Clinical Diabetes
Session Description:
Summary of the diagnosis, classification, aetiology and treatment of
type-1 and type-2 diabetes and the geographic variation of diabetes
Treatment of type-1 diabetes with insulin and diabetic ketoacidosis
Oral agents used for the treatment of type-2 diabetes
The macro and microvascular complications of diabetes are
summarised
Diagnosis of diabetes is very significant as it effects many things e.g. car insurance and
lifestyle. Diagnostic criteria seems to change quite a bit.
Diagnosis of diabetes can be done by doing fasting blood sugar, you can’t do it by a
fingerprick test (as it gives capillary blood sugar), you need a venous blood sugar
sample – it is normally around 5mmol/L, if 6.1<x>7 then above normal, if 7 or above
diabetes.
Another type of test is oral glucose tolerance test, you give them 75g of glucose and
test blood sugar at that time and 2 hours later. If above 11.1mmol/l then diabetes.
- Diagnosis also depends on symptoms, if they have various symptoms (polyuria,
polydipsia, weight loss). Then one of the tests being positive will suffice.
If you’re above normal but not above the diabetic threshold, then it is said you have
impaired glucose tolerance or impaired fasting glycemia.
These mean someone is predisposed to diabetes but by changing lifestyle it can be
prevented.
You also cannot make a diagnosis based on glycosuria (as various conditions can cause
this), fingerprick test (need venous sample), HbA1c (blood sugar attached to RBCs,
gives an average blood sugar level over 3 months, this is useful but can’t do it on its
own).
Types of Diabetes
Type 1 – Beta cell destruction
Type 2 – Insulin resistance and/or insulin deficiency due to beta cell dysfunction
Gestational
Type 1
Develops predominantly in children and young adults, but can occur in all age groups.
There is also marked geographical variation, more common as you go north from the
equator.
This means there must also be some environmental factors.
Commonest cause of Type-1 DM is autoimmune destruction of beta-cells leading to no
beta cell function. There are genetic factors (such as having HLA haplotypes DR3 and
, 4). But not everyone who has these has type 1 DM, this means there is some role of
environmental interaction.
Environmental – Viruses can directly destroy beta cells or by an autoimmune
response. E.g. mumps, coxsackie B, rubella
-Dietary components
-Stress
-Drugs and toxins
But these need to attack someone who is vulnerable, we aren’t 100% sure what causes
it though.
Type 2 Diabetes
The incidence of type 2 DM is rapidly increasing, it is set to double by 2020. There is a
large amount of un-diagnosed diabetes.
Type-2 DM is closely linked to insulin resistance.
There is also geographical variation and ethnic one, in the UK it is much more common
in Indians and African-Caribbean’s.
Its prevalence is closely associated with BMI.
Compared to white patients Indian patients have younger age of onset of type-2
diabetes and earlier proteinuria and renal disease.
Type-2 accounts for most diabetes (85%). Patients do not require insulin to remain
alive, although 20% are treated with insulin to control blood glucose. Incidence is
getting younger.
The treatment for type 1 is evidently insulin! Now we have recombinant human
insulin.
Insulin – Physiology
Insulin acts on adipose tissue, muscle and liver. A lack of insulin results in raised blood
sugar levels. There is breakdown of adipose tissue (FA mobilisation) leading to
diabetic ketoacidosis.
When we give insulin to a patient we try imitate the normal background levels of
insulin, such as below ->
Session Description:
Summary of the diagnosis, classification, aetiology and treatment of
type-1 and type-2 diabetes and the geographic variation of diabetes
Treatment of type-1 diabetes with insulin and diabetic ketoacidosis
Oral agents used for the treatment of type-2 diabetes
The macro and microvascular complications of diabetes are
summarised
Diagnosis of diabetes is very significant as it effects many things e.g. car insurance and
lifestyle. Diagnostic criteria seems to change quite a bit.
Diagnosis of diabetes can be done by doing fasting blood sugar, you can’t do it by a
fingerprick test (as it gives capillary blood sugar), you need a venous blood sugar
sample – it is normally around 5mmol/L, if 6.1<x>7 then above normal, if 7 or above
diabetes.
Another type of test is oral glucose tolerance test, you give them 75g of glucose and
test blood sugar at that time and 2 hours later. If above 11.1mmol/l then diabetes.
- Diagnosis also depends on symptoms, if they have various symptoms (polyuria,
polydipsia, weight loss). Then one of the tests being positive will suffice.
If you’re above normal but not above the diabetic threshold, then it is said you have
impaired glucose tolerance or impaired fasting glycemia.
These mean someone is predisposed to diabetes but by changing lifestyle it can be
prevented.
You also cannot make a diagnosis based on glycosuria (as various conditions can cause
this), fingerprick test (need venous sample), HbA1c (blood sugar attached to RBCs,
gives an average blood sugar level over 3 months, this is useful but can’t do it on its
own).
Types of Diabetes
Type 1 – Beta cell destruction
Type 2 – Insulin resistance and/or insulin deficiency due to beta cell dysfunction
Gestational
Type 1
Develops predominantly in children and young adults, but can occur in all age groups.
There is also marked geographical variation, more common as you go north from the
equator.
This means there must also be some environmental factors.
Commonest cause of Type-1 DM is autoimmune destruction of beta-cells leading to no
beta cell function. There are genetic factors (such as having HLA haplotypes DR3 and
, 4). But not everyone who has these has type 1 DM, this means there is some role of
environmental interaction.
Environmental – Viruses can directly destroy beta cells or by an autoimmune
response. E.g. mumps, coxsackie B, rubella
-Dietary components
-Stress
-Drugs and toxins
But these need to attack someone who is vulnerable, we aren’t 100% sure what causes
it though.
Type 2 Diabetes
The incidence of type 2 DM is rapidly increasing, it is set to double by 2020. There is a
large amount of un-diagnosed diabetes.
Type-2 DM is closely linked to insulin resistance.
There is also geographical variation and ethnic one, in the UK it is much more common
in Indians and African-Caribbean’s.
Its prevalence is closely associated with BMI.
Compared to white patients Indian patients have younger age of onset of type-2
diabetes and earlier proteinuria and renal disease.
Type-2 accounts for most diabetes (85%). Patients do not require insulin to remain
alive, although 20% are treated with insulin to control blood glucose. Incidence is
getting younger.
The treatment for type 1 is evidently insulin! Now we have recombinant human
insulin.
Insulin – Physiology
Insulin acts on adipose tissue, muscle and liver. A lack of insulin results in raised blood
sugar levels. There is breakdown of adipose tissue (FA mobilisation) leading to
diabetic ketoacidosis.
When we give insulin to a patient we try imitate the normal background levels of
insulin, such as below ->
