T2DM Flashcards
List some conditions within the group macrovascular disease
- Ischaemic Heart Disease
- Cerebrovascular Disease (stroke)
- Renal Artery Stenosis
- Peripheral Vacular Disease (PVD)
1) When do microvascular complications occur?
2) List some microvascular complications
1)
- Only in diabetes
2)
- Retinopathy
- Nephropathy
- Neuropathy
In what condition will you get diabetic ketoacidosis?
- In T1DM
- NOT in T2DM
What should a normal fasting sugar be in an oral glucose test?
<6 mmol / L
What should a normal 2-hour glucose be in an oral glucose tolerance test?
< 7.8 mmol / L
What are the boundaries for blood sugar levels in an oral glucose tolerance test in fasting and in 2-hour glucose to consider someone diabetic, and at what level would you always consider someone to be diabetic?
- If glucose > 7 mmol / L at fasting OR…
- If glucose > 11.1 mmol / L at 2-hour glucose OR
- If glucose >11.1 at any point - always considered diabetic
1) Define the intermediate levels in oral glucose tolerance tests at fasting and in 2-hour glucose tolerance tests
2) What risks / indications are indicated by someone having this sugar levels?
1)
- Fasting: 6 - 7 mmol / L
- 2-hour glucose test: 7.8 - 11 mmol / L
2)
- Increased risk of developing diabetes
- Increased macrovascular risk
At what point would microvascular risk occur as suggested by sugar levels in an oral glucose test?
- Once you are deemed diabetic in accordance with the defined boundaries at fasting and in 2-hour glucose tests
Epidemiology of T2DM:
1) What age group is it more common in?
2) What does its prevalence vary based on (i.e. some other factors that affect its prevalence)?
3) Its greatest in particular in people doing what?
1) Elderly
2)
- Ethnicity
- Other environmental factors
3)
- People from ethnicities that have great amounts of rural → urban shift
3 Factors that can play a role in the development of MODY?
- Genes
- Intrauterine environment
- Adult environment
1) What is the genetic basis of MODY?
2) What does the family history for MODY look like, and why?
1)
- Autosomal dominant
- There are 8 hereditary forms of MODY
2)
- Positive family history because of the fact that it is autosomal dominant - if it were recessive, perhaps there may not be immediately positive family history
What is the basic pathophysiological basis for the development of T2DM?
- Genes (unknown) encode…
- Insulin resistance through adipocytokine action
- Leading to ß-cell failure too
How does T2DM lead to…
1) Macrovascular complications
2) Microvascular complications
1)
- The insulin resistance through adipocytokine action leads to metabolic dyslipidaemia and mitogenesis which causes macrovascular symptoms
2)
- ß-cell failure leads to hyperglycaemia and thus microvascular complications
What role does obesity play in the development of T2DM and associated symptoms?
- Obesity contributes to the development of insulin resistance, but genetics is the major causative factor in the development of this resistance
- Adipocytokines released from adipose tissue to cause insulin resistance as well as genetically encoded adipocytokine release
- Adipose tissue release NEFAs which eventually lead to metabolic dyslipidaemia and thus macrovascular complications associated with T2DM
What is T2DM associated with in the neonate?
- Low birth weight / small size
- Due to intra-uterine growth (IUGR) restriction associated with T2DM
Is T2DM monogenic?
No
How have studies shown that there is a likely genetic element to T2DM?
- Monozygotic twin studies show a higher prevalence in identical than non-identical twins (70% and 40% respectively)
Describe the presentation of T2DM
- Heterogenous presentation
- Obesity
- Insulin resistance and insulin secretion deficiency
- Hyperglycaemia
- Dyslipidaemia
- Acute and chronic complications
Describe the pathophysiology for how insulin resistance (as brought on by adipocytokines) leads to hyperglycaemia and metabolic dyslipidaemia (exclude the ketosis aspect)
- Insulin normally directly reduces hepatic glucose ouptut, so resistance increases it, causing hyperglycaemia
- Insulin normally stimulates glucose uptake into muscle tissue, resistance prevents this, causing hyperglycaemia
- TGs are broken down normally in the adipose tissue also, insulin normally prevents NEFAs from being released and entering the liver. Resistance means NEFAs enter the liver and here they can form small-dense VLDL-TG which enters the bloodstream to be cleaved into VLDL - this causes metabolic dyslipidaemia
What is a simple predictor of ischaemic heart disease and why?
- Waist circumference - higher the omental fat (omental adipose tissue), the higher the waist circumference
- Omental adipose tissue releases NEFAs which form VLDL-TG in the liver and thus VLDL in the blood which causes metabolic dyslipidaemia and thus macrovascular complications such as ischaemic heart disease
How might a failing pancreas cause DM?
- Fails to cleave pro-insulin in order to form mature insulin - so immature insulin is ineffective, essentially causing insulin resistance
What metabolic complications can occur in T2DM, and what metabolic complication that occurs in T1DM doesn’t really occur in T2DM?
- Lactic acidosis
- Hyperosmolar symptoms e.g. hyperosmolar hyperglycaemic coma
- Metabolic dyslipidaemia
- Diabetic ketoacidosis does NOT occur
What osmotic symptoms occur in T2DM and why?
- Hyperglycaemia overwhelms the kidney’s ability to reabsorb all glucose molecules so… Glycosuria
- The glucose in the urine in the kidneys takes water with it by osmsosis, leading to… Polyuria
- Hyperglycaemia by osmosis drawing water out of somatic cells and also by causing polyuria leads to… Polydipsia
- Hyperosmolar hyperglycaemic coma
Why can infections be common in someone with T2DM? + What kind of infections might you see?
- Microorganisms thrive in the high glucose conditions
- Yeast etc
