.

4. DIABETES MELLITUS
Metabolic disorder characterized by
hyperglycemia
Resulting from lack of insulin, lack of insulin
effect, or both, abnormalities in carbohydrate,
fat and protein metabolism.
Results in chronic complications including
microvascular, macrovascular, and neuropathic
disorders .
Diabetic mellitus are of two type Primary DM
and Secondary DM.

5. Classification:
I. Primary diabetes mellitus:
• Type 1 absolute insulin insufficiency
• Type 2 insulin resistance
• Gestational diabetes which emerges during pregnancy.
• Potential diabetes mellitus normal GTT but with a family
history of DM
• Latent diabetes mellitus, show diabetic type of GTT curve
without any elevation of blood glucose level.
• Asymptomatic diabetes mellitus
II. Secondary diabetes mellitus: That has a definite cause

6. ETIOLOGY:
1. Heredity
2. Environmental (infection, diet, toxins, stress)
3. Life-style changes in genetically susceptible persons

7. PATHOPHYSIOLOGY:
Type 1 DM
• Autoimmune disorder developing in childhood or early
adulthood.
• Results from autoimmune destruction of the β cells
• Markers include islet cell antibodies, antibodies to glutamic acid
decarboxylase, and antibodies to insulin.
• Rapid rate of β-cell destruction with ketoacidosis is more in
youngsters, in adults ketoacidosis is prevented by sufficient
insulin secretion for many years, often referred to as
(LADA(latent autoimmune diabetes in adults)).
Cont....

8. •In persons genetically susceptible to typeI DM triggering
event,
possibly a viral infection
↓
Production of auto antibodies against the beta cells
↓
Destruction of the beta cells
↓
Decline in and ultimate lack of insulin secretion.
• Insulin deficiency leads to hyperglycemia, enhanced
lipolysis and protein catabolism. These characteristics
occur when more than 90% of the beta cells have been
destroyed.

10. 1. Process of beta cell destruction occurs slowly;
hyperglycemia occurs when 80 – 90% is destroyed;
often trigger stressor event (e. g. illness)
2. Hyperglycemia leads to
a.Polyuria (hyperglycemia acts as osmotic
diuretic)
b. Glycosuria (renal threshold for glucose: 180
mg/dL)
c.Polydipsia (thirst from dehydration from
polyuria)
d.Polyphagia (hunger and eats more since cell
cannot utilize glucose)
e.Weight loss (body breaking down fat and
protein to restore energy source
f.Malaise and fatigue (from decrease in energy)
g.Blurred vision (swelling of lenses from
osmotic effects)
CLINICAL MANIFESTATIONS

11. Type 2 diabetes mellitus :
• Impaired insulin production, inappropriate hepatic
glucose production, or peripheral insulin receptor
insensitivity.
• Genetic factors are significant, and onset is accelerated by
obesity and a sedentary lifestyle.
• Stress can be a pivotal factor.
• “insulin resistance syndrome” or the “metabolic
syndrome.
• Patients with type 2 diabetes are at increased risk of
developing macrovascular complications

12. Type 2 diabetes mellitus :

13. Gestational diabetes
• Placental hormones counteract insulin, causing insulin
resistance.
• Gestational diabetes mellitus is a significant risk factor for
the future occurrence of type 2 diabetes mellitus.
Secondary diabetes mellitus:
• It is a minor type of diabetes mellitus and have a definite
cause of hyperglycemia.
• Damage to pancreas, pancreatic disorder, role of insulin
antagonist, inhibition of insulin secretion are some of the
common cause of secondary type of diabetic mellitus

14. Clinical significance:
• Polyuria
• Polydipsia
• Fatigue
• Weight loss
• Blurred vision
• UTI
Macrovasular disease
• Cardiovascular disease: CHF, MI, stroke, hypertension
• PVD
Microvascular:
• Retinopathy
• Nephropathy
• Neuropathy
Macrovasular & microvascular disease
• Diabetic foot disease

15. General Management Of Diabetes
Check your risk of diabetes
Manage your weight
Exercise regularly
Eat a balanced, healthy diet
Limit takeaway and processed foods
Limit your alcohol intake
Quit smoking
Control your blood pressure
Reduce your risk of cardiovascular disease
See your doctor for regular