Type1 DM Flashcards
What are the two types of DM? And what they tend to be like?
type 1: thin, young, no insulin-not insulin resistant
Type 2: fatter, older-insulin resistant
But not that clear cut in year life
Why is the clinical difference between T1DM and T2DM ambigious?
Type 1 can present late in some patients as LADA (latent autoimmune diabetes in adults)
and Type 2 can present early in some-even childhood (diabetic epidemic)
Also ketoacidosis-can be a feature of T2DM (not only T1)-insulin deficiency by constant irritation (often in black people)
And monogenic diabetes can also change this (MODY)-rare
Also hyperglycemia can be a result of other conditions
Which type of diabetes is most common
T2DM is much more common, then t1, then MODY and LADA
What is the etiology of T1/T2DM
T1 etiology is uncertain-but environement + genes => cause destruction of B-cells
T2 is similar mix but larger gene component-at first insulin resistant and then become insulin deficient as B cells die
What is the pathogenetic path of T1DM?
B cells are the key ofc
AB target the cells and damage them
Early period-slight hyperglyceamia, but some B cells left
But in time loses them all and finish with complete insuin deficiency. can happen fast- ends with hyperglyceamia
Theory that at start of T1DM, intermittent state balance between destruction and proliferation-before complete failure
The AB part means it can be used to diagnose
Why is the immune characteristic of T1DM cause for further concern?
because means patient could be prone to other AID-b12 deficiency, coeliac, addisons, Rhumatoid arthiritis
Relatives could also be at risk
How important is genetic in T1DM?
Well different HLA genes can indicate different chances of patients havig it. DGR3 is important
How important is the environement is in T1DM?
Higher incidence during winter-maybe infections?
Also higher incidence is one part of sardignia. unsure why
But unsure how important is it-or if Abx can be enought to stop it
What are markers that are useful to diagnose t1Dm
For new patients-just after B destruction-islet cells A, insulin AB, GADA AB, IA2A AB -T1 patients tend to have alot more than other people
What are the clinical features of a T1DM patient?
Usually in lean youth, where start with polyuria, polydypsia, nocturia, weight loss (extreme)->tiredness
CAn get vision blur, candida infection
Usually means in hospital arrive dehydrated, cachectic, hyperventilating (metabolic acidocis), Ketone in breath (can smell), glucose and ketone in urine
Describe the several aspects of inuslin deficiency on organ biochemistry
Important organs are liver, muscle and adipose
If deficient in insulin-glucose exreted by liver into blood, and cannot make its way into the muscle (left in blood) at the same time, muscle provides AA for gluconeogenesis for liver-more glucose made and to blood
Also adipose tissue, if insulin deficient, releases glycerol and provides the liver means to make even more glucose
Adipose tissue also provide FA to liver to make ketone bodies (without insulin)-
What are the aims of treatment of t1DM?
avoid early mortality-insulin
avoid co-moribidities (retinopathies, neuropathy, nephropathies, vascular diseases)-these are much longer term (also stroke, MI, and more)
What is the role of diet in T1DM treatment?
Reduce simple carbohydrates intake (low sugar, low fat)-more fibre and more complex carbo
Less important than in t2dm
How do insulin levels vary during the day and how does it vary in T1 and 2 DM?
after each meal, peak production in relation with the size of the meal
Also basal insulin constantly produced
In T1- nothing-so try and mimic the peak (insulin analogues) AND the basal insulin (long acting insulin-zinc bound causes longer acting-or special analogues)
What is an insulin pump? what is the benefits and negatives of it?
Taking long and short acting insulin can be time consuming
small Pump sits on abdomen, and gives basal insulin-but can be increased anytime (when meal or snack)
issue is expensive + no blood glucose sensor (so no feedback)
