Download 10-Endo DM

Dr. Hany Ahmed
Assistant Professor of Physiology (MD, PhD)
Al Maarefa Colleges (KSA) & Zagazig University (EGY)
Specialist of Diabetes, Metabolism and Obesity
Zagazig Obesity Management & Research Unit
At the end of this lecture, students should be able to:
• Define diabetes mellitus.
• Enumerate the types of diabetes mellitus.
• Describe type 1 diabetes mellitus.
• Describe type 2 diabetes mellitus.
• Compare type 1 to type 2 diabetes mellitus.
• Know insulin resistance and its results.
• Discuss the link between obesity and insulin resistance.
• Discuss Characteristic disturbances of diabetes mellitus.
• Know diagnosis of diabetes mellitus.
• Describe the complications of diabetes mellitus.
DIABETES MELLITUS
 The term diabetes mellitus describes a
metabolic disorder of multiple aetiology
characterized by chronic hyperglycaemia with
disturbances of carbohydrate, fat and protein
metabolism resulting from defects in insulin
secretion, insulin action, or both.
 The chronic hyperglycemia of diabetes is
associated with long-term damage, dysfunction,
and failure of different organs, especially the
eyes, kidneys, nerves, heart, and blood vessels.
Types of DIABETES MELLITUS
1- Secondary Diabetes: (↑ anti-insulin hormones)
• Cushing’s syndrome (Cortisol excess).
• Acromegaly (Growth hormone excess).
• Pheochromocytoma (Catecholamine excess).
• Glucagonoma (Glucagon).
2- Primary Diabetes:
• Type I diabetes
• Type II diabetes
• Gestational diabetes
Type I diabetes
10 % of cases of diabetes.
• Immune-mediated diabetes occurs in
childhood, but it may occur at older
age.
• Latent Autoimmune Diabetes in
Adults (LADA) is a form of
autoimmune type I diabetes.
• There is little or no insulin secretion,
as manifested by low or undetectable
levels of plasma C-peptide.
Type II diabetes
90 % of cases of diabetes.
• Age of onset from 35 years
upwards, but it may occur at
younger age.
•Maturity Onset Diabetes of Young
(MODY) is a form of type II that
occurs at age below 25 years.
• Normal or even increased insulin
secretion. Decrease sensitivity of
target cells to insulin i.e. insulin
resistance
Destruction of β -cells due to:
Insulin Resistance may be due to:
a) Auto immune antibodies against a) Abdominal obesity is a big risk
factor.
beta cells.
b) Physical inactivity.
b) Viruses (Coxsackie and Mumps)
c) Aging. d) Genetics.
against beta cells.
Insulin resistance
• A condition in which muscle, fat, and liver cells do
not respond properly to insulin and thus cannot
easily uptake glucose from the bloodstream.
• Over time, insulin resistance can lead to prediabetes and type 2 diabetes as the beta cells fail
to keep up with the body’s increased need for
insulin.
The major contributors to insulin resistance & type II DM
Diabesity
 The link between obesity and insulin resistance:
 Obesity, especially excess fat around the waist, is a
primary cause of insulin resistance.
 Belly fat plays a part in developing chronic, or longlasting, inflammation in the body that decreases insulin
sensitivity.
 Adipocytokines secreted by adipose tissue modulate
response of target tissue to insulin:
I.
Resistin (promotes insulin resistance), increases in
obesity .
II. Adiponectin (increases insulin sensitivity), decreases
in obesity.
• It occurs in about 2% – 5% of all pregnancies and may improve or disappear after
delivery.
• Gestational diabetes is fully treatable but requires careful medical supervision
throughout the pregnancy.
• About 20% – 50% of affected women develop type 2 diabetes later in life.
• Untreated gestational diabetes can damage the health of the fetus or mother.
Characteristic disturbances of diabetes
(Clinical results of insulin deficiency)
1) Hyperglycemia:
* Rise of fasting blood glucose ≥ 126 mg %.
* Rise of post prandial blood glucose ≥ 200 mg %.
2) Glucosuria:
* If blood glucose level rises above renal threshold (=180 mg %)
3) Lipid disturbances:
* lipolysis to supply fatty acids for gluconeogenesis & energy
production   free fatty acids  oxidation of fatty acids for
energy production  formation of ketone bodies 
Ketonaemia  ketoacidosis.
Characteristic disturbances of diabetes
4) Negative nitrogen balance:
•  Protein catabolism  loss of weight.
• Hypoprotienaemia  low resistance to infections.
5) Polyuria & Polydipsia.
6) Dehydration, Na+ & k+ Depletion.
7) Circulatory failure, coma & death if not treated.
Acute complications
(Diabetic coma)
1) Diabetic ketoacidosis
2) Hypoglycemic coma
(Vascular complications)
Advanced glycation end products(AGEs)
AGEs are the addition of a carbohydrate to a protein without the
involvement of an enzyme. The glycation process makes cells stiffer,
less pliable and more subject to damage and premature aging.
AGEs are prevalent in the diabetic vasculature and contribute to
the development of atherosclerosis.
AGEs have a range of pathological effects, such as:
1) Increased vascular permeability & arterial stiffness
2) Inhibition of vascular dilation by interfering with nitric oxide.
3) Oxidizing LDL.
4) Binding cells—including macrophage, endothelial,
and mesangial—to induce the secretion of a variety
of cytokines.
5) Enhanced oxidative stress.
Diagnosis and Classification of DM
Management of Diabetes Mellitus
Management of type 2 DM
• The major components of the treatment of
diabetes are:
A
• Diet and Exercise
B
• Oral hypoglycaemic
therapy
C
• Insulin Therapy
Diabetes Management Algorithm