L18 - T1DM Flashcards
EPIDEMIOLOGY
i) what approx % of adults over 16 have diabetes in the UK?
ii) what is the prevalence?
iii) when is it possible for it to occur? when does it have its peak onset?
iv) does it affect males or females more?
v) does it affect white or BAME more?
vi) is there seasonal variability
vii) is it more prevalent in northern or southern latitudes?
i) 6.7%
ii) 0.5%
iii) can occur at any age but peak onset is in adolescence
iv) affects males and females equally
v) affects white people more than BAME
vi) yes - espec in paeds
vii) higher prevalence in northern latitudes
GENETICS
i) which parents conveys a higher predisposition to their child?
ii) what % of monozygotic twins are affected? what does this show?
iii) what proteins is genetic predispos associated with? which two specific ones?
iv) 90% of T1DM patients from what part of the world are positive for one or both of these proteins?
v) how can T1 and T2DM be differentiated in relation to genetics? how is this done?
i) father
ii) 36% - therefore contrib of both genes and enviro
iii) HLA antigens - DR3-DQ2 and DR4-DQ8
iv) scandinavia
v) look at genetic risk score (GRS)
- look at SNPs that pre dispose to T1DM - how many does each patient have?
PATHOPHYSIOLOGY
i) events in what cells trigger an autoimmune response?
ii) antibodies to which two proteins may appear first?
iii) name two other beta cell antibodies that may appear after this
iv) how are the beta cells overall affected?
i) beta cells
ii) insulin or GAD
iii) IA2 and Zn transporter 8
iv) selective immune beta cell destruction
EVOLUTION OF T1DM
i) how does beta cell mass change as the condition progresses?
ii) what can cause the progression from genetic predispos to insulitis?
iii) what stage is between insulitis and diabetes
iv) name three autoimmune triggers
v) name five other conditions that may be associated with T1DM
i) decreases as condition progresses
ii) environmental trigger
iii) insulitis > pre diab > diabetes
iv) virus (eg coxsackie), endoreticular stress and cytokine release
v) coeliac, addisons, graves, hypothyroidism, pernicious anaemia, hypogonadism, vitiligo
SYMPTOMS
i) what are the 4 T’s?
ii) how may vision be affected? why is this?
iii) why may ketoacidosis occur?
iv) what ketone may cause breath to smell like pear drops?
v) which ketone can lead to DKA?
i) toilet, tired, thinner and thirsty
ii) blurred vision due to glucose in the eye drawing in water
iii) body cant process glucose so starts breaking down fat which can cause ketoacidosis
iv) acetate
iv) D beta hydroxybutyrate
DIAGNOSIS
i) how may age of onset help dx? when is T1DM more commonly seen?
ii) how quick is onset usually?
iii) what other diseases may be of interest
iv) name three antibodies the person may be positive for
v) what protein can be measured to see if the person is making insulin? what is it molecularly? what molar ratio is prod with insulin?
i) age of onset is usually younger than T2DM
ii) quick onset due to beta cell destruction
iii) other autoimmune diseases
iv) GAD, Zn transporter 8 and IA2
v) C-peptide can be measured
- part of pro insulin and is cleaved off (COOH end)
- prod in 1:1 ratio with insulin
T1DM TREATMENT - INSULIN
i) how must it be given? what must it avoid?
ii) give three methods of admin
iii) where should it be injected?
iv) what two types of insulin should be admin? when should each be given? what is this known as?
v) what should the rapid actin insulin reflect?
i) parentally to avoid the GI tract
ii) subcutaneous (most common), inhaled or mucous membranes
iii) into soft tissue to absorb it eg upper arms, thigh, lower abdo or buttock
iv) background long lasting and fast acting injection just before a meal = basal bolus
v) rapid acting insulin should reflect the amount of carbs consumed in a meal
BLOOD GLUCOSE
i) name six things that can affect blood glucose
ii) what blood glucose measurement indicates hypoglycaemia?
iii) name three autonomic symptoms of hypogly
iv) name two neuroglycopaenic symptoms - what causes these? what does a person need when this happens?
i) diet, temperatire, exercise, illness, stress, alcohol, menstrual cycle
ii) blood glucose <4
iii) palpitations, sweating and tremor
iv) confusion and decreased conciousness
- need fast acting glucose eg sweets or lucozade
OTHER TREATMENT METHODS FOR T1DM
i) how does a subcut insulin pump work?
ii) name two disadvantages of a pump? how often does it need to be changed?
iii) what is pancreas transplantation usually paired with? is this common?
iv) what protocol is followed for islet cell transplantation? how does this work? what patients may it be used for?
i) drip feeds in basal insulin
ii) disadv - takes lots of learning and expensive
- changed every few days
iii) usually have panc transplant and kidney transplant although this is uncommon
iv) edmonton protocol for islet cell transplant
- inject beta cells into the liver
- may be useful for patients who have common hypoglycaemia
MONITORING T1DM
i) how many times per day should insulin be checked?
ii) what is CGMS? what does it do?
iii) what is the freestyle libre? why is this good?
iv) what is an ambulatory glucose profile?
v) what can happen if glucose is high? name two ways to monitor this and what each methods detects
vi) what reflects glucose over last three months? what should the target be?
i) at least 4
ii) continous glucose monitoring
- attached sub cut and constantly monitors glucose and alarms if abnormal
iii) flash continuous gluc monitoring - cheap
- measures sub cut glucose (not blood glucose)
iv) ambulatory glucose is last 2 weeks of glucose readings combined into one - gives spread of readings
v) high glucose can cause high ketones
- measure urine for acetoacetate
- measure blood for beta hydroxybutyrate
vi) HbA1c reflects gluc over 3 months (mostly last 6 wks)
- HbA1c affects RBC life span
- target is 48
