Presentation on theme: "What you do this lesson Copy all notes that appear in blue or green Red / White notes are for information and similar notes will be found in your monograph."— Presentation transcript:
What you do this lesson Copy all notes that appear in blue or green Red / White notes are for information and similar notes will be found in your monograph Read up on all diabetes information in your monograph for the next lesson
What is Diabetes mellitus? A failure to control blood glucose levels and an impaired ability to store glucose in the form of liver and muscle glycogen
Symptoms of diabetes mellitus Classic symptoms of diabetes are – Frequent urination, with large volumes of urine (especially at night) Excessive thirst Hunger Weight loss Other symptoms – Fatigue Blurry vision Gum and urinary tract infections Slow healing of skin Genital itching in women
CONTROL OF BLOOD SUGAR LEVELS After a meal excess glucose is stored as glycogen in the liver and skeletal muscles) As glucose levels fall, the liver releases glucose into the blood stream to prevent hypoglycaemia.
Two hormones control this process - Insulin and Glucagon Both are secreted in the pancreas by the Islets of Langerhans Beta (β) cells produce insulin Alpha (a) cells produce glucagon
Control of blood glucose levels by insulin and glucagon
Insulin and its effects Insulin is a protein hormone which binds to specific receptors on the cell membrane of target cells and initiates the following Insulin binds to receptor Activated insulin receptor promotes movement of glucose transporter molecules from intracellular pool to the cell membrane Glucose transporters allow glucose to enter the cell When insulin levels decrease glucose transporters move from cell membrane to intra- cellular storage pool, where they can be recycled
Insulin Affects skeletal muscle, liver and fat cells and stimulates the uptake of glucose by these cells Insulin increases the permeability of muscles to glucose as normally they are not very permeable Liver cells are very permeable but become more so in the presence of insulin and they are also stimulated to increase glycogen formation In obese individuals the number of insulin receptors decreases and therefore glucose uptake is decreased. This reduction in receptors leads to insulin resistance
Glucagon Low blood glucose Alpha cells of pancreas release glucagon Liver breaks down glycogen Glucose released into blood
Complications associated with diabetes – Hypertension Stroke Kidney disease Nerve damage Increased risk of atherosclerosis Impaired vision due to cataracts or damaged retinas.
Diabetes not controlled properly may lead to loss of sight through degeneration of retina.
Forms of diabetes mellitus Type 1 (early onset, insulin dependent diabetes mellitus IDDM) Type 2 (late onset, non-insulin dependent diabetes mellitus NIDDM)
Type 1 (IDDM) Failure of the pancreas to produce adequate amounts of insulin as a result of an autoimmune response Accounts for 5-10% of cases The sympton weight loss is caused by body breaking down fat to supply energy as cells cannot utilise glucose Treatment = regular insulin injections subcutaneously
Type 2 (NIDDM) Accounts for 95% of cases Associated with obesity Plasma insulin levels normal but cells are less sensitive to insulin (insulin resistance) Reduced uptake of insulin into skeletal muscle and fat cells Possibly due to a reduced number of insulin receptors on the cell membrane
In summary insulin is produced but not used efficiently by the cells pancreas compensates by producing more insulin B cells become “worn out” and insulin production decreases Blood glucose increases and diabetes develops
For interactive game on diabetes see ‘My Diabetic Dog’ At the Nobel Prize medical website Click here
Treatment for NIDDM Diet Weight control Adequate exercise Begin an insulin increasing agent Lower blood pressure
Comparison of type 1 and type 2 type 1type 2 Ageunder 20over 40 % of diabeticsless than 10%over 90% appearance of symptomsrapidslow obesity at onsetuncommoncommon β cell no.decreasedvariable Condition of Cells of Isletsinflamednormal Family historyuncommoncommon