Case 5 - Diabetes Flashcards
Identify 1, 2, and 3 from the animation / diagram:
What are the steps A, B and C?
*put in pic*
1 - insulin
2 - insulin receptor
3 - Glut-4 transporter channel
A - Glycolysis
B - Link Reaction
C - Kreb’s / TCA cycle
GLUT-4 insulin regulator glucose channel, found predominantly in fat and muscle:
Where else is the GLUT-4 receptor found?
Adipose tissue
Striated muscle
Heart muscle
Endothelium
Kidney
Neurons
B-cells in the pancreas
Where is glucose actively transported?
Ileum / gut and kidneys
Do GLUT-1, 2, and 3 require insulin to work?
In which tissues are GLUT-1 found?
In which tissues are GLUT-2 found?
In which tissues are GLUT-3 found?
No, they are insulin independent
How many ATPs are generated overall per glucose molecule in aerobic respiration?
Around 30 ATP molecules
What are the functional effects of insulin on the liver, muscle and fat?
Aim = storage
Uptake of glucose for storage as glycogen (glycogenesis) - the liver and muscle
Prevents gluconeogenesis / glycogenolysis - in liver and muscle, also therefore prevents release of amino acids in muscles as muscle is prevented from being broken down
Promotes lipogenesis in fat tissue / prevents lipolysis
What are the causes of Type II diabetes?
What is the tipping point to developing Type II diabetes?
Insufficient insulin production (to counteract the reisstance)
Resistance to insulin in GLUT-4 receptors
Insulin resistance = negative feedback loop with rising blood sugar levels causes the B-cells in the pancreas to release more insulin. But eventually, the B-cells cannot produce enough insulin to meet the requirements, which is the tipping point to developing diabetes
What would the blood results of of Type II diabetes show?
Increased blood glucose levels
More lipolysis, less lipogenesis, so more free fatty acids in blood
More amino acids, more protein breakdown than protein storage
How can obesity develop?
Combination of environmental factors and family history / susceptibility genes
Diet
How can insulin resistance develop? (idek what the q was)
What is the viscious cycle of diabetes?
Adipokines (come from fatty tissues) - toxic actions on some tissues, including B-cells
Visceral fat is more susceptible to insulin resistance
complex pathology - combo of genes / family history, high BGL damages B-cells in pancreas, diabetes leads to lipolysis, breakdown of fat releases adipokines, which are toxic to B-cells …?
Put in pics of wooclap - match 1,2,3,4 with A,B,C,D?
1 - D (impaired glucose tolerance)
2 - B (Impaired fasting glucose)
3 - C (Normoglycaemia)
4 - A (T2DM)
In which sequence did the conditions occur?
What are the normal ranges? *put in pics*
- Normoglycaemia
- Impaired fasting glucose
- Impaired glucose tolerance
- T2MD
UK use 5.5 to 6.9 for fasting glucose levels, so normal = below 5.5 and more than 7 = diabetic range
How to test post-prandial glucose (after eating)?
What is the normal range?
75g sugar given
tests if the body can respong to a big meal - less than 7.8 mmol/l in normal, 7.8-11.1 = IGT, T2MD = above 11.2
Using the table, how can diabetes be diagnosed?
IGT - After a meal = abnormal, but in fasting state = less than 7 (so can be normal levels) = isolated IGT
If after a meal = abnormal, and fasting glucose is also abnormal = IGT and T2MD
IGT or IFG can happen in either order
Ask is they have symptoms - e.g. thirst, lots of peeing, unintended weight loss
Only use the values when present with symptoms
What is pre-diabetes?
What is meant by the terms IFG, IGT, IGR (imparied glucose regulation), non-diabetic hyperglycaemia, and borderline diabetes?
IGR = umbrella term, under which IFG and IGT are found (so IFG and IGT are different things)
What makes IFG and IGT different, pathophysiologically?
IGT = cannot manage glucose after a meal, (after a meal, most glucose goes into muscles), so muscle intolerance to insulin = huge contributor
IFG = resistance in the liver