T1DM Flashcards
ambiguity between T1 and T11
there is autoimmune diabetes leading to insulin deficiency called LADA- similar to T1: monogenic diabetes can also present similarly children may get T11DM ketoacidosis is a feature of late T2DM diabetes may be due to endocrine damage eg cushings/phaeochromocytoma/ALCHOL
pathogenesis of T1DM
autoantibodies against B cells destroy them, causing C peptide BELOW DETECTION- - may be because effector T cells exceed regulator T cells
why immune change in T1DM important
can lead to increased risk of autoimmune disease eg B12 deficiency/addisons, as well as in relatives (family history) antibodies can also be measured for treatment eg islet cell antibodies/insulin antibodies- more prevalent in T1 diabetics
genetic susceptibility
HLA markers on Chr6- DR3/4 alleles increase risk significantly
environmental factors
increased prevalence in winter, possibly due to virus- also more prevalent in different parts of world
symptoms of diabetes
osmotic symptoms (poly/noct/polydipsia) blurry vision thrush (candida infection= rashes) weight loss fatigue
signs of diabetes
dehydration hyperventilation (kussmahls) glycos/ketonuria cachexia (weakness of body)
important organs involved in T1DM
liver, muscle and adipocytes- glucose produced by liver goes into blood, lack of insulin prevents glucose taken into muscle: muscle releases a.a’s, and adipocyte releases glycerol, both of which produce even more glucose in liver, exacerbating hyperglycaemia fatty acids from LIPOLYSIS (NOT glycerol) become ketone bodies (acetoacetate+ hydroxybutyrate) (in liver
aims of treatment of T1DM
prevent early mortality, and long term micro/macrovascular complications (retin/nephro/neuropathy and vascular disease)
diet in T1DM
reduce fat calories, less refined/more complex carbs + more soluble fibre
insulin treatment DIAGRAM
SHORT ACTING insulin given with meals, as well as BACKGROUND insulin (lasts longer)- depending on when meals eaten, there is FLEXIBILITY in insulin treatment insulin pump also given as injecting insulin time consuming- leads to continuous insulin prodcution
islet cell transplants
extract from an individual and given to patient via portal vein- problem is patients are immunosurpressed their whole life
how to monitor treatment+ problems where appropriate
capillary glucose levels (not as accurate as venous glucose levels) CGM’s (continuous glucose monitoring)- alerts you when glucose goes out of target range: works as correlates with lower HBA1C’s HBA1C
explain HBA1C, target+ problem+ why so good
reflection of glucose over 3 months (should be below 42mmol, above 48 is diabetes) as haemoglobin carries glucose- those with anaemia shouldn’t use this, as RBC’s die quickly, so not reflective HBA1C as shows long term glycaemic control- closely linked with microvascular complications
acute effects of T1DM
hyperglycaemia- glucose used by muscle/fat, and liver producing glucose as well metabolic acidosis/ketoacidosis- pH, HCO3- and CO2 low (due to hyperventilation)
hypoglycaemia- define and effects at different glucose elvels
glucose less than 3.6mm- neural issues below 3, unconciousness below 2
who at risk and when most at risk
patients with low HbA1C- occurs pre-lunch and NOCTURNAL (difficult to treat)
why hypoglycaemia occurs
exercise/fasting, alcohol, too much insulin
symptoms of hypoglycaemia
increased SNS- tachycardia, tremor, sweating, cold extremities, anxiety CNS effects- confusion, drowisness, different behaviour, eventual coma
treating hypoglycaemia
orally- simple carbs initially, then complex carbs to prevent glucose crash paraenterally (if conciousness affected)- IV dextrose, glucagon (glucose released from liver)
what causes DKA DIAGRAM
infections mainly, but also not taking insulin, new diagnosis and ischaemic event
bicarbonate generation DIAGRAM
CO2 converted into H2CO3 using CARBONIC DEHYDRATASE- HCO3- goes into blood, and H+ goes into tubule using HK transporter, with help of NA- dehydration= less GFR, so less bicarbonate, so less HCO3- buffering
DIAGRAM henderson hasselbach equation and arterial blood gases
its a metabolic acidosis- low PH, low HCO3- as compensation CO2 goes down too (hyperventilation) anion gap is difference between +ve and -ve ions- a POSITIVE anion gap may be due to DKA (as bicarbonate goes down)
electrolyte issues in DKA
water lost in urine, but also Na and K- acidosis shows high blood K+ but low total body K- this is because K+ mainly intracellular, so acidosis drives out K+
