Discuss the pathophysiology as well as pharmacological management of type-2 diabetes mellitus clients.

You are asked to demonstrate your understanding of the relationship between pathophysiology, clinical manifestations, pharmacological management and client’s disease.

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These questions will be used as a guideline for the assessment of the ‘coverage/accuracy of information’ and coverage of subject matter’ sections of your assignment.

You will need to create a client/person for yourself according to these criteria*.

These questions will require you to answer:

Question 1

The following physiological processes can be used to control blood glucose:

Insulin synthesis & release

Insulin binding is a way to explain the differences between your client and a healthy, non-diabetic individual.

Question 2

Here are some possible consequences of hyperglycaemia that is not controlled long term:Retinopathy

Renal disease. Explain why they may happen in your client/person.

Question 3

The following drugs can be used for the treatment of type II Diabetes Mellitus:



You can choose the best one for your client/person.

You can discuss with your client/person why they should use it by referring back to its mechanism.

Question 4

Answer both questions (a- and (b). (a.) Insulin resistance is possible in people with higher abdominal adiposity.

Explain the pathophysiological reason for this.

(b.) Explain why HbA1c may be used to monitor long-term BGL levels and how it can help manage your client’s or person’s condition.

Answer to Question: BIOH12012 Pathophysiology And Pharmacology

Question 1

Insulin Synthesis & Release

The beta cells in the pancreas have a large amount of insulin synthesis.

The insulin-mRNA can be translated to a single peptide through insertion into the endoplasmicreticulum. This generates proinsulin.

Fu, Gilbert and Liu (2013) said that the main ingredient of proinsulin is exposure to C-peptide endopeptidases.

This allows for the production of mature insulin.

Insulin Binding to Target Tissues

Type 2 diabetes results in insulin resistance due to cellular alternation. This is at the level of the hepatic glucose.

The peripheral targeted tissues are affected by the process of post binding (Berry et. al., 2013).

Post binding defects are the primary cause of type 2 diabetic complications.

Question 2Retinopathy

Retinopathy refers to a disease that occurs due to type 2 diabetes. It causes vision loss and/or impairment.

Mr. Brown runs the risk of being blinded by type 2 diabetes.

Type 2 diabetes is therefore necessary to be treated.

A high level of sugar causes abnormal blood vessels to form inside the retina. (Lovshin Shah, 2017).Renal Disease

Mr. Brown is at higher risk of developing renal disease. This can lead to kidney damage.

Because insulin isn’t produced in sufficient amounts, regulation of blood sugar is hampered.

In this case, the kidneys can become affected, and high-risk cases of kidney failure occur (Coresh et. al., 2014.

The patient must be careful about weight, healthy eating and lifestyle to lessen the effects of diabetes.

Question 3

Insulin and its mechanism of action

Insulin is a peptidehormone.

It is made in the beta cell of the pancreas.

Insulin activates GLUT4, a hormone that helps glucose uptake in the fat cells (Pernicova & Korbonits (2014)).

Insulin production in the body decreases, which causes a drop in glucose uptake. This is when type 2 diabetes symptoms appear.

The insulin contains the single protein that controls the development of the polypeptide chain from endoplasmicreticulum.

The transportation of proinsulin across the trans-Golgi networks causes the formation immaturegranules.

Question 4

A. Pathophysiology Of Insulin Resistance

Insulin resistance is a key factor in type 2 diabetes mellitus pathogenesis and metabolic syndrome.

The main manifestation of insulin resistance in skeletal muscle is the decrease in insulin stimulated glucose synthesis (Blazquez und al., 2014.).

This is the result of decreased glucose transport.B.

Measurement of HbA1c

Red blood cells can survive in the human body for between 8 and 12 week before being renewed.

It is therefore possible to measure the glycated blood hemoglobin. This reflects the average blood sugar (Strack, 2014).

This will have a long-term effect in blood glucose control.

HbA1c is a biochemical marker that helps with type 2 diabetes management.

Refer toBerry, D. C., Jacobs, H., Marwarha, G., Gely-Pernot, A., O’Byrne, S. M., DeSantis, D., … & Croniger, C. M. (2013).

STRA6 is required for the maintenance of vitamin A homeostasis in other tissues than the eyes, but not for retinol bind protein-induced insulin resistant insulin resistance.

Journal of Biological Chemistry. 288 (34), 24528-24539.Blazquez, E., Velazquez, E., Hurtado-Carneiro, V., & Ruiz-Albusac, J. M. (2014).

The brain’s insulin: the pathophysiological implications of central insulin resistance and type 2 diabetes in states. Frontiers in endocrinology, 5, 161.Coresh, J., Turin, T. C., Matsushita, K., Sang, Y., Ballew, S. H., Appel, L. J., … & Green, J. A. (2014).

Falling estimated glomerular filtration rates and increased risk of end-stage kidney disease and death. Jama, 311(24), 2518-2531.

Fu, Z.R Gilbert E., & Liu D. (2013).

Regulation of insulin synthesis and secretion as well pancreatic Beta cell dysfunction in diabetes. Current diabetes reviews, 9(1), 25-53.Lovshin, J. A., & Shah, B. R. (2017).

A population-based study reveals inadequacies in screening for retinopathy in recent immigrants with type 2.

Journal of Diabetes, 31(4), 664-668.Pernicova, I., & Korbonits, M. (2014).

Metformin [mdash] action and clinical implications for diabetes, cancer.

Nature Reviews Endocrinology (10(3)), 143-156.Strack, B., DeShazo, J. P., Gennings, C., Olmo, J. L., Ventura, S., Cios, K. J., & Clore, J. N. (2014).

An analysis of 70,000 patient records in a clinical database reveals the impact of HbA1c on hospital readmissions.

BioMed research International, 2014.

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