Macrovascular Complications of Diabetes: Pathophysiology, Assessment, and Management

Running head: DIABETES
Diabetes
Name of the Student
Name of the University
Author Note

1
DIABETES
Introduction
Diabetes mellitus is a metabolic disorder which is characterised via increase in the
blood glucose level. The pathological hallmark of diabetes mellitus includes macrovascular
and microvascular complications (Chawla, Chawla & Jaggi, 2016). The following essay aims
to discuss the pathophysiology associated with the macrovascular complications followed by
assessment and proper diagnostic criteria for the disease condition and subsequent treatment
and management of the diseased condition.
Macrovascular complications of diabetes: Pathophysiology
The main pathological mechanism of macrovascular complications of diabetes
mellitus (DM) is the development of arthrosclerosis (Bullock & Hales, 2016). Increase in the
blood glucose level creates vasodilation of the blood vessels leading to the chronic injury to
the walls of the arteries. This arterial injury causes inflammation leading to an inflammation
in the walls of the coronary and peripheral vascular system and giving rise to atherosclerosis.
The inflammation in the walls of the tissues of the cardio-vascular system, especially the
walls of the arteries cause oxidation of the lipids which are present in the form of low-density
lipo-protein under the influence of angiotensin II. The lipids in its oxidized form accumulate
in the endothelial walls leading to the narrowing of the arteries further and creating
cardiovascular complications (Bullock & Hales, 2016). The activation of the inflammatory
pathways leads to the stimulation and proliferation of the macrophage and simultaneous
attraction of the T-lymphocyte at the site of inflammation. This activated T-lymphocyte
induces the proliferation of the smooth muscles present inside the arterial walls along with
simultaneous accumulation of collagen inside the arteries. The cumulative effect of these
cause thickening of the walls of the arteries and then narrowing of the arterial diameter which

2
DIABETES
increases the severity of the atherosclerosis and thereby causing macrovascular complications
of diabetes (Marieb & Hoehn, 2015).
According to Chawla, Chawla and Jaggi (2016), diabetes is characterised by
hyperglycemia that is increase in the blood glucose level concentration. Hyperglycemia
promotes the adhesion of the macrophages and other phagocytic cells inside the arterial cells.
The adhesion of monocytes triggers type 1 hypersensitivity reaction under the influence of
the primary hypersensitivity mediators. The deposition of the release of the primary
mediators of the type 1 hypersensitivity reactions narrows the overall diameter of the arteries
further and increases the risk of cardiovascular accidents. Increase in the blood glucose level
cause activation of the matrix-degrading enzyme metalloproteinase which cause rupture of
plaque and arterial remodelling leading thickening of the arteries. Diabetes also causes
increase in the secretion of primary inflammatory mediators and inflammatory cytokines like
C-reactive protein, plasminogen activator, interleukine-6 that leads to activation of the
macrophage extravasations. Macrophage extravasations cause activation of the protein-kinase
pathway and inflict inflammatory reaction and increases vulnerability of developing
macrovascular complications of diabetes (Hartemann et al., 2013).
Increase rate of platelet adhesion and increase in the tendency of hypercoagulability is
another pathophysiology underlying the development of macrovascular complications
(Domingueti et al., 2016). Increased rate of platelet adhesion cause secretion of reactive
oxygen species (ROS). ROS causes increase in the generation of the free radicals with altered
calcium regulation promoting platelet aggregation. Platelet adhesion cause impaired nitric
oxide generation with increase in the secretion of plasminogen activator inhibitor type 1. This
causes fibrinolyisis in diabetic patients. Fibrinolysis causes activation of platelet coagulability
leading to vascular occlusion followed by a series of cardiovascular events. Such conditions
are more common among the patients with type 2 diabetes mellitus (Domingueti et al., 2016).