HND701: Pathophysiology of Diabetes - Complications of Diabetes Assessment 2

HND701: Pathophysiology of Diabetes
HND701
Complications of diabetes
ASSESSMENT 2
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HND701: Pathophysiology of Diabetes
Part 1 “Metabolic Memory”
1.1. Introduction
Metabolic memory is a phenomenon of diabetic vascular stress persisting in
diabetic patients following glucose normalization due to earlier glycemic conditions. In
organs such as the kidney, eyes, and heart, it appears that hyperglycemia is remembered
(Aschner & Ruiz, 2012). This is exhibited in patients who have constantly received
intensive therapy when contrasted with patients who have begun traditional treatment and
after that changed to intensive therapy. Epigenetics can regulate metabolic memory.
1.2. The Body
The write up on metabolic memory is based on the paper “Metabolic Memory
Theory and the Early Treatment of Hyperglycemia in Prevention of Diabetic
Complications” (Testa et al., 2017).
Some epidemiological and imminent studies have demonstrated that the initial control of
hyperglycemia can diminish the risk of diabetes microbial and macrovascular
complexities. A number of experimental evidences support the idea that the danger of the
intricacy of diabetes can be identified with oxidative pressure, non-enzymatic protein
glycation, epigenetic changes, and constant aggravation, which sets up the system for the
"metabolic memory" hypothesis (Jax, 2017).This hypothesis supports the requirement for a
versatile, and aggressive clinical perspective, with the point of normalization of metabolic
control at the earliest. The introduction of therapeutic agents that emerge may also be
valuable.
Hyperglycemia has significant helpful ramifications for the advancement of future
complexities.

HND701: Pathophysiology of Diabetes
It is mandatory for diabetic patients for an early aggressive treatment of this glucose
imbalance. This tight control should also include postprandial hyperglycemia (Gerich,
2010)
as it is accompanied by the formation of explicit reactive species (Oh, 2016) and AGEs, in
plasma as well as intracellular. Another methodology might be to endeavor to reduce the
formation of AGE (RAGE) and the formation of oxidative stress (Khullar, Al-Shudiefat,
Ludke, Binepal and Singal, 2010).
The ability to block AGE formation has already been demonstrated by various drugs. In
vitro, metformin and pioglitazone were shown to prevent the formation of AGE. AT-1
blockers and ACE inhibitors are compounds that control blood pressure, but they can
reduce the formation of AGEs. Telmisartan downregulates levels of RAGE mRNA and
then inhibits the formation of superoxide, while gliclazide has been shown to be useful in
removing "memory". Furthermore, GLP1 receptor agonists have been shown to reduce
inflammation, postprandial hyperlipidemia and coagulation, leading to a beneficial effect
on athero-thrombosis (Swislocki & Jialal, 2016).
Interestingly, weight loss has been shown among nutritional parameters to have a
significant effect on the plasma protein's inflammation profile. The meal sequence also can
be used in postprandial glucose control to increase the incretin secretion]. Finally, aldose
reductase inhibitors such as epalrestat have been shown to guard against peripheral diabetic
neuropathy by mitigating oxidative stress and inhibiting the polyol pathway (Yang et al.,
2016).
1.3. Conclusion

HND701: Pathophysiology of Diabetes
Hyperglycemia can do premature damage to cells in vasculature and target organs that can
in future create diabetes complications. This "metabolic memory" can occur
notwithstanding when glycaemia is effectively controlled. Many queries with respect to the
treatment of diabetes are still unanswered. Early aggressive treatment of hyperglycemia is
significant for this "metabolic memory".
Part 2 “Atherosclerosis”
2.1 Introduction
The process of atherosclerosis involves a gradual reduction of arteries that weaken the
supply of oxygen and tissue supplements (Cold, 2019). Blood flow decreases can lead to
ischemia, causing complications such as angina or irregular claudication. The rupture of
atherosclerotic plaques may also cause intense coagulation form and an unexpected blood
loss to the resulting tissue of the infarction. Finally, the progression of atherosclerosis can
be found in three general ways clinically: a coronary artery ailment, cerebrovascular
disorder and peripheral arterial ailment (Rafieian-Kopaei, Setorki, Doudi, Baradaran and
Nasri, 2014).
2.2 The Body
An activated interface between the circulatory system and the arterial wall is created by
endothelial cells that line veins. Its most obvious function is to give the fluid,
supplementation, gasses and waste between tissue and blood a semi-permeable limit.
Furthermore, endothelial cells monitor different procedures that are less obvious (Cold,
2019).
They have a type of surface which allows the blood's cell components to flow without
sticking to the liner unless a cell disturbance. Endothelial cells emit cytokines that trigger