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CVDM > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What type of insulin does an insulin pump have?

A

Short acting insulin

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2
Q

What regime are insulin injections given in and why?

A

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

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3
Q

How long have islet transplantations been done for?

A

~20 years

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4
Q

Limitations of islet transplantations

A

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

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5
Q

Risk factors for diabetes

A

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

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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

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7
Q

Why does T1D develop?

A

Immune based disease on a background of susceptibility factors

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8
Q

Can T1D be predicted?

A

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

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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

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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

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11
Q

Environmental risk factors for T1D

A

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

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12
Q

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

A

Islet autoantibodies

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13
Q

What percentage of individuals with T1D will have islet autoantibodies?

A

93%

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14
Q

What is Type 1 diabetes?

A

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

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15
Q

Commonest autoantibody in T1D

A

Anti-GAD

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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

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17
Q

What is T2D due to?

A

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

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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

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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

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20
Q

What HbA1c level is diabetes diagnosed at?

A

≥48mmol

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21
Q

Aims of therapy in T1D

A

Prevent hyperglycaemia
Prevent hypoglycaemia
Reduce chronic complications

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22
Q

Aims of therapy in T1D

A

Prevent hyperglycaemia
Avoid hypoglycaemia
Reduce chronic complications

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23
Q

Hyperglycaemia symptoms

A

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

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24
Q

Hypoglycaemia symptoms

A

Pallor
Sweating
Tremor
Palpitations
Nausea
Hunger
Confusion
Coma

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25
Q

What is done in a diabetes annual review assessment?

A

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

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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)

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