T11DM

Question 1

define diabetes

Answer 1

state of chronic hyperglycaema which causes long term damage to tissues eg retina/kidney

Question 2

values of diabetes

Answer 2

fasting glucose greater than 7 T11, lower thaqn 6 normal

Question 3

epi of T11DM

Answer 3

most ppl T11DM rathe than T1- prevalence increasing and becoming younger- largest in ethnic groups going from RURAL to URBAN

Question 4

features of T11- ketoacidosis

Answer 4

doesn’t usually occur- insulin enough to prevent this, but NOT HGO

Question 5

MODY

Answer 5

either produce no insulin, or cannnot sense glucose (glucokinase mutation)- often a family history

Question 6

pathophysiology of T11DM DIAGRAM

Answer 6

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

Question 7

genetic component in t1 vs t11

Answer 7

twin study- in T11, most BOTH had T11DM, thus type 2 has MORE of a genetic component

Question 8

IR vs insulin secretion DIAGRAM

Answer 8

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

Question 9

presentation of T11DM

Answer 9

VARIABLE- but most common things are obesity, issues with IR/secretion, dyslipidemia

Question 10

1st phase vs 2nd phase

Answer 10

impaired glucose tolerance affects 1ST PHASE THE MOST

Question 11

relation between fasting glucose and HGO- why

Answer 11

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

Question 12

DIAGRAM relationship between insulin secretion and sensitivtiy

Answer 12

the less sensitive, the more secreted- in diabetics, at lower sensitivity, less secreted

Question 13

explain omental fat

Answer 13

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

Question 14

effect of gut microbioat

Answer 14

can affect obesity, IR and inflammation

Question 15

presentation of T11DM

Answer 15

osmotic symptoms, infections (high sugar loved by pathogens), heart disease, retinopathy

Question 16

complications of T11DM

Answer 16

microvascular- retin/nephr/neuropathy macro- heart/cerebro/renal artery stenosis metabolic- lactic acidosis (rather than metabolic) complication of treatment- hypoglycaemia

Question 17

diet in T11DM

Answer 17

total calories reduce, less simple/more complex, less fat, more unsaturated, more soluble fibre and less salt (BP)

Question 18

what to monitor in T11DM

Answer 18

weight, glycaemia, BP and dyslipidaemia (LDL/HDL)

Question 19

effect of gastric bypass

Answer 19

stops calories getting into ppl+ modulates appetite hormones

Question 20

metformin- advantage+ side effect

Answer 20

makes insulin more sensitive ie CANNOT cause hypoglycaemia and doesn’t cause weight gain, so very safe- causes some GI side effects

Question 21

how sulphonureas work DIAGRAM

Answer 21

glucose goes into be cell, causing ATP to block K+ channel= Ca2+ rushes in= insulin secretion: sulphonureas block K+ channel DIRECTLY

Question 22

acarbose- how it works + side effect

Answer 22

slows down glucose absorption, allowing insulin secretion to cope- causes flatulence/flatus

Question 23

thiazolidinediones

Answer 23

insulin sensitiser, acting on peripheral and some central insulin inhibitors- causes weight gain but distributes weight from omentum to limbs

Question 24

incretin effect and GLP1

Answer 24

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-

Question 25

SGLT2 inhibitors

Answer 25

increases glycosuria ie pee more glucose out

Question 26

other forms of treatment

Answer 26

ACE inhibitors for BP, and statins for dyslipidaemia

Question 27

most important factor in reducing incidence of T11DM

Answer 27

lifestyl

Question 28

compare T11 vs T1

Answer 28

Type 2 greater prevalence with older age onset more gradual lean vs often obese (due to weight loss) family history common in type 2, less in type 1 insulin low vs variable HLA important in type 1 B cell destroyed vs functioning at start antibodies vs none ketoacidosis vs not usually