DIABETES MELLITUS

• Department of Physiology
• Kiran Medical college, Surat
DIABETES MELLITUS

▪ Diabetes mellitus refers to a clinical syndrome of hyperglycaemia occurring due

to deficiency of insulin.

▪ Diabetes mellitus comprises a group of common metabolic disorders that

share the phenotype of hyperglycemias.
 DIABETES MELLITUS- HISTORY

▪ Term "diabetes" was first coined by

Araetus of Cappodocia . Later, the word
mellitus was added by Thomas Willis
(Britain) in 1675.

▪ 5th and 6th century AD: Sushruta and

Charaka (India) , who had termed it as
‘Madhu-meha
DIABETES MELLITUS

▪ 2019 ≃ 463 million adults (20-79 years) were living with diabetes;
▪ by 2045 ≃ 700 million

▪ India had an estimated 31 million diabetics in 2000

▪ estimated to grow by over 100% to 79 million by 2030
▪ 77 million cases of diabetes in India in 2019
▪ >100 million people in India may have type 2 diabetes by 2030
 DIABETES MELLITUS- CLASSIFICATION

❖Type 1 Diabetes
❖Type 2 Diabetes
❖Other specific types of Diabetes
❖Gestational Diabetes Mellitus
 TYPE-1 DIABETES MELLITUS

▪ Autoimmune destruction of the pancreatic beta cells and insulin deficiency

▪ Insulin depended diabetes mellitus (IDDM)

▪ Usually develops before the age of 20 - Juvenile diabetes

▪ Cause: genetic, infectious or environmental factors
▪ Nature of onset: Rapid
 TYPE-2 DIABETES MELLITUS:

▪ Insulin resistance: Impaired ability of the target cells to respond to insulin

▪ Non-Insulin depended diabetes mellitus (NIDDM)
▪ Insulin: normal or more
▪ precedes an insulin secretory defect
▪ usually develops after age 40
▪ Cause: Overweight, sedentary life, feeding habit, chronic stress,PCOS
 TYPE-2 DIABETES MELLITUS

Mechanism of Insulin Resistance

▪ Obesity: hyperlipidemia, hyperinsulinemia, atherosclerosis (Metabolic syndrome)
▪ Adipokines: group of hormones secreted by fat cells
-Leptin, Adiponectin, Resistin, TNF-α
▪ Defect in Signalling: 2nd messenger system
 OTHER SPECIFIC TYPES OF DM:

▪ Maturity Onset Diabetes of the Young (MODY)

• MODY 1 to MODY 11
• MODY 3 : mutation of HNF-1
• MODY 2 : mutation of glucokinase gene
 OTHER SPECIFIC TYPES OF DM:

▪ Pancreatic disease: pancreatitis, fibrosis, neoplasia

▪ Excess endogenous production:
▪ Acromegaly
▪ Cushing syndrome
▪ Pheochromocytoma
▪ Throtoxicosis
▪ Glucagonoma
▪ Viral infection: Rubella, mumps
▪ Drug induced: corticosteroids, diuretics
▪ Genetic syndromes: Turner, Klinefelter, Down
DM - CLINICAL PRESENTATION

P3
▪ Polyphagia
▪ Polyuria
▪ Polydipsia
DM - CLINICAL PRESENTATION

POLYPHAGIA POLYURIA POLYDIPSIA

 Glucagon Diabetic ketoacidosis
Insulin

Hyperosmolar Hyperglycemic State

(HHS)
 Hyperosmolar Hyperglycemic State
(HHS)

H2 O

H2 O

H2 O
H2O Dehydration
H2 O

H2 O

Increased Urination Dehydration of body

DM - CLINICAL PRESENTATION

Weight Loss Lethargy Blurry vision

Adipose
tissue Lipolysis

Weight loss

Muscle Proteolysis
DM - CLINICAL PRESENTATION

Smell of Acetone Nausea, Vomiting, Abd. pain

Adipose
tissue Lipolysis
Fat
⇩
Fatty acids

Ketone bodies
Acetoacetic acid
B- Hydroxybutyric acid

Ketoacidosis
DM - CLINICAL PRESENTATION

Slow Healing of Wound

DM - CLINICAL PRESENTATION

Vaginal thrush
DM - CLINICAL PRESENTATION

Kussmaul breathing
DM - CLINICAL PRESENTATION

COMA
 DIABETES MELLITUS - COMPLICATIONS

• Diabetic ketoacidosis
• Hyperglycemic Hyperosmolar state
• Hypoglycemia
DIABETES MELLITUS - COMPLICATIONS

Diabetic retinopathy
DIABETES MELLITUS - COMPLICATIONS

Diabetic Neuropathy Diabetic Nephropathy

DIABETES MELLITUS - COMPLICATIONS

Diabetic foot
DIABETES MELLITUS - COMPLICATIONS

Ischemic heart disease

DIABETES MELLITUS - COMPLICATIONS

Stroke
 CLINICAL FEATURES - DIABETES MELLITUS

1. Hyperglycaemia (elevation of blood glucose concentration):- it may lead to-

a) Glycosuria- excretion of glucose in the urine.
b) Polyurea – passage of large amount of urine due to osmotic diuresis.
c) Loss of electrolytes- due to osmotic diuresis.
d) Cellular dehydration- high glucose concentration will increase the
osmotic pressure of extracellular fluid.
e) Polydipsia- excessive drinking of water due to activation of
thirst mechanism by cellular dehydration.
f) Increased caloric loss- due to loss of glucose in urine.
g) Polyphagia- excessive eating due to stimulation of hunger
centre caused by deficient utilization of glucose, and
increased caloric loss also results in compensatory
polyphagia.
h) Loss of body weight:- due to caloric loss & fat & proteins
are being utilized for energy production.
i) Impaired phagocytic function- insulin is essential for
WBC to utilize the glucose. In diabetes due to deficiency of
insulin phagocytic function of WBC will be impaired.
that’s why diabetics are more prone to infections.
j) Non ketotic hyperosmolar coma- osmolarity of blood
goes on increasing with the increasing blood sugar levels.
Such a high osmolarity may cause dehydration in the CNS,
leading to impairment of cerebral functions, the condition is
k/a Non ketotic hyperosmolar coma
k) Glycosylation of proteins- glycosylation refers to addition of
sugar in the structure of proteins.
levels of Glycosylated haemoglobin is used to determine the
long term control of blood sugar in diabetics.
2. Ketosis & Hypertriglyceridaemia:-
• Due to insulin deficiency, utilization of glucose is poor, the
body turns to fats for energy production.
• As a result of lipolysis plasma level of free fatty acids,
triglycerides & ketone bodies will increased.
a) Cellular dehydration- increased ketone bodies in blood will
increase its osmolarity.
b) Ketoacidosis- ketone bodies are strong acids, so ketosis will lead
to acidosis. It will develop rapidly in IDDM due to absolute
deficiency of insulin.
• Features of Ketoacidosis:-
• Rapid & deep respiration k/a kussmaul’s breathing.
• Acetone smell in breath.
• Urine become highly acidic.
• Coma & death due to acidosis & dehydration.
3. Protein catabolism:- it will leads to protein depletion in
the body & muscle wasting.
• Complications of diabetes mellitus:-
i. Predisposition to infections
ii. Acute complications include ketotic coma & nonketotic
hyperosmolar coma.
iii. Chronic complications include-
• Atherosclerosis- deposition of lipids underneath
the tunica intima of blood vessels.
• Microangiopathy- vascular lesion in which the capillary
basement membrane is thicker, probably due to structural
changes caused in tissue proteins by their glycosylation. It may
lead to-
✓Diabetic retinopathy
✓Diabetic nephropathy
✓Diabetic neuropathy.
LABORATORY STUDIES

• Glucose Tolerance Test

• Fasting Blood glucose
• HbA1c
• Urinalysis
• Insulin or C-peptide level
LABORATORY STUDIES

• Glucose Tolerance Test (GTT)

LABORATORY STUDIES
LABORATORY STUDIES

Urinalysis

▪Glycosuria
LABORATORY STUDIES

Urinalysis
▪ pH < 5.5

▪ specific gravity : 1.045 to 1.050

LABORATORY STUDIES

Urinalysis

▪ Ketone bodies: Present

LABORATORY STUDIES

• Insulin assay
• C-Peptide (Blood)
TREATMENT

Lifestyle modification
• Physical exercise • Diabetic diet
• Weight loss
TREATMENT

Anti-diabetic medication:
• Biguanides: Metformin
• Thiazolidinedione: Pioglitazone
• Sulfonylureas: Glipizide, glimepiride
• Meglitinides
• Insulin analog
TREATMENT

Drugs for high cholesterol:

❖ Statins
▪ Atorvastatin
▪ Fluvastatin
▪ Rosuvastatin
TREATMENT

Antihypertensive drug
• Thiazide diuretics
• Calcium channel blockers
• ACE inhibitors
• Beta blockers
TREATMENT

Surgery
• Weight loss surgery
• Pancreas transplant