Macrovascular Complication of Diabetes

Running head: MACROVASCULAR COMPLICATION OF DIABETES
Macrovascular Complication of Diabetes
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MACROVASCULAR COMPLICATION OF DIABETES
Diabetes Mellitus (DM) is a metabolic disorder. It is characterized by hyperglycemia
that generates due to disequilibrium in insulin secretion and/or insulin action. The
pathological hallmark of DM encompasses vasculature leading to microvascular and
macrovascular complications. The microvascular complications like nephropathy and
retinopathy accelerates the chance of developing macrovascular complications, which
promotes atherosclerosis and eventually leads to the development of cardiovascular disease,
peripheral vascular disease and stroke (Marieb & Hoehn, 2015). The following essay aims to
highlight the pathophysiology associated with macrovascular complications of diabetes
followed by assessment and diagnostic criteria. At the end, the essay will explore common
treatment and management principles underlying macrovascular complications of diabetes.
Macrovascular complications: pathophysiology
According to Chilelli, Burlina and Lapolla (2013), the main pathological mechanism
in macrovascular complications in DM mainly involves atherosclerosis. Atherosclerosis
results from chronic injury or inflammation of the wall of arteries present in the coronary or
peripheral vascular system. Inflammation the walls of the arteries cause oxidation of the
lipids from low-density-lipoprotein particles under the action of angiotensin II. The oxidized
lipid particles accumulate in the endothelial walls leading to narrowing (Bullock & Hales,
2016). The activation of the inflammatory pathway causes stimulation and proliferation of
macrophage and attraction of T-lymphocyte at the site of inflammation. The activated T-
lymphocyte induces proliferation of smooth muscle in the arterial walls and simultaneous
collagen accumulation leading to thickening of arteries. The arterial inflammation leads to
narrowing of the arterial walls throughout the body and thereby increasing the chance of
cardiovascular accident (Chilelli, Burlina & Lapolla, 2013).

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MACROVASCULAR COMPLICATION OF DIABETES
Chawla, Chawla and Jaggi (2016) highlighted the pathophysiology underlying the
inflammation in diabetes and subsequent development of macrovascular complications in
details. According to Chawla, Chawla and Jaggi (2016), hyperglycemia provokes monocyte
adhesion to the arterial cells. These monocyte adhserion triggers type 1 hypersensitivity
reaction, promoting the accumulation of the primary mediators of hypersentivity and thereby
causing thickening of the arteries. Increase blood glucose level activates matrix-degrading
enzyme metalloproteinase, which cause plaque rupture and arterial remodelling leading toe
thickening of the arteries. Diabetes also increases the secretion of the primary inflammatory
mediators like C-reactive protein, plasminogen activator inhibitor and interleukine-6 that
cause activation of macrophage and thereby leading to the development of inflammatory
reaction under the influence of protein kinase C (PKC) pathway.
Another underlying pathophysiology behind the development of the macrovascular
complications include increased rate of platelet adhesion and hypercoagulability (Zhang et
al., 2014). Impaired nitric oxide generation, free radical formation in the platelets and altered
calcium regulation promote platelet aggregation cause hypercoagulability. Increased levels of
plasminogen activator inhibitor type 1 impair fibrinolysis in patients with diabetes. The
combination of these cause increased level of platelet coagulability which in turn cause
vascular occlusion and cardiovascular events in type 2 diabetes (Zhang et al., 2014).
Chawla, Chawla and Jaggi (2016) stated that hyperglycemia and insulin resistance are
main reasons behind the development of macrovascular complications of diabetes.
Development of diabetes is inherently associated with hyperglycemia. However, insulin
resistance develops years before hyperglycemia and during the course of time becomes
clinically significant. Obesity plays an important role in the development of insulin resistance
(common among the people with type 2 diabetes). The release of free-fatty acids,

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MACROVASCULAR COMPLICATION OF DIABETES
inflammatory mediators and reactive oxygen species increases the chance of systemic
inflammation and thereby leading to the development of atherosclerosis.
Assessment and diagnostics
The study conducted by Donaghue et al. (2014) highlighted that assessment of
macrovascular complication of diabetes should start after the age of 10. The main screening
methods that are used to highlight the marcrovascular complications include testing the lipid
profile of the individual after every 5 years along with the annual tabulation of blood
pressure. Truong, Maahs and Daniels (2012) highlighted that for type 1 diabetes (T1D)
individuals, with no significant family history of early cardiovascular disease or individuals
who are over 12 years of age, should undergo proper screening of glycemic level after every
5 years. If T1D have family history of cardio-vascular disease then fasting lipid profile must
be used as screening tool for the detection of macrovascular complications. If lipid screening
is found to be abnormal, annual screening is recommended. For type 2 diabetes (T2D), lipid
profile must be done after every 2 years if lipid content of the blood is found within the
permissible range (Truong, Maahs & Daniels, 2012). Other hallmarks apart from blood lipid
concentration, which can be used to detect the tendency of developing macrovascular
complication, include microalbuminuria. Donaghue et al. (2014) stated that microalbuminuria
is confirmed via analysis of two or three samples for a period of three to six months.
Persistent microalbuminuria is found to predict the end stage of the renal failure, which in
turn increases the chance of developing macrovascular disease. Donaghue et al. (2014)
highlighted that loss of nocturnal dipping on round the clock blood pressure monitoring is
regarded as the early marker for the assessment diabetic renal disease which simultaneously
precedes towards microalbuminuria leading the renal hypertrophy and subsequent
development of macrovascular complications.