Increased blood glucose levels Beta cells compensate by increasing insulin output Continued/repeated increase in blood glucose levels

Inability to sustain hyperinsulinemic state Further decline in insulin secretion Increased hepatic glucose production Beta cell exhaustion & failure Continuous increase in serum glucose levels

Diabetes Mellitus II

Increased blood viscosity

Impaired glucose utilization by insulin-sensitive tissues Areas of darkened skin Blurred vision Increased lipolysis and free fatty acid from adipocytes

Sluggish blood flow

Insulin resistance in adipose tissues

Impaired blood supply and tissue perfusion to organs

Activation of RAAS Liver produces angiotensinogen Renin is released by the kidneys Angiotensinogen is converted to Angiotensin I ACE is produced in the lungs Angiotensin I is converted to Angiotensin II

Increased lipid (VLDL, LDL, Triglyceride) synthesis in hepatocytes

Increased level of circulating free fatty acids and other fat cell products

Inflammatory state Inflammatory cells infiltrate adipose tissues Release of cytokines Increased release of matrix metalloproteinase Thinning of fibrous cap Decreased synthesis of collagen Weakening of plaque

Lipid storage (steatosis) in liver

Dyslipidemia (LDL, Trig, HDL)

Lipid accumulation within skeletal myocytes

Formation of atherosclerotic plaques

Ischemia Glutamate released Uptake of glutamate on glutamate receptors Cellular energy failure Ca/Na influx Mitochondrial damage Free radical formation

Release of leukotrine, histamine, prostaglandins and other inflammatory mediators Apoptosis Lipolysis

Proteolysis

Cell membrane and cytoskeletal breakdown

Arachidonic acid production

Weakness of arm Language disturbance Aphasia Ataxia Irritability

Potent Vasoconstriction

Adrenal glands convert Angiotensin II to Angiotensin III Aldosterone production is promoted

Aggregation of atherosclerotic plaque on blood vessels Decreased blood vessel diameter Excessive fat in systemic circulation

Rupture or erosion

Increased blood pressure

Constant increase in blood pressure

Prolonged & uncontrolled BP elevation

Hypertensive Cardiovascular Disease (HCVD)

Hypertension

Platelet Adhesion

Coagulation system is activated

Arteriosclerotic lesions form in the afferent arteriole Fine crackles

Arteriosclerotic lesions form in the efferent arteriole

Platelet Activation

Renal tubule dysfunction

Excessive fat (LDL, triglycerides, cholesterol) accumulate on the arteriosclerotic tubules

Platelet Aggregation

Atherosclerosis on renal tubules develop

Formation of hemostatic thrombi composed of platelets and fibrin

Further impairment of circulatory blood flow and organ perfusion

Dislodgement of thrombus Thrombus is released into the circulation (embolus) Increased myocardial O2 demand Embolus travels towards the cerebral blood vessels

Release of local vasoconstrictors from platelets (thromboxane A and serotonin)

Vasoconstriction Reduction in myocardial O2 supply Chest pain

Acute ischemia

Embolus obstructs cerebral blood vessel (arterial occlusion)

Unstable Angina

Limited O2supply to affected tissues

Inflammatory response

Nausea