Lecture 11 Diabetes

Question 1

*The differences between diabetes insipidus and diabetes mellitus.

Answer 1

Diabetes INSIPIDUS results from a deficiency in anti-diuretic hormone (vasopressin). ADH is necessary for the reabsorption of water from the kidney. This results in copious production of urine.

Diabetes MELLITUS results from an inability to sequester glucose from the blood. As such the glucose levels in the glomerular filtrate are highly elevated. This increased glucose prevents reabsorption of water and hence increased levels of sweet urine.

Question 2

*The causes of diabetes mellitus.

Answer 2

TYPE 1 DIABETES is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. (autoimmune disease) = the body’s immune system attacks and destroys the beta cells.
GENETIC PREDISPOSITION
ENVIRONMENTAL FACTORS such as foods, viruses, and toxins, may play a role BUT NOT PROVEN

TYPE 2 DIABETES (mc)
= insulin resistance, a condition in which the body’s muscle, fat, and liver cells do not use insulin effectively so body produces the hormone but it is defective.
GENETIC PREDISPOSITION =FHx
High risk =
>55yrs
>45yrs OVERWEIGHT
>45yrs HBP
>35yrs Aboriginal/Torres Strait Islander/Pacific Island/Indian subcontinent/Chinese
F given birth to child >4.5 kgs (9 lbs), or had GESTATIONAL DIABETES
POLYCYSTIC OVARIAN SYNDROME

Question 3

*The general differences between type 1 and type 2 diabetes.

Answer 3

Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus
Insulin dependent Insulin independent
Ketosis prone Ketosis resistant
Juvenile onset Adult onset
Growth onset Maturity onset

Question 4

*The symptoms of type 1 diabetes

Answer 4

Diabetic symptoms occur when around 80-90% of the b cells have been destroyed.

POLYURIA (frequent urination)
POLYDIPSIA (excessive thirst)
POLYPHAGIA (excessive hunger)
Sx appear abruptly usually brought on by stress or disease accompanied by
FATIGUE, WEIGHT LOSS AND WEAKNESS
Dx is confirmed by a fasting blood glucose level greater than 126mg/dl.

Question 5

*Metabolic changes associated with type 1 diabetes.

Answer 5

The metabolic abnormalities result from a deficiency of insulin and a relatively high glucagon level and are concentrated in 3 tissues, liver, muscle and adipose tissue.
These abnormalities result in:

1. HYPERGLYCAEMIA = elevated glucose levels caused by an increase in gluconeogenesis in liver coupled by a diminished use in tissues that are unable to take up glucose (muscle, adipose tissue).
2. KETOACIDOSIS = ketosis results from increased mobilisation of fatty acids from adipose tissue, combined with an increase in ketone body synthesis by the liver.
3. HYPERTRIACYLGLYCEROLEMIA = high levels of triglycerides, especially following a meal (postprandial)

Not all fatty acids are disposed of by oxidation or ketone body production by the liver. Excess fatty acids are converted to TAG then packaged into VLDL and there is also an accumulation of chylomicrons from dietary sources.

Question 6

*Treatment for type 1 diabetes.

Answer 6

INSULIN ONLY Tx OPTION

Must be INJECTED WHOLE of the patients LIFE. (not oral)
Types classed = duration of action (short-, medium-, long-).
change of DIET is necessary.
= A healthy diet comprising low-fat, high-fibre, low simple sugar, high complex sugar is recommended.

Question 7

*The role of insulin resistance in type 2 diabetes.

Answer 7

Insulin resistance is the decreased ability of target tissues such as liver, adipose tissue and muscle to respond to normal circulating concentrations of insulin. Obese individuals are most likely to show insulin resistance and eventually compensate for insulin resistance by elevated insulin levels.

Insulin resistance increases with weight gain (and diminishes with weight loss) suggesting fat accumulation is important in development of insulin resistance. These tissues release hormones such as leptin, resistin and adiponectin which may contribute to the development of insulin resistance.

Question 8

*The role of dysfunctional b cells in type 2 diabetes.

Answer 8

Although initially the pancreas is able to secrete elevated levels of insulin to deal with the hyperglycaemia associated with type 2 diabetes, the b cells eventually DETERIORATE and the levels of circulating insulin naturally declines. This deterioration may be accelerated by the toxic effects of sustained hyperglycaemia and elevated free fatty acids associated with disease progression.

Question 9

*The progression of type 2 diabetes.

Answer 9

HYPERGLYCEMIA – caused by increased hepatic glucose production and decreased peripheral usage. Ketosis is minimal because the presence of insulin, even in the presence of insulin resistance, diminishes hepatic ketogenesis.

HYPERTRIACYLGLYCEROLEMIA - Excess fatty acids are converted to TAG then packaged into VLDL and there is also an accumulation of chylomicrons from dietary sources.

Question 10

*Treatment for type 2 diabetes.

Answer 10

MAINTAIN NORMAL GLUCOSE LEVELS to prevent the development of long term complications.

Weight reduction, exercise and dietary modifications often correct the hyperglycaemia although hypoglycaemic agents such as the sulfonylurea class of drugs and insulin therapy may be required to achieve satisfactory plasma glucose levels.

Question 11

Symptoms caused by hypoglycaemia

Answer 11

1. Tachycardia
2. Confusion
3. Vertigo
4. Diaphoresis (excess sweating)
5. Hypersensitivity
6. Lipidystrophy (local atrophy or hypertrophy) of subcutaneous fatty tissue at site of injections