Please describe the pathophysiology of type 2 diabetes mellitus and the pharmacological management that you would recommend for your client.
Your understanding will be demonstrated by demonstrating the connections between pathophysiology and clinical manifestations.
These questions will help you grade your assignment’s ‘coverage and accuracy of information’ sections.
You’ll need to create your client/person according to these criteria*.
Answer the following questions:
These physiological processes are crucial for blood glucose control
Insulin synthesis and release
Insulin binding to target tissue explains how they differ in your client/person in comparison to a healthy person who is not diabetic.
These are the consequences of long-term, poorly controlled hyperglycaemia
Renal disease – Explain why they might occur in your client/person.
These drugs can be used to treat type II diabetes mellitus.
Pick the one that’s most appropriate for you or your client.
Refer to the mechanism of action and discuss why your client/person can use it.
Answer both (a and (b). Insulin resistance may occur in someone with more abdominal adiposity.
This is explained by the pathophysiological reasons.
(b) Explain the reason HbA1c can be used as a long-term measure to control BGL. Also, explain how it will help in managing your client’s disease.
Insulin Synthesis and Release
The beta cells of the pancreas are responsible for the synthesis of insulin.
The insulin mRNA can also be translated into a single peptide by inserting it in the endoplasmic retinal, which creates proinsulin.
Fu, Gilbert, and Liu (2013) stated that proinsulin is mainly derived from exposure to specific endopeptidases which exercise C peptide.
This helps to produce mature insulin.
Insulin binding to the target tissues
Type 2 diabetes is caused by insulin resistance. This occurs because of cellular alternation. Cellular alternation appears at the hepatic level.
Post binding takes place in peripheral targeted tissues (Berry and al., 2013,).
Type 2 diabetes is characterized by post binding defects in peripheral tissues.
Retinopathy, caused by type 2 diabetes, is a condition that causes vision loss or impairment.
Mr. Brown is at risk of becoming blind due to type 2 diabetes.
It is important to treat type 2 diabetes.
Due to high levels of blood sugar, abnormal blood vessels can grow within the retina (Lovshin and Shah, 2017).
Mr. Brown is at greater risk for kidney disease, which can lead to kidney failure.
The regulation of blood glucose is affected by insulin deficiency.
The kidneys become damaged and there is a high risk of developing kidney failure (Coresh, et al. 2014).
To reduce the effects of diabetes mellitus, patients must be mindful about their weight, healthy eating habits, lifestyle and medications.
Insulin and Its Mechanism of Action
Insulin is one peptide hormone.
Insulin is produced in the beta cells of the pancreas. It regulates carbohydrate and fat metabolism.
Insulin activates GLUT4, which aids in glucose uptake in fat cells and muscle (Pernicova & Korbonits 2014).
The body’s insulin production decreases, and the glucose uptake levels drop. Type 2 diabetes symptoms are also seen.
Insulin contains the one peptide that guides the nascent polypeptide chains to endoplasmic retinalum.
When proinsulin is transported to the trans-Golgi network, it forms immature granules.
A. Pathophysiology of Insulin Resistance
Insulin resistance plays a significant role in the pathogenesis of type 2 diabetes mellitus and metabolic syndrome.
Insulin resistance is primarily manifested in skeletal muscle by a decrease in insulin stimulated glycogen synthes (Blazquez and al., 2014).
This is due to decreased glucose transport.
The human body can sustain red blood cells for between 8 and 12 weeks before they are replaced.
The glycated hemoglobin, which measures the average blood glucose, can be measured (Strack and al., 2014).
This has a long-term impact on blood glucose control.
The HbA1c biochemical marker is helpful in managing type 2 diabetes mellitus.
The STRA6 receptor is critical for insulin resistance induced by retinol-binding proteins, but not for vitamin A homeostasis within other tissues than the eye.
Journal of Biological Chemistry 288(34), 24539.
The pathophysiological consequences of insulin in the brain for states with type 2 diabetes, central insulin resistance, and Alzheimer’s disease: Insulin in your brain.
A decline in the estimated glomerular filter rate and the subsequent risk of end-stage kidney disease and death.
Fu, Z., R Gilbert E., and Liu, D. (2013).
Regulation of insulin synthesis, secretion, and pancreatic beta-cell dysfunction in diabetes.
Recent immigrants with type 2 Diabetes are not receiving adequate screening.
Journal of Diabetes and its Related Complications, 31(4): 664-668.
Metformin [mdash] mechanism of action and clinical implications.
Nature Reviews Endocrinology 10(3): 143-156
Analysis of 70,000 patient records from a clinical database to determine the impact of HbA1c measurements on hospital readmissions.
BioMed Research International, 2014.