Introduction to Diabetes Flashcards
Annual screening checks in people with diabetes regarding general health.
Level of knowledge of diabetes
Weight and BMI
Diet and eating habits (Are they eating well and regularly?)
Exercise
Annual screening of glycaemic control.
HBA1c
Glucose monitoring (e.g. FreeStyle Libre)
Medication review
Review of insulin injection site
Annual screening of development of possible complications.
Retinal screening (Retinal photography)
Visual acuity test
Urine albumin:creatinine ratio
Serum urea and electrolytes
eGFR
Examination of feet
FBC
Thyroid function
Liver function
Annual screening of cardiovascular risk.
Smoking status
Blood pressure
Lipid profile
QRISK
Features of vascular disease of the feet in diabetes.
Pale discoloration
Loss of hair
Cool temperature
Absent pulses
Reduced capillary refill time
Evidence of gangrene or infection
Features of neuropathy of the foot in diabetes.
Clawing of toes and loss of plantar arch.
Neuropathic ulcers
Charcot’s joint
Glove and stocking sensory loss
Loss of vibration sense and proprioception and pain
Loss of ankle jerk
Difference between T1DM and T2DM regarding insulin.
T1DM = Severe insulin deficiency
T2DM = Insulin resistance and less severe insulin deficiency
Less common diabetes (1-3%) that is diagnosed under the age of 30 years.
Mutation of single gene also called monogenic mutation.
This used to be called MODY (Maturity-onset diabetes of the young)
Subdivisions of T1DM + the difference.
Type 1A Diabetes is immune-mediated.
Type 1B Diabetes is non-immune mediated.
Pathophysiology of T1DM.
Involves the triggering of a selective autoimmune destruction of the insulin producing cells of a a genetically predisposed individual.
Autoantibodies directed against pancreatic islet constituents appear in the circulation and often predate clinical onset by many years.
Aetiology of T1DM.
Immune-mediated
Idiopathic
Genes involved in T1DM.
In >90% are HLA-DR3 and HLA-DR4 carriers.
Environmental factors that can cause T1DM.
Maternal - Gestational infection or older age
Viral infection - Coxsackie B4
Exposure to dietary constituents - Cow’s milk and deficiency of vitamin D
Environmental toxins
Childhood obesity
Psychological stress
Aetiology of T2DM
Obesity
Diet
Physical inactivity
Genetic susceptibility
Ageing leads to increased incidence
Low weight at birth (poor nutrition early in life impairs beta-cell development)
Why does insulin action diminish in T2DM?
Because of the development of insulin resistance.
What are the metabolic consequences of insulin resistance?
Insulin fails to:
Inhibit hepatic glucose output (gluconeogenesis)
Stimulate glucose uptake into skeletal muscles
Suppress lipolysis in adipose tissue
All of this leads to increased glucose in the bloodl
Will there be any abnormalities in insulin secretion in T2DM?
Yes
Explain what happens to insulin secretion in T2DM.
By the time of diagnosis at least 50% of beta-cell mass and function has been lost.
This is caused by the hyperglycaemia and lipid excess. They are both toxic to beta-cells known as glucotoxicity.
Glucagon levels in T2DM.
Glucagon secretion is increased in T2DM. This leads to increased hepatic glucose output.
Explain the incretin effect.
Response to oral glucose is greater than the response to IV glucose.
This effect is mediated by GLP-1 and GIP.
Explain the major action of GLP-1 and GIP.
Increase glucose-induced beta-cell insulin secretion and suppressing glucagon secretion.
Also slow gastric emptying and induce satiety.
What happens to the incretin effect in T2DM?
It is impaired.
What is monogenic diabetes?
Previously called maturity-onset diabetes of the young (MODY).
Caused by a single gene mutation predominantly affecting beta-cell function.
How can you tell between monogenic diabetes and T1DM?
T1DM does not present in children before 6 months of age.
Infants who develop diabetes at this age are likely to have a monogenic defect.
The reason for knowing about monogenic diabetes is the difference in treatment compared to T1DM and T2DM.
How can monogenic diabetes be treated?
By sulphonylureas instead of insulin.
Why can monogenic diabetes be treated with sulphonylurea instead of insulin like in T1DM?
Because compared to T1DM monogenic diabetes results from defective insulin release and not from beta-cell destruction.
This means that sulphonylureas can help.
Acute presentation of diabetes.
Usually suggestive of T1DM with a triad of symptoms.
Polyuria due to osmotic diuresis
Thirst and polydipsia
Weight loss due to fluid depletion and accelerated breakdown of fat and muscle.
Subacute presentation of diabetes (along with the original triad).
Lack of energy
Visual blurring
Pruritus vulvae (candida)
Balanitis (candida)
Which complications might be the presenting feature?
Staph infection
Retinopathy during a visit to optician
Polyneuropathy
Erectile dysfunction
Arterial disease
Physical examination of diabetes at diagnosis.
Weight loss
Dehydration
Breath may smell of ketones
Acanthosis nigricans (severe insulin resistance)
Hypertension
What is acanthosis nigricans?
Blackish pigmentation of the nape of the neck and axillae.
Diagnostic criteria for diabetes in symptomatic patients.
The classic symptoms + 1 of the following:
Fasting plasma glucose > 7.0 mmol/l
Random plasma glucose > 11.1 mmol/l
HbA1c >6.5% (48 mmol/l)
Diagnostic criteria for diabetes in asymptomatic patients.
Two of the following tests:
Fasting plasma glucose >7.0 mmol/l
Random plasma glucose >11.1 mmol/l
HbA1c >6.5% (48 mmol/l)
If all tests have been done and examination, and there is still uncertainty about diagnosis.
What other test can be done?
75g oral glucose tolerance teset (OGTT)
Diagnostic values of OGTT at fasting.
> 7.0 mmol/l
Diagnostic values of OGTT 2h after glucose.
11.1 mmol/l
There are two further categories of abnormal glucose concentrations.
Which?
Impaired fasting glycaemia (IFG)
Impaired glucose tolerance (IGT)
What are IFG and IGT collective described as?
Pre-diabetes
Definition of impaired fasting glucose.
Fasting plasma glucose between 6.1 and 6.9 mmol/l.
Can glycosuria be used to diagnose diabetes?
No because of the multitude of causes.
What measurements can help determine the type of diabetes?
C-peptide levels
Islet auto-antibodies
Genetic investigations for monogenic diabetes
How to diagnose diabetes in GP setting
Two HbA1c tests of 48 mmol/mol (6.5%) or higher
6 weeks aparts.
Other causes of diabetes.
Steroid induced
Anti-HIV drugs
Newer antipsychotics
Pancreatitis, pancreatic surgery, pancreatic cancer
Haemochromatosis or cystic fibrosis leading to pancreatic destruction
Cushing’s disease
Acromegaly, phaeochromocytoma, hyperthyroidism and pregnancy.
Congenital lipodystrophy or glycogen storage diseases.
Definition of metablic syndrome (syndrome x).
Central obesity (BMI >30 or waist circumference increased with ethnic-specific values)
+ two of…
BP >130/85
Triglycerides >1.7 mmol/L
HDL <1.03(M) or 1.29(F)mmol/L
Fasting glucose >5.6 mmol/L
T2DM
WHO criteria of diagnosing DM.
Symptoms of hyperglycaemia + raised venous glucose detected once (fasting >7mmol/L or random >11.1 mmol/L
or
Raised venous glucose on two separate occasions - fastin >7 mmol/L, random >11.1 mmol/L or OGTT -2h value >11.1mmol/L
or
HbA1c >48 mmol/mol (6.5%). This should be avoided in pregnancy, children, type 1 DM and haemoglobinpathies.
Monitoring glucose control with meal
Fingerprick =>
Before meal = Informs about long-acting insulin doses
After meal = informs about the dose of short-acting insulin
