Give a brief description of diabetes mellitus.
At what age is the onset of type 1/insulin-dependent diabetes?
Is the condition still considered to be type 1 diabetes when insulin dependent diabetes develops/presents >30 years old?
What propensity to develop type 1/insulin dependent diabetes is genetic?
It is unknown EXACTLY how the genetic predisposition to works, but how is it thought to lead to the development of diabetes?
What is 'insulitis'?
What percentage of type 1/insulin dependent diabetics also manifest other organ-specific autoimmune diseases, and what are some examples of these diseases?
Which group of people do environmental triggers produce a stronger effect (with regard to diabetes)?
Describe some environmental triggers for type 1/insulin dependent diabetes.
Describe the pathology of type 1/insulin dependent diabetes.
Describe the clinical features of type 1/insulin dependent diabetes.
What is the basic mechanism of type 1/insulin dependent diabetes?
What is the main difference between type 1 and type 2 diabetes?
Multifactorial genetic inheritance is a key factor in the development of type 2 diabetes. What proportion of development is due to genetic predisposition, and why is this not a certain figure?
List some causes of insulin resistance.
In many type 2 diabetics, what two cellular processes are impaired?
What deficiency can prevent insulin from being released from β cells?
List some possible causes of reduced insulin reception/glucose uptake by cells.
Obesity can contribute towards developing type 2 diabetes but it does not directly cause it. Which group of people are more likely to develop type 2 diabetes?
People who store their fat in certain places can get rid of it more easily through rigorous food consumption control. People who store fat in which areas can get rid of it more easily? And which areas are more difficult to get rid of fat through rigorous food control?
People who store fat in which areas are more likely to develop type 2 diabetes?
Energy metabolism varies greatly between populations and individuals. Explain what this means for obesity and type 2 diabetes.
Describe the pathology seen in type 2 diabetes.
Is diabetes life threatening?
At what age is the onset of type 2 diabetes?
Without insulin, what are the metabolic consequences for an individual?
What type of oxidation do fatty acids undergo in the liver?
Fatty acids enter the blood for transport to the liver from peripheral adipose tissue. What happens to them in the liver?
Ketone bodies can re-enter the circulation and can be used by other tissues, e.g. muscle and brain, for ATP synthesis. However, what can happen from here?
What is metabolic acidosis (in tissues)?
List some possible symptoms of ketone acidosis.
What is anaerobic metabolism, which creates lactate, caused by?
What can happen if lactate leaves the cells and enters the blood?
If untreated, what can ketoacidosis and hypoxia from circulatory collapse lead to? What is the treatment?
What is the equation for glycolysis (words)?
What is lipolysis?
Glycolysis and the Krebs cycle usually generate energy in the form of ATP through oxidative phosphorylation of acetyl CoA. What does lipolysis do?
Although hepatic glucose is still increased as gluconeogenesis is occurring in the liver, the glucose STILL cannot cross the cell membranes in the body. What happens to the fatty acids in β oxidation?
What concentration can CO2/acetone reach in untreated diabetes?
Fatty acid metabolism produces acetyl CoA faster than the Krebs cycle can use it as a substrate. What happens to this extra acyl?
What does the body metabolise after the peripheral adipose tissue?
What can alanine be used to form in gluconeogenesis in the perceived absence of glucose in diabetes?
What physical effects does utilisation of peripheral skeletal muscle tissue have?
Can the glucose produced by skeletal muscle breakdown and gluconeogenesis be used by cells for respiration in untreated diabetes?
The presence of what in the circulation of diabetics will make the blood more viscous?
Why are glycosylated low density lipoproteins (LDLs) made available to blood vessel walls but non-glycosylated LDLs aren't?
What might be the result of LDL deposition in the blood vessels of diabetics?
What risk factor for atherosclerosis and cardiovascular disease is common in adult diabetics?
What is the major cause of death in diabetics?
How is dehydration caused in uncontrolled diabetes?
Dehydration and acidosis can lead to what?
What are the three types of diabetic coma?
List three things that can lead to hypoglycaemia in a diabetic.
Why might a diabetic patient going into a severe hypoglycaemic coma sweat excessively and have a rapid heart rate?
What is the mechanism in the development of a severe hypoglycaemic coma and what can reverse it?
List four consequences of ketoacidosis that can lead to a coma.
What causes the exhaustion in a diabetic patient with ketoacidosis?
Why is there loss of fluid and dehydration in a diabetic patient with ketoacidosis?
Describe the mechanism of a diabetic patient with ketoacidosis going into a coma.
Why are brain cells also starved of oxygen in a coma caused by diabetic ketoacidosis?
Describe the mechanism of a nonketotic hyperosmolar coma, and explain the different between this and a coma resulting from ketoacidosis.
What is protein glycosylation, that occurs with hyperglycaemia?
What sorts of proteins might be involved in protein glycosylation?
What is an initial property of glycosylated proteins that disappears with time?
What happens to glycosylated proteins? What is the overall effect?
In diabetics, what is there a high rate of deposition of, which causes the membranes of vessels and organs to thicken?
What are the effects of the glycosylation of basement membrane proteins?
Why is healing impaired in glycosylation of blood proteins? What can this lead to?
How might tissue necrosis occur as a result of protein glycosylation in diabetes? Where does this commonly occur?
Roughly what proportion of both type 1 and type 2 diabetics develop renal failure?
What does the prevalence of diabetic nephropathy increase roughly in proportion with?
What is the most common reason for kidney transplants in adults?
What is diabetic glomerulosclerosis and what are the two types of it?
List three major manifestations of diabetic glomerulosclerosis.
What is renal disease secondary to in diabetics?
How is diabetic glomerulosclerosis treated?
Name four eye conditions that commonly develop in diabetics. Which is the most devastating?
What is the prevalence of diabetic retinopathy dependent on?
What are the two types of diabetic retinopathy?
Describe the pathogenesis of non-proliferative diabetic retinopathy.
Describe the similarities and differences between non-proliferative and proliferative diabetic retinopathy.
What is the treatment for proliferative/non-proliferative diabetic retinopathy?
What is peripheral neuropathy?
What can cause peripheral neuropathy in diabetics?
What effects does peripheral neuropathy tend to have in diabetics?
What other neuropathies can occur in diabetics and what symptoms may be seen?
Give some reasons why immunity, in particular leukocyte function, is impaired in diabetes.
Which effects of diabetes may increase the risk of infection?
Which type of diabetes is hyperinsulinaemia common in and why?
What can be the effects of hyperinsulinaemia?
What is the clinical presentation of a diabetic patient with hyperinsulinaemia?
What is the treatment for hyperinsulinaemia?
What is a blood glucose test?
What is the normal fasting plasma glucose concentration?
What are the pre-diabetic and diabetic fasting plasma glucose concentrations?
What is a glucose tolerance test?
What is a normal glucose tolerance test result?
What are the pre-diabetic and diabetic results of a glucose tolerance test?
What does the slow response to a glucose tolerance test in pre-diabetic and diabetic patients indicate?
What do fasting plasma glucose and glucose tolerance tests indicate and not indicate about a person?
How might the type of diabetes that a person has be distinguished?
What is C-peptide?
How will the results of a C-peptide assay differ between a type 1 diabetic and a type 2 diabetic?
What might dipstick tests show in a diabetic patient and/or a renal disease patient?
How is type 1 diabetes treated?
How is type 2 diabetes treated?
What has minimising hyperglycaemia been seen to do in type 2 diabetics?
How does exercise minimise hyperglycaemia?
How does weight loss minimise hyperglycaemia?
In which patients might bariatric surgery be recommended as a starting point for type 2 diabetes treatment? In which patients might this not be appropriate?
Who do GLP-1 and GIP do?
What do amylin and insulin do?
How might incretin mimetics, such as exendin-4, be used to treat type 2 diabetes?
Pramlintide mimics amylin. How might this be used in the treatment of type 2 diabetes?
How might drugs which inhibit hepatic glucose release be used in the treatment of type 2 diabetes?
How might drugs which make target tissues more responsive to insulin be used in the treatment of type 2 diabetes?
What property of amylin, other than its ability to reduce digestion and carbohydrate absorption, makes it ideal for use in an obese/inactive type 2 diabetic before bariatric surgery?
Why might insulin be used in the treatment of type 2 diabetes?
List some drug classes that stimulate insulin secretion.
List some drug classes that reduce plasma glucose concentration.
Along with amylin analogs such as pramlinitide, which other drug class reduces intestinal glucose uptake?
What do PPAR activators (or 'glitazones') do in diabetes treatment?