Diabetes Flashcards

(50 cards)

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
What must patients do when administering insulin?
Change injection site Long term use of same injection site causes lipohypertrophy which disrupts insulin absorption
26
What dose of insulin would a 60kg male get for bolus and basal use?
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
What is the 1. insulin carbohydrate ratio (ICR) 2. insulin sensitivity factor (ISF)/ correction factor (CF)?
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
What dose should be changed if a patient is reporting hypo/hyperglycaemia?
Dose before the hypo/hyperglycaemia
29
How much should an insulin dose be changed by?
10%
30
What must you check before changing an insulin dose?
``` Renal function Injection site (lipohypertrophy) Lifestyle changes ```
31
What is the major cause of death in DKA in adults?
Hypokalaemia Aspiration pneumonia Co-morbidities
32
What is the pathophysiology of DKA?
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
How does DKA present?
Polyuria, dehydration, breathlessness, vomiting, abdominal pain, sweet breath
34
What blood tests would you order in suspected DKA? What results would confirm your suspicion?
Urine ketones >3mM Blood glucose > 11mM Bicarbonate <15mM
35
What ketone is used to measure 1. blood ketones 2. urine ketones?
1. ß-hydroxybutarate | 2. acetoacetate
36
Outline management of DKA.
*replace losses* IV fluid IV insulin Potassium ECG monitoring for hyperkalaemia
37
Name 8 symptoms of hypoglycaemia.
``` Tremor Sweating Anxiety Irritability Tachycardia Headache Hunger Blurred vision ```
38
What can cause hypoglycaemia?
Missed meals Exercise Alcohol (increases insulin activity) Over treatment
39
How do you manage hypoglycaemia in a 1. conscious patient 2. unconscious patient
Conscious - 15-20g rapidly absorbed glucose - recheck BG (if abnormal repear step 1) - 15g simple carbohydrate Unconcsious - 1mg subcutaneous glucagon
40
What is hyperglycaemic hyperosmolar syndrome?
Hyperglycaemia causes hyperosmolality without ketoacidosis
41
What is the name given to hyperglycaemia causing hyperosmolality without ketoacidosis?
Hyperoglycaemic hyperosmolar syndrome (HHS)
42
How does hyperglycaemic hyperosmolar syndrome (HHS) present clinically?
Confusion, dehydration and blurred vision over days to weeks
43
What blood tests would you order in suspected hyperoglycaemia hyperosmolar syndrome (HHS)? What results would confirm your suspected diagnosis?
Blood glucose - very high (>30mM) Ketones - none U&Es - hyperosmolar
44
How do you calculate osmolality? What is a normal result?
2([Na]+[K]) + [urea] + [glucose] 285-295
45
Outline management of hyperoglycaemic hyperosmolar syndrome (HHS).
Normalise osmolality with - IV fluid - IV sodium (give insulin if ketones or blood glucose not falling in response to fluids)
46
What are the classes of lactic acidosis? What causes each?
Type A - hypoxia Type B - other (DKA, meformin, liver diseas etc.)
47
How does lactic acidosis present?
Hyperveiltation | Confusion (coma)
48
What is the initial management of lactic acidosis?
IV fluid
49
What is charcot foot?
Arthopathy characterised by degeneration of weight bearing foot joints assoaciated with diabetes
50
What are the different classes of neuropathy in diabates?
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)