T11DM Flashcards
(28 cards)
define diabetes
state of chronic hyperglycaema which causes long term damage to tissues eg retina/kidney
values of diabetes
fasting glucose greater than 7 T11, lower thaqn 6 normal
epi of T11DM
most ppl T11DM rathe than T1- prevalence increasing and becoming younger- largest in ethnic groups going from RURAL to URBAN
features of T11- ketoacidosis
doesn’t usually occur- insulin enough to prevent this, but NOT HGO
MODY
either produce no insulin, or cannnot sense glucose (glucokinase mutation)- often a family history
pathophysiology of T11DM DIAGRAM
genetic condition= IR/ ADIPOCYTOKINES (hormones released by fat cells eg leptin)= pancreas produces IMMATURE insulin= B cell failure (IR wears down genetically susceptible B cell) genes also cause INTRAUTERINE GROWTH RESTRICTION in babies- light babies more likely to have diabetes genes also cause obesity, which increases likelihood of IR IR causes inflammation, mitogenic effects, and dyslipidaemia= MACROVASCULAR effects B cell failure also leads to dyslipidaemia, as well as hyperglycaemia= MICROVASCULAR complications
genetic component in t1 vs t11
twin study- in T11, most BOTH had T11DM, thus type 2 has MORE of a genetic component
IR vs insulin secretion DIAGRAM
ageing leads to more IR- we make less insulin as well, hence T11DM interaction between LACK of insulin and insulin not working, B cells worn down
presentation of T11DM
VARIABLE- but most common things are obesity, issues with IR/secretion, dyslipidemia
1st phase vs 2nd phase
impaired glucose tolerance affects 1ST PHASE THE MOST
relation between fasting glucose and HGO- why
both increase when insulin resistant TG broken down into glycerol and NEFA - glycerol and glycogen become glycose (HGO), NEFA makes VLDL in liver, which goes in blood- glucose goes into omental adipocytes= TG
DIAGRAM relationship between insulin secretion and sensitivtiy
the less sensitive, the more secreted- in diabetics, at lower sensitivity, less secreted
explain omental fat
omental fat broken down in adipocytes- thus glycerol/NEFA go into liver via omental circulation (blood going directly to liver), so omental fat more important than fat in limbs
effect of gut microbioat
can affect obesity, IR and inflammation
presentation of T11DM
osmotic symptoms, infections (high sugar loved by pathogens), heart disease, retinopathy
complications of T11DM
microvascular- retin/nephr/neuropathy macro- heart/cerebro/renal artery stenosis metabolic- lactic acidosis (rather than metabolic) complication of treatment- hypoglycaemia
diet in T11DM
total calories reduce, less simple/more complex, less fat, more unsaturated, more soluble fibre and less salt (BP)
what to monitor in T11DM
weight, glycaemia, BP and dyslipidaemia (LDL/HDL)
effect of gastric bypass
stops calories getting into ppl+ modulates appetite hormones
metformin- advantage+ side effect
makes insulin more sensitive ie CANNOT cause hypoglycaemia and doesn’t cause weight gain, so very safe- causes some GI side effects
how sulphonureas work DIAGRAM
glucose goes into be cell, causing ATP to block K+ channel= Ca2+ rushes in= insulin secretion: sulphonureas block K+ channel DIRECTLY
acarbose- how it works + side effect
slows down glucose absorption, allowing insulin secretion to cope- causes flatulence/flatus
thiazolidinediones
insulin sensitiser, acting on peripheral and some central insulin inhibitors- causes weight gain but distributes weight from omentum to limbs
incretin effect and GLP1
oral glucose rather than intravenous causes more insulin secretion due to GLP1- thus GLP1 agonist can be given to surpress glucagon and stimulate insulin- causes weight loss as more satiety alternatively DPPG-4 inhibitor given= more GLP1-
