Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LCRS Endo > T2DM > Flashcards

T2DM Flashcards

1
Q

what is the simple definition of type 2?

A

state of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues

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

what are the 3 main contributors to T2?

A
  • body weight
  • lipids
  • blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

does ketosis occur in T2DM?

A

T2 is not ketosis prone or mild but it can happen

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

what is the fasting glucose in T2?

A

> 7 mmol/L (normally 6)

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

what is the range between 6 and 7 mmol/L fasting glucose called?

what is the 2 hour response to this called?

A

impaired fasting glucose

impaired glucose tolerance

these people are not diabetic but are on course to be. They are also developing macrovascular complications.

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

which is the more common form of diabetes?

A

type 2

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

who can be affected by T2?

A

adults mostly

children can be too

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

what factor varies the incidence of T2 around the world?

A

ethnicity

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

in which demographics is type 2 greatest?

A

ethnic groups who move from rural to urban lifestyles

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

how many hereditary forms of MODY (uncommon) are there?

inheritance method?

A

1-8 (each type has a specific treatment)

autosomal dominant

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

what mutation causes MODY (Maturity Onset Diabetes of the Young)?

A

glucokinase gene:

transcription factor used by beta cells to recognise glucose concentration leading to ineffective beta cell insulin secretion

  • no obesity caused
  • there will be a positive family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what factors influence the pathophysiology of Type 2?

A

genetics
intrauterine environment (epigenetic changes)
adult environment

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

what are the two errors with insulin in type 2?

A

insulin resistance
insulin secretion deficit (deficiency)

fatty acids also involved

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

what two factors lead to microvascular problems?

A

1) insulin resistance
(causes dyslipidaemia, increased mitogenic pathway, hypertrophy and increase in BP all whilst blood glucose is normal)
atheroma progression
Beta cell failure and eventual insulin loss

2) dyslipidaemia

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

what factor leads to microvascular problems?

A

hyperglycaemia

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

what factor increases the chances of the foetus developing type2?

A

IUGR- intrauterine growth restriction effects the foetus modulating gene expression

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

what is the genetic inheritance pattern in T2?

A

follows an almost autosomal dominant pattern whilst type 1 has less genetic output

T2DM has a great genetic input

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

weight at birth and risk of type 2

A

the lighter the baby, the greater the risk

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

normal changes to insulin with age

A

production decreases with age and we become more resistant to it with age

when resistant and low production bisect, insulin supply does not meet the resistance

the bisection occurs at age 110 in caucasians and sooner in others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the presentation of type 2 DM?

A

 Heterogeneous – there are many forms/causes of T2DM; there isn’t just one T2DM.
 Obesity.
 Insulin resistant and secretion deficient.
 Hyperglycaemia and dyslipidaemia –> acute and chronic complications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the delayed insulin production response called?

A

hyperglycaemia clamp

where people developing type 2 will have some insulin production but they lose their first phase response to glucose so make insulin eventually but it takes longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the first phase response to glucose

A

stored insulin is released when stimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the second phase response to glucose

A

insulin which is produced and secreted over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what causes the increased blood glucose in type 2?

A

hyperglycaemia due to insulin resistance affecting glucose uptake:

  • deficient insulin means glucose can’t move into muscle and metabolising tissue
  • HGO continues to produce glucose even after eating thinking there isn’t enough glucose
  • glucose remains in the blood and reaches high level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what happens with insulin sensitivity with age?

A

insulin sensitivity decreases therefore secretions are increased to compensate

diabetics under-compensate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how are VLDLs present?

A

as fatty acids can not be made into glucose, they are made into atherogenic VLDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The role of obesity in T2DM

A

 More than a precipitant.
 Fatty acids and Adipocytokines are important.
 Central/omental obesity is common - 80% of T2DM.
 Weight reduction is a useful treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

role of gut microbiota in type 2

A

They increase free fatty acids

therefore: associated with obesity, insulin resistance, T2DM, inflammation and adipocytokine pathways.
- Possibly via host signalling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

role of gut bacteria

A

Various lipopolysaccharides are fermented by gut bacteria to short chain FFAs which enter the host circulation and modulate bile acids

30
Q

which is the only drug to reduce weight

A

metformin

31
Q

why does weight increase during diabetes treatment

A

reduction of blood glucose increases appetite

32
Q

how does late T2DM present

A

pancreas makes immature insulin that is dysfunctional

33
Q

what is the clinical presentation of T2DM?

A 
o obesity 
o glycosuria
o polydipsia, polyuria, nocturia
o fatigue 
o blurred vision 
o Infections , thrush
– hyperglycaemia is favourable for bacteria.
o Screening tests.
o Often found at presentation of complications – acute (hyperosmolar coma) or chronic (IHD, retinopathy).
34
Q

where can complications presented arise from?

A

Complications can be:

  • microvascular
  • macrovascular
  • metabolic (much rarer than for T1DM and ketoacidosis)
  • from treatment (hypo attack).
35
Q

what are the management options for T2DM

A
  • education
  • diet
  • pharmacological treatment
  • complication screening.

therefore help symptoms, reduce chance of complications and educate

36
Q

how must the diet be controlled?

A

 Control total calorie intake/increase exercise.
 Reduce fat as proportion of calories and reduce refined carbohydrate (sugar).
 Increase complex carbohydrate, unsaturated fat as proportion of fat and soluble fibre.

37
Q

what 3 things are monitored in treatment?

A
  • weight
  • glycaemia
  • BP
  • dyslipidaemia
38
Q

what drugs are used to treat type 2?

A 
- orlistat 
(pancreatic lipase inhibitor) 
- metformin 
(biguanide-insulin sensitiser)
- sulphonylureas 
(existing pancreas makes more insulin) 
- alpha glucosidase inhibitors 
(delays glucose absorption and boosts first phase) 
- thiazolidinediones
 (acts on adipocytes and insulin sensitiser peripherally in fat and muscle)
- glifozins 
(SLGT-2 inhibitor) 
- GLP-1 agonists + DPP4 inhibitor
 (increase satiety)
39
Q

what class of drugs are insulin sensitisers?

A

biguanide e.g metformin

oral anti-hypertensive drugs

40
Q

example of biguanide

use?

A

metformin (1st line)

  • insulin sensitiser
  • used in the overweight patients where diet alone has not worked out
  • reduce insulin resistance therefore reduced HGO and increases peripheral glucose disposal

has GI side effects

41
Q

side effects of metformin

A

GI side effects
do not use in severe liver/cardiac failure and mild renal failure

GOOD: no weight gain

42
Q

example of sulphonylureas

A

Glibenclamide

43
Q

what is the action of sulphonylureas

A

act on remaining beta cells to increase insulin secretions by blocking ATP sensitive potassium channels and cause influx of calcium

cause weight gain

44
Q

in which patients are sulphonylureas used in ?

A

in lean patients (as it can cause weight gain)

45
Q

side effects of sulphonylureas

A

Hypoglycaemia

weight gain

46
Q

example of alpha glucosidase inhibitor

A

acarbose

slow down glucose absorption and aids first phase

47
Q

action of alpha glucosidase inhibitors

A

prolongs absorption of oligosaccharides

allows insulin secretion to cope following defective first phase insulin

48
Q

side effect of alpha glucosidase inhibitor

A

just as effective as insulin but can cause flatuence

49
Q

example of thiazolidinediones

A

pioglitazone

reduce insulin resistance

50
Q

what is the action of thiazolidinediones?
what are the effects?

why is there peripheral weight gain?

A

peroxisome proliferator-activated receptor agonist (PPAR-GAMMA):

  • sensitises insulin peripherally
  • improves glycaemia and dyslipidaemia
  • good vascular outcomess
  • prevent MI
  • adipocytes are rearranged so weight gain is peripheral rather than central

NB gemfibrozil (a lipid lowering fibrate agonises the PPAR-ALPHA receptor)

51
Q

what are the side effects of thiazolidinediones e.g. proglitazone?

A

hepatitis

heart failure

52
Q

examples of GLP-1

A

exenatide

liraglutide

53
Q

Where is GLP-1 secreted from normally?

in response to what?

A

L-cells in response to nutrients in the gut (incretin effect)

54
Q

what is the action of GLP-1

A

main: incretin effect

stimulates insulin and suppresses glucagon and increases satiety

55
Q

what is GLP-1 broken down by?

how is this clinically relevant?

A

DPP-4 (gliptins)

therefore has a short half life
therefore DPP-4 inhibitors can be used to prolong the action go GLP-1 analogues

56
Q

GLP-1 drug

A

injected
long acting GLP-1 agonist
decreases glucagon and glucose
leads to weight loss

57
Q

what are DPP-4 inhibitors?

A

Gliptins (anti-glucagon effect)

  • increase half life of exogenous GLP-1 so it can have its incretin effect
  • neutral effect on weight
58
Q

what does empagliflozin (gliflozins) do?

A

inhibits Na-glucose transporter (SLGT-2 inhibitor)
increase glycosuria by affecting PCT of the kidney

reduce mortality
reduce HF due to sodium transport effect in the heart

59
Q

what are the contributors to major problems of diabetes?

A

1) high BP- 90% of T2 patients have issues

2) dyslipidaemia- high cholesterol, TG and less HDLs –> macrovasc complications

60
Q

what is the incretin effect?

A

oral glucose has a greater metabolic effect

more insulin produced in response to oral load of glucose than IV glucose

61
Q

what is the most successful intervention in Type 2 diabetics?

A

lifestyle changes including dietary over metformin

62
Q

which groups of people need to be identified as high risk of diabetes?

A

gestational diabetes (temporary pregnant diabetics)

impaired glucose tolerance people

63
Q

why is Type 2 hard to screen?

A

doesn’t present until complications have arisen

64
Q

what effect will statins have?

A

for ischaemic heart disease to reduce LDLs and increase HDLs

but increases chance of t2Dm development and myositis

65
Q

what effect does metformin have?

A

insulin sensitiser:

  • decreases HGO
  • increased sensitivity to insulin

side effects: diarrhoea, nausea, abdominal pain and lactic acidosis.

no weight gain

66
Q

what effect does sulphonylurea have compared to metformin?

A

sulphonylurea increases insulin secretion

metformin is an insulin sensitizer.

67
Q

how can weight increase during DM treatment be tackled?

A

give GLP-1 to stimulate incretin effect for increased insulin secretion and increases satiety.

68
Q

what is the incretin effect? is the incretin effect present in diabetic?

A

The incretin effect is defined as the increased stimulation of insulin secretion elicited by oral as compared with intravenous administration of glucose under similar plasma glucose levels.

Patients with type 2 diabetes have been demonstrated to exhibit an almost total loss of incretin effect (don’t respond with increased insulin when ingesting glucose)

69
Q

how can the incretin effect induced by GLP-1 be enhanced?

A

DPP4-Inhibitors

– reduce breakdown of GLP-1

70
Q

what do DPP4-Inhibitors do?

A

inhibit breakdown of GLP-1 so the incretin effect is done on diabetics (which they lack)

LCRS Endo (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions