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The Patient > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What cBG is hypoglycaemia?

A

<2.5mmol/L

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2
Q

What cBG is normoglycaemia?

A

3-5mmol/L fasting

7-8mmol/L post-prandial

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3
Q

What cBG is hyperglycaemia?

A

> 10mmol/L

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4
Q

How is insulin synthesised?

A

From proinsulin. 23 amino acids removed to make insulin

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5
Q

Insulin half life

A

3-5 mins

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6
Q

What do the different cells in the Islets of Langerhans produce

A 
β-cells; release insulin
α-cell; release glucagon
δ-cells; release somatostatin
ε-cells; release ghrelin
PP-cells; release pancreatic polypeptide
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7
Q

How is insulin release triggered by presence of glucose?

A
  1. Uptake by B cells
  2. K channels close, depolarisation
  3. Ca2+ influx
  4. release of insulin
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8
Q

How is insulin release triggered by gut hormones?

A
  1. rise in serum GLP-1
  2. activation of GLP-1 receptor on B cells
  3. cell signalling
  4. insulin release
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9
Q

What is ghrelin?

A

Hunger hormone

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10
Q

What effect does insulin have on cells?

A
  1. binds to insulin receptor on cell surface
  2. conformation change, switch on kinase activity of receptor (phosphorylates)
  3. activates many processes in the cell - cascade
  4. activates (and increases number of) transporters in the membrane, to increase glucose uptake
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11
Q

How does insulin reduce blood sugar?

A
  • increased glucose uptake into cells
  • convert glucose to glycogen
  • decrease glycogen breakdown
  • increase fat stores
  • increase protein production
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12
Q

Which systems increase food intake (towards hyperglyc.)?

A

GI tract and CNS (through hunger)

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13
Q

Which systems increase glucose production?

A

Liver and adipocytes

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14
Q

Which systems increase glucose reabsorption?

A

Kidneys

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15
Q

Which tissues increase glucose utilisation?

A

All of them. Especially liver and skeletal muscle

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16
Q

Which systems increase glucose storage?

A

Liver and adipocytes

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17
Q

Which systems increase glucose loss?

A

kidneys

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18
Q

How to adipocytes control blood glucose?

A

Lipolysis, glucose uptake, leptin

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19
Q

Definition of Diabetes?

A

When the pancreas doesn’t produce enough insulin, or the body cannot use it. Leads to hyperglycaemia

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20
Q

Non-medical causes of hypoglycaemia?

A
  • inadequate food intake
  • insulin overdose
  • sulfonylurea overdose
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21
Q

Medical causes of hypoglycaemia?

A
  • insulinoma
  • hyperinsulinism
  • nocturnal hypo with T1
  • gastric bypass associated hypo
  • transient neonatal hypo
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22
Q

Symptoms of hypoglycaemia?

A

Autonomic: hunger, sweating, shaking, heart rate increased, nausea, headache
Neuroglycopaenic: confusion, drowsiness, odd behaviour, incoherent speech, poor co-ordination

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23
Q

When to use glucagon therapy?

A

Severe hypoglycaemia when oral glucose not possible or desired

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24
Q

What form is glucagon therapy in?

A

Injection (iv, im, sc). Must be reconstituted

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25
Q

Side effects of glucagon therapy?

A

Headache and nausea

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26
Q

What is diazoxide therapy?

A

For severe hypoglycaemia. Reverses the depolarisation effect that glucose has on B cells

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27
Q

Side effects of diazoxide?

A

Anorexia, nausea, vomiting, hypotension, oedema, tachycardia, arrhythmia, hypertrichosis (prolonged use)

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28
Q

4 T’s of Type 1 Diabetes?

A

Toilet, Thirst, Tired, Thinner

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29
Q

How do the majority of T1 diabetics present?

A

Diabetic ketoacidosis (DKA)

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30
Q

What is DKA?

A

Response to absense of insulin

  • hyperglycaemia
  • increased urine output - dehydration
  • suppressed lipolysis –> ketones
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31
Q

Why is DKA dangerous?

A

profound acidosis (often <7), severe dehydration

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32
Q

Symptoms of DKA

A

tachypnoea, altered mental state (drowsiness/coma, mistaken for drunkenness), nausea, vomiting, abdo pain

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33
Q

Fluid Resuscitation in DKA

A

First hour - isotonic only, give slowly (rapid leads to cerebral oedema and death)

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34
Q

Insulin administration in DKA

A

Given on a sliding scale (0.05-0.1unit/kg/hour), monitor cBG hourly, maintenance fluid once cBG <15

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35
Q

DKA Maintenance fluid amount in adults?

A

Max 2L / day

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36
Q

What fluid should be given for DKA management?

A

isotonic, glucose containing, with KCl (for kidneys, insulin lowers potassium)

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37
Q

At what point can you reduce iv insulin in DKA?

A

<3mmol/L (increase glucose and insulin if not dropping)

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38
Q

Correct order of treatment once a DKA patient is ready to eat?

A
  1. Eat and give sc insulin
  2. wait 30 minutes
  3. stop glucose iv
  4. stop insulin sliding scale
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39
Q

DKA in children - fluids?

A

50% volume of normal.
10kg - 2mL/kg/hour, 10-40kg - 1mL/kg/hour. >40kg, 40mL/hour (not weight based).

Replace deficit over 48 hours not 24

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40
Q

When to start sc insulin in children with DKA?

A

cBg <14mmol/L, ketones <3mmol/L, resolved acidosis, oral fluids tolerated

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41
Q

What are the complications of DKA?

A

fatality 0.15-0.31% of children. Most common cause is cerebral oedema (>4mL/kg/h, hypotonic fluid).

symptoms: bradycardia, dilated pupils, altered mental state

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42
Q

What insulin regimens are available for T1 Diabetics?

A

Basal bolus or biphasic

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43
Q

What is basal bolus insulin?

A

Long acting insulin OD or BD, plus rapid acting insulin with meals

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44
Q

What types of insulins are available for basal bolus?

A

Rapid acting, short acting, intermediate acting, long acting, super long acting

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45
Q

Onset time of short acting insulin?

A

30 mins - 1 hour

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46
Q

Peak time for short acting insulin?

A

2-3 hours

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47
Q

Duration of action for short acting insulin?

A

8-10 hours

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48
Q

Examples of short acting insulins?

A

Human Actrapid, Humulin S, Insuman Rapid

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49
Q

Onset time of rapid acting insulins?

A

5-15 mins

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50
Q

Structural changes to rapid acting insulins?

A

Changed last few amino acids - quicker penetration through s/c tissue

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51
Q

Peak time for rapid acting insulins?

A

30-90 mins

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52
Q

Duration of action for rapid acting insulins?

A

4-6 hours

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53
Q

Examples of rapid acting insulins?

A

Humalog (insulin lispro), Novorapid (insulin aspart), Apidra (insulin glulisine)

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54
Q

What is the insulin balancing act?

A

Decreased BG: exercise and insulin

Increased BG: Food and stress hormones

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55
Q

Onset time of intermediate acting insulins?

A

2-4 hours

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56
Q

Peak time for intermediate acting insulins?

A

4-10 hours

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57
Q

Duration of action for intermediate acting insulins?

A

12-18 hours

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58
Q

Examples of intermediate acting insulins?

A

Human insulatard
Humulin 1
Insuman Basal

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59
Q

Onset time of long acting insulins?

A

2-4 hours

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60
Q

Peak time of long acting insulins?

A

no peak, mimics basal output in non-diabetics

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61
Q

Duration of action of long acting insulins?

A

20-24 hours

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62
Q

Examples of long acting insulins?

A

Insulin Glargine (Lantus or Abasaglar), Detemir (Levemir)

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63
Q

NICE indication for ultra long acting insulins?

A

3rd line when other long acting have failed

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64
Q

Duration of action of ultra long acting insulins?

A

up to 42 hours

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65
Q

When are ultra long acting insulins beneficial?

A

Troublesome nocturnal hypos, or non-adherent patients who forget their insulin

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66
Q

When is non-human insulin used?

A

Rarely. Only for patients who have used historically, or unable to tolerate human insulin

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67
Q

When should blood glucose be monitored?

A

before meals, before bed

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68
Q

Blood glucose monitoring requirements for driving?

A

Check before, then every 2 hours

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69
Q

Which dose would need to be adjusted if cBG was abnormal before breakfast?

A

evening long acting

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70
Q

Which dose would need to be adjusted if cBG was abnormal before dinner?

A

lunch quick acting

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71
Q

How much support should patients get in the first 6 months?

A

lots. help with dose titration based on cBG diaries

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72
Q

When can’t patients move to self adjustment?

A

Non-adherent or those on biphasic insulins

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73
Q

What does DAFNE stand for?

A

Dose Adjustment For Normal Eating

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74
Q

What does DAFNE involve?

A

Calculating insulin dose based on carb content of meals

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75
Q

What are the benefits of DAFNE?

A

Saves NHS money, patients can eat more freely, reduced complications, reflects natural insulin response

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76
Q

What is biphasic insulin made up of?

A

Short or rapid acting insulin in a protamine suspension

Some in a complex so isn’t immediately released

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77
Q

Onset time for biphasic insulins?

A

approx 30 minutes

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78
Q

Duration of action of biphasic insulins?

A

12 hours

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79
Q

Peak time for biphasic insulins?

A

1-2 hours

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80
Q

What patients is biphasic insulin suitable for?

A

Those that struggle with multiple injections, those unable to carb count

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81
Q

Examples of biphasic insulins?

A

Humulin M3, Insuman Comb 15,25, 50, Humalog Mix 25, 50, Novomix 30

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82
Q

Biphasic insulin regime?

A

2 injections a day, breakfastand evening meal

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83
Q

What is hypoglycaemia for people with medication controlled diabetes?

A

<4mmol/L

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84
Q

What to do when diabetic patient is hypoglycaemic?

A

Lucozade or other sugary drink, meal or snack.

If in hospital, dextrose tabs/glucogel, meal or snack.

If unconscious, Glucagon IM followed by 10% glucose 100mL/h

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85
Q

What 4 things need to be remembered on Sick days?

A

S - sugar. check every 2-3 hours
I - insulin. continue to avoid DKA
C - carbs. continue to take sugar to avoid hypo.
K - ketones. check urine, take rapid acting if present. drink plenty of water.

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86
Q

What route is insulin administered via?

A

S/c injection

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87
Q

Which insulins should always be timed with food?

A

short, biphasic or intermediate

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88
Q

When in relation to meals should insulin be given?

A

30 mins before, rapid acting can be given 5 mins after

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89
Q

When can IV insulin be given?

A

in hospital for close control - DKA or peri-op

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90
Q

How to remove air from the needle?

A

Eject 2 units

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91
Q

What angle should it be injected?

A

90 degrees

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92
Q

What types of insulin device can you get?

A

refillable pens, pre-filled pens, single use needles + vials (rarely used out of hospital)

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93
Q

Variations in insulin needles?

A

different lengths and thicknesses available. higher gauge = thinner needle.

some patients prefer short needles, others require longer ones

94
Q

Benefits of needles that cover themselves?

A

good for needle phobics, safer for others administering to prevent injury

95
Q

When should continuous sc infusion be considered?

A
  • disabling hypos in attempt to reach target HbA1c
  • HbA1c >69mmol/mol on MDI therapy, despite high care level
  • patient (or carer) must have commitment and competience
96
Q

Definition of disabling hypoglycaemia?

A

repeated and unpredictable episodes, persistent anxiety, significant impact on life

97
Q

What is type 2 diabetes?

A

chronic hyperglycaemia due to insulin resistance and impairment of insulin secretion

98
Q

Why does hyperglycaemia worsen T2 diabetes?

A

can impair B cell function and increase insulin resistance, so cycle of hyperglycaemia and worsening state

99
Q

What is IGT?

A

Impaired glucose tolerance (prediabetes). insulin scretion/resistance and BG are increasing, but not yet in diabetic levels

100
Q

When does T2D beome insulin dependent instead of resistant?

A

when insulin resistance becomes so high and secretion stops

101
Q

Genetics and T2 risk?

A

1st degree - 5-10x increase, 90% concordance in identical twins

102
Q

Ethnicity and T2 risk?

A

increased risk south asians, chinese, afro-caribbean, black african

103
Q

Gender and T2 risk?

A

females more likely than men

104
Q

Weight and T2 risk?

A

more men than women classified as obese, but more women than men have high waist circumference.

BMI: 1cm/m2 increases risk by 8.4%
WC: 1cm increases by 3.5%

105
Q

What is epigenetics?

A

Underlying genetic risk factors and environment that favours development of disease

106
Q

How does T2 present?

A

often asymptomatic, picked up in routine screening, or patient has complications.

some patients - increased thirst, urination

107
Q

Diagnostic criteria for T2?

A

fasting cBG >7mmol/L

HbA1c ≥48mmol/mol

108
Q

Prediabetes diagnostic criteria?

A

Fasting cBG <7mmol/mol

2 hour venous BG after 75g load 7.8-11.1mmol/L

109
Q

Treatment for T2D?

A

Diet, exercise, medication (that order).

Diet has most effect, followed by exercise

110
Q

Goals from adjusting diet for T2D?

A

5-10% weight reduction short term, long term - normal BMI.

111
Q

Good food choices for T2?

A

oily fish, complex carbs, high fibre, low fat dairy

112
Q

Poor food choices for T2?

A

saturated and trans fats, simple carbs, food aimed at diabetics

113
Q

Exercise goals for type 2?

A

150 mins/week moderate, or 75 mins intense

plus muscle strengthening 2x week

(any is better than none)

114
Q

What do sulfonylureas target?

A

stimulates insulin release from B cells - inhibits ATP sensitive K channel

115
Q

Examples of sulfonyl ureas?

A

Short acting: gliclazide, glipizide, tolbutamide, glimepiride
Long acting: glibenclamide

116
Q

Which sulfonylureas are preferred?

A

Short acting as lower hypo risk. gliclazide most common

117
Q

When should sulfonylureas be taken?

A

Always with food. don’t take if no meal

118
Q

Dosing information for gliclazide?

A

start 40mg with breakfast

up to 160mg BD with meals

119
Q

Advantages of sulfonylureas?

A

Can be OD or BD, quickly lowers cBG soimproves symptoms, fewer GI effects than metformin

120
Q

Disadvantages of sulfonylureas?

A

Can cause hypos, can cause weight gain, need some pancreas function, unpredictable in renal impairment and the elderly, need to monitor liver function

121
Q

What are meglitanides?

A

same mechanism as sulfonylureas, different B cells. less likely to cause hypos. repaglinide/nateglinide. not often used in UK

122
Q

What class is pioglitazone?

A

Thiazolidinediones. only one licensed in UK

123
Q

What does pioglitazone target?

A

Decreases peripheral insulin resistance. increases glucose utilistation in muscles and adipose, and decreases glucose production in liver.

124
Q

Pioglitazone dosing info?

A

Start 15mg OD, max 45mg OD

125
Q

Advantages of pioglitazone?

A

OD dosing, low risk of hypo, suitable in renal impairment

126
Q

Disadvantages of pioglitazone?

A

Linked to bladder cancer, heart failure and fracture risk (CI), liver monitoring required, weight gain, can take 3-6 months to show benefit

127
Q

What class is metformin?

A

Biguanide. First line!

128
Q

What does metformin target?

A

Inhibits gluconeogenesis in the liver, increase glucose utilisation in peripheral tissues

129
Q

Metformin dosing info?

A

start 500mg OD, max 1g TDS (rarely go over 2g)

130
Q

Alternative form metformin suitable when?

A

Modified release may improve GI side effects

131
Q

Advantages of metformin?

A

Cheap, weight neutral, low hypo risk

132
Q

Disadvantages of metformin?

A

GI effects, lactic acidosis risk (avoid if other risk factors e.g. post MI, sepsis), short t1/2 so TDS, not suitable in renal impairment,

133
Q

Metformin dose adjustment in renal impairment?

A

half dose when eGFR gets to 45 (caution), stop when 30 (CI)

134
Q

What class is acarbose?

A

Alpha glucosidase (UK only)

135
Q

What does acarbose target?

A

inhibits enzymes that convert poly - monosccharides, slows glucose absorption

136
Q

Acarbose dosing info

A

start 50mg OD, increase daily to TDS. max 200mg TDS

have to chew, take with meals

137
Q

Side effect of acarbose?

A

GI side effects, poorly tolerated

138
Q

Which classes of antidiabetic target GLP-1 hormone?

A

GLP-1 agonists, DPP-1 inhibitors

139
Q

What does GLP-1 do?

A

Gut derived incretin hormone, stimulates insulin release and suppresses glucagon production. also inhibits gastric empyting and suppresses appetite

140
Q

What do GLP-1 agonists do?

A

Stimulate insulin secretion and cause minor delay in gastric emptying - reduced hunger

141
Q

What forms of GLP-1 agonists are there?

A

Exenatide, liraglutide, lixisenatide (daily)

albiglutide, dulaglutide, lond acting exenatide (weekly)

s/c injections

142
Q

What are the criteria for GLP-1 agonist use?

A
  • BMI >35 (adjusted for non-europeans)
  • BMI < 35 but psychological/medical problems associated with weight
  • BMI <35 but insulin is unsuitable due to occupation
143
Q

What must patients demonstrate in order to continue use of GLP-1 agonists?

A

Weight loss and improved HbA1c

144
Q

Advantages of GLP-1 agonists?

A

Weight loss, once a day (or week) preparations, rarely cause hypos, suitable in moderate renal impairment

145
Q

Disadvantages of GLP-1 agonists?

A

Injections, severe GI effects are common, can cause pancreatitis

146
Q

What do DPP-4 inhibitors target?

A

block rapid degradation of GLP-1

147
Q

Examples of DPP-4 inhibitors?

A

sitagliptin, vildagliptin, saxagliptin, alogliptin (all need dose adjustment in renal impairment)
linagliptin (suitable in all renal functions)

148
Q

Advantages of DPP-4 inhibitors?

A

Once a day, no weight gain, low hypo risk, suitbale in renal impairment

149
Q

Disadvantages of DPP-4 inhibitors?

A

commonly causes Gi effects, rash and UTIs, risk of pancreatic inflammation

150
Q

What do SGLT-2 inhibitors target?

A

block active transport (reabsorption) of glucose in glomerular filtrate

151
Q

Renal requirements for SGLT-2 inhibitors?

A

Don’t start if eGFR <60

Stop when eGFR <45

152
Q

Examples of SGLT-2 inhibitors?

A

Canagliflozin, empagliflozin (cheapest), dapagliflozin

153
Q

Advantages of SGLT-2 inhibitors?

A

Weight loss, can lower BP, low risk of hypo

154
Q

Disadvantages of SGLT-2 inhibitors?

A

Thrush and UTIs (especially on starting treatment), only effective if good renal function, lower BP can increase fall risk, safety concerns around AKI and DKA

evidence of increased amputation incidence with canagliflozin

155
Q

NICE guidance on SGLT-2 inhibitors?

A

only as part of dual therapy when patient is unable to take sulfonylureas - due to hypo risk, intolerance or contraindications

156
Q

Step 1 of NICE guidelines for T2 drug therapy?

A

When HbA1c >48mmol/mol, metformin

157
Q

Step 2 of NICE guidelines for T2 drug therapy?

A

When HbA1c >58mmol/mol, add ONE OF:
DPP-4 inhibitor, Sulfonylurea, pioglitazone, SGLT-2 inhibitor

53mmol/mol HbA1c target

158
Q

Step 3 of NICE guidelines for T2 drug therapy?

A

Triple therapy:

  • metformin + DPP-4i + SU
  • metformin + pioglitazone + SU
  • metformin + pioglitazone or SU + SGLT-2i

if not effective, consider metformin + SU + GLP-1 (criteria)

Consider insulin therapy

159
Q

First step of insulin treatment in T2?

A

Basal insulin only - start with NPH (intermediate) BD

long acting insulin can be given for patients having hypos that restrict dose increases, or are unable to administer themselves and nurse is needed

160
Q

Second step of insulin treatment in T2?

A

Basal bolus regime or biphasic - HbA1c >75mmol/mol

161
Q

1st step if metformin is contraindicated or not tolerated?

A

HbA1c >48mmol/mol
DPP-4i, pioglitazone or SU
SGLT-2i if DPP-4i not possible

HbA1c targets: 48mmol/mol (53 if SU)

162
Q

2nd step if metformin contraindicated or not tolerated?

A

HbA1c >58mmol/mol

  • DPP-4i + pioglitazone OR SU
  • pioglitazone + SU

aim for 53mmol/mol

163
Q

3rd step if metformin contraindicated or not tolerated?

A

insulin therapy

164
Q

% HbA1c reduction with lifestyle changes?

165
Q

% HbA1c reduction with metformin?

166
Q

% HbA1c reduction with insulin?

167
Q

% HbA1c reduction with Pioglitazone?

168
Q

% HbA1c reduction with GLP-1 agonist?

169
Q

% HbA1c reduction with DPP-4i?

170
Q

% HbA1c reduction with SGLT-2i?

171
Q

Main aims of medicines optimisation in diabetes?

A

blood sugar control and reducing complications

172
Q

Types of microvascular complications?

A

retinopathy, nephropathy and neuropathy

173
Q

What is diabetic retinopathy?

A

micro-thrombi in retina, blocks capillaries

174
Q

What are the three mechanisms of retinopathy?

A
  1. increased retinal blood flow due to impaired autoregulation
  2. increased sorbitol production - osmolarity and swelling leads to cell rupture
  3. glycosylation end products (e.g. glucose + amino acid) results in vasculature damage
175
Q

What is proliferative retinopathy?

A

New blood vessels form and leak blood into vitreous - blocking light

176
Q

What is non-proliferative retinopathy?

A

No new vessels form, damage occurs to existing ones

177
Q

Is diabetic retinopathy treatable?

A

No - irreversible

Laser treatment can help to slow the progress

178
Q

What is diabetic neuropathy?

A

High blood sugars lead to reduced blood flow and death of nerves - most common is peripheral neuropathy

179
Q

Symptoms of neuropathy?

A

Pain, unusual sensations, complete loss of sensation

180
Q

Treatment for neuropathy?

A

Topical - capsacin
Antidepressants - amitriptyline, duloxetine, nortriptyline
Anticonvulsants - gabapentin, pregablin (lyrica only licesned)

181
Q

Order of treatment for diabetic neuropathy?

A

Topical agent first, then patient choice for systemic

182
Q

Why are regular foot and eye checks necessary?

A

To monitor for foot ulcers and retinopathy

183
Q

How to diabetic foot ulcers arise?

A

Lack of sensation (neuropathy) increases risk of damage to feet
high blood sugar increases infection risk, poor blood flow delays healing
poor antibiotic penetration
often leads to amputation

184
Q

What is diabetic nephropathy?

A

Nephrons become thickened and scarred due to chronic hyperglycaemia, ineffectiveness

185
Q

Treatment for nephropathy?

A

Blood pressure control - ACE or ARB

186
Q

Macrovascular complications associated with diabetes?

A

High insulin levels lead to atherosclerosis
diabetes related dyslipidaemia

leads to MI, stroke, vascular disease

187
Q

Prevention of macrovascular complications?

A

Control BP, cholesterol
aspirin if evidence of CVD
obviously glucose control

188
Q

Blood pressure targets for T2?

A

140/80
130/80 if kidney, eye or cerebrovascular damage

ACE inhibitor (CCB for black or pregnant patients)

189
Q

When to offer atorvastatin to T1D?

A

20mg

older than 40, diabetes for >10y, established nephropathy or otehr CVD risk factors

190
Q

When to offer atorvastatin to T2D?

A

anyone scoring over 10% on QRISK

191
Q

Goals of statin treatment in diabetics?

A

reduce HDL by 40% in 3 months - titrate dose as needed

192
Q

What is glaucoma?

A

a blanket term for several conditions caused progressive neuropathy, leading to optic nerve damage, visual loss and eventual blindness

usually due to impaired drainage of aqueous humour (imbalance of production and drainage)

193
Q

What are the risk factors for glaucoma?

A

(usually asymptomatic)

  • raised IOP (>21)
  • family history
  • race (black, asian, hispanic)
  • hypertension, CV disease
  • migraine
194
Q

What are the two types of glaucoma?

A

Open angle, closed angle

most drugs are to manage open angle

195
Q

Where in the eye is aqueous humour produced?

A

Ciliary epithelium

196
Q

Where does aqueous humour sit within the eye?

A

Anterior chamber

197
Q

What rate is aqueous humour produced?

A

2.75microL/min

198
Q

Where does aqueous humour drain?

A

Between iris muscle and trabecular meshwork (into here), then down into Schlemm’s canal

angle must be sufficient for drainage to occur, and this is where the types come from

199
Q

What is a normal Intra-occular pressure?

A

around 16 mmHg (up to 20)

200
Q

What are the goals of glaucoma treatment?

A

Reduce IOP to 16-20mmHg
Drug to have sufficient duration of action (for compliance)
Provide preservation of vision, no loss of effect over time, compatibility with other treatments (comorbid), no topical or systemic side effects

201
Q

How is aqueous humour formed?

A

Aq. substances and ions transported from blood into occular cells, to produce humour which is then released into the posterior chamber

202
Q

What are the first choice treatment for glaucoma and why?

A

Prostaglandins

Have a unique mechanism for decreasing IOP - increase outflow

203
Q

What are examples of the prostaglandin analogues?

A

Latanoprost, Travoprost, Tafluprost (esters, converted to acid as absorbed across cornea - prodrug)

204
Q

How to prostaglandin analogues work to treat glaucoma?

A

Analogues of Prostaglandin F2a, and act on the FP receptor (dont use PGE as shorter half life than F)

reduce the outflow of aqueous humour

205
Q

What effect do the prostaglandin analogues for glaucoma have on the FP receptor?

A

The FP receptor is a GPCR, which is coupled with GåQ

activates phospholipase C, which increases production of diacylglycerol and inositol phosphate

206
Q

Where are the FP receptors found?

A

ciliary body/muscle and sclera, iris sphincter, trabecular meshwork cells (little effect here as damaged due to glaucoma)

207
Q

Benefits of using prostaglandin analogues?

A

Long duration of action, lower IOP by up to 35%, well tolerated (good compliance)

208
Q

Example of a prostamide analogue?

A

Bitamoprost

209
Q

How to prostamide analogues differ from prostaglandin analogues?

A

Not prodrug - analogues of prostamide F2alpha

slightly more effective, because work on both prostamide and FP receptors

210
Q

What is the mechanism of action of prostaglandin analogues?

A

Increased uveoscleral outflow (reduces resistance by remodelling the extracellular matrix:

  • increase matrix metalloproteinases
  • degrades collagen
  • decreases resistance of ciliary muscle and sclera to increase outflow
211
Q

What are some side effects of PG analogues?

A
  • red eye (initial)
  • increased pigmentation in iris, eyelashes and perocular skin
  • eyelash growth
  • precipitate or worsen cystoid macular oedema in aphakic eyes
  • light sensitivity
  • C/I in pregnancy (theoretical general effect on cell division)
212
Q

What is the mechanism of action of beta blockers for glaucoma?

A

blocks cAMP:
cAMP activates the cotransporter than transports ions in pigmented epithelial cells, controls Cl efflux in non-pigmented
- blocking these processes reduces the aq. humour production

  • decreased ion concentration
  • decreased fluid gradient
  • better balance of production and drainage
213
Q

What are the advantages of beta blockers for glaucoma treatment?

A

well tolerated, rapid onset, effective in 75% of patients, lower IOP by 20-30%, compatible with other drugs, OD or BD administration

214
Q

What are the disadvantages of beta blockers for glaucoma treatment?

A

can have effect on the other eye also, systemic side effects, efficacy declines over time

215
Q

What side effects can occur from beta blockers for glaucoma treatment?

A

generally systemic:
bradycardia, hypotension, vascoconstriction, impotence etc
C/I in heart block/failure

bronchial effects - constriction - C/I in asthma and other airways disease

diabetic - masks hypoglycaemia

216
Q

What are fixed dose combinations?

A

Preparations that contain both drugs, as combinations can be more effective than singular ones

217
Q

What are the benefits of fixed dose combinations?

A

patient compliance, reduced preservative exposure, no washout effect for second drop
cheaper for patient (one charge), cheaper treatment

218
Q

What are carbonic anhydrase inhibitors?

A

INhibit carbonic anhydrase in ciliary epithelium - which produces bicarbonate needed for aq humour production

decreased ion conc leads to decreased fluid gradient

219
Q

What are the systemic carbonic anhydrase inhibitors?

A

Acetazolamide (not absorbed topically) - used only in emergencies

used in open angle glaucoma, secondary glaucoma, or peri-op for closed angle

side effects limit use

220
Q

What are the side effecs of acetazolamide?

A

sulfonamide derivative so increased risk of allergy and blood disorders

enzyme is present throughout body so effect on GI tract, diuresis, acid/base balance disturbance, drowsiness, depression, parasthesias

221
Q

How were topical carbonic anhydrase inhibitors developed?

A

modified acetazolamide to improve lipid solubility (for corneal absorption) and reduce side effects by increasing selectivity for CA-II enzyme

222
Q

Examples of topical carbonic anhydrase inhibitors?

A

Dorzolamide and brinzolamide

223
Q

When are topical carbonic anhydrase inhibitors indicated?

A

adjunct with beta blockers or PG analogues

sole therapy if patient cannot tolerate beta blockers

224
Q

What % reduction in IOP can you expect from topical carbonic anhydrase inhibitors?

225
Q

What are ethe side effects of topical carbonic anhydrase inhibitors?

A

burning/stinging (pH brinzolamide drops 7.5, pH dorzolamide drops 5.6-6.0)

Blurred vision, conjunctival hyperaemia, transient myopia, blepharitis, allergic conjunctivitis

taste disturbances, dry mouth, headache

226
Q

Alpha-2 receptor agonist use for glaucoma?

A

same as beta blockers/ stimulated alpha-2 receptors reduce cAMP so subsequently aq humour production (receptors on ciliary, corneal and conjunctival epithelial cells)

also decreases blood flow so less ultrafiltration (from vasoconstriction)

increases uveo-scleral outflow (thought to be from increased PGs from alpha stimulation)
potentially neuroprotective

227
Q

Examples of alpha-2 agonists in glaucoma treatment?

A

Brimonidine and Apraclonidine

b. is more selective for alpha-2
apraclonidine is only for short term use as can cause tachyphylaxis, used post laser surgery to prevent IOP rise

228
Q

Side effects of alpha-2 agonists?

A

local: blurred vision, stinging/burning, photophobia
systemic: hypotension, drowsiness, fatigue, dry mouth, taste disturbances

229
Q

What type of drug is pilocarpine?

A

Parasympathomimetic

230
Q

What is the mechanism of pilocarpine for glaucoma treatment?

A 
Contract ciliary muscle
Pulls scleral spur
Opens trabecular meshwork
Increases trabecular outflow
Decreases IOP
231
Q

What is the main problem with using pilocarpine for glaucoma?

A

Only lasts about 6 hours so multiple daily doses - compliance issue

The Patient (8 decks)

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