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Yr 4 - CCC > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the ideal blood glucose conc?

A

4.4-6.1 mmol/l

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2
Q

Where is insulin produced?

A

Beta cells in the Islets of Langerhans in the pancreas

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3
Q

What is insulin?

A

An anabolic hormone

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4
Q

Insulin reduces blood sugar levels in what 2 ways?

A

1) Causes cells in body to ABSORB glucose from blood and use it as FUEL

2) Causes muscle & liver cells to ABSORB glucose from blood and STORE it as GLYCOGEN

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5
Q

How does a lack of insulin affect glucose levels?

A

Hyperglycaemia (as cells cannot take up and use glucose)

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6
Q

Where is glucagon produced?

A

Hormone produced by the alpha cells in the Islets of Langerhans in the pancreas

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7
Q

Is glucagon an anabolic or catabolic hormone?

A

Catabolic (breakdown)

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8
Q

What is glucagon released in response to?

A

a) low blood sugar levels
b) stress

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9
Q

Glucagon INCREASES blood sugar levels in what 2 ways?

A

1) glycogenolysis –> tells liver to break down stored glycogen into glucose

2) gluconeogenesis –> tells liver to convert proteins & fats into glucose

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10
Q

What is T1D?

A

An autoimmune metabolic disorder in which the immune system targets and destroys the insulin-producing cells of the pancreas.

Without insulin, the cells of the body cannot absorb glucose from the blood and use it as fuel.

Therefore, the cells think there is no glucose available. Meanwhile, the glucose level in the blood keeps rising, causing hyperglycaemia.

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11
Q

What is T1D characterised by?

A

Persistent hyperglycaemia (random plasma glucose >11mol/L) due to defects in insulin secretion, insulin action, or both.

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12
Q

Cause of T1D?

A
  • Unclear
  • There may be a genetic component, but it is not inherited in any clear pattern.
  • Certain viruses, such as the Coxsackie B and enterovirus, may trigger it.
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13
Q

What is the classic triad of symptoms of hyperglycaemia?

A

1) Polyuria (excess urine)

2) Polydipsia (excess thirst)

3) Weight loss (mainly through dehydration)

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14
Q

In patients with undiagnosed T1D, how may they typically present?

A

In diabetic ketoacidosis (DKA)

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15
Q

How can the risk of complications of T1D be reduced?

A

By keeping circulating glucose levels to as near to normal as possible.

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16
Q

Patients with T1D may present with hypoglycaemia, hyperglycaemia, or DKA.

Give some symptoms of hypoglycaemia

A
  • Tremor
  • Sweating
  • Dizziness
  • Pallor
  • Reduced consciousness, coma and death if severe
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17
Q

Management of moderate hypoglycaemia?

A

Rapid acting glucose (e.g. lucozade) + slower acting glucose (e.g. biscuits and toast)

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18
Q

2 management options for severe hypoglycaemia?

A

1) IV dextrose
2) IM glucagon

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19
Q

What is ketogenesis? When does it occur?

A

What - production of ketones, liver takes fatty acids and converts them to ketones

When - insufficient glucose supply and glycogen stores are exhausted e.g. prolonged fasting

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20
Q

What are ketones?

A

Ketones are water-soluble fatty acids that can be used as fuel.

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21
Q

Can ketones cross the BBB?

A

Yes - and can be used by the brain

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22
Q

How are ketone levels measured?

A

Urine –> dipstick test
Blood –> ketone meter

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23
Q

What is characteristic breath smell of people in ketosis?

A

Acetone smell to breath

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24
Q

How do ketones affect blood pH?

How is this buffered in healthy people?

A

Ketones make blood more acidic.

In healthy people, the kidneys buffer ketones so the blood does not become acidotic.

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25
Q

What occurs in DKA?

A

Insulin deficiency results in release of free fatty acids from adipose tissue (lipolysis) –> hyperglycaemic ketosis.

This results in a life-threatening metabolic acidosis.

Characterised by:
1) Uncontrolled hyperglycaemia
2) Metabolic acidosis
3) Increased body ketone concentration

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26
Q

What are the 3 most common scenarios for DKA to occur?

A

1) Initial presentation of T1D

2) Existing T1 diabetic who is unwell for another reason, often infection

3) An existing T1 diabetic who is not adhering to their insulin regime

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27
Q

What are the 3 key features of DKA?

A

1) Ketoacidosis
2) Dehydration
3) Potassium imbalance

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28
Q

What are some precipitating factors for DKA?

A
  • Infection
  • Discontinuation of insulin (unintentional or deliberate).
  • Inadequate insulin
  • Cardiovascular disease - eg, stroke or myocardial infarction
  • Drug treatments e.g. steroids, thiazides, SGLT2 inhibitors
  • Psychological stress e.g. pregnancy, trauma or surgery
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29
Q

What is ketoacidosis?

A

1)Without insulin, the body’s cells cannot recognise glucose, even when there is plenty in the blood, so the liver starts producing ketones to use as fuel.

2) Over time, there are higher and higher glucose and ketones levels.

3) Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.

4) Over time, the ketone acids use up the bicarbonate, and the blood becomes acidic. This is called ketoacidosis.

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30
Q

How does DKA lead to dehydration?

A
  1. high blood glucose levels (hyperglycaemia) overwhelm the kidneys
  2. glucose leaks into the urine
  3. the glucose in the urine draws water out by osmotic diuresis
  4. This causes increased urine production (polyuria) and results in severe dehydration
  5. Dehydration results in excessive thirst (polydipsia).
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31
Q

How does insulin normally affect potassium?

A

Drives potassium INTO cells (i.e. lowers serum potassium)

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32
Q

How does diabetes/DKA affect potassium levels?

A

Without insulin, potassium is not added to and stored in cells.

The serum potassium can be high (or normal as the kidneys balance blood potassium with the potassium excreted in the urine).

However, total body potassium is LOW because no potassium is stored in the cells.

When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, leading to fatal arrhythmias.

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33
Q

How does diabetes/DKA affect total body potassium?

A

LOW total body potassium - as no potassium is stored in the cells

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34
Q

How can starting treatment for diabetes/DKA affect potassium levels?

A

When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly as potassium is taken up into cells, leading to fatal arrhythmias.

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35
Q

Symptoms of DKA?

A
  • Polyuria, polydipsia –> dehydration
  • N&V
  • Acetone-smelling breath (‘pear drops’ smell)
  • Weight loss
  • Hypotension
  • Altered consciousness
  • Abdominal pain
  • Kussmaul respiration (deep hyperventilation)
  • Symptoms of underlying trigger (i.e. sepsis)
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36
Q

Features of DKA:

A
  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis (with a low bicarbonate)
  • Potassium imbalance
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37
Q

A diagnosis of DKA requires what 3 criteria?

A

1) hyperglycaemia e.g. blood glucose level >11 mmol/L

2) ketosis e.g. blood ketones >3 mmol/L

3) acidosis e.g. pH <7.3

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38
Q

What are the main principles of management of DKA?

A

ABCDE assessment & escalate early –> life-threatening

Most dangerous aspects are 1) dehydration, 2) potassium imbalance, and 3) acidosis.

Priority –> fluid resuscitation to correct these.

FIG-PICK:

  • Fluid resuscitation –> IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
  • Insulin –> fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
  • Glucose –> closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
  • Potassium –> add potassium to IV fluids and monitor closely (e.g., every hour initially)
  • Infection –> treat underlying triggers such as infection
  • Chart fluid balance
  • Ketones –> monitor blood ketones, pH and bicarbonate
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39
Q

Example of fluid resuscitation in DKA management:

A

1st hour –> 1 litre 0.9% sodium chloride (saline)

For the remaining time –> 0.9% sodium chloride 1L with potassium chloride

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40
Q

What is your priority management in DKA?

A

Fluid resus

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41
Q

Give some signs of gross deydration

A
  • Dry mucous membranes.
  • Decreased skin turgor/skin wrinkling.
  • Sunken eyes.
  • Slow capillary refill.
  • Tachycardia with weak pulse.
  • Hypotension.
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42
Q

Describe the breathing in DKA

A
  • Can be tachypnoea
  • Can be Kussmaul respiration (very deep, slowly rhythmic breathing)
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43
Q

How should insulin be given in DKA?

A

Fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)

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44
Q

When should a glucose infusion be given in DKA?

A

when blood glucose is less than 14 mmol/L

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45
Q

Before stopping the insulin and fluid infusions in DKA, what should you ensure?

A

1) Ketosis and acidosis should have resolved
2) They should be eating and drinking
3) They should have started their regular subcutaneous insulin

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46
Q

What are key potential complications during DKA treatment?

A

1) Hypoglycaemia
2) Hypokalaemia
3) Cerebral oedema, particularly in children
4) Pulmonary oedema 2ary to fluid overload or acute respiratory distress syndrome

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47
Q

Who is cerebral oedema during DKA management more common in ?

A

Children

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48
Q

Under normal circumstances, what should the rate of potassium infusion not exceed?

Why?

A

10 mmol/hour - as there is a risk of inducing an arrhythmia or cardiac arrest

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49
Q

In DKA, what should the rate of potassium infusion not exceed?

A

Rates up to 20 mmol/hour may be used

There must be expert supervision with cardiac monitoring and through a central line (rather than a peripheral cannula).

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50
Q

When there is doubt about whether a patient has type 1 or type 2 diabetes, what 2 investigations can be done?

A

Checking for autoantibodies and serum C-peptide

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51
Q

What are the 3 types of autoantibodies in T1D?

A

1) Anti-islet cell antibodies
2) Anti-GAD antibodies
3) Anti-insulin antibodies

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52
Q

What is serum c-peptide a measure of?

A

A measure of insulin production:
- It is low with low insulin production
- It is high with high insulin production

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53
Q

What 4 factors are involved in long-term T1D management?

A

1) SC insulin

2) Monitoring dietary carbohydrate intake

3) Monitoring blood sugar levels upon waking, at each meal and before bed

4) Monitoring for and managing complications, both short and long term

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54
Q

What are 2 potential insulin regimes in T1D management?

A

1) Basal-bolus regime

2) Insulin pumps

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55
Q

What does a basal-bolus regime of insulin involve a combination of?

A

1) Background, long-acting insulin

2) Short-acting insulin

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56
Q

When is short-acting insulin injected in T1D management?

A

injected 30 minutes before consuming carbohydrates (e.g., at meals)

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57
Q

When is background, long-acting insulin injected in T1D?

A

injected once a day

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58
Q

Why should T1D patients cycle their insulin injection sites?

A

Injecting into the same spot can cause lipodystrophy (where the subcutaneous fat hardens).

Areas of lipodystrophy do not absorb insulin properly from further injections.

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59
Q

What should you check if a patient is not responding to insulin as expected?

A

Ask where they inject and check for lipodystrophy.

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60
Q

What are insulin pumps?

A

What –> Insulin pumps are small devices that CONTINUOUSLY infuse insulin at different rates to control blood sugar levels.

How they work –> The pump pushes insulin through a small plastic tube (cannula) inserted under the skin.

The cannula is replaced every 2 – 3 days, and the insertion sites are rotated to prevent lipodystrophy and absorption issues.

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61
Q

Advantages of insulin pumps?

A
  • Better blood sugar control
  • More flexibility with eating
  • Less injections
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62
Q

Disadvantages of insulin pumps?

A
  • Difficulties learning to use the pump
  • Having it attached at all times
  • Blockages in the infusion set
  • A small risk of infection
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63
Q

What are the 2 types of insulin pumps?

A

1) Tethered pump
2) Patch pump

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64
Q

What is a tethered pump?

A

Devices with replaceable infusion sets and insulin. They are usually attached to the patient’s belt or around the waist with a tube connecting the pump to the insertion site. The controls for the infusion are on the pump itself.

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65
Q

What is a patch pump?

A

Patch pumps sit directly on the skin without any visible tubes. When they run out of insulin, the entire patch pump is disposed of, and a new pump is attached. A separate remote usually controls patch pumps.

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66
Q

A pancreas transplant is one potential management option in T1D.

However, the procedure carries significant risks, and life-long immunosuppression is required to prevent rejection.

Who is it reserved for?

A

1) patients with severe hypoglycaemic episodes
2) patients also having kidney transplants

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67
Q

What does a pancreas implant involve?

A

A pancreas transplant involves implanting a donor pancreas to produce insulin.

The original pancreas is left in place to continue producing digestive enzymes.

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68
Q

Why is the original pancreas left in place in a pancreas transplant?

A

to continue producing digestive enzymes.

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69
Q

What are 2 surgical options in severe T1D?

A

1) pancreas transplant
2) islet transplantation

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70
Q

What is an islet transplantation?

A

Islet transplantation involves inserting donor islet cells into the patient’s liver.

These islet cells produce insulin and help in managing diabetes.

However, patients often still need insulin therapy after islet transplantation.

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71
Q

What monitoring is needed in T1D?

A

1) HbA1c (every 3-6 months)

2) Capillary blood glucose (daily)

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72
Q

How often is HbA1c measured in T1D?

A

It is measured every 3 to 6 months to track the average sugar levels.

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73
Q

What is HbA1c?

A

HbA1c measures glycated haemoglobin (which is how much glucose is attached to the haemoglobin molecule).

It reflects the average glucose level over the previous 2-3 months.

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74
Q

What is glycated haemoglobin?

A

how much glucose is attached to the haemoglobin molecule

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75
Q

How is HbA1c measured?

A

Lab blood test

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76
Q

How is capillary blood glucose measured?

A

Finger prick test - can be measured using a blood glucose monitor, giving an immediate result

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77
Q

Give 3 options for glucose monitoring in T1D

A

1) Capillary blood glucose (finger-prick test)

2) Flash glucose monitors (e.g., FreeStyle Libre 2)

3) Continuous glucose monitors (CGM)

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78
Q

What are flash glucose monitors?

A

They use a SENSOR on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue.

The sensor records the glucose readings at short intervals, so you get an excellent impression of what the glucose levels are doing over time.

The user needs to use their mobile phone to swipe over the sensor and collect the reading.

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79
Q

How often do need to change flash glucose monitors (e.g., FreeStyle Libre 2)?

A

Sensors need replacing every 2 weeks for the FreeStyle Libre system.

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80
Q

If hypoglycaemia is suspected, why is a flash glucose monitor not appropriate?

A

There is a 5-minute lag behind blood glucose.

The 5-minute delay means it is necessary to do capillary blood glucose testing if hypoglycaemia is suspected.

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81
Q

How do continuous glucose monitors (CGM) work?

A

Similar the flash glucose monitors in that a sensor on the skin monitors the sugar level in the interstitial fluid.

However, continuous glucose monitors send the readings over bluetooth and do not require the patient to scan the sensor.

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82
Q

What is a closed loop system in T1D management? What is it a combination of?

A

Also called an artificial pancreas.

Combination of:
1) continuous glucose monitor
2) an insulin pump

The devices communicate to automatically adjust the insulin based on the glucose readings.

Patients still need to input their carbohydrate intake and adjust the system to account for strenuous exercise.

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83
Q

What are the 2 major short term risks in T1D?

A

1) Hypoglycaemia
2) Hyperglycaemia (and DKA)

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84
Q

What can cause hypoglycaemia in T1D patients?

A
  • Too much insulin
  • Not consuming enough carbohydrates
  • Not processing carbs correctly e.g. malabsorption, diarrhoea or vomiting
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85
Q

What may hyperglycaemia without DKA in patients with T1D indicate?

A

May indicate that insulin dose needs to be increased

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86
Q

Management of hyperglycaemia?

A
  • Essential to exclude DKA
    -Short episodes of hyperglycaemia do not necessarily require treatment. Insulin injections can take several hours to take effect and repeated doses could lead to hypoglycaemia.
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87
Q

Long term complications of T1D can be separated into microvascular, macrovascular and infection-related.

What are the macrovascular complications?

A
  • Coronary artery disease –> a significant cause of death in diabetics
  • Peripheral ischaemia –> causes poor skin healing and diabetic foot ulcers
  • Stroke
  • Hypertension
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88
Q

What predisposes to diabetic foot ulcers in T1D?

A

Peripheral ischaemia

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89
Q

What are the microvascular complications in T1D?

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis
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90
Q

Main kidney disease seen in T1D?

A

Glomerulosclerosis

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91
Q

Infection-related complications of T1D?

A
  • UTIs
  • Pneumonia
  • SSTIs, particuarly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis
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92
Q

Pathophysiology behind T2D?

A

1) Repeated exposure to glucose and insulin

2) Cells in the body become resistant to the effects of insulin

3) More and more insulin is required to stimulate the cells to take up and use glucose.

4) Over time, the pancreas becomes fatigued and damaged by producing so much insulin, and the insulin output is reduced.

5) This leads to chronic hyperglycaemia.

I.e. combination of insulin resistance and reduced insulin production.

93
Q

Complications of T2D?

A

Same as T1

94
Q

Modifiable risk factors for T2D?

A
  • Obesity
  • Sedentary lifestyle
  • High carbohydrate (particularly sugar) diet
95
Q

Non-modifiable risk factors for T2D?

A
  • Older age
  • Ethnicity (Black African or Caribbean and South Asian)
  • Family history
96
Q

Which ethnicities have a higher risk of T2D?

A

Black African or Caribbean and South Asian

97
Q

Presenting features of T2D?

A
  • Tiredness
  • Polyuria and polydipsia
  • Unintentional weight loss
  • Opportunistic infections (e.g., oral thrush)
  • Slow wound healing
  • Glucose in urine (on a dipstick)
98
Q

What is acanthosis nigricans?

What is it associated with?

A

Acanthosis nigricans is characterised by the thickening and darkening of the skin (giving a “velvety” appearance), often at the neck, axilla and groin.

It is often associated with insulin resistance.

99
Q

What is pre-diabetes?

A

Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes.

100
Q

What HbA1c indicates pre-diabetes?

A

42-47 mmol/mol

101
Q

What HbA1c level indicates T2D?

A

48 mmol/mol or above

102
Q

To confirm a diagnosis of T2D, when is the HbA1c repeated?

A

Repeated after 1 month to confirm the diagnosis (unless there are symptoms or signs of complications).

103
Q

Management of T2D recommendations:

A

1) A structured education program
2) Low-glycaemic-index, high-fibre diet
3) Exercise
4) Weight loss (if overweight)
5) Antidiabetic drugs
6) Monitoring and managing complications

104
Q

What is the HbA1c target for new type 2 diabetics?

A

48 mmol/mol

105
Q

What is the HbA1c target for patients requiring MORE THAN 1 antidiabetic medication?

A

53 mmol/mol

106
Q

How often is the HbA1c measured in T2D?

A

The HbA1c is measured every 3 to 6 months until under control and stable.

107
Q

1st line medical management of T2D?

A

Metformin

108
Q

Give stepwise medical management of T2D

A

1st line –> metformin

2nd line -> Dual therapy: add sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor

3rd line options –> Triple therapy (with metformin and two of the second line drugs) or insulin therapy

109
Q

Management of T2D patients with existing cardiovascular disease or heart failure?

A

Settle them on metformin.

Then add an SGLT-2 inhibitor (e.g., dapagliflozin).

N.B. NICE suggest considering an SGLT-2 inhibitor in patients with a QRISK score above 10%.

110
Q

What does triple therapy in T2D involve?

A

metformin and two of the second-line drugs (e.g. sulfonylurea and SGLT-2 inhibitor)

111
Q

1st line treatment of patients with T2D at high risk of cardiovascular disease?

A

SGLT-2 inhibitors alongside metformin

112
Q

What is the significant potential side effect of SGLT-2 inhibitors?

A

DKA

113
Q

When triple therapy fails in T2D, and the patient’s BMI is above 35 kg/m2, what can you do?

A

there is the option of switching one of the drugs to a GLP-1 mimetic (e.g., liraglutide).

114
Q

Give some examples of an SGLT-2 inhibitor

A
  • dapagliflozin
    -empagliflozin
  • canagliflozin
  • ertugliflozin
115
Q

How does metformin work?

A

Metformin increases insulin sensitivity and decreases glucose production by the liver.

116
Q

What class of drug is metformin?

A

Biguanide

117
Q

Can metformin cause weight gain?

A

No (may cause some weight loss)

118
Q

Can metformin cause hypoglycaemia?

A

No

119
Q

What are the 2 notable side effects of metformin?

A

1) GI symptoms e.g. pain, nausea, and diarrhoea (dose dependent)

2) Lactic acidosis (e.g., secondary to AKI)

120
Q

What can be offered to patients on metformin with GI side effects?

A

Patients with gastrointestinal side effects with standard-release metformin can try modified-release metformin.

121
Q

What suffix do SGLT-2 inhibitors end with?

A

-gliflozin

122
Q

Mechanism of action of SGLT-2 inhibitors?

A

1) The sodium-glucose co-transporter 2 protein is found in the proximal tubules of the kidneys –> acts to reabsorb glucose from the urine back into the blood.

2) SGLT-2 inhibitors block the action of this protein, causing more glucose to be EXCRETED in the urine

3) Loss of glucose in the urine lowers the HbA1c, reduces the blood pressure, leads to weight loss and improves heart failure

123
Q

Function of the sodium-glucose co-transporter 2 protein in the proximal tubules of the kidneys?

A

It acts to reabsorb glucose from the urine back into the blood.

124
Q

Notable side effects of SGLT-2 inhibitors?

A
  • Hypoglycaemia (when used with insulin or sulfonylureas)
  • Glycosuria (glucose in the urine)
  • Increased urine output and frequency
  • Genital and urinary tract infections (e.g., thrush)
  • Weight loss
  • Diabetic ketoacidosis, notably with only moderately raised glucose
  • Lower-limb amputation may be more common in patients on canagliflozin (unclear if this applies to the others)
  • Fournier’s gangrene (rare but severe infection of the genitals or perineum)
125
Q

Can SGLT-2 inhibitors cause weight gain?

A

No - can cause weight loss

126
Q

Can SGLT-2 inhibitors cause hypoglycaemia?

A

Yes

127
Q

Which SGLT-2 inhibitor can increase risk of lower limb amputation?

A

canagliflozin

128
Q

What is Fournier’s gangrene?

A

rare but severe infection of the genitals or perineum

129
Q

Why can SGLT-2 inhibitors increase frequency of UTIs and genital thrush?

A

due to lots of sugar passing through the urinary tract

130
Q

What class of drug is Pioglitazone?

A

thiazolidinedione

131
Q

Mechanism of Pioglitazone?

A

It increases insulin sensitivity and decreases liver production of glucose.

132
Q

Does Pioglitazone cause hypoglycaemia?

A

No, not typically

133
Q

What are the notable side effects of Pioglitazone?

A
  • Weight gain
  • Heart failure
  • Increased risk of bone fractures
  • Small increase in risk of bladder cancer
134
Q

Can Pioglitazone cause weight gain?

A

Yes

135
Q

Which diabetic medication can cause increase in the risk of bladder cancer?

A

Pioglitazone

136
Q

Which diabetic medication can increase risk of bone fractures?

A

Pioglitazone

137
Q

What is the most common sulfonylurea?

A

Gliclazide

138
Q

Mechanism of Sulfonylureas?

A

Sulfonylureas stimulate insulin release from the pancreas.

139
Q

What are the 2 notable side effects of Sulfonylureas?

A

1) Weight gain
2) Hypoglycaemia

140
Q

What are incretins?

A

hormones produced by the gastrointestinal tract

141
Q

When are incretins secreted?

What is their role?

A

They are secreted in response to large meals and act to reduce blood sugar

142
Q

Via what 3 mechanisms can incretins reduced blood sugar?

A

1) Increasnig insulin secretion
2) Inhibiting glucagon production
3) Slowing absorption by the GI tract

143
Q

What is the main incretin?

A

Glucagon-like peptide-1 (GLP-1).

144
Q

What are incretins inhibited by?

A

An enzyme called dipeptidyl peptidase-4 (DPP-4).

145
Q

How can incretins be used in T2D management?

A

1) DPP-4 inhibitors (i.e. stopping inhibition of incretins)

2) GLP-1 mimetics (i.e. mimicking action of incretin)

146
Q

Mechanism of DPP-4 inhibitors in T2D?

A

DPP-4 inhibitors block the action of DPP-4, allowing increased incretin activity.

147
Q

Give 2 examples of DPP-4 inhibitors

A

1) sitagliptin
2) alogliptin

148
Q

Do DPP-4 inhibitors cause hypoglycaemia?

A

No

149
Q

What are the 2 notable side effects of DPP-4 inhibitors?

A

1) Headaches
2) Low risk of acute pancreatitis

150
Q

Mechanism of GLP-1 mimetics in T2D?

A

GLP-1 mimetics imitate the action of GLP-1.

151
Q

Give 2 examples of GLP-1 mimetics?

A

1) exenatide
2) liraglutideo

152
Q

How are GLP-1 mimetics given?

A

SC injections

153
Q

Which GLP-1 mimetic can be used for weight loss in non-diabetic obese patients?

A

Liraglutide

154
Q

Give 3 notable side effects of GLP-1 mimetics

A

1) Reduced appetite
2) Weight loss
3) Gastrointestinal symptoms, including discomfort, nausea and diarrhoea

155
Q

Give different types of insulin used in T2D management

A

1) Rapid-acting insulins

2) Short-acting insulins

3) Intermediate-acting insulins

4) Long-acting insulins

5) Combinations insulins

156
Q

Give an example of a rapid-acting insulin

A

NovoRapid

157
Q

When do rapid acting insulins start working? How long do they last?

A

Start - after around 10 mins

Last - around 4 hours

158
Q

Give an example of a short-acting insulin

A

Actrapid

159
Q

When do short acting insulins start working? How long do they last?

A

Start - 30 mins

Last - 8 hours

160
Q

Give an example of an intermediate-acting insulin

A

Humulin I

161
Q

When do intermediate acting insulins start working? How long do they last?

A

Start - 1 hour

Last - 16 hours

162
Q

Give an example of a long-acting insulin

A

Levemir and Lantus

163
Q

When do intermediate acting insulins start working? How long do they last?

A

Start - 1 hour

Last - 24 hours

164
Q

What do combination insulins contain (T2D)?

A

Contain a rapid-acting and intermediate-acting insulin

165
Q

Examples of combination insulins:

A
  • Humalog 25 (25:75)
  • Humalog 50 (50:50)
  • Novomix 30 (30:70)

In brackets is the ratio of rapid-acting to intermediate-acting insulin:

166
Q

Diabetes OSCE tip

A

A common exam scenario involves discussing the possibility of starting insulin with an HGV driver. Patients treated with insulin must fulfil very strict criteria to carry on driving, so starting insulin has enormous implications for professional drivers. This can be a motivating factor for improving diet, exercise and taking medications to improve diabetes control and avoid insulin.

167
Q

Key complications of T2D?

A
  • Infections (e.g., periodontitis, thrush and infected ulcers)
  • Diabetic retinopathy
  • Peripheral neuropathy
  • Autonomic neuropathy
  • Chronic kidney disease
  • Diabetic foot
  • Gastroparesis (slow emptying of the stomach)
  • Hyperosmolar hyperglycemic state
168
Q

What is the 1st line medical management of HTN in patients of any age with type 2 diabetes?

A

ACE inhibitors

169
Q

In CKD in patients WITHOUT diabetes, at what albumin-to-creatinine ratio (ACR) are ACEi started?

A

ACR above 30 mg/mmol in patients without diabetes

170
Q

In CKD in patients WITH diabetes, at what albumin-to-creatinine ratio (ACR) are ACEi started?

A

albumin-to-creatinine ratio (ACR) above 3 mg/mmol

171
Q

In patients with CDK and T2D, what is given when the albumin-to-creatinine ratio (ACR) is above 30 mg/mmol (i.e. in addition to the ACE inhibitor)?

A

SGLT-2 inhibitors

172
Q

What class of drug can be used to manage erectile dysfunction in T2D?

A

Phosphodiesterase‑5 inhibitors (e.g., sildenafil or tadalafil)

173
Q

Gastroparesis is one complication of T2D.

What is the medical management?

A

Prokinetic drugs (e.g., domperidone or metoclopramide)

N.B. These medications are used with caution due to cardiac side effects.

174
Q

What are the 4 pharmacological options for neuropathic pain (e.g., diabetic neuropathy) in T2D?

A

1) Amitriptyline – a tricyclic antidepressant
2) Duloxetine – an SNRI antidepressant
3) Gabapentin – an anticonvulsant
4) Pregabalin – an anticonvulsant

175
Q

What class of drug is Amitriptyline

A

tricyclic antidepressant

176
Q

What class of drug is duloxetine

A

SNRI antidepressant

177
Q

What class of drug is gabapentin

A

anticonvulsant

178
Q

What class of drug is pregabalin

A

Anticonvulsant

179
Q

What is Hyperosmolar hyperglycemic state (HHS)?

A

a rare but potentially fatal complication of type 2 diabetes.

180
Q

What characterises HHS?

A

1) hyperosmolality (water loss leads to very concentrated blood)

2) hyperglycaemia

3) absence of ketones (distinguishing it from ketoacidosis)

181
Q

Presentation of HHS?

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Weight loss
  • Tachycardia
  • Hypotension
  • Confusion
182
Q

Management of HHS?

A

IV fluids and careful monitoring

183
Q

How can HHS be distinguished from ketoacidosis?

A

HHS –> absence of ketones

DKA –> lots of ketones

184
Q

What is diabetic nephropathy?

A

People with diabetes are at increased risk of renal atherosclerosis, urinary tract infections, papillary necrosis and glomerular lesions - eg, from basement membrane thickening and glomerulosclerosis.

185
Q

What is the principal feature of diabetic neuropathy?

A

Proteinuria

This develops insidiously, starting as intermittent microalbuminuria before progressing to constant proteinuria and occasionally nephrotic syndrome.

186
Q

Define microalbuminuria.

What is ACR?

What is albumin concentration?

A

There is albumin present in urine (indicates kidney damage).

Albumin:creatinine ratio (ACR) greater than or equal to 2.5 mg/mmol (men) or 3.5 mg/mmol (women),

Albumin concentration greater than or equal to 20 mg/L.

187
Q

Define proteinuria

A

ACR greater than or equal to 30 mg/mmol or albumin concentration greater than or equal to 200 mg/L

188
Q

ACR in microalbuminuria vs proteinuria?

A

Microalbuminuria –> >/= 2.5 mg/mmol (men) or 3.5 mg/mmol (women)

Proteinuria –> >/= 30 mg/mmol

189
Q

In all patients with confirmed nephropathy (including those with microalbuminuria alone) and type 1 diabetes, what medication should be started?

A

ACEi –> and titrated to FULL DOSE

(if ACEi not tolerated, use ARB)

190
Q

What should be offered to all adults with type 2 diabetes and CKD with an ACR over 30mg/mmol who are taking the highest tolerated dose of ACE inhibitor or ARB?

A

an SGLT2 inhibitor

Or considered for those with an ACR between 3-30 mg/mmol.

191
Q

What is the most importance management of kidney disease in diabetics?

A

Antihypertensives

192
Q

What is the most common cause of peripheral neuropathy in the world?

A

Diabetes

193
Q

Risk factors for diabetic neuropathy?

A
  • Smoking
  • Age >40
  • History of periods of poor glycaemic control.
  • Prevalence increases with increased duration of diabetes.
  • People with signs of neuropathy are likely also to have evidence of diabetic nephropathy and diabetic retinopathy.
  • Hypertension.
  • Coronary heart disease.
194
Q

There are different types of diabetic neuropathy: peripheral, sensory, autonomic and motor.

What symptoms are seen in peripheral neuropathy?

A
  • Touch, pain and temperature sensation and proprioception in lower limbs in a glove and stocking distribution (i.e. hands and feet)
  • Loss of ankle jerks and, later, knee jerks.
195
Q

Are sensory or motor nerves affected more in diabetic neuropathy?

A

Sensory

196
Q

Describe distribution of sensory loss in diabetic neuropathy

A

Glove and stocking

197
Q

Are hands or feet affected first in diabetic neuropathy

A

Feet (hands are only affected in severe long-standing neuropathy)

198
Q

Prevalence of peripheral neuropathy in type 1 vs type 2 diabetes?

A

Equal prevalence in types 1 and 2.

199
Q

Diabetic neuropathy can also present as acute peripheral neuritis.

What symptoms may be seen?

A
  • Often abrupt onset and not related to duration of diabetes.
  • Can resolve completely.
  • Burning foot pain, often worse at night.
  • Associated with poor glycaemic control but sometimes initially follows establishing good glycaemic control.
  • Examination may be normal apart from hyperaesthesia.
200
Q

Give some risk factors for diabetic autonomic neuropathy

A
  • HTN and dyslipidaemia
  • More common in females
201
Q

Presentation of diabetic autonomic neuropathy?

A

Cardiac e.g. resting tachycardia, postural hypotension, exercise intolerance

Genitourinary e.g. impotence, sexual dysfunction, urinary hesitancy, overflow incontinence

GI e.g. N&V, abdo distension, diarrhoea

202
Q

What is the main motor presentation of diabetic neuropathy?

A

Proximal motor (diabetic amyotrophy):

Severe pain and paraesthesiae in the upper legs, with weakness and muscle wasting of the thigh and pelvic girdle muscles.

203
Q

How is BMI calculated?

A

BMI = weight (kg) / height (m) squared

204
Q

BMI range for the following categories:

1) underweight
2) normal
3) overweight
4) obese class 1
5) obese class 2
6) obese class 4

A

1) <18.49
2) 18.5-25
3) 25-30
4) 30-35
5) 35-40
6) >40

205
Q

What is the step-wise management of obesity?

A

1) conservative: diet, exercise
2) medical: orlistat, liraglutide
3) surgical

206
Q

What class of drug is liraglutide?

A

Incretin mimentic (GLP-1 receptor agonist)

207
Q

What class of drug is orlistat?

A

Pancreatic lipase inhibitor

208
Q

How does orlistat work in weight loss?

A

Orlistat works by preventing around a third of the fat from the food you eat being absorbed. The undigested fat is not absorbed into your body and is passed out with your poo.

209
Q

How does liraglutide work in weight loss?

A

work by making you feel fuller and less hungry.

210
Q

Adverse effects of orlistat?

A

Faecal urgency/incontinence and flatulence.

211
Q

Criteria for using orlistat in obesity?

A

It should only be prescribed as part of an overall plan for managing obesity in adults who have:

1) BMI of 28 kg/m^2 or more with associated risk factors, or

2) BMI of 30 kg/m^2 or more

3) continued weight loss e.g. 5% at 3 months

212
Q

How long is orlistat usually used for in obesity?

A

<1 year

213
Q

How is liraglutide given?

A

given as a once daily subcutaneous injection

214
Q

Which diabetic medication can cause weight loss?

A

Glucagon-like peptide-1 (GLP-1) mimetic: liraglutide

215
Q

Bariatric surgery can be divided into restrictive operations, malabsorptive opertions, and mixed operations.

What is normally the first-line intervention in patients with a BMI of 30-39kg/m^2?

A

Laparoscopic-adjustable gastric banding (LAGB): this is a primarily restrictive operation

216
Q

1st line management of T2D stepwise approach:

A

1) Assess CVS risk - does patient have established CVD/high risk of CVD/chronic heart failure?

2a) If no –> metformin

2b) If yes –> metformin, once established add SGLT-2 inhibitor

217
Q

What class of drug is added to metformin in patients with T2DM who have high risk CVD/established CVD/chronic HF?

A

SGLT-2 inhibitor (-gliflozin)

218
Q

What can you switch metformin to if it is not tolerated (e.g. to GI side effects)?

A

modified release metformin

219
Q

What can you give if metformin is contraindicated:

a) if risk of CVD/HF
b) if no risk of CVD/HF

A

a) SGLT-2 monotherapy

b) DPP-4 inhibitor or Pioglitazone or Sulfonylurea (SGLT-2 may be used if certain NICE criteria met)

220
Q

2nd line therapy in T2D?

A

Metformin plus any one of:

  • DPP-4 inhibitor
  • Pioglitazone
  • Sulfonylurea
  • SGLT-2 inhibitor (if criteria met)

E.g. metformin + DPP-4 inhibitor

221
Q

3rd line therapy in T2D?

A

Add another drug (from 2nd line therapy list) e.g. Metformin + DPP-4 inhibitor + sulfonylurea

OR

Start insulin based treatment

222
Q

At any point in T2D management, if CVD risk changes (e.g. QRISK >10%), what should be added?

A

SGLT-2 inhibitor

223
Q

4th line therapy in T2D?

A

If triple therapy not effective or tolerated, consider switching one of the drugs for a GLP-1 mimetic (if BMI >/= 35) or insulin (occupational implications)

224
Q

How does peripheral neuropathy in diabetes typically present?

A
  • Sensory loss but NOT motor loss.
  • Sensory loss typically results in a ‘glove and stocking’ distribution, with the lower legs affected first due to the length of the sensory neurons supplying this area.
  • Painful diabetic neuropathy is also a common problem
225
Q

What is the 1st line treatment of peripheral neuropathy in diabetes?

A

Managed as neuropathic pain:

1st line: amitriptyline, duloxetine, gabapentin or pregabalin

If the first-line drug treatment does not work try one of the other 3 drugs.

226
Q

What are the 2 different types of diabetic neuropathy?

A

1) peripheral neuropathy

2) GI autonomic neuropathy

227
Q

How does GI autonomic neuropathy present?

A

1) gastroparesis:
- erratic blood glucose control, bloating and vomiting

2) chronic diarrhoea

3) GORD:
- caused by decreased lower esophageal sphincter (LES) pressure

228
Q

What are management options for gastroparesis as a result of GI autonomic neuropathy in diabetes?

A

prokinetic agents:
- metoclopramide
- domperidone
- erythromycin

229
Q
A

Yr 4 - CCC (54 decks)

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