Brainscape's Knowledge GenomeTM

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


See full index

CVDM > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What type of insulin does an insulin pump have?

A

Short acting insulin

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

What regime are insulin injections given in and why?

A

Basal bolus regime to try and mimic the body’s normal response

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

How long have islet transplantations been done for?

A

~20 years

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

Limitations of islet transplantations

A

Requires cadaveric islets
Patients need to go on immunosuppressants
Reserved for those with severe hypoglycaemia

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

Risk factors for diabetes

A

HLA type
Family history
Levels of anti-islet antibodies in the blood

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

What is a closed-loop system in treatment of diabetes and what does it involve?

A

It is basically an artificial pancreas
It uses real time glucose data to affect the insulin administration from the insulin pump, but is not licensed at the moment

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

Why does T1D develop?

A

Immune based disease on a background of susceptibility factors

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

Can T1D be predicted?

A

Partially
Can sometimes predict whether or not someone will develop diabetes but can’t predict when

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

Epidemiology of T1D

A

Highest incidence in individuals of European descent and rates increasing in Europe
Peaks at age 5-7 and again at puberty
Highest incidence in Scandinavian and Northern European cohorts

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

Genetic risk factors for T1D

A

Polygenic
HLA genes on chromosome 6 lead to 50% increased risk (HLA class II)
>40 genes identified

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

Environmental risk factors for T1D

A

Viral infection
North/South hypothesis - vitamin A/vitamin D exposure

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

What is currently the only available marker of islet autoimmunity in T1D?

A

Islet autoantibodies

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

What percentage of individuals with T1D will have islet autoantibodies?

A

93%

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

What is Type 1 diabetes?

A

An autoimmune disorder of beta cell destruction which results in a state of absolute insulin deficiency

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

Commonest autoantibody in T1D

A

Anti-GAD

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

Diagnosis of T1D

A

Fasting blood glucose ≥7mmol/L
Random blood glucose ≥11.1mmol/L and symptoms
Often the type of diabetes diagnosed on symptoms alone but if in doubt check autoantibodies

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

What is T2D due to?

A

Progressive loss of beta-cell insulin secretion frequented on the background of insulin resistance

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

What is gestational diabetes?

A

Diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation

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

What is idiopathic T1D?

A

When patients have permanent insulinopenia and are prone to DKA but there is no evidence of beta cell autoimmunity

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

What HbA1c level is diabetes diagnosed at?

A

≥48mmol

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

Aims of therapy in T1D

A

Prevent hyperglycaemia
Prevent hypoglycaemia
Reduce chronic complications

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

Aims of therapy in T1D

A

Prevent hyperglycaemia
Avoid hypoglycaemia
Reduce chronic complications

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

Hyperglycaemia symptoms

A

Thirst
Tiredness
Blurred vision
Weight loss
Polyuria
Nocturia
Fungal infections
Altered cognitive function, mood state, information processing and memory

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

Hypoglycaemia symptoms

A

Pallor
Sweating
Tremor
Palpitations
Nausea
Hunger
Confusion
Coma

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

What is done in a diabetes annual review assessment?

A

Weight
Blood pressure
HbA1c
Renal function
Lipids
Retinal screening
Diabetic foot assessment

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

Devices to administer insulin

A

Syringe
Disposable pen
Re-usable cartridge pen
Continuous subcutaneous insulin infusion pump

27
Q

Prandial insulin analogues:
Examples
Onset
Peak action
Duration

A

Examples - Novorapid, Humalog, Apidra
Onset of action - 10-15 minutes
Peak action - 60-90 minutes
Duration - 4-5 hours

28
Q

Prandial soluble insulin:
Examples
Onset
Peak action
Duration

A

Examples - Humulin S, Actarapid
Onset of action - 30-60 minutes
Peak action - 2-4 hours
Duration - 5-8 hours

29
Q

Isophane basal insulins:
Examples
How long do they act?
What is the peak action?

A

Examples - Insulatard, Humulin I
Intermediate/long acting
Peak activity 4-6 hours after administration

30
Q

Analogue basal insulins:
Examples
How often should they be given?

A

Examples - Lantus, Levemir
May be given once or twice a day

31
Q

True or false:
People with cystic fibrosis can develop their own cystic fibrosis form of diabetes

A

True - usually found in severe mutations

32
Q

Autoimmune conditions that may be associated with diabetes

A

Thyroid disease
Coeliac disease
Pernicious anaemia
Addison’s disease
IgA deficiency

33
Q

Indications for pancreas transplantation in a patient with diabetes

A

Imminent or ESRD due to receive or with kidney transplant
Severe hypoglycaemia/metabolic complications
Incapacitating clinical or emotional problems

34
Q

4 key steps in islet transplantation

A

Pancreas donation and retrieval
Islet isolation
Islet culture
Islet transplantation

35
Q

What causes monogenic diabetes?

A

Mutations in a single gene - they are Mendelian disorders

36
Q

Is monogenic diabetes autosomal or recessive?

A

Can be either

37
Q

What is the most common form monogenic diabetes?

A

MODY - mature onset diabetes of the young

38
Q

Is MODY autosomal dominant or autosomal recessive?

A

Dominant

39
Q

Is MODY insulin dependent?

A

No

40
Q

What is the age of onset in MODY?

A

Usually <25 years

41
Q

Clinical diagnosis of MODY

A

3 generation FH
One family member diabetes <25
Non-insulin dependent

42
Q

What are the three groups of MODY?

A

Those with mutations in glucokinase gene
Those with mutations in transcription factors
Those with MODY but we do not know the gene

43
Q

What is the function of glucokinase?

A

Converts glucose into glucose-6-phosphate

44
Q

When does MODY with glucokinase mutations present?

A

Birth

45
Q

Describe insulins secretion in someone with glucokinase mutation

A

There is a right shift of the insulin sensing curve
They will sense normal glucose as e.g. 7 compared to 5
They produce just as much insulin as someone who doesn’t have diabetes, no defect in beta cell function

46
Q

When does MODY with transcription factor mutations present?

A

Teenage years or early adulthood

47
Q

True or false:
Transcription factor MODY is a progressive disease?

A

True

48
Q

In glucokinase MODY, there is stable/unstable hyperglycaemia

A

Stable

49
Q

How is glucokinase MODY treated?

A

Diet treatment

50
Q

Where are the mutations in transcription factor MODY?

A

HNF-1alpha, HNF-1beta, HNF4-alpha

51
Q

How is transcription factor MODY treated?

A

1/3 diet, 1/3 OHA, 1/3 insulin

52
Q

Which diabetes drugs do patients with transcription factor MODY respond well do?

A

Sulphonylureas

53
Q

Mutations present in neonatal diabetes

A

KCNJ11, ABCC9

54
Q

How do the mutations present in neonatal diabetes affect the body?

A

Causes K channels to be unresponsive to ATP, leading to them remaining open and the beta cell remains hyper polarised and there is no insulin secretion

55
Q

True or false:
Neonatal diabetes is insulin dependent?

A

False - not necessarily. Can use sulphonylureas to close the channel

56
Q

Lipids and liver fat biochemical biomarkers that are increased and decreased in T2DM

A

Increased - ALT, TG (triglycerides)
Decreased - HDL

57
Q

Inflammatory biochemical biomarkers that are increased in T2DM

A

CRP
IL-1
IL-6
IL-18
MCP-1

58
Q

Ferritin is increased/decreased in T2DM

A

Increased

59
Q

Adiponectin is increased/decreased in T2DM

A

Decreased

60
Q

What percentage of diabetes is T2D?

A

90-95%

61
Q

Aims of management in T2DM?

A

Treat symptoms
Prevent microvascular complications
Prevent cardiovascular complications

62
Q

How much weight loss can result in remission of T2DM?

A

10-15%

63
Q

Advice on healthy eating for T2DM

A

Normal intake of unrefined carbs, reduced intake of unrefined sugars
Reduce fat intake
Increase fruit and veg intake
Reduce salt
Safe and sensible alcohol consumption

64
Q

Factors leading to failure to reach glycemic targets in T2DM

A

Female
Younger
Obese
Not at lipid or BP targets
Poor adherence to meds, lifestyle
Reluctance to intensify treatment

CVDM (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions