucose production Metformin
a-glucosidase inhibitor Decrease GI glucose absorption Acarbose,
Dipeptidyl peptidase IV Prolong endogenous GLP-1 action Saxagliptin,
inhibitorsb Sitagliptin,
Vildagliptin
Insulin secretagogues: Increase insulin secretion Gliclazide,
Sulfonylureasb Glibenclamide,
Glimepiride
Thiazolidinedionesb Decrease Insulin resistance, Increase Rosiglitazone,
glucose utilization Pioglitazone
Parenteral
Insulin Increase Glucose utilization, Decrease
Hepatic glucose production, and other
anabolic actions
GLP-1 receptor Increase Insulin, decrease glucagon, Exenatide, liraglutide
agonistsb slow gastric emptying, satiety
GLYCEMIC TARGET
General Goal: HbA1c <7
FBS 72 - 126 mg/dl
2h PPG 90 – 180 mg/dl
Capillary Fasting 80 – 130mg/dl
PPBG < 180
GLYCEMIC TARGET
For: Newly diagnosed
Relatively young (age <60)
No complications
No risk factors for hypoglycaemia
General Goal: HbA1c <6.5
FBS < 110 mg/dl
2h PPG < 145 mg/dl
