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Pharmacy Year 3 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the value for hypoglycaemia?

A

<2.5mmol/L

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2
Q

What is the value for hyperglycaemia?

A

> 10mmol/L

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3
Q

What are the values for normoglycaemia?

A

3-5mmol/L - healthy fasting value

7-8mmol/L - post prandial

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4
Q

Describes the events of hyperglycaemia

A

Rise in blood sugar from eating carbohydrate rich food
Insulin release from beta cells in pancreas
Insulin exerts an effect on different tissues in the body
As a result of insulin release, blood sugar reduces

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5
Q

Describe the events of hypoglycaemia

A

Low blood sugar levels from overnight or deliberate fasting
Glucagon is released
Glucagon promotes endogenous glucose production, increasing availability of glucose in the blood
Raises blood sugar levels

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6
Q

What is insulin?

A

A protein hormone derived from pro-insulin

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7
Q

Where is insulin synthesised?

A

Beta cells - in the islets of Langerhans

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8
Q

When would insulin be complexed with zinc?

A

When used for slow release formulations

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9
Q

What is insulins half life?

A

3-5 mins

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10
Q

How does insulin lower blood sugar?

A

Binds to insulin receptors on tissues

Insulin receptor is a dimer - insulin binding triggers a conformation change
Endogenous kinase protein is switched on

Receptor becomes active and has kinase activity

Transport protein switched on - becomes active and transports glucose across cell membrane

Signalling cascade leads to more transporters in the cell membrane

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11
Q

How does insulin promote hypoglycaemia?

A 
Increases transport of glucose into cells
Converts glucose to glycogen
Decreases glycogen breakdown
Increases fat stores
increases protein production
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12
Q

Glucose levels lean towards hyperglycaemia when…

A

Food intake is increased
Glucose is produced
Glucose is reabsorbed

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13
Q

Glucose levels lean towards hypoglycaemia when…

A

Glucose is utilised
Food intake decreases
Glucose is stored
Glucose is lost

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14
Q

What is diabetes?

A

A chronic disease which occurs when the pancreas doesn’t produce enough insulin OR when the body can’t used insulin produced effectively.

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15
Q

What are the non-medical causes of hypoglycaemia?

A

Inadequate, irregular food intake
Insulin overdose
Sulphonylurea overdose

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16
Q

What are the medical causes of hypoglycaemia?

A 
Insulinoma
Hyperinsulinism
T1DM
Post-gastric bypass hypoglycaemia 
Transient neonatal hypoglycaemia
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17
Q

What is glucagon used for?

A

Severe hypoglycaemia when oral glucose is not possible / desired
Given by injection

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18
Q

What is diazoxide therapy used for?

A

Recurrent hypoglycaemia
Inhibit glucose action on beta cells to stop insulin release
- Eudemine 50mg tablets (Proglychem brand)

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19
Q

What are the presenting symptoms of T1DM?

A 
Polyuria
Polydipsia
Fatigue/lethargic
Weight loss
DKA
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20
Q

What happens in response to the absence of insulin in T1DM diabetic ketoacidosis?

A

Increase in glycogenesis and gluconeogenesis and reduced glucose uptake by tissues

Increased urine output

Suppressed lipolysis

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21
Q

What are the symptoms of DKA?

A

Tachypnoea
Altered mental state
N&V
Abdominal pain

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22
Q

What needs to be done in the first 4 hours of someone presenting with DKA?

A

Fluid resuscitation - isotonic fluids only and given slowly
Insulin infusion
Maintenance fluid
Reintroduce food and drink

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23
Q

When should a DKA patient be switched to maintenance fluid?

A

Once cBG is <15mmol/L

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24
Q

At what point should a DKA patient be given s/c insulin?

A

30 mins before stopping insulin infusion

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25
Q

When should insulin be started in a child with DKA?

A

cBG <14mmol/L
Ketones <3mmol/L
Resolved acidosis
Oral fluids are tolerated

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26
Q

Basal bolus insulin regime:

A

Long acting in the evening or BD

3 doses of short/rapid acting during the day before meals (based on carb intake)

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27
Q

Biphasic insulin regime:

A

2 biphasic doses, morning and tea time

Dose split depends on biggest meal

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28
Q

Describe rapid acting insulin and give examples

A

Mimics pancreases
Onset 5-15 mins, peak 30-90min, duration 4-6 hours

Novorapid - Insulin Aspart
Humalog - Insulin lispro
Apidra - Insulin glulisine

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29
Q

Describe short acting insulin and give examples

A

Soluble
Onset 30mins-1hour, peak 2-3 hours, duration 8-10 hours

Human Actrapid - human insulin
Humulin S - human insulin
Insuman rapid - human insulin

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30
Q

Describe intermediate acting insulin and give examples

A

Isophane insulin
Onset 2-4 hours, peak 4-10 hours, duration 12-18 hours

Human insulatard
Humulin I
Inusman Basal

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31
Q

Describe long acting insulin and give examples

A

Flat insulin profile
Onset 2-4 hours, duration 20-24 hours, no peak as it mirrors basal insulin out put in non-diabetics

Lantus & Abasaglar - Insulin glargine
Levemir - Determir

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32
Q

Describe ultra long acting insulin and give examples

A

3rd line use. OD administration fives flattest insulin profile. Up to 42 hours duration

Tresiba - Insulin degludec
Toujeo - Insulin glargine 300 units/ml

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33
Q

What are the symptoms of hypoglycaemia in medication controlled diabetes?

A

<4mmol/L cBG
Hunger, tremor, sweating, palpitation

Odd behaviour drowsiness, visual disturbance, seizures

Headache and nausea

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34
Q

What is used to replace glucose in hospitalised patients?

A

Conscious - dextrose tabs/glucogel

Unconscious - glucagon IM followed by 10% glucose 100ml/hr

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35
Q

When should insulin be injected? What are the exceptions to this?

A

Half an hour before meals

Except: insulin lispro, aspart or glulisine - these can be given 5 mins before eating

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36
Q

Define disabling hypoglycaemia

A

Repeated and unpredictable occurrence of hypos that results in persistent anxiety about recurrence and is associated with adverse effects on quality of life

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37
Q

What is used in the treatment of disabling hypoglycaemia?

A

Continuous s/c insulin infusion

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38
Q

When should continuous insulin infusion be considered?

A

Attempts to achieve HbA1c with daily injections results in disabling hypoglycaemia

HbA1c is still high (>69mmol/L) on multiple daily injections despite high level of care

Patient has commitment and competence to use

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39
Q

What is classed as good diabetes management?

A 
Low cBG
Low HbA1c
Reduced episodes of hypoglycaemia
Reduced episodes of hyperglycaemia
No hospitalisations 
Reduces complications and mortality
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40
Q

When is tight control needed?

A

Benefits outweigh risk

Long term benefits outweigh short term side effects

41
Q

When is less tight control needed?

A

Risk outweighs benefits

Little change of long term benefit

42
Q

What is HbA1c?

A

The amount of glucose attached to Hb in RBC.
It is a good measure of average blood glucose for the last <6 months and it is a good predictor of heart attack, amputation and microvascular complications.

43
Q

What is HbA1c a poor predictor of?

A

Early death, other heart disease, stroke or foot ulcers

44
Q

What is the normal HbA1c value?

A

<42 mmol/ml - normal

45
Q

What is the HbA1c value for pre diabetes?

A

42-47 mmol/ml

46
Q

What is the HbA1c value for good diabetes control?

A

<58 mmol/ml

47
Q

What is the HbA1c value for moderate diabetes control?

A

58-70 mmol/ml

48
Q

What is the HbA1c value for poor diabetes control?

A

> 70 mmol/ml

49
Q

Which drug is first line for diabetes?

A

Metformin

50
Q

Describe the MoA of biguanides

A

Inhibit gluceoneogenesis in the liver, results in lower hepatic glucose production
Increases insulin mediated glucose utilisation in peripheral tissues

51
Q

Give an example of a biguanide and its dosage regime

A

Metformin
Start dose 500mg OD
Max dose 1g TDS

52
Q

When is metformin contraindicated and used with caution?

A

C/I if eGFR <30ml/min/1.73m2

Caution if eGFR <45ml/min/1.73m2

53
Q

What can a patient do to avoid the severe GI side effects that come with metformin?

A

Take with meals

54
Q

What are the advantages biguanides?

A

Cheap
Weight neutral
Low risk of hypos

55
Q

What are the disadvantages biguanides?

A

Can cause GI side effects
Rarely causes lactic acidosis
Short half life - take TDS
Need reasonable renal function

56
Q

Describe the MoA of sulfonylureas

A

Directly stimulate insulin release from beta cells by stimulating ATP sensitive potassium channels

57
Q

Give examples of short and long acting sulfonylureas

A

Short acting: gliclazide, glipizide, toltubamide, glimepride

Long acting: glibenclamide

58
Q

What needs to be monitored when a patient is on sulfonylureas?

A

Liver function - can lead to hepatitis

59
Q

What are the advantages sulfonyureas?

A

OD or BD
Quickly lowers cBG
Fewer GI side effects

60
Q

What are the disadvantages sulfonylureas?

A

Can cause hypos
Weight gain
Needs residual pancreatic function
Unpredictable in renal impairment and in the elderly

61
Q

Describe the MoA of thiazolidinediones

A

Increase insulin sensitivity and reduce glucose production from the liver. They act on adipose and muscle tissues to increase glucose utilisation

62
Q

Give an example of a thiazolidinedione

A

Pioglitazone

Starting dose 15mg

63
Q

What are the advantages of tiazolidindiones?

A

OD
Low hypo risk
Suitable in renal impairment

64
Q

What are the disadvantages of tiazolidindiones?

A

Associated with heart failure, increased risk of bladder cancer and fractures
Causes weight gain
Liver toxicity
3-6 months to show benefit

65
Q

How do meglitanides differ from sulfonylureas?

A

Work in the same way but on different beta cells

66
Q

Give 2 examples of meglitanides

A

Repaglinide an nareglinide

67
Q

Describe the MoA of alpha glucosidase inhibitors

A

Inhibit enzymes that convert complex polysaccharide carbohydrates into monosaccarides. They have a dose dependent effect.

68
Q

Give an example of an alpha glucosidase inhibitor

A

Acarbose

69
Q

Describe the MoA of GLP 1 agonists

A

Stimulate insulin release from pancreas and suppresses glucagon secretion. Also inhibit gastric emptying and reduce appetite

70
Q

Give examples of daily and weekly GLP 1 agonists

A

Daily: exenatide, liraglutide, lixisenatide
Weekly: albiglutide, dugladtide, long acting exenatide

71
Q

Describe the MoA of DPP-4 inhibitors

A

Block rapid degradation of GLP 1

72
Q

Give examples of DPP-4 inhibitors

A

Sitagliptin
Vildagliptin
Saxagliptin
Alogliptin

73
Q

Give advantages of DPP-4 inhibitors

A

OD
No weight gain
Can be used in renal impairment

74
Q

Give disadvantages of DPP-4 inhibitors

A

Cause GI side effects, rash and UTIs

Rarely causes pancreatic inflammation

75
Q

Describe the MoA of SGLT-2 inhibitors

A

Block active transport of glucose from glomerular filtrate.

76
Q

When should SGLT-2 inhibitors be stopped?

A

when eGFR <45ml/min

77
Q

Give examples of SGLT-2 inhibitors

A

Canagliflozin
Empagliflozin
Dapagliflozin

78
Q

What are the advantages of SGLT-2 inhibitors?

A

Can cause weight loss
Reduces blood pressure (1-3mmHg)
Low risk of hypos

79
Q

What are the disadvantages of SGLT-2 inhibitors?

A 
Thrush and UTIs when starting
Needs reason renal function 
Lower BP can increase fall risk 
Risk of DKA
Risk of KI and foot ulcers
80
Q

What type of insulin is first line and why?

A

Basal insulin
Needs less frequent blood testing, lower hypo risk, and no carb counting. Give as OD or BD injections which are immediate or long acting

81
Q

What drug combinations can be used in poor diabetes control?

A

Metformin, DPP-4 inhibitor & sulfonylurea

Metformin, pioglitazone & sulfonyurea

Metformin, sulfonylurea & SGLT-2 (not dapaligflozin)

Metformin, pioglitazone & SGLT-2 (not dapaligflozin)

82
Q

What are the diabetic microvascular complications?

A

Retinopathy (proliferative or non-proliferative)
Neuropathy
Nephropathy

83
Q

What causes diabetic retinopathy? How can it be treated?

A

High blood sugar makes blood more coagulable - this is an issue in retina due to fine blood vessels. Capiliaries become blocked.
Proliferative: new vessels form & leak blood
Non-proliferative: no new vessels form

No drug treatment but laser therapy burns leakages

84
Q

What causes diabetic neuropathy? How can it be treated?

A

Increased blood sugar leads to reduced blood flow and death of nerves. Peripheral neuropathy is most common.

Topical: capsaicin
Antidepressants: duloxetine or amitriptyline/nortriptyline
Anticonvulsants: gabapentin or prcegablin

85
Q

What causes diabetic foot ulcers?

A

It is a complication of neuropathy, lack of sensation increases risk of damage to feet.
Increased blood sugars increase infection risk and decrease healing

86
Q

What causes diabetic nephropathy? How can it be treated?

A

Nephrons are thickened and scarred making them less effective. Kidney function deteriorates.

Treatment involves good BP control with ACE or ARBs

87
Q

How can macrovascular complications be prevented?

A

Control cholesterol - atorvastatin
Control BP - Aspirin 75mg, CCB, ACEI
Control blood sugar

88
Q

What is T2DM?

A

Chronic hyperglycaemia due to insulin resistance and impairment of insulin secretion relative to requirements

89
Q

What are the T2DM risk factors?

A 
Genetics
Ethnic background
Increased age
Female
Obesity
Poor food choices/sedentary lifestyle 
Smokers
90
Q

What are the presenting symptoms of T2DM?

A 
Always hungry
Vaginal infections
Numbness and tingling of feet
Frequent urination 
Wounds that won't heal
Unexplained weight loss
Blurred vision
Always tired
Increased thirst
91
Q

How can T2DM be treated with diet?

A

Eat foods: high in fibre, low GI sources of carbs, low fat dairy products, oily fish
Avoid: saturates and trans fatty acids, simple carbs and food aimed at diabetics

92
Q

How can T2DM be treated with exercise?

A 
Active daily 
150 mins a week of moderate activity and 75mins intense activity 
Muscle strengthening 2x a week
Stop smoking 
Avoid sitting for long periods of time
93
Q

Which drugs reduce sugar through enhanced insulin secretion?

A

Sulfonylureas and Meglitanides

94
Q

Which drugs reduce peripheral insulin resistance?

A

Metformin and pioglitazone

95
Q

Which drugs delay carbohydrate absorption?

A

Acarbose and GLP 1 agonists

96
Q

Which drugs reduce hepatic glucose output?

A

Metformin, pioglitazone, DPP-4 inhibitors and GLP 1 agonists

97
Q

Which drugs reduce glucose rey-take from glomerular filtrate?

A

SGLT 1 inhibitors

98
Q

Which drugs enhance the action of incretin?

A

GLP 1 agonists and DPP-4 inhibitors

Pharmacy Year 3 (11 decks)

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