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Endo yr 2 > type 2 diabetes > Flashcards

type 2 diabetes Flashcards

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1
Q

pathophysiology of type 2 diabetes

A

COMBINATION of insulin resistance (the unique characteristic) and beta cell failure that result in hyperglycaemia

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2
Q

how is the resultant chronic hyperglycaemia initially managed? can it be reversable?

A

diet/ weigh loss yes it can

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3
Q

is diet sufficient management long term?

A

no, glu lowering needed, including insulin

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4
Q

what diseases may trigger diabetes presentation?

A

pancreatic damage or other endocrine disease

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5
Q

observations on the prevalence of t2d

A

varies enormously across ehtnic gorups
greatest in ethnic groups that move form rural to urban lifestyle

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6
Q

what are the changes observed in the epidimeology of t2 diabetes?

A

prevalence incr in general from past

diab occuring and being diagnosed younger

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7
Q

how many stages are there in the t2d spectrum and what are the 3 factors that are different in each ?

A

3 stages: 1) normal, 2) intermediate 3) type 2 diabetes
and the three factors are: 1) fasting glucose levels 2) imparied glu tolerance 3) hba1c

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8
Q

range values for fasting glu, imparied glu tolerance and hba1c for the 3 stages of disease

A

fasting glu: 6 <intermid stage <7 mmol/L

(when equal to 6 and 7 included in the other respective categories)

impaired glu tol: 7.7</=mid<11 mmol/L

hbaic: 42</= mid< 48

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9
Q

at which disease stage is insulin prod the highest/ peaks? What is the overall pattern

A

intermediate: peak (low before and drops even lower than before- can even reach 0 during t2d)

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10
Q

what is the pattern of insulin resistance level?

A

zero at normal , slowly increases in intermediate, plateaus at t2d

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11
Q

what is the clinical term for the intermediate stage

A

pre-diabetic hyperglycaemia or pre-diabetes

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12
Q

what is the term for fasting glucose levels at the intermediate stage?

A

Impaired fasting glycaemia

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13
Q

what is the term for impaired glu tolerance at intermediate stage?

A

impaired glu tolerance

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14
Q

when can you diagnose diabetes?

A

diabetic random glu and symptoms of diabetes

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15
Q

(see slide 12) why do t2d patients present at earlier stages of b cell function loss compared to t1d patients?

A

Because even at 50% loss (in contrast to 80% loss for average presentation in type 1) you are resistant so the 50% that are working are not enough bc theres resistance while theres no resist for type 1

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16
Q

what is a clinical scenario of diabetes where this point of the resistance acting as a catalyst for your presentation even with not that huge losses of b cells?

A

pregnancy

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17
Q

what is this phenomenon of not enough insulin production to overcome insulin resistance called?

A

RELATIVE insulin deficiency

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18
Q

why does the hyperglycemia encountered in t2d usually does not cause ketosis?

A

bc of RELATIVE insulin def. bc there IS insulin to inhibit ketone body production in liver, its just that the target cells in body are resistant to it but it EXISTS in circulation so can still inhibit ketone bodies.

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19
Q

when can type 2 diab get ketosis?

A

after theyve had infection in pancreas, diabetes for very long and pancr is shutting down- no glu prod cytotoxic or lipotoxic (from too much lip not being conv to ketone bod bc too much insulin perhaps?) pancr (10-20 yrs),

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20
Q

is it better to stop insulin in someone with long term type 2 (maybe u see theyre on low dose and want to spare them the lifestyle burdain) or better to keep?

A

ITS CRUCIAL CRUCIAL to keep the isnulin treatment bc the longer into the disease the higher risk

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21
Q

4 categories of pathophysiology of type 2

A

1) genes
2) intrauterine environment/ adult environment
3) insulin resistance and insulin secretion defects
4) fatty acids (role in pathogenesis AND complications)

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22
Q

in what ways is type 2 diabetes variable?

A

1) heterogenous (means theres different causes for it:)
2) people develop it at variable BMI, ages and progress differently

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23
Q

what risks does gestational diabetes have?

A

incr. risk of mother and child having normal diabetes
mother: pancreas already has some resistance so …
child: either epigenetic changes or bc of following a certain lifestyle of mother/ family

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24
Q

what is a hyperglycemic clamp?

A

when they give you a specific amount of glucose IV for a continuous time frame to measure your body’s responding insulin production. (basically used to measure b cell function)

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25
difference between standard glu tolerance test and hyperglycemic clamp?
GTT measures GLUCOSE after EATING usualllly a sugary drink after having FASTED, aim is to see if body can lower glu levels, used to DIAGNOSE diabetes, more natural repsonce observation. clamp is more artificial way, not used for diagnosis.
26
what is observed in insulin production after givinf the iv glu challeneg to t2d vs normal?
spike in insulin prod immediately after glu challenge given in normal vs minimal insul prod in t2d
27
2 basic mechanisms of low insulin causing increased FPG (fasting plasma glucose levels)? (and the official terms)
1) glucose cant enter target cells eg peripheral muscles (impaired-insulin mediated glucose disposal) 2) gluconeogenesis not inhibited by insulin anymore, glucagon is allowed to act on liver : hepatic glucose production is increased (excessive glucagon-mediated glucose output)
28
what are two ways/ terms to describe glucose not being able to enter tafrget cells due to low/ resistance to insulin?
impaired insulin- mediated glucose disposal reduced metabolic clearance rate of glucose
29
what event does Cori cycling refer to?
the excessive amounts of glucose in blood converted to lactate which then returns to the liver to be metabolized back to glucose
30
what event could explain early morning increase in FPG in the progression to T2DM
cori cycling from previous nights meal
31
2 more mechanisms of Further increasing FGP in diabetes.
Inadequate insulin action also causes an increased flux of substrates – glycerol and free fatty acids – to the liver, resulting in increased gluconeogenesis. Inappropriate glucagon secretion induces continued glucose production by stimulating glycogenolysis (release of glucose from glycogen, its stored form) (in addition to already mentioned gluconeogenesis)
32
ABOVE WHAT FPG levels is HGP more evident (in mg/dl)
>140
33
American Diabetes Association’s diagnostic criterion for FPG?
>/= 126 mg/dl
34
look at ipad for relationship between insulin resistance and secretion
35
3 other lipid/ adipocyte related consequences of low insulin
insulin normally incr the conversion of trig to gly and nefa so they can enter adipocytes. now not conv, stay in blood also insulin stimulates transporter allowing glu to enter adipocytes also promotes recombination of gly and nefa in adipocyte so they can leave again
36
does glucagon have an effect on muscle cell glucose transporters (that llow glu into cell?)
yes, inhibits them
37
what is monogenic vs polygenic diabetes?
monogenic: MODY (maturity onset diabetes of the young) - single gene mutation causes it, ur born with it polygenic: you have polymorphisms that incr risk, may develop later DEPENDING on other factors
38
is the proportion of environmental / genetic factors influencing t2d onset relatively fixed for df people?
no, very variable may have low gen risk and low env: low general or very low env and very high genetic
39
what is the usual cause of a lean person having t2d?
problem with pancreas b cells insulin production
40
how are GWAS done for diabetes related nucleotide changes?
u get people with t2d and controls and look at Nucleotide changes present in type 2 diabetes group but not controls
41
average percentage risk of diabetes with one single nucleotide polymorphism
1.2%
42
average absolute risk of diabetes with 40 nucleotide polymorphisms
11.2% (prevalence)
43
what % of t2diabetics are obese?
80%
44
what components/ mechanism of obesity make it major risk factor for t2d?
Fatty acids and adipocytokines important Central (subcutaneous) vs visceral )(problem) obesity
45
what are some other factoras that have been correlated/ associated with t2d?
1) Perturbations (αναστατώσεις) in gut microbiota 2) fermentation of Bacterial lipopolysaccharides to short chain FA, 3) bacterial modulation of bile acids 4) Inflammation, signaling metabolic pathways 5) Intra-uterine growth retardation
46
what is did hales et al 1991 show abt intra uterine growth retardation and t2 diabetes
Weight at age 1 year <8.16kg, 22% had type 2 diabetes or IGT (impaired glucose tolerance) Weight age 1 year >12.25 kg, 6% had type 2 diabetes or IGT (meaning, more underweight children at 1yr get t2d)
47
typical t2d symptoms
Hyperglycaemia Overweight Dyslipidaemia (can have) osmotic symptoms (fewer) With complications Insulin resistance Later insulin deficiency infections,
48
what are the complicaitons associated with t2d and at what stage of disease do thwy happen
later in disease more long term renal failure (diabetic nephropathy) nerve disease arteriosclerosis stroke (HYPEROSMOLAR BLOOD- VISCOUS- BLOOD CLOTS- STORKE) eye disease ( diabetic retinopathy, GLAUCOMA, CATARACT) diabetic foot (eventually u feel numb and stuff in your feet) heart damage stroke
49
acute t2d presentaiton
hyperosmolar hyperglycaemic state
50
chronic t2d presentaiton
(complications linked) ischaemic heart disease, retinopathy
51
firs tline t2d diagnosis
1x HBA1C> 48 AND symptoms OR 2X HBAC> 48 IF NO SYMPOTMS
52
WHAT COMplication does hyperosmolar hyperglucemic state commonly present wotih?
renal failure
53
why is there not ketogenesis and lipolysis in hyperglycaemic hyperosmolar patients ( clearly there have insulin problem)?
because even though insulin not enough for supression of hyperglyc, it IS ENOUGH TO SUPRESS ketogenesis (->acidosis) and lipolysis
54
what is a common history of presenting complaint for hyperosmolar hyperglycaemic state
some identifyable percipitating event such as infection or MI
55
what are two common areas of management in t1 and t2 d
- giving insulin (t1 always: basal-bolus treatment- t2d: maybe give later in disease) -structured education
56
unique type 1 and 2management strategies
t1d: technology self monitoring glu t2d diet oral medication
57
things to do in t2d consultation
glucose monitor (hbac1) medications check weight assessment blood pressure dyslipidaemia (cholesterol profile) complications check
58
dietary recommendations and education 6 pricnciples
total calories control reduce calories as fat reduce calories as refined carbohydrate decr sodium increase calories as complex carbohydrate increase soluble fibre
59
what doe metformin do?
1) reduce hepatic glucose production - 2) improve insulin sensitivity (also increases peripheral glucose disposal)
60
what do thiozolidinediones do (pioglitazone) ? what is their medical name?
2) improve insulin sensitivity (mainly peripheral ) -Peroxisome proliferator-actived receptor agonists PPAR-γ
61
advantages/ disadvantages of pioglitazone and what type of
disadv Adipocyte differentiation modified, weight gain but peripheral not central Side effects of older types hepatitis, heart failure may cause wight incr adv: Improvement in glycaemia and lipids
62
what to sulphonylureas do? (DPP4 inhibitors GLP-1 Agonists) and how specifically?
boost insulin secretion. -normally glucose gets in b cell by glut 2, converted to atp, blocks K channel, K stays in cell, stimulates ca channel, ca flows in, stimulates insulin secretion - bc theres no glucose coming into cell, atp cant vlock k channel so this drUg does this instead (plays role of ATP)
63
what does Alpha glucosidase inhibitor SGLT-2 inhibitor do?
Inhibit carbohydrate gut absorption Inhibit renal glucose resorption
64
what problems does weigh loss help?
all the problems
65
what category of srugs is metformin under
biguanide
66
when is metformin given
when first line/ dietary hasnt worked
67
metformin side effects and when is it contraindicated
GI side effects Contraindicated in severe liver, severe cardiac or moderate renal failure
68
what is a common side effect of glucose lowering therapies? how is emtformin bit diff?
wight gain, metformin: can weigh loss
69
WHAT IS GLP-1 (glucagon like peptide -1)
Gut hormone Secreted in response to nutrients in gut Transcription product of the gene coding for proglucagon (precursor of glucagon) , mostly from L-cell
70
what does glp-1 do molecularly and clinically ?
Stimulates insulin, suppresses glucagon Used in treatment of diabetes mellitus liraglutide, semaglutide ↑ satiety (feeling of ‘fullness’). (weight loss) injectable daily or weekly
71
why does glp1 have short half life?
due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)
72
what is the incretin effect and why do we care
The relative increase in insulin in response to oral glucose relative to intravenous glucose is known as the incretin effect. Relevant for treatment T2dm.
73
examples of GLP-1 agonists
Liraglutide, Semaglutide
74
DPP-4 inhibitor (gliptin) and what does it do molecularly and clinically?
Increase half life of exogenous GLP-1 Increase [GLP-1] Decrease [glucagon] Decrease [glucose] Neutral on weight
75
what do SGLT2 INHIBITORS DO molecularly and clinically
inInhibits Na-Glu transporter, increases glycosuria HbA1c lower 32% lower all cause mortality 35% lower risk heart failure Improve CKD
76
SGLT2 INHIBITORS examples of drugs
Empagliflozin, dapagliflozin, canaglifloz
77
dif between remission and cure
n summary, "treatment" involves the active management and care provided to address a medical condition, while "remission" describes the state in which the signs and symptoms of the condition have significantly improved or disappeared.
78
APPROAches to achieve remission of t2d
Gastric bypass surgery has the potential to induce remission of type 2 diabetes DIRECT Study / DROPLET study: very low-calorie diet (800 kcal/day) for 3-6 months has the potential to induce remission, which appears to be sustained at 2 years
79
other aspects of t2d management? and how
Blood Pressure management Hypertension very common in T2DM Clear benefits for reduction esp with use of ACE-inhibitors Lipid management Total cholesterol raised Triglycerides raised HDL cholesterol reduced Clear benefit to lipid-lowering therapy

Endo yr 2 (11 decks)

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