Diabetes Flashcards

1
Q

What is the major cause of death in DKA in children?

A

Cerebral oedema

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2
Q

What must you ask in any child presenting with vague symptoms?

A

Polyuria, polydipsia, nocturnal enuresis

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3
Q

What is T1DM?

A

Autoimmune destruction of pancreatic ß-cells by anti-GAD and anti-islet cells. Causes hyperglycaemia.

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4
Q

How does T2DM present?

A

Polyuria, polydipsia, fatigue

In obese person

Often in older person

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5
Q

How does T1DM present?

A

Polyuria, polydipsia, fatigue

Weight loss

Often in younger person

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6
Q

What is T2DM?

A

Insulin resistance from chronic hyperglycaemia

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7
Q

How do you diagnose diabetes mellitus?

A

Random glucose > 7mmol

Fasting glucose > 11mmol

Glucose tolerance test > 11mmol

(repeat tests required)

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8
Q

What autoantibodies are associated with T1DM?

A

Anti-GAD

Anti-islet cell

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9
Q

What is c-peptide and would it be raised in T1DM and/or T2DM?

A

Measure of endogenous insulin production

Low in T1DM
Normal/high in T2DM

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10
Q

Name a rapid acting insulin.

A

Novorapid

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11
Q

Name a long acting insulin

A

Lantus

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12
Q

What insulin regimen are most T1DM patients on and what does it consist of?

A

Basal bolus

Long acting basal insulin (lantus)

Short acting insulin (novoarpid) taken before meals

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13
Q

What should the HbA1c target be in

  1. most diabetics?
  2. young diabetics?
A
  1. 53mmol/mol

2. 48mmol/mol

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14
Q

What is HbA1c?

A

Glycalated haemoglobin

Measures average glucose levels in blood in last 6-8 weeks

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15
Q

What should diabetic patients blood glucose targets be before meals?

A

6mM (4-7mM)

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16
Q

What is the pathogenesis of T2DM?

A

Fat and fatty acid produce inflammatory mediators which inhibit insulin receptor substrate 1 which inhibits insulin function resulting in insulin resistance.

The ß-cells compensate for this by over-secreting insulin but these eventually fatigue resulting in ß-cell dysfunction

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17
Q

What are the main chronic complications of T2DM?

A

Macrovascular

  • MI
  • Stroke

Microvascular

  • neuropathy
  • retinopathy
  • nephropathy
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18
Q

What is the stepwise treatment pathway in diabetes mellitus?

A
  1. Lifestyle modification
  2. Lifestyle + oral monotherapy
  3. Lifestyle + combined therapy
  4. Lifestyle + injected therapy
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19
Q

What is involved in a diabetic review?

A

Ask about lifestyle

Visual acuity
Leg/foot exam
Urinalysis
HbA1c
U and Es
Cholesterol
Measure BMI
Blood pressure
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20
Q

8 months old boy presents with polyuria, polydipsia and failure to thrive. What is the diagnosis?

A

Maturity onset diabetes of the young (MODY)

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21
Q

Name 2 genes which are mutated in MODY and which MODY types they cause.

A

Hepatocute nuclear factor
- MODY1/3/5

Glucokinase
- MODY2

22
Q

What is MODY treated with?

A

Sulphonylureas

23
Q

Patient with BMI 31 presents with polydipsia, polyuria and lethargy. They are autoantibody positive and non-insulin requiring. What is the diagnosis?

A

Latent onset diabetes of adulthood (LADA)

24
Q

How do you diagnose LADA?

A

Elevated pancreatic autoantibodies (anti-GAD, anti-islet cell)

Non-insulin requiring at diagnosis

25
Q

What must patients do when administering insulin?

A

Change injection site

Long term use of same injection site causes lipohypertrophy which disrupts insulin absorption

26
Q

What dose of insulin would a 60kg male get for bolus and basal use?

A

60kg person gets 18 units insulin a day (weight times 0.3)

18 units divided equally between basal and bolus

Basal - 9 units

Bolus - 9 units (3 units per meal)

27
Q

What is the

  1. insulin carbohydrate ratio (ICR)
  2. insulin sensitivity factor (ISF)/ correction factor (CF)?
A
  1. units of insulin requires to clear x grams of carbohydrate
    ICR=1:10, 1unit insulin clears 10g carbohydrate
  2. units insulin required to reduce blood glucose by x mM
    ICF=1:2, 1 unit insulin lowers BG by 2mM
28
Q

What dose should be changed if a patient is reporting hypo/hyperglycaemia?

A

Dose before the hypo/hyperglycaemia

29
Q

How much should an insulin dose be changed by?

A

10%

30
Q

What must you check before changing an insulin dose?

A
Renal function
Injection site (lipohypertrophy)
Lifestyle changes
31
Q

What is the major cause of death in DKA in adults?

A

Hypokalaemia
Aspiration pneumonia
Co-morbidities

32
Q

What is the pathophysiology of DKA?

A

Lack on insulin prevents glucose moving into cells starving them of energy which causes them to release stress hormones.

Stress hormones produce more glucose and breakdown lipids which forms ketone bodies.

Ketone bodies are acidic and cause ketoacidosis.

33
Q

How does DKA present?

A

Polyuria, dehydration, breathlessness, vomiting, abdominal pain, sweet breath

34
Q

What blood tests would you order in suspected DKA? What results would confirm your suspicion?

A

Urine ketones >3mM

Blood glucose > 11mM

Bicarbonate <15mM

35
Q

What ketone is used to measure

  1. blood ketones
  2. urine ketones?
A
  1. ß-hydroxybutarate

2. acetoacetate

36
Q

Outline management of DKA.

A

replace losses

IV fluid
IV insulin
Potassium

ECG monitoring for hyperkalaemia

37
Q

Name 8 symptoms of hypoglycaemia.

A
Tremor
Sweating
Anxiety
Irritability
Tachycardia
Headache
Hunger
Blurred vision
38
Q

What can cause hypoglycaemia?

A

Missed meals

Exercise

Alcohol (increases insulin activity)

Over treatment

39
Q

How do you manage hypoglycaemia in a

  1. conscious patient
  2. unconscious patient
A

Conscious

  • 15-20g rapidly absorbed glucose
  • recheck BG (if abnormal repear step 1)
  • 15g simple carbohydrate

Unconcsious
- 1mg subcutaneous glucagon

40
Q

What is hyperglycaemic hyperosmolar syndrome?

A

Hyperglycaemia causes hyperosmolality without ketoacidosis

41
Q

What is the name given to hyperglycaemia causing hyperosmolality without ketoacidosis?

A

Hyperoglycaemic hyperosmolar syndrome (HHS)

42
Q

How does hyperglycaemic hyperosmolar syndrome (HHS) present clinically?

A

Confusion, dehydration and blurred vision over days to weeks

43
Q

What blood tests would you order in suspected hyperoglycaemia hyperosmolar syndrome (HHS)?

What results would confirm your suspected diagnosis?

A

Blood glucose - very high (>30mM)

Ketones - none

U&Es - hyperosmolar

44
Q

How do you calculate osmolality?

What is a normal result?

A

2([Na]+[K]) + [urea] + [glucose]

285-295

45
Q

Outline management of hyperoglycaemic hyperosmolar syndrome (HHS).

A

Normalise osmolality with

  • IV fluid
  • IV sodium

(give insulin if ketones or blood glucose not falling in response to fluids)

46
Q

What are the classes of lactic acidosis?

What causes each?

A

Type A - hypoxia

Type B - other (DKA, meformin, liver diseas etc.)

47
Q

How does lactic acidosis present?

A

Hyperveiltation

Confusion (coma)

48
Q

What is the initial management of lactic acidosis?

A

IV fluid

49
Q

What is charcot foot?

A

Arthopathy characterised by degeneration of weight bearing foot joints assoaciated with diabetes

50
Q

What are the different classes of neuropathy in diabates?

A

Peripheral (distal symmetric aesthesia, proprioception loss)

Focal (one/group of dysfunctional nerve(s)

Proximal (proximal lower limb pain progressing to weakness)

Autonomic (increased sympathetic nervous action eg gastroparesis)