Understanding Type 1 Diabetes Mellitus

The case of the 10 year old boy, who experienced symptoms of abdominial pain, starving frequently but still does not gain any weight. He was then given a dipstick test. This is for urine and glucose test. After obtaining the result, it shows that he has higher level of glucose as compared to healthy children. Therefore, he has been diagnose as type 1 diabetes mellitus. Thus, he must take insulin frequently. The question is, what type 1 diabetes mellitus is? What is the cause, signs, symptoms and risk factor of type 1 diabetes mellitus? What pathophysiology of type 1 diabetes mellitus? Hoe do insulin respond to the human body? What is pharmacodynamics and pharmacokinetics between insulin and human body?Finally, what is the side effect of insulin treatment?

TYPE 1 DIABETES MELLITUS

OUTLINE

Type 1 mellitus is a persistent extreme disease in which the pancreas absorbs little or no insulin and is excluded from insulin-based diabetes known as juvenile diabetes. Insulin is a compound that can be used to produce energy in sugar (glucose) cells to transform glucose into glycogen to store it in the liver. Various factors can contribute to type 1 diabetes, including genetics and certain infections. While type 1 diabetes is usually seen in children or teenagers, it can also occur in adults. Despite the latest technology, there is still no cure for type 1 diabetes mellitus. However, it can be controlled by insulin, a balanced diet, and blood sugar control activities to prevent further complications.

CAUSES

There is still no clear source of type 1 diabetes. Your own immune system is usually incorrectly attacked and destroyed, with insulin-producing pancreatic cells usually struggling against harmful bacteria and viruses. Further causes of this disease may be inherited genetics from parents or grandparents with the same type of disease (type 1 mellitus) and viral exposure and other environmental factors.

INCIDENT

About 108 million (1980) people living with diabetes are increasing gradually from the World Health Organisation (WHO) to 422 million (2014). Global prevalence of diabetes has increased rapidly in 18 years, from 4.7% (1980) to 8.5% (2014) among adults 18 years of age. The incidence of diabetes is higher relative to high-income countries in low-and middle-income nations.

In 1980, around 108 million people are having diabetes and it increasing gradually until 422 million in 2014. The statement is from World Health Organisation. Global prevalence of diabetes has increase so fast in only for 18 years from 4.7% to 8.5%. this percentage is among adults above 18 years old. The disease is spreading more across the low and middle income nations as compared to higer income countries. In Asia, Malaysia has the most diabetes patient for over 3.6 millions. Malaysia is also one of the biggest diabetic patient across the world.

RISK FACTOR

The risk factor for type 1 diabetes mellitus includes family history, which is if any member of your family, including parents and siblings, has type 1 diabetes mellitus, you also have a greater chance of having it. Then, the external conditions surrounding you, including flu. Therefore you should always look after your hygiene. After that, the existence of autoantibodies which are killing immune system cells. Such autoantibodies will give you a better risk of enduring the disorder. Typically you only get it because your family has it. But not everyone who has these autoantibodies has diabetes.

PATHOPHYSIOLOGY

The culmination of lymphocytic infiltration and destruction of beta cells that secrete insulin in the Langerhan pancreatic islet is a consequence of type 1 diabetes mellitus. As the number of beta cells decreases, insulin secretion often decreases until insulin is sufficient to maintain normal blood glucose levels. Hyperglycemia can evolve and, after 80-90 percent of Beta cells die, diabetes may be identified. In patients, exogenous insulin is needed. Catabolism is abolished, ketosis is stopped, hyperglucagonemia is decreased and lipid and protein synthesis is regulated.

In addition, autoimmunity is considered a primary factor in the pathophysiology of type 1 diabetes mellitus. Viral protein antibodies in a genetically sensitive person could be caused by a viral infection. This causes the same antigenic autoimmune reaction as beta cell molecules.

About 85 percent of patients with form 1 have circulating islet cell antibodies. In fact, anti-insulin antibodies are detected prior to insulin therapy. Glutamic acid decarboxylase (GAD), an enzyme found in pancreatic beta cells, is the most common antibody found in islet cells.

Type 1 diabetes mellitus incidence is growing in patients with many autoimmune diseases. Graves disease, Hashimoto thyroiditis, and Addison 's disease, for example. Both Pilia et al observed a higher prevalence of insular cell antibodies as well as antiGAD antibodies in patients with autoimmune thyroiditis.

Work used Philippe et al. computed tomography ( CT) tests, Glucagon stimulation test results and fecal elastase-1 measurements to support the drop in the pancreatic volume of diabetic individuals. This research, which included the same for both types of diabetes mellitus, may further explain the profound exocrine dysfunction associated with diabetes mellitus.

DR and DQ in human leukocyte antigen ( HLA) genes with class II polymorphisms are the primary genetic determinants of type 1 diabetes mellitus. Any 95 percent of patients with type 1 have either HLA-DR3 or HLA-DR4 diabetes mellitus. The chance of diabetes mellitus is slightly higher among such heterozygotes relative to homozygotes. A may grouping for HLA-DQs can also be considered.

SIGNS AND SYMPTOMS

Symptoms and symptoms may occur quickly and suddenly with type 1 diabetes mellitus. This may involve increasing tiredness, frequent urination, bed-weighting of unwet children the previous night, daily malnutrition, unexplained weight loss, irritability and mental changes, tiredness and excessive weariness, and blurred vision.

PHARMACOKINETIC AND PHARMACODYNAMIC OF INSULIN

ABSORPTION

Insulin is injected directly into the bloodstream through a subcutaneous infusion. A small part of the transport is carried out by the Lymph Network. Absorption of insulin into the bloodstream following a subcutaneous injection is the rate that limits the stage of insulin operation. This absorption is not consistent with T50 per unit heterogeneity, which means that it is time to consume 50 per cent of the insulin dose that is specific in one person from ~25 per cent and in patients up to 50 per cent. Various rates of insulin absorption at various locations (abdomen, deltoid, cement, and thighs) are often related to shifts in blood flow. It has a 2-fold quicker effect than other rising subcutaneous abdominal insulin absorption sites. The safety importance of this is that doctors will avoid administering insulin doses spontaneously at various body places. For starters, this position would be used daily for this injection if the patient needs insulin in his thigh at noon. The abdomen is the ideal injection site since it is the least susceptible to the symptoms that affect insulin absorption.

Factors that usually change the local blood flow to affect the absorption of insulin in the subcutaneous tissue. The absorption rate can also be improved by factors that increase the flow of subcutaneous blood. Factors that affect insulin absorption are listed below: injection area planning, local massage, temperature, jet injectors, lipahypertrophy, insulin blends, injection location, physical state (soluble vs. suspension), insulin dose.

ELIMINATION

The primary organ of insulin depletion is the kidneys and liver. In fact, hepatitis is reduced by between 50% and 60% of the insulin released into the portal vein by the pancreas and the kidney degrades by between 35% and 45%. Injections of exogenous insulin are no longer immediately transferred through the portal chamber, thus increasing the degradation profile. The kidney is more important for insulin degradation with SQ insulin than for approximately 30 to 40 per cent of liver degradation.

Renal impairment may decrease the clearance of insulin and extend its action because the kidneys are involved. This reduced clearance can be observed both in the normal production and administration of exogenous insulin and in the creation of endogenous insulin. Generally, renal activity should be reduced dramatically before it is critically necessary. Deterioration in renal function leads to a slowdown in the demand for exogenous insulin and an increased risk of hypoglycaemia.

PHARMACODYNAMIC

Pharmacodynamics is the initiation, height and duration of the results. This may vary between insulin preparations. Insulin Pharmacodynamics relates to the oxidative function of insulin. Available insulins are categorized as fast-acting, short-acting, mid-acting, and long-acting insulin commercially active. Areas of intra-patient or inter-patient heterogeneity are described in terms of introduction, height and length. The time-action pattern for the same insulin will be best measured in patients who are still controlling blood glucose.

ADVERSE EFFECT OF INSULIN THERAPY

Hypoglycemia, headache, flu-like symptoms, weight gain, lipoatrophy, itching, rash and injection site reactions are common adverse reactions to insulin therapy. Extreme side effects from insulin use include severe hypoglycaemia, allergic reactions and anaphylaxis.

REFERENCES

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