Pathophysiology of diabetes and hypertension
Pathophysiology of Diabetes Mellitus:
Insulin Resistance
In type 2 diabetes mellitus, insulin resistance occurs primarily within the muscles, liver, and fat tissue, leading to decreased glucose uptake and utilization.
β-Cell Dysfunction
There is a relative impairment in insulin secretion by pancreatic β-cells, contributing to hyperglycemia.
Increased Hepatic Glucose Production
Due to insulin resistance, the liver inappropriately releases glucose into the blood, exacerbating hyperglycemia.
Lipotoxicity
Increased breakdown of lipids within fat cells contributes to insulin resistance and β-cell dysfunction.
Incretin Deficiency/Resistance
There is resistance to and lack of incretin effect, hormones that enhance insulin secretion in response to meals.
Hyperglucagonemia
Elevated glucagon levels in the blood contribute to increased hepatic glucose production.
Renal Sodium and Water Retention
Increased retention of salt and water by the kidneys can contribute to hypertension in diabetic patients.
Central Nervous System Dysregulation
Inappropriate regulation of metabolism by the central nervous system may play a role in the development of type 2 diabetes.
Genetic Factors
Genetic predisposition influences insulin secretion and action, affecting individual susceptibility to diabetes.
Inflammation
Chronic low-grade inflammation contributes to insulin resistance and β-cell dysfunction.
Pathophysiology of Hypertension:
Increased Peripheral Resistance
Structural narrowing of small arteries and arterioles leads to increased resistance to blood flow, elevating blood pressure.
Renin-Angiotensin-Aldosterone System (RAAS) Activation
Overactivity of the RAAS leads to vasoconstriction and sodium retention, contributing to hypertension.
Sympathetic Nervous System Overactivity
Enhanced sympathetic tone increases heart rate and vascular resistance, elevating blood pressure.
Endothelial Dysfunction
Impaired endothelium-derived nitric oxide production reduces vasodilation, promoting vasoconstriction.
Sodium Retention
Kidney dysfunction leads to impaired sodium excretion, increasing blood volume and pressure.
Genetic Factors
Genetic predisposition affects blood pressure regulation mechanisms, influencing hypertension risk.
Obesity
Excess adipose tissue elevates blood pressure through mechanisms like increased RAAS activity and sympathetic overactivity.
Insulin Resistance
Common in metabolic syndrome, it contributes to hypertension through sympathetic activation and sodium retention.
Inflammation:
Chronic low-grade inflammation contributes to endothelial dysfunction and vascular stiffness, promoting hypertension.
Vascular Remodeling
Structural changes in blood vessels, including increased wall thickness, reduce lumen diameter, raising vascular resistance.