Brainscape's Knowledge GenomeTM

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


See full index

BRS YR2 > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

What is type 2 diabetes?

A
  • condition with the combination of insulin resistance and beta cell failure in hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the WHO classify T2DM?

A
  • genetic risk + obesity
  • insulin resistance
  • relative insulin deficiency
  • hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is latent autoimmune diabetes in adults(LADA)?

A
  • autoimmune diabetes leading to insulin deficiency present later in life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can monogenic diabetes present phenotypically?

A
  • T1DM

- T2DM

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

When can T2DM present?

A

Can present in all decade of life

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

When is the prevalence of T2DM greatest?

A

ethnic groups that move from rural > urban lifestyle

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

What fasting glucose levels indicate T2DM?

A

> =7mmol/L

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

What 2hr glucose tolerance test results indicate T2DM?

A

> =11mmol/L

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

What random glucose levels indicate T2DM?

A

> =11.1mmol/L

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

What can be used to diagnose T2DM?

A
  • random glucose (high)

- symptoms of diabetes

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

Why does T2DM not cause ketosis under normal circumstances?

A

due to T2DM being a relative insulin deficiency

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

What happens in long-duration T2 diabetes?

A
  • beta-cell failure may progress to complete insulin deficiency
  • usually on insulin, DO NOT STOP (ketoacidosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the biggest contributory factor to the development of type 2 diabetes?

A

both

  • beta cell failure
  • insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a normal fasting glucose levels?

A

<=6mmol/L

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

What does it mean if fasting glucose levels are between 6-7mmol/L?

A

Impaired fasting glycaemia

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

What 2hr glucose tolerance test results are normal?

A

<7.7mmol/L

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

What HbA1c levels indicate type 2 diabetes?

A

> =48mmol/mol

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

What HbA1c levels are normal?

A

<42mmol/mol

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

What does 2hr glucose tolerance test result between 7.7-11 mmol/L are normal?

A

Impaired glucose tolerance

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

What does HbA1c levels between 42-48mmol/mol mean?

A

pre-diabetes or non-diabetic hypergylcaemia

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

What happens to insulin during T2 diabetes?

A
  • max insulin resistance

- reduced insulin production

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

What happens to insulin during the intermediate stage of developing T2 diabetes

A
  • increasing resistance

- maximum insulin production

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

What is a rapid way to diagnose T2 diabetes?

A

random glucose (>11.1), and symptoms

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

What happens to beta cell mass when developing T2DM?

A

already reduced at time of diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does a relative insulin deficiency mean?

A

insulin is produced by pancreatic beta-cells but not enough to overcome insulin resistance

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

When does ketosis typically form?

A

when there is no insulin

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

What makes the tissues resistance to the action of insulin?

A

a mix of:

  • adipose cytokines (adipokines)
  • internal adiposity (fatty acids)
  • pro-inflammatory state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is diabetes heterogenouses?

A

variable:

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

What is one of the first signs of developing T2DM?

A

the loss of the first phase insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the impact of the loss of first phase insulin release?

A
  • less uptake of glucose into skeletal muscle

- hepatic glucose production is increased due to a reduction in insulin action and an increase in glucagon action.

31
Q

What is the impact of high glucose?

A
  • impaired insulin-mediated glucose disposal

- excessive glucagon-mediated glucose disposal

32
Q

What is the relationship between insulin secretion and insulin sensitivity in T2DM?

A

Low insulin sensitivity, low insulin secretion

33
Q

What are the consequences of insulin resistance?

A
  • increased hepatic glucose production
  • adipocytes, increased fatty acid uptake, and triglycerides form unhealthy lipids (usually inhibited insulin)
  • less glucose muscle uptake
34
Q

What does monogenic mean?

A

single gene mutation (eg; MODY)

inevitable development

35
Q

What does polygenic mean?

A

polymorphisms increasing the risk of diabetes

factor dependent

36
Q

What types of mutations cause T2DM?

A

polygenic

37
Q

What causes T2DM?

A
  • genetic risk

- strong environmental factor(precipitant)

38
Q

What is the role of obesity in T2DM?

A
  • major risk factor

- 80% of T2DM are obese

39
Q

What is central obesity?

A

excess fat in the abdominal area

40
Q

What are other factors implicating developing T2DM?

A
  • pertubations in microbiota

- intra-uterine growth retardation (little when born)

41
Q

How does T2DM present?

A
  • hyperglycaemia
  • overweight
  • dyslipidaemia
  • fewer osmotic symptoms (blurred vision, polyuria…)
  • complications (eg retinopathy)
  • insulin resistance
  • later insulin deficiency
42
Q

What are the risk factors of T2DM?

A
  • age
  • high BMI
  • ethnicity
  • PCOS
  • family history
  • sedentary
43
Q

What is the first line test for diagnosis?

A

HbA1c
1 x HbA1c >=48mmol with symptoms
or
2 x HbA1c >=48mmol asymptomatic

44
Q

What is an acute metabolic decompensation?

A

life threatening state due to hyperglycaemia

in T2DM hyperosmolar hyperglycaemic state

45
Q

What is an acute metabolic decompensation?

A

life threatening state due to hyperglycaemia

in T2DM hyperosmolar hyperglycaemic state

46
Q

What is hyperosmolar hyperglycaemic state?

A

unchecked gluconeogenesism and osmotic diuresis

47
Q

How does hyperosmolar hyperglycaemic state present?

A

common with renal failure

unlikely to present with acidosis

48
Q

Why does a hyperosmolar hyperglycaemic state occur?

A

insufficient insulin for prevention of hyperglycaemia but sufficient insulin for suppression of lipolysis and ketogenesis

49
Q

How do you manage T2DM?

A
  • diet + physical activity
  • oral medication
  • education
  • insulin later
  • remission/reversal
50
Q

What are the complications associated with T2DM?

A
  • retinopathy
  • neuropathy
  • nephropathy
  • cardiovascular problems
51
Q

How do you prevent the complications associated with T2DM?

A
  • good cholesterol
  • good HbA1c
  • good blood pressure
52
Q

What is involved in a T2DM consultation?

A
  • glucose levels
  • weight assessment
  • blood pressure
  • cholesterol profile
  • complications screening
53
Q

How do you check on glucose levels for a consultation?

A
  • HbA1c

- if on insulin, glucose monitor

54
Q

How do you screen for the complications associated with T2DM?

A
  • foot check
  • retinal screening
  • urine test
55
Q

What are the dietry recommendations for T2DM?

A 
- calorie control 
reduce:
- fat
- refined carbohydrates
- sodium
increase
- complex carbohydrates
- soluble fibre
56
Q

What treats all 4 aspects for T2DM pathophysiology?

A

weight loss

57
Q

What can be used to treat the excess hepatic glucose production in T2DM?

A

metformin

58
Q

What can be used to increase insulin sensitivity in T2DM?

A
  • metformin

- thiozolidinediones

59
Q

What can be used to boost insulin secretion?

A
  • sulphonylureas
  • DPP4 inhibitors
  • GLP-1 agonists
60
Q

What can be used to inhibit carbohydrate gut abosrption and renal glucose absorption to reduce the excess glucose in circulation?

A
  • alpha glucosidase inhibitor

- SGLT-2 inhibitor

61
Q

What is Metformin?

A

Biguanide

insulin sensitiser

62
Q

When is metformin used?

A 
first line 
(if dietry/lifestyles changes have made no difference)
63
Q

What does metformin do?

A
  • reduced hepatic glucose output

- increases peripheral glucose disposal

64
Q

What are the side effects of metformin?

A

GI side effects

65
Q

When is metformin contraindicated?

A
  • severe liver failure
  • servere cardiac failure
  • moderate renal failure
66
Q

How do sulphonylureas increase insulin release?

A

bind to the ATP sensitive potassium channel causing it to close and causing it to produce insulin (independent of glucose/ATP)

67
Q

What is Pioglitazone?

A 
insulin sensitiser (through peripheral tissues)
Peroxisome proliferator-activated receptor agonists.
68
Q

How does Pioglitazone work?

A

modifies adipocyte differentiation, causing production of peripheral fat not central when weight is gained.

69
Q

What are the side effects of Piogiltazone>

A
  • hepatitis

- heart failure

70
Q

What is GLP-1?

A

a hut hormone that is secreted in response to
nutrients
transcription production from L cells

71
Q

What does GLP-1 do?

A
  • simulates insulin, suppreses glucagon

- increased satiety

72
Q

What do GLP-1 agonists do?

A

(Liraglutide, Semaglutide)
decrease glucagon, decrease glucose
weight loss

73
Q

What do SGLT-2 inhibitors do?

A

inhibits the Na-Glu transporter, increases glycosuria

- lowers HbA1c

74
Q

What is the effect of treatment on beta cell failure?

A

nothing

BRS YR2 (70 decks)

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