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BRS YR2 > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

What is type 1 diabetes?

A
  • autoimmune condition where insulin-producing beta-cells in the pancreas are destroyed by the immune system
  • result is partial or complete insulin deficiency > hyperglycaemia
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2
Q

What classifies type 1 diabetes?

A

autoimmune destruction of islets > absolute insulin deficiency

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3
Q

What is latent autoimmune diabetes in adults (LADA)?

A

autoimmune diabetes leading to insulin deficiency presents later in life

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4
Q

Why is the autoimmune basis of type 1 diabetes important?

A
  • increased prevalence of other autoimmune diseases

- increased complete destruction of beta-cell

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5
Q

Which HLA-DR alleles increase the risk of diabetes significantly?

A

DR3, DR4

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6
Q

What are the possible environmental factors in developing type 1 diabetes?

A

NO causation relationship

  • enteroviral infections (koksaki virus)
  • cow’s milk protein exposure
  • seasonal variation
  • changes in microbiota
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7
Q

Key characteristic of type 1 diabetes?

A

Ketones in urine

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8
Q

What is needed to stop ketonegenesis?

A

Insulin

Basal bolus insulin regimen

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9
Q

What can be a trigger for DM?

A
  • pancreatic damage

- endocrine disease

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10
Q

What is MODY?

A

when there is a single genetic defect that has caused the development of diabetes

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11
Q

When can T1DM develop?

A

at any decade of life

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12
Q

How does T1DM develop?

A
  • genetic predisposition
  • precipitating event
  • asymptomatic beta cell decline
  • no C-peptide present
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13
Q

What do you use to measure insulin production in T1DM?

A

C-peptide

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14
Q

What produces C-pepetide?

A

the conversion of pro insulin (from beta cells) to insulin - cleavage product

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15
Q

Why do we measure C-peptide?

A

people with T1DM will be taking insulin and therefore will have normal levels if insulin is measured

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16
Q

What happens after the precipitating event?

A
  • immune activation leads to beta cell attack

- development of single autoantibodies

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17
Q

What can be seen on microscope in islet cells?

A
  • immune cells concentrated in islet cell

- after attack, much lower numbers of immune cells

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18
Q

Why is the immune aspect important?

A
  • increased risk of other autoimmune diseases
  • complete destruction of B-cells
  • autoantibodies and immune modulation offer possible novel treatments
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19
Q

How long does the asymptomatic stage last?

A

dependent on how aggressive the immune response is (more steep in children, gradual in adults)

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20
Q

Why does the immune activation occur?

A

due to a defect in both the innate and adaptive immune system

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21
Q

What happens in immune activation?

A
  • CD4+T lymphocytes identify autoantigen
  • CD4+ cells activated CD8+ cells
  • CD8+ travel to islets and lyse b-cells
  • increased by pro-inflammatory cytokine release
  • worsened by defects in regulatory T cells, failure to suppress autoimmunity
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22
Q

Are all b-cells destroyed in the development in T1DM?

A

SOME produce small amounts of insulin therefore NO

BUT, insulin is still needed

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23
Q

What is the effect of the remaining insignificant insulin production?

A

fewer, less severe complications associated with T1DM

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24
Q

What are the symptoms associated with T1DM?

A
  • polyuria
  • nocturia
  • polydipsia
  • blurred vision
  • recurrent infections (thrush)
  • weight loss
  • fatigue
    (short duration)
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25
Q

When does ketoacidosis occur?

A
  • low/no insulin

- acute insulin resistance due to counter-regulatory response (adrenalin…)

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26
Q

When are pancreatic autoantibodies are detected?

A

in the sera of people of T1DM

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27
Q

What are the pancreatic antibodies in response to proteins from b-cells?

A
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase (GADA)
  • Insulinoma-associated-2 autoantibodies (IA-2A) Zinc transporter 8 (ZnT8)
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28
Q

What are the signs of T1DM?

A
  • dehydration
  • cachexia
  • hyperventilation
  • smell of ketones (pear drop)
  • glyosuria
  • ketonuria
29
Q

Why does blurred vision occur in T1DM?

A

high glucose levels cause osmotic shifts in the eyeball

30
Q

What is the diagnosis of T1DM based on?

A
  • clinical features
  • presence of ketones
    occasionally:
  • pancreatic autoantibodies
  • C-peptide
31
Q

What are the effects of insulin deficiency?

A
  • proteinolysis (AA)
  • hepatic glucose output
  • lipolysis (NEFA + triglycerides)
32
Q

What happens to NEFA’s?

A

oxidised in the liver to produce ketone bodies, which are acidic and can accumulate causing diabetic ketoacidosis

33
Q

Which ketone bodies are involved in ketoacidosis?

A
  • acetyl CoA
  • acetoacetate
  • acetone + 3 OH-B
34
Q

What are the aims when treating T1DM?

A
  • maintain glucose levels w/o hypo
  • restore insulin profile
  • prevent acute metabolic decompensation
  • prevent micro and macrovascular complications
35
Q

Why does high glucose cause weight loss?

A
  • osmotic diuresis
  • dehydration
  • no calorie retention
  • muscle breakdown for energy
36
Q

What does MODY stand for?

A

Maturity Onset Diabetes of the Young

37
Q

What are the acute complications associated with T1DM?

A

diabetic ketoacidosis

38
Q

What are the chronic microvascular complications associated with T1DM?

A
  • retinopathy
  • neuropathy
  • nephropathy
39
Q

What are the chronic macrovascular complications associated with T1DM?

A
  • ischaemic heart disease
  • cerebrovascular disease
  • peripheral vascular disease
40
Q

What are the complications associated with the treatment of T1DM?

A

hypoglycaemia

41
Q

How do you manage T1DM?

A

SELF-MANAGED

  • insulin treatment
  • dietary support
  • education
  • technology
  • transplantation
42
Q

What are the 2 different types of insulin?

A
  • short/quick-acting/with meals

- long-acting/basal/background

43
Q

What is short/quick-acting insulin/with meals?

A
  • human insulin (exact molecular replica)

- Insulin analogue (Lispro, Aspart, Glulisine)

44
Q

What is long-acting/basal/background insulin?

A
  • bound to Zn or protamine (neutral protamine hagedorn, NPH)

- Insulin analogue (Glargine, Dermitir, Degludec)

45
Q

What is a typical basal bolus regime?

A

1) long acting (1 x daily - morning)

2) short acting

46
Q

What cannot be replicated using basal bolus?

A
  • basal profile between meals is not flat

- only one peak in the longacting phase of the insulin

47
Q

What does an insulin pump do?

A

continuous delivery of short-acting insulin analogue into s/c space

48
Q

What is the advantage of using an insulin pump?

A
  • program insulin to deliver different amounts across the day
  • variable basal rates
  • extended boluses
  • greater flexibility
49
Q

What is included in the structured education programs for T1DM?

A
  • dose adjustment for carbohydrate content
  • training on carbohydrate counting
  • substitute refined carbohydrates for complex carbohydrates
50
Q

What is involved in an artificial pancreas/closed-loop?

A

glucose monitor + insulin pump

  • real time continuous glucose sensor
  • calculate insulin requirement
  • pump delivers the calculated insulin
51
Q

What is a hybrid closed-loop system?

A

when eating, must intervene with pump especially when eating refined carbohydrates

52
Q

What happens in islet cell transplants?

A
  • isolate human islets from pancreas
  • transplant into hepatic portal vein
  • required life long immunosuppression
53
Q

What happens in simultaneous pancreas and kidney transplants?

A
  • better survival of pancreas graft when transplanted with kidneys
  • requires life-long immunosuppression
54
Q

What are the limitations of transplants?

A
  • donor availability

- life-long immunosuppression complications

55
Q

How can you monitor glucose levels?

A
  • capillary (finger prick) blood glucose measurement

- continuous glucose monitoring

56
Q

What does a HbA1c show?

A
  • glycated haemoglobin (glucose+haemoglobin)
  • irreversible reaction
  • reflects last 3 months
  • measured every 3-4months
57
Q

What are the acute complications associated with T1DM?

A
  • diabetic ketoacidosis
  • uncontrolled hyperglycaemia
  • hypoglycaemia
58
Q

When does diabetic ketoacidosis occur in established T1DM?

A
  • acute illness
  • missed insulin doses
  • inadequate insulin doses
59
Q

How do you diagnose diabetic ketoacidosis?

A
  • pH <7.3
  • ketones increased (urine or blood)
  • HCO3- <15mmol/L
  • glucose >11mmol/L
60
Q

What measurement is deemed as hypoglycaemia?

A

<3.6mmol/L (variable 3.5-4)

61
Q

What is the effect of frequent (too many) hypoglycaemia?

A
  • exhaustion
  • confusion
  • tremors
  • palpitations
  • sweating
  • hunger
  • somnolence
  • inco-ordination
  • seizures
  • coma
62
Q

How many hypoglycaemic episodes is normal?

A

2/week

63
Q

What quantifies severe hypoglycaemia?

A

an episode that requires 3rd party help

64
Q

When does hypoglycaemia become a problem?

A
  • excessive frequency
  • impaired awareness (unable to detect low blood sugar)
  • nocturnal hypoglycaemia
  • recurrent severe hypoglycaemia
65
Q

What are the risks of hypoglycaemia?

A
  • seizure/coma/death
  • emotional impact
  • impair driving
  • impaired day-to-day function
  • cognition impacts
66
Q

What is not useful to identify a hypoglycaemic episode?

A

HbA1c

67
Q

What increases the risk of hypoglycaemia?

A
  • exercise
  • missed meals
  • inappropriate insulin regime
  • alcohol intake
  • low HbA1c
  • lack of training on dose adjustment
68
Q

What can be done to support problematic hypoglycaemia?

A
  • insulin-pump therapy
  • different insulin analogues
  • revisit carbohydrate counting/education
  • psychological support
  • transplantation

BRS YR2 (70 decks)

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