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BRS ENDOCRINOLOGY > 1b T1DM > Flashcards

1b T1DM Flashcards

1
Q

What is T1DM?

A

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

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2
Q

What does the resultant hyperglycaemia result in?

A

the need for life long insulin treatment

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3
Q

What are the triggers of type 1 diabetes which can lead to an autoimmune destruction of islets?

A

Environmental triggers
Genetic risk

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4
Q

How does T1DM lead to hyperglycaemia?

A

Absolute insulin deficiency

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5
Q

What is MODY?

A

Maturity Onset Diabetes of the Young

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6
Q

What is C-peptide?

A

A cleavage product of pro-insulin

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7
Q

What is pro insulin cleaved into?

A

Insulin and C peptide

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8
Q

What happens in the stages A and B of the diabetes onset graph?

A

Normal B cell Mass results in normal insulin production

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9
Q

What happens at stage C in the diabetes onset graph?

A

Genetic predisposition

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10
Q

What happens after the C stage in the diabetes onset graph?

A

Progressive loss of insulin release, glucose levels normal and then eventually Overt diabetes

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11
Q

What happens in the G stage of diabetes in the graph?

A

Overt diabetes, C peptide Present

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12
Q

What happens in the H stage of diabetes in the graph?

A

No C peptide and no insulin present

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13
Q

What are the pancreatic Beta cells attacked with?

A

Pancreatic autoantibodies = immune activation

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14
Q

Why is the immune basis of T1DM important?

A
  • Increased risk of other autoimmune conditions
  • Risk of autoimmunity on relatives
  • More destruction of Beta Cells
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15
Q

Are all the beta cells destroyed in T1DM?

A

No = some people with type 1 diabetes continue to produce insulin but not enough to negate the need for insulin therapy

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16
Q

Which HLA-DR genes pose a significant risk to the genetic susceptibility of Diabetes?

A

DR3 and DR4

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17
Q

What are four environmental factors which might contribute to the implications of T1DM?

A
  • Enteroviral infections
  • Cow’s milk protein exposure
  • Seasonal variation
  • Changes in microbiota
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18
Q

Where are pancreatic autoantibodies detectable?

A

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

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19
Q

What are four examples of pancreatic autoantibodies which are detectable?

A
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase (GADA) – widespread
    neurotransmitter
  • Insulinoma-associated-2 autoantibodies (IA-2)
  • Zinc transporter 8 (ZnT8)
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20
Q

What are the 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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21
Q

What are the signs of T1DM?

A

dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

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22
Q

What is the diagnosis of T1DM based on?

A

CLINICAL FEATURES and presence of ketones

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23
Q

What are the effects of insulin deficiency on the muscle?

A

Proteinolysis resulting in more Amino acid

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24
Q

What are the effects of lack of insulin on the liver?

A

Hepatic glucose output increases resulting in more glucose

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25
Q

what are the effects of lack of insulin on the fat cells?

A

Lipolysis increases resulting in more NEFA

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26
Q

Describe how ketone bodies are produced?

A

NEFA taken into the liver
Beta Oxidation - Fatty Acyl CoA is converted into Acetyl CoA which is then made into Acetoacetate, Acetone and 3 Beta-hydroxybutyrate (ketone bodies)

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27
Q

What are ketone bodies?

A

Fuel source in times of starvation

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28
Q

Why can ketone bodies become problematic?

A

they are acidic, therefore too many results in the blood becoming more acidic and an accumulation of H+

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29
Q

what is the effect of insulin on beta oxidation?

A

insulin inhibits it, stimulated by glucagon

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30
Q

What is the treatment for someone with T1DM?

A

Insulin for life

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31
Q

What are the treatment aims for someone with T1DM?

A
  • Maintain glucose levels without excessive
    hypoglycaemia
  • Restore a close to physiological insulin profile
  • Prevent acute metabolic decompensation
  • Prevent microvascular and macrovascular
    complications
32
Q

What are the acute complications of hyperglycaemia?

A

Diabetic ketoacidosis

33
Q

What are the macrovascular complications of T1DM?

A
  • Ischaemic heart disease
  • Cerebrovascular disease
  • Peripheral vascular disease
34
Q

What are the microvascular complications of T1DM?

A

Retinopathy
Neuropathy
Nephropathy

35
Q

What word is used to describe T1DM treatment?

A

Self - Management

36
Q

What are the compensatory mechanisms for Hypoglycaemia?

A

Glucagon
Catecholamines
Cortisol
growth hormones

37
Q

How many phases does the prandial peak have?

A

2 Phases - first and second phase insulin release

38
Q

What are the key characteristics of the physiological insulin profile?

A
  1. Basal insulin has a flat profile
  2. Prandial peak has 2 phases
  3. Insulin is never completely suppressed
39
Q

What is the basal Bolus Regime?

A

Treatment for T1DM
- Short / quick acting insulin with meals = Bolus
- Background long lasting insulin = Basal

40
Q

What are the two types of short acting (Bolus) insulin?

A
  1. Human insulin - exact molecular replicate of human insulin
  2. Insulin Analogue
41
Q

What is an example of a short acting human insulin?

A

Actrapid

42
Q

What are examples of short acting insulin analogues?

A

Lispro
Aspart
Glulisine

43
Q

What is an insulin analogue?

A

Recombinant = one or two amino acids have been changed in order to increase absorption

44
Q

Why is c peptide measured rather than insulin?

A

C peptide has a longer half life

45
Q

What are the two types of background insulin?

A
  1. Bound to zinc or protamine
  2. Insulin analogues
46
Q

What is the name of the insulins which are bound to zinc or protamine?

A

Neutral Protamine Hagedorn, NPH

47
Q

What is the typical basal Bolus regime?

A

TDS (three times/day) short-acting
Once daily long-acting

48
Q

What is insulin pump therapy?

A

Continuous delivery of short-acting insulin analogue - delivery of insulin into the subcutaneous space

49
Q

What are the benefits of insulin pump therapy?

A

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

50
Q

What are the characteristics of a insulin from a pump?

A

Variable basal rates
Extended boluses
Greater flexibility

51
Q

What is the dietary advice which should be given to patients with diabetes?

A
  • Dose adjustment for carbohydrate content of food.
  • All people with type 1 diabetes should receive training for carbohydrate counting
  • Where possible, substitute refined carbohydrate
    containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index)
52
Q

What course are all people with a diagnosis of diabetes given?

A

Structured Education programme on how to administer their insulin

53
Q

What is the closed loop system?

A

Artificial insulin delivery:

  • Algorithm to use glucose value to calculate insulin requirement
  • Pump delivers insulin
  • Results in a change in glucose
  • real time continuous glucose sensor
54
Q

What are the side effects of a islet cell transplantation?

A

Requires life-long immunosuppression

55
Q

Why are pancreas transplants often done with kidney?

A

Better survival of pancreas graft when
transplanted with kidneys

56
Q

what are the limitations of transplantation?

A

availability of donors, complications of lifelong immunosuppression

57
Q

How are glucose levels monitored?

A

Capillary (finger prick) blood glucose monitoring
Continuous glucose monitoring

58
Q

What is HbA1c a measurement of?

A

Glycated haemaglobin -

59
Q

Why is HbA1c useful?

A

Reflect last 3 months (red blood cell lifespan) of glycaemia

60
Q

what is the relationship between glucose levels and HbA1c levels?

A

linear relationship

61
Q

What four things can affect HbA1c levels?

A
  1. Erythropoesis
  2. Altered Haemaglobin
  3. Glycation
  4. Erythrocyte production
62
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

63
Q

What are the three acute complications of T1DM?

A
  1. Diabetic ketoacidosis
  2. Uncontrolled hyperglycaemia
  3. Hypoglycaemia
64
Q

What are the criteria needed for DKA diagnosis?

A

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

65
Q

Which types of diabetes can ketoacidosis occur in?

A

both

66
Q

what is the numerical definition of hypoglycaemia?

A

<3.6 mmol/L

67
Q

What is severe hypoglycaemia?

A

any event requiring 3rd party assistance

68
Q

What are the adrenergic symptoms of hypoglycaemia?

A

*Tremors
*Palpitations
*Sweating
*Hunger

69
Q

What are the neuroglycopaenic symptoms of hypoglycaemia?

A

*Somnolence
*Confusion
*Incoordination
*Seizures, coma

70
Q

When does hypoglycaemia become a problem?

A
  1. Excessive frequency
  2. Impaired awareness (unable to detect low
    blood glucose)
  3. Nocturnal hypoglycaemia
  4. Recurrent severe hypoglycaemia
71
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

72
Q

What are risk factors for hypoglycaemia?

A

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

73
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
74
Q

What is the acute management plan for someone with a hypo who is alert and orientated?

A

Oral Carbohydrates
Rapid acting;
juice / sweets

75
Q

What is the acute management plan for someone with a hypo who is drowsy / confused but swallowing is intact?

A

Buccal Glucose
Glucogel
Complex Carbohydrates

76
Q

Describe the development of type 1 diabetes?

A
  • starts with genetic predisposition
  • precipitating event - virus, stressful event
  • triggers autoimmune process
  • loss of beta cells
  • insulin production decreases rapidly
  • become hyperglycaemic
  • however not all beta cells are destroyed

BRS ENDOCRINOLOGY (20 decks)

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