Diabetes Mellitus:

Etiology predisposing factors

- Genetic, autoimmune response, viruses -environmental factors, diet, age, obesity, lifestyle

IDDM (type I) NIDDM (type II)

Individual both exposed to etiology and PF impaired insulin secretion

Autoimmune response to Beta cells diminished intracellular reaction

Damaged beta cells = decrease insulin insulin less effective to stimulate glucose uptake
by the tissue

Unchecked glucose Glucose from food cannot be stored in Inability of glucose to cross cellular membrane to
production in the liver the liver be use for energy

Increase glucose in the blood stream = hyperglycemia Stimulation of hunger center due to
less glucose. = polyphagia
Increase blood viscosity leading to arthrosclerosis of the
vessels Fat breakdown for energy = wasting of
lean body mass leading to wt. loss
EYES HEART

Damage to the decrease blood supply = base Fat metabolism in the liver = ketone formation
membrane of the retina ISCHEMIA and accumulation in the blood leading to
Diabetic Ketoacidosis
Decrease blood supply
Respiratory system compensates to metabolic acidosis = kausmaull’s
= DIABETIC RETINOPHATY BLINDNESS
breathing and acetone breathe
 Kidneys cannot reabsorb all the filtered glucose in the
blood
Glycoprotein cell wall deposits
Increase osmotic pressure = execration of large
amount of body fluids leading to POLYURIA and
GLYCOSURIA

Dehydration occurs

Hypotension leading to HYPOVOLEMIA

Small vessel disease DIABETIC NEPHROPATHY

If disease complicates, it would lead to RENAL

DIABETIC NEUROPATHY SHUTDOWN leading to END STAGE RENAL
FAILURE
-Symmetrical loss of sensation
-Numbness and tingling of extremities
-Wasting of intrinsic muscles
 Diabetes mellitus

Destruction of BETA CELLS of the pancreas

Failure to produce insulin Excess glucagon production

Elevated blood glucose Production of glucose from fat and protein

stores
Increased osmolarity due to
glucose leading to polydipsia, Wasting of lean body mass
polyuria, polyphagia leading to acidosis, ketone
Chronic elevation of blood formation, weight loss and
glucose fatigue

Glycoprotein cell wall deposits

Diabetic neuropathy Small vessel disease Accelerated atherosclerosis Impaired immune function

-symmetrical loss of - diabetic nephropathy -hypertension

protective sensation = end stage renal failure -increase LDH levels - infection
-numbness and tingling of the - diabetic renopathy -coronary artery disease - delayed wound
extremities = loss of vision healing
-wasting of intrinsic muscles
-charcol changes in joints