Module 2 Assignment: Type 1 Diabetes Mellitus and Immune Disorders

This assignment explores immune system disorders, specifically focusing on Type 1 Diabetes Mellitus as an autoimmune disease. It delves into the pathophysiology of the disease, explaining how the autoimmune response destroys the beta cells of the pancreas, leading to decreased insulin production and subsequent glucose dysregulation. The assignment also details the treatment modalities available, including various types of insulin and the importance of a multidisciplinary approach to manage the disease and its complications. Furthermore, it includes an interview with a patient who has lived with Type 1 Diabetes for many years, discussing the impact of the disease on their life and the challenges they face. The assignment concludes by emphasizing the significance of understanding immune system dysregulation and its impact on human health, highlighting the need for lifelong management of Type 1 Diabetes and the importance of early detection and appropriate treatment to prevent complications such as retinopathy. The assignment also highlights the importance of evidence-based practice in the management of type 1 diabetes.

Running head: MOD 2 ASSIGNMENT 1
Module 2 Assignment: Immune System Disorders
Your Name
Rasmussen College
NUR2063: Essentials of Pathophysiology
Instructor Desautels
Month Day, 2020

MOD 2 ASSIGNMENT 2
Module 2 Assignment: Immune System Disorders
Immune system disorders occur due to a dysregulation in the immune system resulting in
an abnormal immune response. There are several diseases that can result from this dysregulation
such as allergies and autoimmune diseases. Autoimmune diseases such as type 1 diabetes
mellitus and systemic lupus erythematosus result from the immune system responding against its
own antigen or antigens. The autoimmune disease then occurs when the autoimmune response
leads to organ or tissue damage and the physiological function of the organ is disturbed. There is
certain criterion that has to be fulfilled to prove that the autoimmune disease resulted from an
immune response. Criteria such as prove that auto reactive T cells or autoantibodies with
specificity for the affected organ are found reliably in the disease. This essay will discuss type 1
diabetes mellitus as an autoimmune disease and explain its pathophysiology, its treatment and
expected outcomes (Mosaic of Autoimmunity, 2018).
Pathophysiology of type 1 Diabetes Mellitus
Type 1 diabetes mellitus results from an autoimmune response that destroys the beta cells
of the pancreas leading to decreased production of insulin. Type 1 diabetes mellitus commonly
occurs in the age below 14 years and less commonly above this age and therefore it was
commonly referred as Juvenile diabetes. Due to destruction of the beta cells there are
consequently abnormally low levels of insulin and high levels of glucose in the blood (Paschou
et al. 2018). Insulin produced by these cells regulates the levels of glucose in blood by pumping
glucose into cells. Cytotoxic T lymphocytes infiltrate and cause macrophage activation in the
endocrine pancreas. Consecutively there is delayed type hypersensitivity that results into release
of cytokine and antibody release. Lytic enzymes and the released cytokines from the activated
macrophages cause destruction of beta cells of the pancreas. Beta cell specific antibodies can

MOD 2 ASSIGNMENT 3
mediate beta cell destruction either through antibody mediated compliment lysis or antibody
dependent cellular cytotoxicity. There is absolute insulin deficiency and therefore glucose
production by the liver is unopposed (Burrack, Martinov & Fife, 2017). This type of diabetes is
insulin dependent and therefore patients with this disease have to take insulin throughout their
life either by using insulin pumps or injections. The classic symptoms that a person with type
1diabetes mellitus would present with are polyuria, polydipsia, and polyphagia and unexplained
weight loss. Polyuria results from osmotic fluid loss because the maximum reabsorptive capacity
of the kidney tubules is exceeded leading to loss of glucose in urine. This phenomenon is known
as glycosuria and polydipsia occurs to replace the excess lost fluid and maintain fluid balance.
The person with type 1 diabetes mellitus loses weight because the body burning muscles and the
adipose tissue to counter the glucose insufficiency in the cells. Diabetic ketoacidosis,
retinopathy, diabetic foot and diabetic foot are some of the main complications associated with
type 1 diabetes mellitus (Jameson & Groot, 2015).
Treatment of type 1 Diabetes Mellitus
There are several treatment modalities that are available for treatment of type 1 diabetes
mellitus as it is a lifelong treatment that requires a multidisciplinary approach. A
multidisciplinary approach is required because there are several complications that can arise
from the disease and there different specialists such as ophthalmologists, renal physicians
dietitians are needed in the management of type 1 diabetes mellitus patients. This patient use
insulin for life and many of them two or more injections with dose adjustments made according
to the blood glucose levels (Donner & Sarkar, 2019). Treating a type 1 diabetes mellitus patient
requires that age of the patient be highly considered when establishing glycemic goals, with
targets for bedtime, hemoglobin A1C and pre-prandial levels. The set objectives for these patients

MOD 2 ASSIGNMENT 4
are to achieve a hemoglobin A1C level below 7.5% in the pediatric age group and below 7% in
adult age.
There are several types of insulin that are used by type 1 diabetes mellitus patients and they
include rapid acting like lispro, short acting, intermediate acting and long acting insulin. The
rapid acting has a rapid onset action and are absorbed quickly once injected and short duration of
action. The rapid acting Lispro can be used before a meal together with neutral protamine
Hagedorn (NPH) but not the regular where the NPH has an inhibition effect (Silver et al. 2018).
Regular insulin is an example of short acting whose duration action can last up to twelve hours.
NPH which is an intermediate insulin type has an onset of action of around two hours and can act
for duration of up to 24 hours (Saleem & Sharma, 2019). Insulin glargine is a long acting insulin
type that can maintain blood glucose levels for more than 24 hours and can therefore be given
once daily in some patients. There are cases when different types of insulin can be administered
together in a single preparation by mixing measured doses of the two insulin types in the same
syringe. The major side effects of the treatment modalities are hypoglycemia due to excess influx
of glucose and hypokalemia because of the glucose potassium ion exchange that occurs when
glucose is pumped into cells (Coca et al. 2017).
Interview
Mr. Johnson was the patient interviewed in this assignment who is currently 46 years old and
states that he was retired from his job where he worked as a mechanic. Mr. Johnson states that he
has type 1 diabetes mellitus. He reports that he has had the disorder since he was 11 years old.
Mr. Johnson states that he cannot carry out his activities of daily living independently because

MOD 2 ASSIGNMENT 5
over the last five years he is becoming progressively blind. This is because of retinopathy which
is a complication associated with type 1 diabetes mellitus (Nentwich & Ulbig, 2015). He has
been using lispro and neutral protamine Hagedorn. Mr. Johnson states that he underwent an eye
surgery 24 years ago but the eye problem is back and his currently having an appointment with
his ophthalmologist two weeks from to discuss the treatment options available for him. He states
that there is a time he overdosed his medication and went into a coma which could be due to
hypoglycemia which is a side of the medication he is using (DeFronzo et al. 2016).
Conclusion.
In conclusion it is evident that dysregulation of the immune system leads to abnormal response
that can lead to many immune disorders. Autoimmune diseases like type 1 diabetes mellitus
which has been discussed results from immune destruction of the beta cells in the pancreas that
produce insulin. Type 1 diabetes mellitus is treated by lifelong administration of insulin which
exists in different types. The different available treatment modalities are aimed at insulin that
cannot be produced by the pancreas to control the blood glucose levels.
References.
Burrack, A. L., Martinov, T., & Fife, B. T. (2017). T Cell-Mediated Beta Cell Destruction:
Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes. Frontiers in
endocrinology, 8, 343. https://doi.org/10.3389/fendo.2017.00343

MOD 2 ASSIGNMENT 6
Coca, A., Valencia, A. L., Bustamante, J., Mendiluce, A., & Floege, J. (2017). Hypoglycemia
following intravenous insulin plus glucose for hyperkalemia in patients with impaired
renal function. PloS one, 12(2).
DeFronzo, R., Fleming, G. A., Chen, K., & Bicsak, T. A. (2016). Metformin-associated lactic
acidosis: current perspectives on causes and risk. Metabolism, 65(2), 20-29.
Donner, T., & Sarkar, S. (2019). Insulin–pharmacology, therapeutic regimens, and principles of
intensive insulin therapy. In Endotext [Internet]. MDText. com, Inc..
Jameson, J. L., & Groot, L. J. D. (2015). Endocrinology: Adult and Pediatric E-Book.
MOSAIC OF AUTOIMMUNITY: The novel factors of autoimmune diseases revisited. (2018).
Place of publication not identified: ELSEVIER ACADEMIC Press.
Nentwich, M. M., & Ulbig, M. W. (2015). Diabetic retinopathy - ocular complications of
diabetes mellitus. World journal of diabetes, 6(3), 489–499.
https://doi.org/10.4239/wjd.v6.i3.489
Paschou, S. A., Papadopoulou-Marketou, N., Chrousos, G. P., & Kanaka-Gantenbein, C. (2018).
On type 1 diabetes mellitus pathogenesis. Endocrine connections, 7(1), R38–R46.
https://doi.org/10.1530/EC-17-0347
Saleem, F., & Sharma, A. (2019). NPH Insulin.
Silver, B., Ramaiya, K., Andrew, S. B., Fredrick, O., Bajaj, S., Kalra, S., Charlotte, B. M.,
Claudine, K., & Makhoba, A. (2018). EADSG Guidelines: Insulin Therapy in
Diabetes. Diabetes therapy : research, treatment and education of diabetes and related
disorders, 9(2), 449–492. https://doi.org/10.1007/s13300-018-0384-6