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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
What is done in a diabetes annual review assessment?
Weight Blood pressure HbA1c Renal function Lipids Retinal screening Diabetic foot assessment
26
Devices to administer insulin
Syringe Disposable pen Re-usable cartridge pen Continuous subcutaneous insulin infusion pump
27
Prandial insulin analogues: Examples Onset Peak action Duration
Examples - Novorapid, Humalog, Apidra Onset of action - 10-15 minutes Peak action - 60-90 minutes Duration - 4-5 hours
28
Prandial soluble insulin: Examples Onset Peak action Duration
Examples - Humulin S, Actarapid Onset of action - 30-60 minutes Peak action - 2-4 hours Duration - 5-8 hours
29
Isophane basal insulins: Examples How long do they act? What is the peak action?
Examples - Insulatard, Humulin I Intermediate/long acting Peak activity 4-6 hours after administration
30
Analogue basal insulins: Examples How often should they be given?
Examples - Lantus, Levemir May be given once or twice a day
31
True or false: People with cystic fibrosis can develop their own cystic fibrosis form of diabetes
True - usually found in severe mutations
32
Autoimmune conditions that may be associated with diabetes
Thyroid disease Coeliac disease Pernicious anaemia Addison's disease IgA deficiency
33
Indications for pancreas transplantation in a patient with diabetes
Imminent or ESRD due to receive or with kidney transplant Severe hypoglycaemia/metabolic complications Incapacitating clinical or emotional problems
34
4 key steps in islet transplantation
Pancreas donation and retrieval Islet isolation Islet culture Islet transplantation
35
What causes monogenic diabetes?
Mutations in a single gene - they are Mendelian disorders
36
Is monogenic diabetes autosomal or recessive?
Can be either
37
What is the most common form monogenic diabetes?
MODY - mature onset diabetes of the young
38
Is MODY autosomal dominant or autosomal recessive?
Dominant
39
Is MODY insulin dependent?
No
40
What is the age of onset in MODY?
Usually <25 years
41
Clinical diagnosis of MODY
3 generation FH One family member diabetes <25 Non-insulin dependent
42
What are the three groups of MODY?
Those with mutations in glucokinase gene Those with mutations in transcription factors Those with MODY but we do not know the gene
43
What is the function of glucokinase?
Converts glucose into glucose-6-phosphate
44
When does MODY with glucokinase mutations present?
Birth
45
Describe insulins secretion in someone with glucokinase mutation
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
When does MODY with transcription factor mutations present?
Teenage years or early adulthood
47
True or false: Transcription factor MODY is a progressive disease?
True
48
In glucokinase MODY, there is stable/unstable hyperglycaemia
Stable
49
How is glucokinase MODY treated?
Diet treatment
50
Where are the mutations in transcription factor MODY?
HNF-1alpha, HNF-1beta, HNF4-alpha
51
How is transcription factor MODY treated?
1/3 diet, 1/3 OHA, 1/3 insulin
52
Which diabetes drugs do patients with transcription factor MODY respond well do?
Sulphonylureas
53
Mutations present in neonatal diabetes
KCNJ11, ABCC9
54
How do the mutations present in neonatal diabetes affect the body?
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
True or false: Neonatal diabetes is insulin dependent?
False - not necessarily. Can use sulphonylureas to close the channel
56
Lipids and liver fat biochemical biomarkers that are increased and decreased in T2DM
Increased - ALT, TG (triglycerides) Decreased - HDL
57
Inflammatory biochemical biomarkers that are increased in T2DM
CRP IL-1 IL-6 IL-18 MCP-1
58
Ferritin is increased/decreased in T2DM
Increased
59
Adiponectin is increased/decreased in T2DM
Decreased
60
What percentage of diabetes is T2D?
90-95%
61
Aims of management in T2DM?
Treat symptoms Prevent microvascular complications Prevent cardiovascular complications
62
How much weight loss can result in remission of T2DM?
10-15%
63
Advice on healthy eating for T2DM
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
Factors leading to failure to reach glycemic targets in T2DM
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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