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Y2 - BRS - Endo > Type 1 Diabetes > Flashcards

Type 1 Diabetes Flashcards

1
Q

What causes type 1 diabetes?

What does type 1 diabetes result in?

A

An autoimmune condition in which insulin-producing beta-cells in the pancreas are attacked and destroyed by the immune system

The result is a partial or complete deficiency of insulin production, which results in hyperglycaemia
The resultant hyperglycaemia requires life-long insulin treatment

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2
Q

What are the different types of diabetes?

A 
Type 1 Diabetes
Type 2 Diabetes
Hybrid forms
Other
Unclassified
During pregnancy
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3
Q

What is LADA?

A

Latent autoimmune diabetes in adults

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4
Q

Can T2DM present in childhood?

Can diabetic ketoacidosis feature of T2DM?

How can monogenic diabetes present?

A

Yes

Yes - although more typical in type 1

Phenotypically as Type 1 or Type 2 diabetes (eg. MODY, mitochondrial diabetes)

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5
Q

What event might diabetes present after?

A

Following pancreatic damage or other endocrine disease

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6
Q

How does the evidence showing that type 1 diabetes presenting in adulthood challenge clinicians?

A

Clinicians are faced with a challenge, trying to differentiate adult-onset type 1 diabetes from the much large numbers of cases of type 2 diabetes

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7
Q

What are the stages of development of type 1 diabetes?

A

Genetic predisposition

Potential precipitating event

Overt immunological abnormalities; normal insulin release

Progressive loss if insulin release; glucose normal

Overt diabetes; C-peptide present

No C-peptide present

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8
Q

What do we measure when looking at beta cell function?

A

C-peptide cleaved from pro-insulin

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9
Q

Why is the immune basis of T1DM important?

A

Increased prevalence of other autoimmune disease

Risk of autoimmunity in relatives

More complete destruction of B-cells

Auto antibodies can be useful clinically

Immune modulation offers the possibility of novel treatments (not there yet)

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10
Q

Summarise immunology of T1DM?

A

Primary step is the presentation of auto-antigen to autoreactive CD4+ T lymphocytes

CD4+ cells activate CD8+ T lymphocytes (cytotoxic)

CD8+ cells travel to islets and lyse beta-cells
expressing auto-antigen

Exacerbated by release of pro-inflammatory cytokines

Underpinned also, by defects in regulatory T-cells that fail to supress autoimmunity

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11
Q

Are all the beta cells destroyed in T1DM?

A

Not always, some beta cells escape the immune response

Some people with type 1 diabetes continue to produce small amounts of insulin and have C-peptide

Not enough to negate the need for insulin therapy

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12
Q

What is HLA?

What HLA is associated with diabetes?

A

Human Leukocyte antigen

HLA-DR = If you have these polymorphisms you are 6x more likely to develop T1DM

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13
Q

What are the environmental factors involved with T1DM?

A

Multiple factors implicated, but causality has not been established

Enteroviral infections
Cow’s milk protein exposure
Seasonal variation
Changes in microbiota

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14
Q

When are auto-antibodies detectable?

Are auto-antibodies needed for diagnosis?

A

Detectable in the sera of people with Type 1 diabetes at diagnosis

Not generally needed for diagnosis in most cases

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15
Q

When are pancreatic auto-antibodies made?

A

Made when the beta cells content is exposed

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16
Q

What are the different types of pancreatic auto-antibodies ?

A 
Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)
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17
Q

What are symptoms of T1DM?

A 
Excessive urination (polyuria)
Nocturia
Excessive thirst (polydipsia)
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue
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18
Q

Why does T1DM lead to blurry vision?

A

Glucose goes into eyeball

Causes osmotic change in lens

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19
Q

What are the signs of T1DM?

A 
Dehydration
Cachexia
Hyperventilation
Smell of ketones
Glycosuria
Ketonuria
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20
Q

What are the 4 Ts of T1DM?

A

Toilet
Thirsty
Tired
Thinner

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21
Q

How is T1DM diagnosed based on clinical features?

What ketone bodies are produced in T1DM?

A

Ketones

Acetyl CoA
Acetoacetate
Acetone + 3 OH-B

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22
Q

What happens with insulin deficiency?

A

Proteinolysis
Hepatic glucose output
Uninhibired lipolysis

23
Q

What are the aims of treatment in type 1 diabetes?

A

Maintain glucose levels without excessive hypoglycaemia

Restore a close to physiological insulin profile

Prevent acute metabolic decompensation

Prevent microvascular and macrovascular complications

24
Q

What is the only thing can prevent patients from taking insulin for life?

A

Transplant

25
Q

What are the acute complications of hyperglycaemia?

What are the microvascular chronic complications of hyperglycaemia?

What are the macrovascular chronic complications of hyperglycaemia?

A

Diabetic ketoacidosis

Retinopathy
Neuropathy
Nephropathy

Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

26
Q

How is T1DM managed?

A

Is self-managed with:

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

27
Q

What are the main features of physiological profile of insulin?

A

Basal insulin has a flat profile

Prandial peak has two phases

Insulin is never completely suppressed

28
Q

What are the different types of insulin with meals?

A

(short / quick-acting insulin)

Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine)
29
Q

What are the different types of long-acting insulin?

A 
Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)
30
Q

What is the typical regime for taking insulin?

A

Typical basal bolus regime

Background and meal times
3x a day but can be more with snacks

31
Q

What are the main features of insulin pump therapy?

A

Continuous delivery of short-acting insulin analogue e.g. novorapid via pump

Delivery of insulin into subcutaneous space

Programme the device to deliver fixed units / hour throughout the day (basal)

Actively bolus for meals

32
Q

What is CSII?

A

Alternative name for pump therapy

Continuous subcutaneous insulin infusion

33
Q

What are the principles of dietary advice for T1DM?

What are the NICE guidelines for diet and T1DM?

A

Dose adjustment for carbohydrate content of food.
All people with type 1 diabetes should receive training for carbohydrate counting

All people with type 1 diabetes should be offered a Structured Education Programme
e.g. DAFNE but many others
5 day course on skills and training in self-management

34
Q

What substitutes should be made in diet?

A

Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index

35
Q

What is the closed-loop/artificial pancreas?

A

Real-time continuous glucose sensor
Algorithm to use glucose value to calculate insulin requirement
Insulin pump delvers calculated insulin
Change in glucose

36
Q

What are Hybrid closed loop systems?

A

Not quite closed loop

The pump still needs to be told before a meal

Available on NHS

37
Q

What are the two types of transplant?

What are the main features of these?

A

Islet cell transplants - isolate human islets from pancreas of deceased donor
Transplant into hepatic portal vein
Requires life-long immunosuppression

Simultaneous pancreas and kidney transplants - better survival of pancreas graft when transplanted with kidneys
Requires life-long immunosuppression

38
Q

Why are transplants not more frequently used?

A

Limited organ availability

Pancreas is not generally viable

Risks of long-term immunosuppressants

39
Q

What are the aims of transplantation?

A

Try to restore physiological insulin production to the extent that insulin can be stopped

Even if incomplete, often results in better control

40
Q

How do you measure glucose levels?

A

Capillary (finger prick) blood glucose monitoring

Continuous glucose monitoring (restricted availability, NICE guidelines)

41
Q

What are the main features of HbA1c?

What are the limitations of HbA1c?

A

Reflect last 3 months (red blood cell lifespan) of glycaemia
Biased to the 30 days preceding measurement
Glycated NOT glycosylated (enzymatic)
Therefore linear relationship
Irreversible reaction

Not perfect
Things affect it

42
Q

What is used to guide insulin doses?

A

Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months

Based on results, increase or decrease insulin doses

43
Q

What are the main features of diabetic ketoacidosis?

A

Can be a presenting feature of new-onset type 1 diabetes
Occurs in those with established type 1 diabetes
Acute illness
Missed insulin doses
Inadequate insulin doses
Life-threatening complication
Can occur in any type of diabetes

44
Q

How is diabetic ketoacidosis diagnosed?

A

pH <7.3, ketones increased (urine of capillary blood), HCO3- <15 mmol/L and glucose >11 mmol/L

45
Q

What are the main features of hypoglycaemia?

A

To some extent an inevitable feature of the self-management of type 1 diabetes
‘Lost normal physiology and homeostasis’
May become debilitating with increased frequency
Numerical definition (variable) <3.6 mmol/L
Severe hypoglycaemia: any event requiring 3rd party assistance

46
Q

What are the symptoms of a hypo?

A

Adrenergic

  • Tremors
  • Palpitations
  • Sweating
  • Hunger

Neuroglycopaenic

  • Somnolence
  • Confusion
  • Incoordination
  • Seizures, coma
47
Q

What defines low glucose?

When does hypoglycaemia become a problem?

A

< 3.5 mmol/L

Excessive frequency
Impaired awareness (unable to detect low blood glucose)
Nocturnal hypoglycaemia
Recurrent severe hypoglycaemia

48
Q

What are the risks of hypoglycaemia?

A 
Seizure / coma/ death (dead in bed)
Impacts on emotional well-being
Impacts on driving
Impacts on day to day function
Impacts on cognition
49
Q

What are the risk factors for a hypoglycaemia?

A 
Exercise
Missed meals
Inappropriate insulin regime
Alcohol intake
Lower HbA1c
Lack of training around dose-adjustment for meals
50
Q

What are the strategies to support problematic hypoglycaemia?

A

Indication for insulin-pump therapy (CSII)
May try different insulin analogues
Revisit carbohydrate counting / structured education
Behavioral psychology support
Transplantation

51
Q

How do you acutely manage a hypoglycaemia when they are alert and orientated?

A

Oral carbohydrates
Rapid acting juice/sweets
Sandwich (longer acting)

52
Q

How do you acutely manage a hypo when they are Drowsy / confused but swallow intact?

A

Buccal glucose
e.g. Hypostop / glucogel
Complex carbohydrate

53
Q

How do you acutely manage a hypo when they are unconscious or concerned about swallow?

A

IV access

20% glucose IV

Y2 - BRS - Endo (22 decks)

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