This document summarizes the clinical features and morphology of diabetes mellitus. It discusses the types of diabetes, including type 1 which typically requires insulin and type 2 which is more common in older and obese individuals. The classic triad of symptoms for diabetes are polyuria, polydipsia, and polyphagia. Long-term complications result from damage to blood vessels and tissues from hyperglycemia, such as nephropathy, retinopathy, neuropathy, and accelerated atherosclerosis. Morphological changes include a reduction in pancreatic islet cells, amyloid deposition, thickening of basement membranes, and lesions in the kidneys like glomerular sclerosis.

1. CLINICAL FEATURES AND
MORPHOLOGY OF DIABETES
MELLITUS
-D.VIGHNESH (5TH SEM)

2. OVERVIEW
• Type 1 Diabetes:
Now known to occur at any age, in the initial years not much exogenous insulin
is required. After the b-cell destruction occurs (although prolonged), insulin
requirement increases drastically
• Type 2 Diabetes:
Typically seen in 40 years or older and obese adolescents. Diagnosis is made
generally after a routine blood testing.
• Classic triad of Diabetes:
Onset marked by Polyuria, Polyphagia and Polydipsia, when sever, Diabetic
Ketoacidosis

3. SEQUELAE OF METABOLIC
DERANGEMENTS
• Acute complications:
Most common precipitating factor:
failure to take insulin, giving rise to
increased action Of glucagon,
causing osmotic diuresis and
dehydration (DKA). Second most
common being activafion of
ketogenesis
• Chronic complication:
Damage to large and medium sized
muscular arteries by hypercalcemia

4. CHRONIC COMPLICATIONS
Formation of Advanced Glycated End products (AGE) are formed as a
result of nonenzymatic reactions between intracellular glucose derived
dicarbonyl precursors.
• Get accelerated in the presence of a specific receptor (RAGE) that is
expressed on inflammatory cells (macrophage and T cells), endothelium
and vascular smooth muscles
Detrimental effects include:
• Release of cytokines and growth factors
• Generation of ROS
• Increased procoagulant activity
• Enhanced proliferation of vascular smooth muscle cells

5. LONG TERM COMPLICATIONS
OF DIABETES (OVERVIEW)

6. MORPHOLOGY
• PANCREAS:
Reduction in number of islets
Leukocytic infiltration in islets
Reduction in islet cell mass (type 2 diabetes)
Amyloid deposition
• DIABETIC MACROVALVULAR DISEASE:
Endothelial dysfunction
Accelrated atherosclerosis (aorta)
Myocardial Infafction and gangrene of lower extremities

7. • HYALINE ARTERIOSCLEROSIS:
Associated with hypertension, seen in older patients
• DIABETIC MICROANGIOPATHY:
Diffused thickening of basement membrane
Capillaries are more leaky than normal
Underlies the development of:
• Nephropathy
• Retinopathy
• Neuropathy

8. • DIABETIC NEPHROPATHY: (Prime target)
Three lesions are encountered:
• Glomerular lesions
• Renal vascular lesions
• Pyelonephritis with necrotising papillitis
Most important lesions being
Membrane thickening, Diffuse mesangial
Sclerosis and Nodular Glomerulosclerosis

9. • DIABETIC OCULAR COMPLICATIONS:
Eye is profoundly affected in Diabtes Mellitus, leads to opacification of lens, causing
Cataract
Retinal Vasculopathy and Proliferative Diabetic retinopathy is seen, may lead to even
permanent blindness
• DIABETIC NEUROPATHY:
Present in 50% of patients and 80% of them have clinical
manifestations for more than 15 years.
Other than these, Diabetics are most susceptible to
• Infections of skin
• Tuberculosis
• Pneumonia
• Renal Vascular insufficiency
• Cerebrovascular accidents

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