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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
  • Auto antibodies can be useful clinically
  • Immune modulation offers the possibility of novel treatments
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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 urine in type 1 diabetes?

A

Ketones in urine

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8
Q

What is needed to stop ketogenesis?

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 monogenic diabetes?

A

when there is a single genetic defect that has caused the development of diabetes e.g. MODY

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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 cleavage of pro insulin (from beta cells) into insulin

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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

How long does the asymptomatic stage last?

A

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

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19
Q

Why does the immune activation occur?

A

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

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20
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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21
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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22
Q

What is the effect of the remaining insignificant insulin production?

A

fewer, less severe complications associated with T1DM

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23
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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24
Q

When does ketoacidosis occur?

A
  • low/no insulin
  • acute insulin resistance due to counter-regulatory response (adrenaline)
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25
Q

Where are pancreatic autoantibodies detected?

A

in the serum of people with T1DM

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26
Q

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

A
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase antibodies (GADA)
  • Insulinoma-associated-2 autoantibodies (IA-2A)
  • Zinc transporter 8 (ZnT8)
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27
Q

What are the clinical signs of T1DM?

A
  • dehydration
  • cachexia (muscle wasting)
  • hyperventilation
  • smell of ketones (pear drop)
  • glycosuria
  • ketonuria
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28
Q

Why does blurred vision occur in T1DM?

A

high glucose levels cause osmotic shifts in the eyeball

29
Q

What is the diagnosis of T1DM based on?

A
  • clinical features
  • presence of ketones
    occasionally
  • pancreatic autoantibodies
  • C-peptide
30
Q

What are the effects of insulin deficiency?

A
  • proteinolysis (AA)
  • increased hepatic glucose output
  • lipolysis (NEFA/free fatty acids + triglycerides)
31
Q

What happens to NEFAs/free fatty acids?

A

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

32
Q

Which ketone bodies are involved in ketoacidosis?

A
  • acetyl CoA
  • acetoacetate
  • acetone + 3 OH-B
33
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
34
Q

Why does high glucose cause weight loss?

A
  • osmotic diuresis
  • dehydration
  • no calorie retention
  • muscle breakdown for energy
35
Q

What does MODY stand for?

A

Maturity Onset Diabetes of the Young

36
Q

What are the acute complications associated with T1DM?

A

diabetic ketoacidosis

37
Q

What are the chronic microvascular complications associated with T1DM?

A
  • retinopathy
  • neuropathy
  • nephropathy
38
Q

What are the chronic macrovascular complications associated with T1DM?

A
  • ischaemic heart disease
  • cerebrovascular disease
  • peripheral vascular disease
39
Q

What are the complications associated with the treatment of T1DM?

A

hypoglycaemia

40
Q

How do you manage T1DM?

A

SELF-MANAGED

  • insulin treatment
  • dietary support
  • education
  • technology
  • transplantation
41
Q

What are the 2 different types of insulin?

A
  • short/quick-acting/with meals
  • long-acting/basal/background
42
Q

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

A
  • human insulin (exact molecular replica)
  • Insulin analogue (Lispro, Aspart, Glulisine)
43
Q

What is long-acting/basal/background insulin?

A
  • bound to Zn or protamine (neutral protamine hagedorn, NPH)
  • Insulin analogue (Glargine, Dermitir, Degludec)
44
Q

What is a typical basal bolus regime?

A

1) short acting Actrapid (human insulin) 3 x daily
2) longacting once daily

45
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
46
Q

What does an insulin pump do?

A

continuous delivery of short-acting insulin analogue into subcutaneous space

47
Q

What is the advantage of using an insulin pump?

A
  • program insulin to deliver different amounts across the day
  • variable basal rates
  • actively bolus for meals
  • greater flexibility
48
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
49
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
50
Q

What happens in islet cell transplants?

A
  • isolate human islets from pancreas
  • transplant into hepatic portal vein
  • required life long immunosuppression
51
Q

What happens in simultaneous pancreas and kidney transplants?

A
  • better survival of pancreas graft when transplanted with kidneys
  • requires life-long immunosuppression
52
Q

What are the limitations of transplants?

A
  • donor availability
  • life-long immunosuppression complications
53
Q

How can you monitor glucose levels?

A
  • capillary (finger prick) blood glucose measurement
  • continuous glucose monitoring
54
Q

What does a HbA1c show?

A
  • glycated haemoglobin (glucose+haemoglobin)
  • irreversible reaction
  • reflects last 3 months of glycaemia
  • measured every 3-4months
55
Q

What are the acute complications associated with T1DM?

A
  • diabetic ketoacidosis
  • uncontrolled hyperglycaemia
  • hypoglycaemia
56
Q

Which events can cause diabetic ketoacidosis in established T1DM?

A
  • acute illness
  • missed insulin doses
  • inadequate insulin doses
57
Q

How do you diagnose diabetic ketoacidosis?

A
  • pH <7.3
  • ketones increased (urine or blood)
  • HCO3- <15mmol/L
  • glucose >11mmol/L
58
Q

What measurement is deemed as hypoglycaemia?

A

<3.6mmol/L (variable 3.5-4)

59
Q

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

A
  • exhaustion
  • confusion
  • tremors
  • palpitations
  • sweating
  • hunger
  • somnolence
  • inco-ordination
  • seizures
  • coma
60
Q

How many hypoglycaemic episodes is normal?

A

2/week

61
Q

What quantifies severe hypoglycaemia?

A

an episode that requires 3rd party help

62
Q

When does hypoglycaemia become a problem?

A
  • excessive frequency
  • impaired awareness (unable to detect low blood sugar)
  • nocturnal hypoglycaemia
  • recurrent severe hypoglycaemia
63
Q

What are the risks of hypoglycaemia?

A
  • seizure/coma/death
  • emotional impact
  • impair driving
  • impaired day-to-day function
  • cognition impacts
64
Q

What is not useful to identify a hypoglycaemic episode?

A

HbA1c

65
Q

What increases the risk of hypoglycaemia?

A
  • exercise
  • missed meals
  • inappropriate insulin regime
  • alcohol intake
  • low HbA1c
  • lack of training on dose adjustment
66
Q

What can be done to support problematic hypoglycaemia?

A
  • insulin-pump therapy
  • different insulin analogues
  • revisit carbohydrate counting/education
  • psychological support
  • transplantation
67
Q

What is the managment of hypoglycaemia in a person who is alert and orientated?

A
  • oral carbohydrates
  • juice or sweets
  • sandwich
68
Q

What is the acute managment of hypoglycaemia in a person who is drowsy/confused but can still swallow?

A
  • buccal glucose
  • glucogel
  • complex carbohydrates
69
Q

What is the acute managment of hypoglycaemia in a person who is unconscious or may not be able to swallow?

A
  • IV access
  • 20% IV glucose

BRS YR2 (67 decks)

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