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endo - yr2 > type 2 diabetes > Flashcards

type 2 diabetes Flashcards

1
Q

definition of dm *

A

state of chronic hyperglycaemia sufficient to casue long term damage to specific tissues, notably retina (retinopathy), kidney (nephropathy) nerves and arteries (micro and macrovascular disease)

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2
Q

when is it abnormal that ketones are high *

A

when sugar is high - ie in t1dm

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3
Q

what are the characteristics associated with t2dm *

A

weight (central adiposy), lipids (athrogenic lipid profile) and bp

some people more about the bp/lipids than sugar

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4
Q

what are the cut offs for diabetes *

A

fasting glucose: <6 normal, 6-7 impaired fasting glucose, >7 dm

glucose tolerance test: <7.8 normal, 7.8-11.2 impaired glucose tolerance, >11.1 dm

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5
Q

what is the significance of aving impaired fasting glucose or impaired glucose tolerance *

A

wont have microvasc consequences

will ahve macrovascular disease -atheroma

at risk of dm

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6
Q

describe the epi of t2dm *

A

dm is prevelent - 10% at 60yr - mostly t2 - increasing in every population and predicted to continue increasing

associated with increasing age but aslo in children - occuring and being diagnosed earlier

prevalence varies between countries

greatest in ethnic gps that move from rural to urban lifestyle - with given set of genes - NOT a disease of lifestyle - genetic condition accelarated by lifestyle

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7
Q

summarise the pathophysiology of t2dm *

A

affected by genes, intrauterine env (predict the adult env which fascilitates the onset fo diabetes ie exercise and activity) and adult env - almost autosomal dominant but dont know the genes involved

insulin resistance and insulin secretion defects - deficiency is not absolute - enough present to switch of ketone production

fatty acids important in the pathogenesis and complications - damage the b cells

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8
Q

what is MODY *

A

maturity onset diabetes of young

uncommon

genetic condition that leads to t2dm, know the genes - but is not t2dm - help predict pathophysiology of t2dm

severeal hereditory forms (1-8) - single gene defects

autosomal dom

ineffective b cell insulin production - cant produce insulin/cant sense glucose

because of mutation in transcription factor genes, glucokinase gene

positive FH

no obesity

specific treatment

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9
Q

explain the processes that lead to t2dm *

A

genes mean determined to get dm - they operate through insulin resistance and adipocytokines released from fat cells - insulin resistance wears down B cell as they have to produce more insulin = b cell failure

intrauterine growth restriction - ie lack of calories in utero modulate gene expression for rest of childs life

with genes obestity and fatty acids cause progression to insulin resistance

insuilin resistance causes metabolic and mitogenic problems - dyslipidaemia = progression to atheroma and macrovascular disease

eventually and slowly = b cell failure - cant make enough insulin for resistance - make dyslipidaemia and metabolic effects worse - cause hyperglucaemia and microvascular complications

b cell failure means you need insulin treatment - become absolutely deficient

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10
Q

how do we know that there is a genetic influence in t2dm *

A

there is concordance between monozygous twins of 70-90% - ie if 1 has it the otehr will too, if not it is temporal - havent got it yet - autosomal dominant

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11
Q

is there a genetic component of t1dm *

A

yes but more env is involved than in t2 - these environmental factors are yet to be discovered

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12
Q

how is fetal growth associated with impaired glucose tolerance *

A

low birth weight = more likely to have dm

because low weight means had protein restriction in utero - proteins important for the development of panc

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13
Q

effect of insulin treatment in t1 and t2 *

A

t1 - give insulin and blood sugar doest rise

t2 - insulin has no effect on blood sugar - probably have high insulin anyway - making it to try to overcome resistance

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14
Q

describe how insulin levels and hence dm is affected by age *

A

as age - insulin secretion ccapacity decreases, and you become more insulin resistant

one day wont make enough insulin for resistance - in dm this happens in lifetime, most people, without dm, would die first

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15
Q

describe the presentation of t2dm *

A

heterogenous - sugar, cholesterol and bo involved

obesity common

insuil resistance and secretion deficient

hyperglycaemia and dyslipidaemia - have mroe ldl cholesterol

acute - hyperosmolar complications

and chronic ccomplications - present with blindness/mi - too late

infections eg in urine - bacteria love the sugar

osmotic sympptomes - polydipsea and polyiurea

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16
Q

describe how insulin secretion differs at differnet stages of glucose tolerance *

A

normally have peak of 1st phase insulin and then more is made

in IGT - have smaller 1st peak and then less over hours

in t2DM - vhronically not enough insulin made

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17
Q

effect of t2dm on hgo *

A

unable to stop hgo - so high therefore fasticgg plasma glucose is high

have impaired insulin mediated glucose disposal - difficult to get it into muscle when insulin resistant

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18
Q

describe how the normal response to insulin resistance increase with aging differs from dm response *

A

normally - prroduce more insulin to cope

in dm cant make this insulin - cross the centiles off insulin secretion/sensitivity relationship

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19
Q

describe the mechanism of the pathophysiology of t2dm *

A

main store of energy is TG in fat - TG break down into glycerol and nefa - go to the liver - mainly from omental fat in direct circulation

2 glycerol molecules form glucose - gluconeogenesis

glycogen is broken down in liver - glycogenolysis

hgo doesnt decrease

glucose leaves liver but cant enter the muscle - because insulin resistant = high serum glucose

nefa in liver cant make glucose = converted to small dense vldl colesterol - atherogenic lipid profile

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20
Q

how is fat involved in t2dm *

A

endocrine organ - release factors that are important in the mecanism

they are a means to howw the change in metabolism occurs

adiponectins are of particular interest - reduce insulin resistance and are predictive of dm

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21
Q

how is obesity involved in t2dm *

A

more than precipitant

mechanism of dm is related to obesity

fatty acids and adipocytokines importany

central/omental obesity important - these cells are more met active, and endocrine make more factors here, and drain directly to live r

80% people wioth t2 are obese - more than in normal pop/t1

weight reduction is a useful treatment - improves usgar and maybe results in remission

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22
Q

how is the gut micorbiome involved in dm *

A

microbiome important for normal metabolism

FA released by biome - could enter omental circ and alter liver met - associates with obesity more than dm - this is association rather than causation

bacterial liposacchharides ferment to short cain fa nad bacteria modulatee bile acides - this causes inflammation and alters signalling metabolic pathways

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23
Q

what is a side effect of dm treatment - what is the exception *

A

weight gain

metformin exception - is weight neutral - can cause weight loss - so this is 1st line

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24
Q

how does insulin cause weight gain *

A

stop losing sugar in urine

sugar must go somewhere = weight gain

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25
Q

what affects the interrelation between insulin resistance and secretion that is involved in dm *

A

intrauterine env affect, adipocytokinesm diet and exercise (bring forward resistance if bad) and microbiome insulin resistance

genes affect insulin secretion

failing panc makes more immature insulin - doesnt work properly

medication can be used to try to prevent point where secretion doesnt match resistance

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26
Q

what are the complications if t2dm *

A

microvascular - retinopathy, nepropathy, neuropathy (because of damage to blood supply to distal nerves) - cause morbidity not mortality

metabolic - lactic acidosis, hyperosmolar - these are less likely than in T1

macrovascular - IHD, CVD, renal artery stenosis, PVD (peripheral vascular disease)- mortality anad morbidity

treatmeent can cause hypoglycaemia

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27
Q

what are the 4 things that need to be considered for management of t2dm *

A

education - prevent probleems later

diet

pharm

complicayion screening - before perm damage

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28
Q

why treat t2dm *

A

prevent the symptoms - polyuria and dipsia - good at this

reduce chance of acute metabolic complications

reduce chance of long term complications

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29
Q

what is the recommended diabetic diet *

A

control total calories and exercise - weight

reduced refined carbs

increase complex carb - rice

reduce fat as proportion of calories- less insulin resistance

increase unsat fat as proportion of fat - prevent ihd

increase soluble fibre - longer to absorb carbs

address salt - reduce bp risk

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30
Q

what are the 4 areas to target for dm treatment *

A

weight - orlistat - GI lipase inhibitor - prevent fat absorption

glycaemia

bp

dyslipidaemia

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31
Q

how does gastric bypass help diabetes *

A

improves dm control

adverse events and nutritional deficiency are increased gut peptides modulate energy in take and modulate feeling of fullness- with surgery food makes less contact with the gut which means you reduce energy intake

less calorie intaje

32
Q

describe metformin as a treatment for diabetes *

A

biguanide

insulin sensitiser

give to overweight people with dm where diet alone has not succeeded

reduces insulin resistance - centrally and peripherally = reduced hgo and increases peripheral glucose disposal

doesnt cause weight gain or hypoglycaemia because insulin is not increased

GI side effects inc bloating, abdo discomfort, diarrhoea so titrate the dose and build it up - but well tolerated - safe to sue on everyone with dm

contraindications - severe liver, cardiac or mild renal failure (GFR <30)

33
Q

describe how insulin release is regulated *

A

glucose enter B cell - undergo metabolism = ATP

ATP blcok ATP sensitive K channel - stop K enter

Ca enter through VSCC

stimulate insulin release

34
Q

what is the mechanism of sulfonylureas *

A

act in the B cell adn stimulate insulin secretion

eg glibenclamide

they block the k channel in B cell = insulin release, missing out the glucokinase step

therefore insulin can be secreted even when B cells dont recognise glucose

have to have functional B cells

35
Q

describe sulphonylureas *

A

they are insulin secretagogues

give to lean pts with dm where diet alone has not succeeded

side effect - hypoglycaemia and weight gain

36
Q

what is the action of a glucosidase inhibitors *

A

reduce glucose absorption in the gut

37
Q

describe acarbose *

A

a glucosidase inhibitor

prolongues the absorption of oligosaccharides

allows insulin secretion to cope following defective 1st phase insulin - sugar enters body over 2hrs rather than 2omins

as effective as metformin

sugar is fermented in large bowel = SE - flatus

38
Q

describe thiazolidinediones *

A

make insulin work better - insulin sensitisor centrally, but mainly peripherally

peroxisome proliferator-activated receptor agonists PPAR-y

eg pioglitazone

adipocyte differentiation is modified - weight gain but peripheral not central - better place to ave fat in terms of dm

improvement in glycaemia and lipids

better vascular outcomes

SE of older types - hepatitis and heart failure

39
Q

what do GLP1 and DPP4 do *

A

GLP-1 is given itself or DPP4 inhibitor (gliptins) act in GLP1

benefit endogenous b cells and have an anti-glucagon effect

40
Q

wat is the mechanism of SGLT2 inhibitors *

A

act on PCT increase glucosurea - pts get rid of more glucose

41
Q

what is the different insulin response when glucose is given orally or via injection *

A

orally - have incretin effect - big surge of insulin because of gut peptides

42
Q

describe glucagon like peptide 1 - GLP1 *

A

secreted in response to nutrients in the gut

transcription product of the proglucagon gene - mostly from the L cell

stimulates insulin, suppresses glucagon - increases satiety

restore B cell sensitivity

increase satiety

restore B cell glucose sensitivity

reduces sugar and is effective for weight loss

short half life - rapid degradation by dipeptidyl peptidase 4 (DPPG-4)

43
Q

describe GLP1 agonists and give examples *

A

eg exenatide, liraglutide

injected

long acting

decrease glucagon and glucose

= weight loss

44
Q

describe gliptins *

A

DPPG-4 inibitors

oral

not as effective as glp1 agonist - used because more tolerable than injections

increase glp1

=decrease glucagon adn glucose

neutral on weight

45
Q

describe empaglifoxin *

A

SGLT-2 inhibitor

inhibit na-glucose transporter = glucosuria

effects na transport in heart

reduce hba1c

lower all cause mortality

lower risk of heart failure

46
Q

is medication overall curative *

A

no - B cell func will continue to decline and they will need insulin eventually

47
Q

what is the difference in insulin treatment between young anad old people *

A

old people unlikely to get complications as a result of their dm so dont need to have as tight control

young people - want to prevent complications so want to control as close to normal as possible

48
Q

other than sugar what else do you aim to control in dm *

A

bp - clear benefits to treatment

diabetic dislipidaemia - in dm have high cholesterol, high TG, low hdl - give statin = reduce stroke and mi and increase lifespan

49
Q

what do you need to consider when making a screening tool for dm *

A

what is the problem you are screening for - mortality, morbidity and cost

screen - specifics, which test and for who

diagnosis - use fasted glucose or stimulated

people at high risk?

what is the treatment for people you screen

50
Q

whhat is the most effective treatment for dm *

A

diet and exercise - expensive - need personal trainors and dieticians

51
Q

wat is the time scale for the onset of t2dm *

A

gradual

52
Q

is there a fh in t1/t2

A

common in t2

uncommon in t1

53
Q

where is t1 and t2 common *

A

t1 - north europe

t2 - not europe

54
Q

is there HLA association is t2 *

A

no

55
Q

what is the serum insulin in t1 *

A

low or absent

56
Q

describe subutramine *

A

for weight loss

act on brain to reduce energy intake

taken off market

57
Q

describe rimonabant *

A

cannibinoid inhibitor for weight loss

taken off market

58
Q

what would the cause be of recurrrent boils

A

skin absesses because of infection because immune system down

59
Q

what does it mena if the Hba1c is igh *

A

had dm for a while- not recently

becasue of the lifespan or red cells

60
Q

what level of LDLs do you want *

A

<2

61
Q

what level of HDL do you want *

A

>1

62
Q

what do you wnat your total cholesterol to be *

A

<4

63
Q

what is metabolic syndrome *

A

syndrome predisposes you to dm, fatty liver and MI

criteria: waist circum >94cm men or 80cm women, high TG, low HDL, hhigh BP or t2dm

64
Q

what can you sue to asssess teh patients risk of having a heart attack

A

QRISK3 - if pts see their risk it increases compliance to treatment

65
Q

what can patients do to reduce risk with t2dm *

A

engage in lifelong program 0f self management - lose weightm stop smoking, diet, exercise, enrole in structured education program - 5 day training

have food wit low glycaemic index - sugar spike not as high

reduce fatty acids

high fibre

Diabetes Education and Self Management for Ongoing and Newly Diagnosed - DESMOND

66
Q

what is teh target HBA1c *

A

48 if on 1 drug

59 if on 2

67
Q

what effect would you wnat to see on an antihypertensive eg ace inhibitors *

A

aim for 140/80 unless complications - then 130/80

68
Q

side effect of ace inhib and alternative *

A

cough

so use angiotensin 2 receptor blocker

69
Q

what regular checks should a person with dm have *

A

HbA1c

lipids

BP

pulses of feet

monopathy to check sensation in feet - here checking fro peripheral vascualr disease and neuropathy

check eyes for retinopathy, this is annual

kidneys - protein in urine (microalbuminuria before see actual protein), urea creatinine

70
Q

why is rising obesity increasing dm prevalence *

A

body needs certain amount of insulin for the body mass and number of cells - more mass = pancreas works harder to produce more insulin

if lose weight - can go into remission

71
Q

why might you gain weight when you have been diagnosed for dm *

A

sulphonylureas - increase insulin = increased glucose stored

scared of hypos so overeat

might stop smoking - and smoking suppresses the appetite

72
Q

how would you treat a diabetic pt that is putting on weight *

A

use a GLP1 analogue eg liraglutide - decreases glucagon, and gastric emptying - dfeel fuller - reduced eating

DPP4 inhibitor - reduce breakdown of our own GLP-1

bariatric surgery if >35 BMI wit hypertension/dm (or >30 BMI if asian - have higher risk at lower BMI)

73
Q

what are te outcomes of bariatric surgery *

A

25% weight los at 10 years from te baraitric surgery

30% t2dm remission in 5 years

74
Q

complication of bariatric surgery *

A

malabsorption - need to follow up every pt

75
Q

definition of t2dm *

A

impaired insulin utilization coupled with the body’s inability to compensate with increased insulin production

76
Q

aetiology of t2dm *

A

genetic predisposition

aggravated by being overweight, sedentary and aging

endo - yr2 (24 decks)

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