Predispposing factors: Age: 63 Hereditary

Precipitating factors: Diet Lifestyle Hypertension Diabetes

High glucose in blood

Impaired fnxnign of insulin glucose by adipokines

Over Compensatation of pancreas

Enters blood by glucokinase

Adipon ectin

Leptin

Restin

Exhaustion

Form atp

Negative Feedback Inhibit insulin metabolism Decrease insulin production

Close K channel

Impairment

Insulin Resistance

Type 2 diabetes millitus

Intracellular hypoglycemia

Extracellular hyperglycemia

Glycolysis and Gluconeogenesis

Shunting of glucose polyol pathway or the sorbitol aldose reductase

Glycoprotein cell wall deposit

Sorbitol to fructose

Plaque deposition in lumen of blood

vessels

Accumulation of sorbitol in the basement membrane of the cells and between that uses sorbitol pathway

Accelerated atherosclerosis

Basement membrane thickened

Atherosclerotic Aorta

Cell receives inadequate oxygen and nutrition and retained waste products

Narrowing of blood vessels

Ischemia in the kidney

Decrease blood flow circulation

Tissue injury

Activation of RAAS

ACE

Aldosterone
Diabetic nephropathy

Vasoconstrictio n

Water retention

Increased BP

Hypertension

Thickening hyalinization of vessel walls Narrowing of the arteriols Vascular structure thicken

Decrease perfussion

Damage to nephron

Hypertensive Nephrosclerosis

Tubular damage

Tubular damage

glumerosclerosis

GFR

proteinuria

Renal blood

Stage I DIMINISHED RENAL RESERVE GFR 50%

Increase permeability of glomerular capillaries

Increase NA macula densa

albuminuria

Increase intrarenal tension

hypoalbumininemia Decrease renal blood flow Decrease plasma oncotic pressure Decrease plasma volume

Decrease glomerular filtration rate

Further loss of nephron functioning

Accumulation of solutes

Stage II RENAL INSUFFICIENCY GFR 20-50%

BUN, Creatinine levels begin to rise

Remaining nephrons undergo changes to compensate for those damaged nephrons

Filtration of more concentrated blood by the remaining nephrons

Hypertrophy of nephrons

Intolerance and exhaustion of the remaining nephrons

Further damage of the nephrons

80-90% damage

Stage III RENAL FAILURE GFR 10-20%

Impaired kidney function and Uremia - Reduction in renal capillaries -Scarring of Glomeruli - Atrophy & Fibrosis of Renal tubules > 90 % of kidney damage

Malfunction of RAAS

Nitrogenous wastes impairs platelets

Decreased Erythropoietin Production

Toxins impair immune system

Toxins affect CNS

Na & H2O retention Continuous decline in renal function

Decreased Urine Output Oliguria

Increased blood pressure

Edema

Decreased Immune system

Pulmonary Edema, Peripheral Edema

Risk for superinfection

Hypertension

Bleeding Tendencies

Uremic Encephalopathy

ANEMIA
Stage IV END-STAGE RENAL DISEASE (ESRD) GFR <10% Sepsis -changes in mentation/ psychiatric symptoms -irritability -fatigue -insomnia

Nonspecific injury to Arterial wall

Increase work load

Continuous Multisystem Affectation

Desquamation of endothelial lining Heart pumps forcefully Increased Permeability Lipids and platelets assimilate into the area Oxidized LDL attracts monocytes and the macrophages to the site Plaques begin to form from cells which imbed into the endothelium Enlargement of the muscle
Multiple Organ Failure

Left Ventricular Hypertrophy

DEATH

Lipids are engulfed by the cells and smooth muscle cellls develop

CORONARY ARTERY DISEASE(formation of atheromas)

Decreased Coronary tissue perfusion

Coronary Ischemia

Anaerobic Metabolism PAIN (Angina Pectoris/ Acute MI)

Production of Lactic Acid