Diabetes Type 2 Flashcards

1
Q

What factors cause insulin resistance?

A

Genetic risk

Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is LADA?

A

Latent autoimmune diabetes in adults

  • need be aware aware that there are cases where diabetic ketoacidosis is a feature of T2DM, and it may be present in the youth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is monogenic diabetes?

A

Can present phenotypically as type 1 or type 2 e.g. MODY mitochondrial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which country as the highest projected prevence?

A

India

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Whats a normal fasting glucose vs a T2 fasting glucose?

A

<6mmol/L

vs

> 7mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a normal 2 -hr glucose vs a T2?

A

<7.7 mmol/L

vs

> 11mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens to Beta cell function after T2DM?

A

If treatment is started, function % may increase by a very small %. then it will decrease a few years after being on treatment steadily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does it mean to have relative deficiency of insulin?

A

Insulin is being produced but not enough to overcome insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In which cases may T2DM have complete insulin deficiency?

A

Long duration T2, beta cell failure may progress to complete deficiency

Usually they are started on Insulin at this point and do not stop as they are at risk of ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can genetics cause B cell failure *as a factor of T2?

A

IUGR or involving obesity/fatty acids which are both affected by genetics

Can cause insulin resistance adipocytokines

And these cause B cell failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens to first phase insulin in T2?

A

is lost : plasma levels do not shoot up although they start slightly higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does T2 diabetes affect skeletal muscle uptake?

A

Less glucose uptake due to reduced insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How to T2DM affect hepatic glucose production?

A

Increased due to a reduction in insulin action and increase in glucagon action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What physiological processes contribute to a high fasting plasma glucose in T2DM?

A
  • impaired glucose removal
  • Increased hepatic production
  • inability to oxidise and store in muscles due to bad insulin

= reduction in metabolic clearance rate of glucose

–> excess glucose turned into lactate which enters Cori cycle and turns back into glucose * this results in the increased fasting glucose e.g. from last nights meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can glucagon result in hepatic glucose production in T2DM?

A

excessive glucagon mediated glucose output cause gluconeogenesis

and this is supported by inadequate insulin which causes an influx of substances like glycerol and free fatty acids to live also increasing gluconeogensis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does the graph of insulin sensitivity by insulin secretion look like and how does this differ for T2DM

A

Reciprocal graph

Those people have ‘fallen off the curve’ and for a given degree of insulin sensitivity they secrete less insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which inflammatory adipokines are in excess?

A

TNF-a IL-6

Glucocorticoids

Visfatin

Adiponectin

Endocannabinoids

Leptin

Resistin

Apelin

Fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does TNF-a IL-6 do in T2DM?

A
  • -> lipolysis
  • -> VLDL secretion
  • -> insulin R

decreases adiponectin expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does adiponectin do in T2DM?

A

Decrease insulin resistance and is predictive of diabetes

20
Q

What does Visfatin do in T2DM?

A

Visceral fat

Decreased insulin R in whole body

21
Q

What does Glucocorticoids do in T2DM?

A
  • -> 11B HSD-1 in fat
  • -> fat cell size and IR

–> glucose BP lipids

22
Q

What does ENdocannabinoids do in T2DM?

A

Insulin inhibits expression in fat

fat resistance > circulating EC ?

23
Q

What does Leptin do in T2DM?

A

Elevated in obesity

resistance increases in body, muscle, liver

appetitie decreaser

metabolic rate increaser

24
Q

What does resistin do in T2DM?

A

Elevated in obesity and T2DM

Insulin resistance in whole body and liver

Liver TG secretion increaser

25
Q

What do fatty acids do in T2DM?

A
Elevated in obesity and T2DM
--> IR Whole body muscle and liver 
decreases B cell function
--> Liver TG secretion
--> Organ fat, oxidative stress
26
Q

What does Apelin do in T2DM?

A

Insulin stimulates expression in fat

elevated in hyperInsulin

Cardiovascular effects

27
Q

What is SNPs?

A

single nucleotide polymorphisms

  • each individual SNP has only a mild effect on risk
  • cumulative effect of all SNPs have a bigger effect
28
Q

What are the presentations of T2DM?

A
  • Hyperglycaemia
  • Overweight
  • Dyslipidaemia
  • Fewer osmotic symptoms
  • With complications
  • Insulin resistance
  • later insulin deficieny
29
Q

What is considered during the diagnosis of Type 2?

A

Osmotic symptoms
Infections
Screening test
At presentation of complication

All above can be reasons to look into diagnostic testing:

  • 1 HbA1c with symptoms
  • 2 HbA1c is asymptomatic
30
Q

What type of complications may a potential diabetic present with?

A

Acute: Hyperosmolar hyperglycaemic state

Chronic : ischaemic heart disease, retinopathy

31
Q

Which type of px present with hyperosmolar hyperglycaemia state?

A

Renal failure

insulin is insufficient to stop hyperglycaemia but enough to suppress lipolysis + ketoacidosis

often identifiable precipitating event e.g. infection, MI

32
Q

What is checked during a T2DM consultation?

A

Glycaemia HbA1c, medication review

Weight assessment

Blood pressure

Dyslipidaemia- cholesterol profile

Screening for complications

33
Q

Why is Metformin given?

A
  • Reduces the excess hepatic glucose production
  • lowers the glucose resistance of insulin so increases sensitivity
  • GI side effects
34
Q

What does Thiozolidinediones do?

A
  • lowers the glucose resistance of insulin so increases sensitivity
35
Q

What do Sulphonylureas,
DPP4-inhibitors.
GLP-1 Agonists do?

A

Boost insulin secretion

36
Q

What does Alpha glucosidase inhibitor and SGLT-2 inhibitor do?

A

inhibit carb gut absorption and inhibit renal glucose resorption to reduce excess glucose in circulation

37
Q

What is metformin contraindicated?

A

Severe liver, severe cardiac, moderate liver failure

38
Q

What is the mechanism of action of sulphonylureas?

A

Bind to ATP sensitive potassium channel and close it, independent of glucose releasing insulin

39
Q

What is Pioglitazone?

A

Peroxisome proliferator-activated receptor agonists

peripheral adipocyte differentiation modified = insulin sensitizer

glycaemia and lipid improvements

vascular outcomes

side effects of older types hep, heart failure

40
Q

Which glucose lowering therapy causes most weight gain?

A

Thiozolidinediones

41
Q

What is GLP-1?

A

glucagon like peptide

gut hormone secreted in response to nutrients

transcription product of pro glucagon gene, from L cell

increases satiety

short half life due to rapid degradation from enzyme dipeptidyl peptidase-4

used in DM treatmentq

42
Q

What effects do GLP-1 agonists have?

A

decrease glucagon
decrease glucose
weight loss

  • injectable
  • e.g:
    liraglutide, semaglutide
43
Q

What is Gliptins?

A

DPPG-4 inhibitor (inhibits enzyme)

increases half life of exogenous GLP-1

Increases GLP-1

Decrease glucagon
decrease glucose

neutral on weight

44
Q

What do SGLT-2 inhibitors do?

A

inhibits Na-Glu transporter, increases glycosuria

e.g.

Empagliflozin, Canagliflozin, Deapagliflozin

HbA1c lower

lowers all cause mortality and heart failure

improve CKD

45
Q

What may allow remission of T2DM?

A

Gastric bypass surgery

very low cals - 800 daily for 3-6 months can induce remission

46
Q

Why is lipid management important?

A

Total cholesterol raised
Triglycerides raised
HDL cholesterol reduced
Clear benefit to lipid-lowering therapy