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My MRCP > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What different tests do we have for DM? [6]

A
  • Random Glc test
  • Fasting Glc test
  • HbA1c test
  • Oral Glucose Tolerance Test (OGTT)
  • Blood & Urine Ketones
  • Urine glucose
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2
Q

All DM tests are indicative of DM, which tests are considered diagnostic and what values would indicate diabetes? [4]

A

Fasting Venous Plasma Glc > 7mmol/l
Random Venous plasma Glc > 11.1mmol/l
OGTT >11.1mmol/l after 2 hours
HbA1C > 48mmol/mol

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3
Q

Explain the OGTT [3]

What result is abnormal? [1]

A

1) Take a fasting glucose
2) Give them oral glucose load
3) Test again after 2 hours

If its still raised then its +ve for diabetes (should normally return to normal within 1 hour of ingesting glucose)

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4
Q

What do we need to diagnose Diabetes Mellitus? [2]

A

2 +ve diagnostic tests (fasting or random glucose, OGTT or HbA1c)

OR

1 +ve diagnostic test + Symptoms

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5
Q

What is HbA1c? [3]

A

Glycated Haemoglobin [1]

Sugar in the blood binds to haemoglobin, the amount that does is directly proportional to the total amount of Glucose. [1]
So HbA1c levels reflect the level of glucose in the blood over the last 8-12w [1]

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6
Q

When can we not use an HbA1c test? [7]

A
  • Children or young people
  • Pregnant women
  • The acutely ill
  • Meds that affect glucose e.g. CCS or antipsychotics
  • Acute pancreatic damage
  • Renal Failure
  • HIV infection

Basically anything that would alter recent glucose levels renders HbA1c useless

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7
Q

How would you diagnose DKA? [2]

A

Clinical diagnosis and blood/urine ketone testing.

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8
Q

Describe the biochem results of a patient with DKA? [4]

A

1) High glucose
2) Low Bicarbonate (kessmauls resp)
3) Low Na+ (diluted by movement of water)
4) High urea, potassium & Creatinine (dehydration reduces excretion)

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9
Q

When would you want to test C-peptide? [2]

A

If a patient was having recurrent hypoglycemia. Test their insulin levels to see if thats the source and its raised.
When insulin is self-injected, laboratory studies will show high plasma insulin levels in combination with low plasma C-peptide levels during the hypoglycemic episode. With sulfonylurea consumption, the clinical picture may mimic an insulinoma with high plasma levels of both C-peptide and insulin; a positive drug screen can render the diagnosis.

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10
Q

What would you want to monitor to keep an eye out for long-term complications? [3]

A

Urine Albumin/creatinine Ratio (for nephropathy)

Lipids & BP for CV disease

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11
Q

Investigations DKA

  • Initial [5]
  • After the patient is stable what additional investigations would you order? [3]
A

Inititial Investigations:

  • ABCs
  • Vital Signs
  • IV access
  • Clinical Assessment
  • Glucose fingerprick test

First Investigations:

  • Lab Blood Glucose to confirm
  • ABGs (Low CO2 from hyperventilation & acidosis)
  • Urinalysis and blood ketones
  • U&E + FBC
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12
Q

Prediabetes definition

Also known as…

A

impaired glucose levels which are above the normal range but not high enough for a diagnosis of diabetes mellitus

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13
Q

How do we define prediabetes through investigations? [3]

A
  1. patients identified at high risk should have a blood sample taken
  2. a fasting plasma glucose of 6.1-6.9 mmol/l or
    - an HbA1c level of 42-47 mmol/mol (6.0-6.4%)

So normal is <6 mmol/l and 41 HbA1c on fasting glucose
DM is >7 mol/l and 48 HbA1c is DM on fasting plasma

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14
Q

How do you identify high risk people in the first instance before investigating for prediabetes?

A

all adults aged 40 and over, people of South Asian and Chinese descent aged 25-39

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15
Q

Management of prediabetic patients [3]

NICE guidelines 2012

A
  • lifestyle modification: weight loss, increased exercise, change in diet
  • at least yearly follow-up with blood tests is recommended
  • metformin for adults at high risk ‘whose blood glucose measure (fasting plasma glucose or HbA1c) shows they are still progressing towards type 2 diabetes, despite their participation in an intensive lifestyle-change programme’
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16
Q

Impaired fasting glucose vs Impaired glucose tolerance

A

impaired fasting glucose (IFG) - due to hepatic insulin resistance
impaired glucose tolerance (IGT) - due to muscle insulin resistance
*patients with IGT are more likely to develop T2DM and cardiovascular disease than patients with IFG

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17
Q

Impaired fasting glucose definition

Impaired glucose tolerance definition

A
  • a fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)
  • impaired glucose tolerance (IGT) is defined as:
    1. fasting plasma glucose less than 7.0 mmol/l AND
    2. OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
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18
Q

What is the mainstay and first line options of Type 1 treatment? [2]

A

Lifestyle changes and Insulin!

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19
Q

How is insulin delivered? [2]

Why is it delivered any other route

A

By SC or IV

Because its a polypeptide inactivated by the GI tract so it doesnt work orally

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20
Q

What are the types of insulin? [5]

A
  • Rapid acting
  • Short Acting
  • Intermediate Acting
  • Long acting
  • Continuous SC insulin infusion (CSII)
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21
Q

What changes the time insulin takes to take effect? [2]

A

Soluble insulin associates into hexamers in SC fat.

  • It needs to dissociate into monomers in order to diffuse into capillaries.
  • Altering the structure/solubility of insulin affects how long it takes to dissociate
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22
Q

Describe a twice daily insulin regime [1]

Timings [2]

A 
Mix of rapid and intermediate acting insulin 
Before breakfest (BB) &amp; before tea (BT)
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23
Q

Describe a thrice daily insulin regime? [1]

Timings [2]

A

Mix of rapid and intermediate BB

Rapid BT

Intermediate Bbed

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24
Q

Describe a 4x daily insulin regime? [2]

A

Mix of: Short acting insulin BB, BL & BT

Then Intermediate Bbed or long acting insulin at a fixed time once per day

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25
Q

How is Type 2 Diabetes treated?

Name drugs from 1st to 3rd line

A

Lifestyle modifications
1st line - Metformin (OHG)
2nd line - A Sulphonyurea (E.g. glimepiride)
3rd line - A thiazolidinedione (e.g. pioglitazone) (aka Glitazones)

Further 3rd line meds include:
DPP-IV inhibitors - SGLT-2 inhibitors - GLP-1 agonist - Insulin

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26
Q

What does metformin do? [1]

A

It increases insulin sensitivity

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27
Q

What aspects of hypoglycemia is it important to educate patients on? [4]

A
  • How to test their blood sugar
  • How to recognise the signs of a hypo
  • How to treat it
  • How to avoid it
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28
Q

Treatment of hypoglycaemia
Give 3 options for non-hospital and hospital settings
Follow up [1]

A

Rapid acting carb e.g. 200ml of fruit juice
OR 1mg IM glucagon
OR if in hospital then 80ml 20% glucose

Follow up with a long acting carbohydrate

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29
Q

How do patients avoid based on causes of hypoglycemia? [4]

A
  • Blood glucose monitoring
  • Rotate & check injection sites
  • Review diet (carb counting)
  • Maybe change the insulin regime
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30
Q

What are the rules for driving and Hypos?

What are the contraindications for driving that the DVLA impose on diabetics [2]

A

Diabetics have to check their glucose within 2 hours of driving [1] and repeat on long journeys [1]
They should carry short acting carbs in the car
If they can’t recognise a hypo [1] or have >1 severe hypo a year they can’t drive [1]

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31
Q

How would we advise a patient to deal with DKA at home? [6]

A

1) They think they’re getting symptoms
2) Test their ketones
3) +ve? Test Blood Glc
4) Elevated? Take an extra insulin dose
5) still high after 4 hours? Take another dose
6) Call diabetes team, notify them of possible DKA

32
Q

How do we treat DKA? [7]

A

Fluid replacement 0.9% NaCl 1L for 1st hour
- Once BM <15 mmol/l start 5% dextrose infusion
Insulin:
- IV infusion 0.1 unit/kg/hour
- Continue long acting insulin usual dose
- Stop short acting insulin
Correct hypokalaemia

33
Q

Management of DM complications

How do we manage diabetic nephropathy? [4]

A
  • Glycaemic control
  • BP control
  • ACE inhibitor slows progression & treats BP
  • CVD risk factor control
34
Q

Diarrhoea is a potential diabetic autonomic neuropathy, how do you treat it? [1]

A

Loperamide (i.e. imodium)

35
Q

Gastric stasis and vomiting is a potential diabetic autonomic neuropathy, how do you treat it?

A

Domperidone.

Dopamine antagonist that acts as an antiemetic and progastrokinetic

36
Q

Postural Hypotension is a potential diabetic autonomic neuropathy, how do you treat it? [3]

A

Advice: avoid getting up to quickly

NSAIDS or Fludrocortisone

37
Q

Erectile dysfunction is a potential diabetic autonomic neuropathy, how do you treat it? [1]

A

Phosphodiesterase inhibitors e.g. Viagra

38
Q

Management of peripheral neuropathy

  • Rx [2]
  • Non pharmacological [3]
A

Pain relief:

  • Capsaicin cream
  • Amitriptyline

Protection of feet from ulceration:

  • Fitted footwear
  • Regular podiatry visits
  • Foot screening and risk assessment
39
Q

How do we treat maculopathy? [3]

A

Grid laser therapy
Glc Control
BP control

40
Q

Treatment: proliferative retinopathy [2]
Describe rationale for each [4]
Natural progression if untreated [2]

A

We can do a vitrectomy if theres a vitreous haemorrhage

Laser photocoagulation destroys ischaemic retina [1] , reducing Endothelial Growth Factors [1] causing the new vessels to regress [1]

If untreated, scarring can occur which can lead to retinal detachment.

41
Q

CV risk reduction is an example of primary prevention [4]

A

Lifestyle mods
Control BP to <130/80
Smoking cessation services
Statin therapy - simvastatin for over 40 and in younger patients with significant complications

42
Q

Package of care for people with T2DM [11]

A
  • Blood glucose levels (annually)
  • Blood Pressure (annually)
  • Blood Lipids (annually)
  • Eyes Screened (annually)
  • Feet checked (annually)
  • Kidney function (annually)
  • Weight
  • Smoking Cessation Support
  • Individual Care plan
  • Education Course
  • Emotional and psychological support
43
Q

Targets HBA1C depend on management:
Lifestyle AND/OR metformin only
Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)

A

Lifestyle AND/OR metformin only:
- Target for 48

Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)
- Target for 53

44
Q

Fluid replacement regime in DKA admission with systolic BP >90 mmHg (for 19 hours)

A 
1L over 1st hour 0.9% NaCl
1L over next 2h 0.9% NaCl with KCl
- Another 1L over next 2h
- Another 1L over next 4h
- Another 1L over next 4h
- Another 1L over next 6h
45
Q 
Main complication of treating DKA in young people
Specific age range
Symptoms
Onset
Mx
A

Fluid therapy can cause cerebral edema so slower infusion is needed

  • 18-25yo
  • need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc
  • Usually occur 4-12h after commencement of treatment
  • CT head and senior review
46
Q

Goals of management of HHS

What NOT to do…

A
  1. Normalise the osmolality (gradually)
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)

Don’t use insulin in first instance, fluid replacement alone can facilitate a gradual decline in BM and plasma osmolarity. Because most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.

47
Q

Fluid replacement in HHS [2]
Aim?
What is a safe rate of fall of plasma glucose? [2]

A

Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid.
2nd line if unresponsive: 0.45% NaCl

Aim: achieve positive balance of 3-6L by 12h, replace remaining losses within next 12h

A safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended. The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.

48
Q

Complications of HHS treatment
When can you expect total normalization?
What target blood glucose is used?

A

Cardiovascular collapse
Central pontine myelinolysis

Complete normalisation of electrolytes and osmolality may take up to 72 hours.

A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.

49
Q

Why can insulin treatment cause cardiovascular collapse?

A

Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.

50
Q

When would insulin be indicated in HHS?

What ROA and dose of insulin would be recommended?

A

If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture).

The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.

51
Q

Potassium in HHS

A

Patients with HHS are potassium deplete but less acidotic than those with DKA so potassium shifts are less pronounced
Hyperkalaemia can be present with acute kidney injury
Replace as required

52
Q

What are the drugs used for Type 2? (1st/2nd/3rd line)

A
53
Q

How does Metformin Work?

A

It increases insulin sensitivity

54
Q

Pros [4] & Cons of Metformin [3]

A
  • Well tolerated
  • Effective
  • Weight neutral
  • Improves mortality & CV complications

Cons:

  • GI side effects
  • Vit B12 malabsorption
  • Lactic Acidosis
55
Q

What do Sulphonyureas do? [2]

Give an example

A

Glimepiride

Blocks ATP-sensitive K+ channels leading to increased insulin secretion

56
Q

Pros [4] and cons of Sulphonyureas? [2]

Contraindications [4]

A

Pros:

  • Rapid action so good for the acutely ill
  • Well tolerated
  • Rapid titration

Cons:

  • Risk hypo
  • Weight gain
  • Contraindicated in pregnant/breastfeeding
  • Cautioned in renal/hepatic disease
57
Q

MOA Thiazolidinediones[2]

Give an eg

A

Pioglitazone

Increases insulin sensitivity in muscle/fat/liver by acting on PPar gamma receptors

58
Q

Pros [2] and cons [4] of Thiazolidinediones

A
  • Effective for insulin resistance
  • Safe with CV system

Cons:

  • Weight gain
  • Fluid retention
  • Increases bone turnover -> fractures
  • Bladder cancer
59
Q

Example of a DPP-IV inhibitor and how they work?

A

Saxagliptin

DPP-IV is an enzyme that breaks down incretin hormones.
Inhibitors extend incretin half-lives.
Incretin hormones cause glucose dependant insulin release and glucagon inhibition

60
Q

Pros and cons of DPP-IV?

A
  • Well tolerated
  • Usuable in renal impairment
  • Weight neutral
  • No Hypo risk

Cons:

  • Small effects
  • CI in pregnancy/breastfeeding
  • PAncreatitis/pancreatic cancer
  • Nausea
61
Q

Example and function of SGLT-2 inhibitors? [3]

A

Gliflozins e.g. empagliflozin

Inhibit Sodium Glucose Transporter 2 in the proximal tubule of the kidney.

Thus increases Glc & Na excretion in urine

62
Q

Effects of SGLT-2 inhibitors?

A

Diuretic Effect - Postural hypotension & dehydration

Glucouric Effect - Weight loss from pissing out so many calories

Na Excretion - Lowers BP

Greater risk of urogenital infections

63
Q

Which Type 2 meds are injectable and which ones oral?

A

Oral:

  • Metformin
  • Sulphonyureas
  • Thiazolidinediones
  • DPP-IV inhibitors
  • SGLT2 Inhibitors

Injected:

  • Insulin
  • GLP-1 analogue
64
Q

Example and function of GLP-1 analogues?

A

Liraglutide
GLP-1 is an incretin hormone.

DPP-IV resistant analogues are injected (which cause Glc dependant Insulin release & glucagon inhibition) which have a much longer biological half-life.

65
Q

What drugs can replace sulphonyurea’s as 2nd line Type 2 treatment if neccessary? [3]

A
  • Thiazolidinediones e.g. pioglitazone
  • DPP-IV inhibitors e.g. Sitagliptin
  • SGLT-2 inhibitors e.g. Empagliflozin
66
Q

How do DPP-IV inhibitors work? [4]

A

They inhibit DPP-IV, an enzyme that breaks down incretin hormones [1]

This prolongs the life of incretins [1] allowing them to cause Glc Dependant Decrease in Glucagon [1] release and Increase in Insulin Release [1]

67
Q

Pros [4] and cons [4] of DPP-4 inhibitors?

A

Pros

  • Well tolerated
  • Weight Neutral
  • Works in renal impairment
  • No hypoglycaemic risk

Cons:

  • small effect
  • CI in pregnant/breastfeeding
  • risk of pancreatitis/pancreatic cancer
  • Nausea
68
Q

How do GLP-1 analogues work? [3]

A

Similar to DDP-IV inhibitors.
GLP-1 is an incretin [1], the analogues are resistant to DPP-4 degradation [1] so have a longer half life causing:
- Glc dependant insulin release and glucagon inhibition [1]

69
Q

Pros [1] & Cons [1] of GLP-1 Analogues?

A

Pros - Do cause some weight loss for those overweight

Cons - Nausea (by delaying gastric emptying)

70
Q

Example of each Type 2 drug? [5]

A

Biguanides - Metformin

Sulphonyureas - Glimepiride

Thiazolidinediones - Pioglitazone

DPP-IV inhibitors - Saxagliptin

GLP-1 Analogue - Liraglutide

71
Q

T2DM patients on metformin
Indications to start?
HbA1c rises to 58 mmol/l [3]

A

Metformin is 1st line if HbA1c has risen to 48mmol/mol on lifestyle measures.

HbA1c remains 58mmol/mol: triple therapy or consider insulin therapy
- Eg METFORMIN + GLIPTIN + SULFONYLUREA

72
Q

Further management of T2DM for second line therapy

A
73
Q

T2DM patients who can’t tolerate metformin: what to do when HbA1c rises to 58 mmol/mol?

When would insulin therapy be considered?

A

• GLIPTIN + PIOGLITAZONE

If despite double therapy, HbA1c remains at 58 mmol/mol

74
Q

When starting insulin therapy what must be continued?

A

Continue metformin

75
Q

If triple therapy is not effective, management of T2DM

A

If triple therapy is not effective or tolerated consider switching one of the drugs for a GLP-1 mimetic:
* BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
* BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
* only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

My MRCP (43 decks)

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