Overview of Diabetes Mellitus
Diabetes
Mellitus (D.M) refers to a group of diseases that affect how your body uses
blood sugar.Glucose is an important source of energy for the cells that make up
your muscles and tissues. It's also the main source of energy for brain.
Diabetes
Mellitus is associated with abnormalities in carbohydrate, fat and protein
metabolism.
D.M may
result in chronic complications including microvascular, macrovascular and
neuropathic disorders.
Main types of D.M
- Type 1 D.M.
- Type 2 D.M.
- Gestational D.M.
- Type 1 D.M: associated with immune system mediated destruction of Beta cells of pancreas, it is also associated with absolute insulin deficiency.
- Type 2 D.M: it is caused by insulin resistance, it is associated with relative insulin deficiency.
- Gestational D.M: any degree of glucose intolerance first recognized during pregnancy.
Normal insulin actions
- Suppress hepatic glucose production.
- Stimulate glucose uptake by tissues.
- Suppress glucagon release.
- Suppress lipolysis and increase synthesis of fatty acids from glucose in the adipose tissues.
- Increase synthesis of amino acids from glucose in the muscles.
Normal bolus/basal insulin secretion
- Bolus insulin is secreted in response to increased blood glucose levels(after each meal).
- Basal insulin is secreted continuously in small amounts (not related to meals),it also prevents the increase of fasting blood sugar (FBS), conversion of fatty acids to glucose in adipose tissues, conversion of amino acids to glucose in muscles and production of glucose in the liver.
Normal insulin secretion
Early phase
insulin secretion
Secretion of
pre-formed insulin from the pancreas ( occurs after meals and continue for
5-15 minutes.
Late phase insulin secretion
Secretion of newly formed insulin from the pancreas (occurs after 15
minutes of beginning of insulin secretion).
Role of glucagon,
amylin and incretin hormones in glucose regulation process
Role of glucagon
- Promote glycogen breakdown (glycogenlysis) in the liver.
- Inhibit glycogen synthesis (glycogenesis) in the liver.
- Promote glucose synthesis (gluconeogenesis) in the liver.
Role of amylin
- Reduce glucagon secretion.
- Slows gastric emptying rate (GER), thus slows glucose absorption.
- Increase satiety.
Role of incretin
- Increase insulin release.
- Reduce glucagon release.
Type 1 Diabetes Mellitus
- Is it associated with destruction of Beta cells by autoimmune antibodies (stimulus is unknown) in genetically susceptible patients.
- Symptoms start to appear when about of 80-90% of beta cells are destroyed (overt D.M).
Possible triggers of type 1 D.M
- Cow’s milk or lack of breastfeeding.
- Some viruses.
- Vitamin D deficiency.
Clinical presentation of type 1 D.M
- Polyuria.
- Polydipsia.
- Glucosuria.
- Weight loss.
- Ketoacidosis.
- Ketonuria.
- Ketonemia.
- Recurrent infections.
Honeymoon period
It is the apparent remission in patients with type 1 D.M within days or
weeks after the initial diagnosis and implementing treatment which is reflected
by decreased blood glucose concentration and markedly decreased insulin requirements.
Type 2 Diabetes mellitus
Risk factors of type 2 D.M
- Family history (firs degree family member).
- Obesity (specially central obesity).
- Physical inactivity.
- HDL levels less than 35mg/dL or Triglycerides levels more than 250mg/dL.
- Hypertension.
- History of gestational D.M.
- History of polycystic ovarian syndrome (PCOS).
Insulin resistance
It is defined as the impaired response of tissues
(primarily liver, muscles and adipose tissues) to insulin, resulting in
impaired glucose utilization and entering to tissues which leads to
compensatory increase in insulin secretion from beta cells.
Insulin resistance causes
- Decreased insulin receptors.
- Decreased insulin receptors affinity to insulin.
- Defect in insulin signaling.
- Defect in post-receptors mechanisms.
Consequences of insulin resistance
- Hyperglycemia.
- Hyperinsulinemia.
Clinical presentation of type 2 D.M
- Polyuria.
- Polydipsia.
- Polyphagia.
Note:
The symptoms are mild (may be not noticed by the patient) and D.M is
diagnosed incidentally during a routine physical examination.
Diagnosis of type 2 D.M
American Diabetic Association (ADA) diagnostic criteria for D.M
D.M is diagnosed if one of the following is present:
- Glycosylated hemoglobin (A1C) of 6.5% or more.
- Fasting blood glucose of 126mg/dL or more.
- Two hour plasma glucose more than 200mg/dL during an oral glucose tolerance test (OGTT).
- If the patient is present with classic symptoms of hyperglycemia or hyperglycemic crisis and has a random plasma glucose concentration more than 200mg/dL.
Normal and diabetic values of glycosylated hemoglobin (A1C), fasting plasma glucose (FPG) and oral glucose tolerance test (OGTT):
Complication of D.M
Acute complications of D.M
- Diabetic ketoacidosis “DKA” (more common in type 1 D.M patients).
- Hyperosmolar hyperglycemic state “HHS” ( more common in type 2 D.M patients).
Long term complication of D.M
Long term diabetic patients develop microvascular and macrovascular complications.
- Microvascular complications of D.M are risk of developing retinopathy, neuropathy and nephropathy.
- Macrovascular complications of D.M are risk of developing stroke, cardiovascular disease (CVD) and peripheral vascular disease (PVD).
Management and treatment of D.M
The drugs used in the treatment of D.M are discussed in the following assay:
References
- Pharmacotherapy principles and practice 4 edition.
- PubMed.
- Mayoclinic.
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