T1DM Flashcards
T1DM
DM is the pathological and metabolic state caused by inadequate insulin action
to be thought of as a vascular disease
selective autoimmune destruction of insulin secreting B cells in the pancreas
risk of developing T1DM if family have it
genetics counts for 1/3 of the risk in T1DM
larger risk in mono and di zygotic twins, HLA identical siblings and if both parents have it
concordance is only 30% in identical twins, indicating environmental influence
(genetics plays a much larger part in T2DM)
is the genetic risk larger in T1 or T2 DM
T2DM
HLA genes
represent around half of familial risk
the highest risk genotype is DR3-DQ2/DR4-DQ8
95% of those diangosed with T1DM under the age of 30 have one or both of the genotypes
there is no HLA association in T2DM
describe the development of T1DM
- there is a genetic predisposition, influenced by foetal risk factors
- immune dysregulation leads to insulitis and beta cell injury
- this can lead to pre diabetes, which eventually leads to overt diabetes
- environmental triggers and factors can accelerate/cause this progression
risk factors in foetal life
infection
age
ABO mismatch
birth order
auto-immune trigger factors
viral infection
vitamin D deficiency
dietary factors
environmental toxins
= pre-diabetes (can last for months to years)
accelerating factors for development of T1DM
infection
insulin resistance
puberty
diet/weight
stress
diagnosis of DM
fasting glucose ≥ 7
random glucose ≥ 11.1
and symptoms of hyperglycaemia OR repeat test
what are the clinical features of hyperglycaemia
hyperglycaemia causes an osmotic diuresis, which causes dehydration: polyuria and polydipsia (excessive thirst)
unexplained weight loss
visual blurring
genital thrush
lethargy and somnolence
increase in appetite
ensuresis
symptom of polyuria due to hyperglycaemia
- inability to control urination (bed-wetting)
could be a sign of diabetes in children
why is there unexplained weight loss
insufficient insulin also stops glucose from entering the tissues, meaning they have to break down fats for energy
increased lipolysis (FA release from adipose tissue).
what is a possible presentation of DM
acute short sightedness
later in life develop cataracts, glaucoma etc and diabetic retinopathy
why is there visual blurring
high levels of glucose in the blood can be absorbed by the lens of the eye, which changes its shape
the lens will return to its normal shape once normal glycaemic control has been established
what is lethargy and somnolence associated with
poor glycaemic control - go away once this is established
investigation: urine glucose
normally there is no glucose in the urine, if there is too much in the blood it will be excreted via the urine
tested for using urinalysis
random glucose
not diagnostic of diabetes, ≥11.1 mmol/L
diagnostic with symptoms, resting and fasting raised
OR
fasting and resting raised on 2 separate occasions
elevated HbA1c
≥48mmol/L
HbA1c
glycated haemoglobin
during its life a Hb molecules will slowly react and attach (non-enzymatically) to glucose present in the cell - forming glycated Hb
if patient has chronically high blood glucose they will have more HbA1c
used to measure long term blood glucose control in known diabetics as a way of evaluating the effectiveness of their management
what is high HbA1c often a sign of
non compliance
in what situations can HbA1c vary and be unreliable
haemolytic anaemia, acute or chronic blood loss, pregnancy
describe the limitations of HbA1c
descibe the target levels for HbA1c
normal = 42 mmol/L
pre- diabetes = 42-47 mmol/L
target in diabetic patients = 48 mmol/L in younger patients, 53 mmol/L in others
dangerous = >75 mmol/L
islet autoantibodies
suggest T1 rather than T2
GAD 65, IA2 and IAA
