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brs (phase 1b) > (endo) type I diabetes mellitus > Flashcards

(endo) type I diabetes mellitus Flashcards

1
Q

summarise the pathophysiology of T1DM

A

autoimmune destruction of the beta cells of the islets of Langerhans
= leads to partial/complete insulin deficiency
= hyperglycaemia (requiring life-long insulin treatment)

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2
Q

explain how type 1 diabetes mellitus leads to hyperglycaemia

A

environmental trigger + genetic risk
= autoimmune destruction of beta cells
= absolute insulin deficiency
= hyperglycaemia

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3
Q

explain how type 2 diabetes mellitus leads to hyperglycaemia

A

genetic risk + obesity
= insulin resistance
= relative insulin deficiency
= hyperglycaemia

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4
Q

when does each type of diabetes normally present?

A

T1DM = ‘juvenile’ type diabetes, present in early years

T2DM = adult-type of diabetes

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5
Q

what term describes autoimmune diabetes leading to insulin deficiency that presents later in life?

A

when T1DM symptoms present later in life

= LADA (latent autoimmune diabetes in adults)

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6
Q

what term describes when T2DM symptoms present earlier on in life?

A

MODY = maturity-onset diabetes of the young

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7
Q

what is LADA?

A

when T1DM symptoms, that normally present earlier in life, actually present later in adulthood

= autoimmune diabetes that can lead to insulin deficiency

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8
Q

which type of diabetes is DKA a complication of normally?

A

normally = T1DM but can also be a feature of T2DM

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9
Q

define monogenic diabetes

A

diabetes caused by mutations (changes) in a single gene - that has phenotypic features of both T1 + T2DM

(as opposed to T1/T2DM that are caused by multiple gene defects + environmental trigger)

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10
Q

what are the types of monogenic diabetes?

A
  • MODY (mature-onset diabetes of the young)
  • mitochondrial diabetes
  • neonatal diabetes mellitus
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11
Q

what is MODY?

A

mature-onset diabetes of the young

= diabetes that acts like T2DM but found in younger patients BUT limits the body’s ability to produce insulin

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12
Q

what is beta cell mass indicative of?

A

how much insulin-producing capacity there is

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13
Q

what happens to C-peptide levels as T1DM develops?

A

decrease gradually until no C-peptide is available

due to lack of insulin production when there are no functional beta cells

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14
Q

why are insulin levels not measured in patients with diabetes?

A

patients w diabetes are usually on insulin

= so cannot measure endogenous insulin levels as they will be skewed by exogenous insulin

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15
Q

how are insulin levels measured in patient and why?

A

best way = measure C-peptide levels

as C-peptide is produced in equimolar quantities to endogenous insulin specifically, so do not have to worry about exogenous insulin skewing the readings

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16
Q

what is C-peptide?

A

the cleavage product of proinsulin, the precursor molecule to insulin

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17
Q

explain briefly the development of type 1 diabetes mellitus

A

genetic risk + environmental trigger
= immune activation that causes beta cells to be attacked
= immune response wherein autoantibodies are developed
= T1DM

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18
Q

why is the immune basis of T1DM important?

A

1) the presence of one autoimmune condition increases the risk of other autoimmune diseases
2) risk of autoimmune disease is increased in relatives (of T1DM patients)
3) autoantibodies are clinically useful (for diagnosis + treatment)
4) more complete destruction of B-cells

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19
Q

briefly explain the immunology behind autoimmunity

A

1) the APCs, B cells, initially present the autoantigen to autoreactive CD4+ T cells
2) CD4+ T cells will in turn activate CD8+ T cells
3) CD8+ T cells will then travel to the islets and lyse the beta-cells expressing the auto-antigen in question
4) exacerbated by the release of pro-inflammatory cytokines

– occurs due to defects in the regulatory T-cells that fail to suppress autoimmunity –

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20
Q

to what extent do T1DM patient experience insulin deficiency?

A

most patient w severe, long-standing T1DM do not have any functional beta cells
= so no insulin produced

BUT

some people continue to produce small amounts of insulin but not enough to negate the need for insulin therapy

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21
Q

which allele in the human genome mediates the genetic susceptibility to T1DM?

A

HLA-DR allele

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22
Q

the development of T1DM requires both a genetic predisposition AND an environmental trigger

what potential environmental factors can trigger the development of T1DM?

A

possible environmental factors:

  • enteroviral infections
  • cow’s milk protein exposure
  • seasonal changed
  • changes in microbiota

(genetic: HLA-DR allele)

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23
Q

which autoantibodies are commonly detected in the sera of patients w T1DM?

A
  • IAA (insulin autoantibodies)
  • GADA (glutamic acid decarboxylase)
  • IA-2A (insulinoma-associated-2 autoantibodies)
  • Zn-T8 (zinc-transporter 8)
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24
Q

what is the diagnosis of type 1 diabetes mainly based on?

A
  • clinical symptoms
  • glycosuria, ketonuria
  • ketonaemia
  • pancreatic autoantibody presence
  • C-peptide levels
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25
Q

what are the symptoms of type 1 diabetes?

A
  • polyuria
  • polydipsia
  • nocturia
  • weight loss
  • fatigue
  • recurrent infections (e.g. thrush)
  • blurring of vision
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26
Q

what are the signs of type 1 diabetes?

A
  • glycosuria
  • ketonuria
  • ketonaemia
  • smell of ketones
  • hyperventilation
  • dehydration
  • cachexia
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27
Q

what are the four Ts of type 1 diabetes?

A
  • toilet
  • thirst
  • thinner
  • tired
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28
Q

what do doctors aim for in patients w T1DM?

A

1) maintain glucose levels with insulin without excessive hypoglycaemia
2) restore normal insulin profile
3) prevent microvascular and macrovascular complications of diabetes

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29
Q

list the acute and chronic complications of hyperglycaemia

A

A) acute = DKA

B) chronic

1) microvascular = neuropathy, nephropathy, retinopathy
2) macrovascular = ischeamic heart disease, cerebrovascular disease, peripheral vascular disease

C) of the treatment itself = hypoglycaemia

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30
Q

what are the microvascular complications of hyperglycaemia?

A

neuropathy, nephropathy, retinopathy

31
Q

what are the macrovascular complications of hyperglycaemia?

A

ischeamic heart disease, cerebrovascular disease, peripheral vascular disease

32
Q

summarise how T1DM is managed

A
  • basal-bolus insulin regime
  • regular glucose monitoring
  • structured education
  • technology
  • transplantation
33
Q

describe the physiological insulin profile

A

1) insulin levels are never completely suppressed = always have basal insulin release
2) three prandial peaks for breakfast, lunch and dinner (dependent on an individual’s meal times)
3) each prandial peak has two phases

34
Q

what are the phases of insulin release?

A

each prandial peak has two phases:

1) first phase insulin release (immediately after food - lasts 10 mins)
2) second phase insulin release (after first peak - lasts for 2-3 hours)

35
Q

what is first phase insulin release?

A

the secretion of insulin immediately after the ingestion of food
= lasts 10 mins approx

36
Q

what is second phase insulin release?

A

the secretion of insulin after the first peak

= lasts approx 2-3 hours

37
Q

what are the two types of insulin available to manage diabetes?

A

1) with meals (short-acting, quick)

2) background (long-acting, basal)

38
Q

what is a typical basal bolus insulin regime?

A

1) once daily dose of long-acting insulin
2) thrice daily dose of quick-acting insulin (with meals)

OR

1) thrice daily dose of quick-acting insulin
2) twice daily intermediate-acting insulin

39
Q

what is insulin pump therapy?

A

continuous subcutaneous insulin infusion

where insulin is continuously delivered via a pump into the subcutaneous space (basal + bolus)

40
Q

how does insulin pump therapy work?

A

a pump injects insulin into the subcutaneous space
- both basal per hour unit insulin + bolus during meal times

= can be programmed to do so

41
Q

which structured education programme is offered to all patients w T1DM?

A

DAFNE usually

= 5 day course on skills and training in self-management

42
Q

what dietary advice is usually given to patients w T1DM?

A

1) carbohydrate counting - adjuct insulin dose based on carb content of food
2) carb substitution - try and substitute sugary, high glycaemic index foods with complex carbs (low glycaemic index, starchy)

43
Q

what is a closed-loop system?

A

= a loop that acts like an artificial pancreas controlling insulin dose based on glucose levels in the blood

44
Q

explain how a closed-loop/artificial pancreas works

A

1) glucose sensor = real-time continuous glucose sensor
2) algorithm uses glucose value to calculate the insulin requirement
3) appropriate insulin dose is administered by the pump

45
Q

which two types of transplants are available for severe T1DM patients?

A

1) islet cell transplants

2) simultaneous pancreas & kidney transplant

46
Q

what is an islet cell transplant?

A

a transplant wherein islet cells, isolated from the pancreas of a deceased donor, are isolated + transplanted into the patient’s hepatic portal vein

= requires life-long immunosuppression

47
Q

why are simultaneous pancreas & kidney transplant preferred over islet transplants?

A

better survival of pancreas graft when it is transplanted with the kidneys

= requires life-long immunosuppression

48
Q

what are the main limitations of pancreas transplantation?

A

1) limited availability of donors
2) requirement of life-long immunosuppression
3) failure of procedure

49
Q

what is the main aim of pancreas transplantation?

A

aim to restore normal, physiological insulin production to the extent that insulin can be stopped

50
Q

how are glucose levels monitored?

A

1) continuous glucose monitoring (sensor)
2) capillary blood glucose (finger prick)
3) HbA1c (a bigger picture of the last three months)

51
Q

what is HbA1c and why is it measured?

A

level of glycated haemoglobin
= reflects the last three months of glycaemia

(essentially forms when haemoglobin is bound to glucose = irreversible reaction)

52
Q

how are insulin doses determined?

A
  • self-monitoring of blood glucose at home (capillary blood glucose, finger-prick test)
  • HbA1c test every 3-4 months

= adjust insulin doses accordingly

53
Q

what are the acute complications of T1DM?

A

1) diabetic ketoacidosis
2) uncontrolled hyperglycaemia
3) hypoglycaemia

54
Q

in patients w T1DM, how can uncontrolled hyperglycaemia arise?

A

if patient misses a once daily long-acting basal dose of insulin

= uncontrolled hyperglycaemia

55
Q

what is diabetic ketoacidosis and why does it occur?

A

an acute complication of T1DM wherein due to a lack of insulin (missed/inadequate dose)

= increased compensatory ketogenesis
= more ketone bodies in the blood increases the acidity of the blood to dangerous levels
= life-threatening

56
Q

who is most commonly affected by DKA?

A

1) T1DM patients
2) new-onset T1DM patients
3) T2DM patients

57
Q

how is DKA diagnosed?

A

1) pH < 7.3
2) ketones +++ (urine/capillaty blood)
3) HCO3- <15 mmol/L
4) glucose >11 mmol/L

58
Q

what are possible causes of DKA?

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

what glucose level is expected in DKA?

A

a level of >11 mmol/L is expected

60
Q

what are the possible causes of hypoglycaemia in patients w T1DM?

A

an acute complication of T1DM when

= too much insulin is injected (too large a dose given for the quantity of food eaten)

61
Q

which complication of T1DM is most likely if a dose is missed?

A

DKA

alongside uncontrolled hyeprglycaemia

62
Q

which complication of T1DM is most likely if a dose is too much?

A

hypoglycaemia

63
Q

why are hypoglycaemia episodes dangerous in patients w T1DM?

A

one/two episodes = normal

but if they are recurrent = patient may become accustomed to the symptoms + fail to recognise them unless levels fall dangerously low

64
Q

define hypoglycaemia numerically

A

glucose = <3.6 mmol/L

65
Q

how is hypoglycaemia treated?

A

administer glucose

66
Q

what are the symptoms of hypoglycaemia?

A

adrenergic = tremors, palpitations, sweating, hunger

neuroglycopaenic = seizures, coma, confusion, incoordination, somnolence

67
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

68
Q

what are the risks of hypoglycaemia?

A
  • impacts of cognition, driving, day-to-day function, emotional wellbeing
  • seizure, coma, death
69
Q

who is at risk of a hypoglycaemic episode?

A

all people w T1DM but especially those w:

  • inappropriate insulin regime
  • lack of training around dose-adjustment for meals
  • missed meals
  • lower HbA1c, alcohol intake, exercise
70
Q

what are the possible strategies to support problematic hypoglycaemia?

A
  • indication for insulin-pump therapy (CSII)
  • revisit carbohydrate counting/structured education
  • behavioural psychology support
  • transplantation
71
Q

how is hypoglycaemia acutely managed in patients who are alert and orientated?

A
  • oral carbohydrates
  • rapid-acting = juice, sweets
  • long-acting = sandwich
72
Q

how is hypoglycaemia acutely managed in patients who are are drowsy/confused BUT their swallow is intact?

A
  • buccal glucose

- complex carbohydrates

73
Q

how is hypoglycaemia acutely managed in patients who are are drowsy/confused BUT their swallow is NOT intact?

A
  • IV access
74
Q

how is hypoglycaemia acutely managed in patients who are are deteriorating/difficult IV access?

A

consider IM/SC glucagon administration

brs (phase 1b) (71 decks)

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