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endocrinology lectures phase 2 > type 1 diabetes > Flashcards

type 1 diabetes Flashcards

1
Q

presenting features of diabetes

A
  • Thirst
    osmotic activation of hypothalamus
  • Polyuria
    osmotic diuresis
  • Weight loss and fatigue
    lipid and muscle loss due to
    unrestrained gluconeogenesis
  • Hunger
    Lack of useable energy source
  • Pruritis vulvae and balanitis
    Vaginal candidiasis
    Chest / skin infections
  • Blurred vision
    Altered acuity due to uptake of glucose/water into lens
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2
Q

suggestive features of type 1 diabetes

A
  • Onset in childhood / adolescence
  • Lean body habitus
  • Acute onset of osmotic symptoms
  • Prone to ketoacidosis
  • High levels of islet autoantibodies
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3
Q

can type 1 diabetes occur at any age

A

yes

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4
Q

what does the spectrum of type 1 diabetes depend on

A

on the rate of β-cell destruction

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5
Q

3 clinical features of newly diagnosed type 1 diabetes

A
  1. weight loss
  2. Short history (weeks) of severe symptoms
  3. Moderate or large urinary ketones

Any 2 of these three features indicate Type 1 diabetes and are an indication for immediate insulin treatment at ANY age

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6
Q

when does type 1 diabetes onset

A

childhood/adolescne

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7
Q

when does type 2 diabetes onset

A

usually over 30s

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8
Q

is type 2 diabetes genetic

A

yes almost 100% concordance in identical twins

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9
Q

suggestive features of type 2 diabetes

A
  • Usually presents in over-30s
  • Onset is gradual
  • FH is often positive
  • Almost 100% concordance in identical twins
  • Diet, exercise and oral medication can often control hyperglycaemia; insulin may be required later in the disease
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10
Q

distinguishing factors between type 1 and 2 diabetes

A

Type 2 is diagnosed in younger patients, including childhood

Type 1 patients can be obese

Uncontrolled Type 2 can present with weight loss and ketouria

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11
Q

what to do if in doubt

A

treat with insulin

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12
Q

commonest age of type 1 diabetes diagnosis

A

5 - 15 years
but can occur at any age

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13
Q

prevalence of type 1 diabetes

A

Relatively rare (prevalence of 3/1000 among children and adolescents)

~370,000 in the UK

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14
Q

risk of developing type 1 diabetes if the mother has it

A

2%

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15
Q

risk of developing type 1 diabetes if the father has it

A

8%

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16
Q

risk of developing type 1 diabetes if both parents has it

A

up to 30%

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17
Q

risk of developing type 1 diabetes if a brother or sister has it

A

10%

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18
Q

risk of developing type 1 diabetes if a non identical twin has it

A

15%

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19
Q

risk of developing type 1 diabetes if an identical twin has it

A

40%

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20
Q

what happens to index if a family member of a child has t1 diabetes

A

If a family member has diabetes then the index case is less unwell compared to sporadic cases

Less autoimmunity in familial vs sporadic cases

Parents diagnosed 13% of the time after the birth of the index child

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21
Q

are offspring of affected fathers more unwell or affected mothers?

A

Offspring of affected fathers are more unwell than those of affected mothers, with longer duration of symptoms, more than twice as likely to present in ketoacidosis.

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22
Q

what is autoimmunity associated with

A

antibodies and other autoimmune diseases

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23
Q

what antibodies is autoimmunity associated with

A

Anti GAD
Pancreatic islet cell Ab
Islet antigen-2 Ab
ZnT8

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24
Q

what other autoimmune diseases is autoimmunity associated with

A

Hypothyroidism
Addisons
Coeliac disease

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25
Q

what happens if the diagnosis for type 1 diabetes is missed

A

fat metabolism

formation of ketone bodies

26
Q

why does missed diagnosis cause fat metabolism

A

Reduced insulin leads to fat breakdown and formation of glycerol (a gluconeogenic precursor) and free fatty acids

27
Q

why does missed diagnosis cause formation of ketone bodies

A

Free fatty acids (FFA) impair glucose uptake

Are transported to the liver, providing ‘energy’ for gluconeogenesis

Are oxidised to form ketone bodies (beta hydroxy butyrate, acetoacetate and acetone)

28
Q

why does absence of insulin cause ketoacidosis

A

Absence of insulin and rising counterregulatory hormones leads to increasing hyperglycaemia and rising ketones

Glucose and ketones escape in the urine but lead to an osmotic diuresis and falling circulating blood volume

29
Q

what do ketones cause

A

anorexia and vomiting

30
Q

how does ketoacidosis lead to death

A

Vicious circle of increasing dehydration, hyperglycaemia and increasing acidosis eventually lead to circulatory collapse and death

31
Q

characteristrics of diabetic ketoacidosis

A

Hyperglycaemia (plasma glucose usually <50 mmol/l)

Raised plasma ketones (urine ketones > 2+)

Metabolic acidosis – plasma bicarbonate < 15 mmol/l

32
Q

causes of diabetic ketoacidosis

A

Intercurrent illness
- infection
- myocardial infarct

Treatment errors – stop/reduce insulin dose

Previously undiagnosed diabetes

Unknown

33
Q

diabetic ketoacidosis triad

A

Hyperglycaemia
Ketones
Acidosis

34
Q

symotopms of dieabteic ketoacidosis

A

develop over days
polyuria and polydipsia
nausea and vomiting
weight loss
weakness
abdominal pain (confused with surgical abdomen)
Drowsiness / confusion

35
Q

signs of diabetic ketoacidosis

A

hyperventilation (Kussmaul breathing)
dehydration (average fluid loss 5-6 litres)
hypotension
Tachycardia
coma

36
Q

biochemical diagnosis of diabetic ketoacidosis - hyperglycaemia

A

hyperglycaemia (<50 mmol/l)

37
Q

biochemical diagnosis of diabetic ketoacidosis - K+

A

K+ – high on presentation despite total body K+ deficit (due to acute shift of K out of cell with acidosis), subsequently fall with insulin and rehydration, anticipate fall in K+

38
Q

biochemical diagnosis of diabetic ketoacidosis - HCO3-

A

HCO3- <15 mmol/l

39
Q

biochemical diagnosis of diabetic ketoacidosis - urea and creatinine

A

urea and creatinine - raised due to pre-renal failure

40
Q

biochemical diagnosis of diabetic ketoacidosis - urinary ketones dipstick

A

urinary ketones dipstix >2+ ketones
blood ketones >3.0

41
Q

management of diabetic ketoacidosis

A

rehydration (3L first 3 hrs)

insulin (inhibits lipolysis, ketogenesis, acidosis, reduces hepatic glucose production, increase tissue glucose uptake)

replacement of electrolytes (K+)

treat underlying cause

Treatment must be started without delay

Follow DKA protocol in hospital

42
Q

complications of diabetic keto acidosis

A

cerebral oedema (deterioration in conscious level)
children more at risk

adult respiratory distress syndrome

thromboembolism – venous and arterial

aspiration pneumonia (in drowsy/comatose patients)

death

43
Q

aims of tretment with type 1 diabetes

A

Relieve symptoms and prevent ketoacidosis

Prevent microvascular and macrovascular complications

44
Q

how much life do people with type 1 diabetes lose

A

On average, people with Type 1 diabetes lose 8 years of life (mostly from cardiovascular disease)

45
Q

how many t1 diabetes patients develop diabetic nephropathy

A

Around 30% in the UK will develop diabetic nephropathy

46
Q

impact of diabetic nephropathy

A

Those with nephropathy tend to develop proliferative retinopathy and severe neuropathy with major effect on quality of life

47
Q

key goal of type 1 diabetes treatment

A

To restore the physiology of the beta cell

48
Q

what needs to be done to restore physiology of beta cell to treat t1 diabetes

A

Insulin treatment
- Twice daily mixture of short/medium acting insulin
- Basal bolus, (once or twice daily medium acting insulin plus pre meal quick acting insulin)

Ability to judge CHO intake

Awareness of blood glucose lowering effect of exercise

All combined to keep blood glucose close to normal (and so prevent diabetic complications)

49
Q

what do innapropiatley high insulin levels confer

A

high risk of hypoglycaemia

Acute deprivation of glucose within the brain leads to cerebral dysfunction (loss of concentration, confusion, coma)

50
Q

physiological defences to hypoglycaemia

A

Release of glucagon, adrenaline

51
Q

symptoms of hypoglycaemia

A

Symptoms of
Sweating, tremor, palpitations (autonomic activation)
Loss of concentration, ‘hunger’

52
Q

what happens to hypoglycaemia when glucose level is 4.6 mM

A

inhibition of insulin secretion

53
Q

what happens to hypoglycaemia when glucose level is 3.8 mM

A

counter-regulatory hormone release (glucagon and adrenaline)

54
Q

what happens to hypoglycaemia when glucose level is 3.8 - 2.8 mM

A

autonomic symptoms
- sweating, tremor, palpitations

55
Q

what happens to hypoglycaemia when glucose level is <2.8 mM

A

neuroglycopenic symptoms
- confusion, drowsiness, altered behaviour, speech difficulty, incoordination

56
Q

what happens to hypoglycaemia when glucose level is <1.5 mM

A

severe neuroglycopenic
- convulsions, coma, focal neurological deficit ie hemiparesis

57
Q

what is the dilemma for people with type 1 diabetes

A

Setting higher glucose targets will reduce the risk of hypoglycaemia but increase the risk of diabetic complications

Setting lower glucose targets will reduce the risk of complications but increase the risk of hypoglycaemia

58
Q

what factors make it difficult for people with diabetes to sustain effective self management

A
  • Risk of hypoglycaemia
  • Too arduous a treatment
  • Risk of weight gain
  • Interference with lifestyle
  • Lack of sufficient training from diabetes teams
59
Q

what should diabetes treatment reduce the risk of

A
  • cardiovascular morbidity and mortality
  • chronic kidney disease
  • microvascular complications
60
Q

what are incretins

A

hormones secreted by intestinal endocrine cells in response to nutrient intake
Incretins influence glucose hom

61
Q

how do incretins influence glucose homeostasis

A

via multiple actions including glucose-dependent insulin secretion, postprandial glucagon suppression, and slowing of gastric emptying

62
Q
A

endocrinology lectures phase 2 (17 decks)

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