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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
When should insulin be started in a child with DKA?
cBG <14mmol/L Ketones <3mmol/L Resolved acidosis Oral fluids are tolerated
26
Basal bolus insulin regime:
Long acting in the evening or BD | 3 doses of short/rapid acting during the day before meals (based on carb intake)
27
Biphasic insulin regime:
2 biphasic doses, morning and tea time | Dose split depends on biggest meal
28
Describe rapid acting insulin and give examples
Mimics pancreases Onset 5-15 mins, peak 30-90min, duration 4-6 hours Novorapid - Insulin Aspart Humalog - Insulin lispro Apidra - Insulin glulisine
29
Describe short acting insulin and give examples
Soluble Onset 30mins-1hour, peak 2-3 hours, duration 8-10 hours Human Actrapid - human insulin Humulin S - human insulin Insuman rapid - human insulin
30
Describe intermediate acting insulin and give examples
Isophane insulin Onset 2-4 hours, peak 4-10 hours, duration 12-18 hours Human insulatard Humulin I Inusman Basal
31
Describe long acting insulin and give examples
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
32
Describe ultra long acting insulin and give examples
3rd line use. OD administration fives flattest insulin profile. Up to 42 hours duration Tresiba - Insulin degludec Toujeo - Insulin glargine 300 units/ml
33
What are the symptoms of hypoglycaemia in medication controlled diabetes?
<4mmol/L cBG Hunger, tremor, sweating, palpitation Odd behaviour drowsiness, visual disturbance, seizures Headache and nausea
34
What is used to replace glucose in hospitalised patients?
Conscious - dextrose tabs/glucogel | Unconscious - glucagon IM followed by 10% glucose 100ml/hr
35
When should insulin be injected? What are the exceptions to this?
Half an hour before meals | Except: insulin lispro, aspart or glulisine - these can be given 5 mins before eating
36
Define disabling hypoglycaemia
Repeated and unpredictable occurrence of hypos that results in persistent anxiety about recurrence and is associated with adverse effects on quality of life
37
What is used in the treatment of disabling hypoglycaemia?
Continuous s/c insulin infusion
38
When should continuous insulin infusion be considered?
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
39
What is classed as good diabetes management?
``` Low cBG Low HbA1c Reduced episodes of hypoglycaemia Reduced episodes of hyperglycaemia No hospitalisations Reduces complications and mortality ```
40
When is tight control needed?
Benefits outweigh risk | Long term benefits outweigh short term side effects
41
When is less tight control needed?
Risk outweighs benefits | Little change of long term benefit
42
What is HbA1c?
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
What is HbA1c a poor predictor of?
Early death, other heart disease, stroke or foot ulcers
44
What is the normal HbA1c value?
<42 mmol/ml - normal
45
What is the HbA1c value for pre diabetes?
42-47 mmol/ml
46
What is the HbA1c value for good diabetes control?
<58 mmol/ml
47
What is the HbA1c value for moderate diabetes control?
58-70 mmol/ml
48
What is the HbA1c value for poor diabetes control?
>70 mmol/ml
49
Which drug is first line for diabetes?
Metformin
50
Describe the MoA of biguanides
Inhibit gluceoneogenesis in the liver, results in lower hepatic glucose production Increases insulin mediated glucose utilisation in peripheral tissues
51
Give an example of a biguanide and its dosage regime
Metformin Start dose 500mg OD Max dose 1g TDS
52
When is metformin contraindicated and used with caution?
C/I if eGFR <30ml/min/1.73m2 | Caution if eGFR <45ml/min/1.73m2
53
What can a patient do to avoid the severe GI side effects that come with metformin?
Take with meals
54
What are the advantages biguanides?
Cheap Weight neutral Low risk of hypos
55
What are the disadvantages biguanides?
Can cause GI side effects Rarely causes lactic acidosis Short half life - take TDS Need reasonable renal function
56
Describe the MoA of sulfonylureas
Directly stimulate insulin release from beta cells by stimulating ATP sensitive potassium channels
57
Give examples of short and long acting sulfonylureas
Short acting: gliclazide, glipizide, toltubamide, glimepride | Long acting: glibenclamide
58
What needs to be monitored when a patient is on sulfonylureas?
Liver function - can lead to hepatitis
59
What are the advantages sulfonyureas?
OD or BD Quickly lowers cBG Fewer GI side effects
60
What are the disadvantages sulfonylureas?
Can cause hypos Weight gain Needs residual pancreatic function Unpredictable in renal impairment and in the elderly
61
Describe the MoA of thiazolidinediones
Increase insulin sensitivity and reduce glucose production from the liver. They act on adipose and muscle tissues to increase glucose utilisation
62
Give an example of a thiazolidinedione
Pioglitazone | Starting dose 15mg
63
What are the advantages of tiazolidindiones?
OD Low hypo risk Suitable in renal impairment
64
What are the disadvantages of tiazolidindiones?
Associated with heart failure, increased risk of bladder cancer and fractures Causes weight gain Liver toxicity 3-6 months to show benefit
65
How do meglitanides differ from sulfonylureas?
Work in the same way but on different beta cells
66
Give 2 examples of meglitanides
Repaglinide an nareglinide
67
Describe the MoA of alpha glucosidase inhibitors
Inhibit enzymes that convert complex polysaccharide carbohydrates into monosaccarides. They have a dose dependent effect.
68
Give an example of an alpha glucosidase inhibitor
Acarbose
69
Describe the MoA of GLP 1 agonists
Stimulate insulin release from pancreas and suppresses glucagon secretion. Also inhibit gastric emptying and reduce appetite
70
Give examples of daily and weekly GLP 1 agonists
Daily: exenatide, liraglutide, lixisenatide Weekly: albiglutide, dugladtide, long acting exenatide
71
Describe the MoA of DPP-4 inhibitors
Block rapid degradation of GLP 1
72
Give examples of DPP-4 inhibitors
Sitagliptin Vildagliptin Saxagliptin Alogliptin
73
Give advantages of DPP-4 inhibitors
OD No weight gain Can be used in renal impairment
74
Give disadvantages of DPP-4 inhibitors
Cause GI side effects, rash and UTIs | Rarely causes pancreatic inflammation
75
Describe the MoA of SGLT-2 inhibitors
Block active transport of glucose from glomerular filtrate.
76
When should SGLT-2 inhibitors be stopped?
when eGFR <45ml/min
77
Give examples of SGLT-2 inhibitors
Canagliflozin Empagliflozin Dapagliflozin
78
What are the advantages of SGLT-2 inhibitors?
Can cause weight loss Reduces blood pressure (1-3mmHg) Low risk of hypos
79
What are the disadvantages of SGLT-2 inhibitors?
``` 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
What type of insulin is first line and why?
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
What drug combinations can be used in poor diabetes control?
Metformin, DPP-4 inhibitor & sulfonylurea Metformin, pioglitazone & sulfonyurea Metformin, sulfonylurea & SGLT-2 (not dapaligflozin) Metformin, pioglitazone & SGLT-2 (not dapaligflozin)
82
What are the diabetic microvascular complications?
Retinopathy (proliferative or non-proliferative) Neuropathy Nephropathy
83
What causes diabetic retinopathy? How can it be treated?
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
What causes diabetic neuropathy? How can it be treated?
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
What causes diabetic foot ulcers?
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
What causes diabetic nephropathy? How can it be treated?
Nephrons are thickened and scarred making them less effective. Kidney function deteriorates. Treatment involves good BP control with ACE or ARBs
87
How can macrovascular complications be prevented?
Control cholesterol - atorvastatin Control BP - Aspirin 75mg, CCB, ACEI Control blood sugar
88
What is T2DM?
Chronic hyperglycaemia due to insulin resistance and impairment of insulin secretion relative to requirements
89
What are the T2DM risk factors?
``` Genetics Ethnic background Increased age Female Obesity Poor food choices/sedentary lifestyle Smokers ```
90
What are the presenting symptoms of T2DM?
``` 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
How can T2DM be treated with diet?
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
How can T2DM be treated with exercise?
``` 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
Which drugs reduce sugar through enhanced insulin secretion?
Sulfonylureas and Meglitanides
94
Which drugs reduce peripheral insulin resistance?
Metformin and pioglitazone
95
Which drugs delay carbohydrate absorption?
Acarbose and GLP 1 agonists
96
Which drugs reduce hepatic glucose output?
Metformin, pioglitazone, DPP-4 inhibitors and GLP 1 agonists
97
Which drugs reduce glucose rey-take from glomerular filtrate?
SGLT 1 inhibitors
98
Which drugs enhance the action of incretin?
GLP 1 agonists and DPP-4 inhibitors

Pharmacy Year 3 (11 decks)

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