Communication- OTC advice

Question 1

How to choose the correct product

Answer 1

Be logical, think about:
Patient characteristics, indication and contra-indications, formulation, dose, patient preference, red flag symptoms, evidence base, licensing considerations, referral criteria

Question 2

What info should you provide?

Answer 2

If a product is recommended (be familiar with OTC guide): what is it, instructions for use, possible side effects, special storage instructions, what to do if symptoms get worse/ don’t improve with a clear timeline
If patient is referred: explain why you are making a referral, emphasise importance

Question 3

The sensation of pain is increased by:

Answer 3

Discomfort, fatigue, fear, sadness, boredom, insomnia, anxiety, anger, depression, loneliness

Question 4

The sensation of pain is decreased by:

Answer 4

Sleep, sympathy, companionship, rest, understanding, diversional activities, antidepressants (if appropriate)

Question 5

Features of acute pain

Answer 5

Usually raid in onset
Usually identifiable cause
Limited duration
Tends to get better
Biological significance

Question 6

Features of chronic pain

Answer 6

Not necessarily an identifiable cause
Large emotional component
Unpredictable duration
Does not get better
None or negative meaning

Question 7

Pain is transmitted through 3 different levels:

Answer 7

Peripheral: activation and release of pain mediators- nociception
Dorsal horn of the spinal cord- pain gating
The brain (thalamus, limbic and cortical systems)- pain perception

Question 8

Nociceptive

Answer 8

Stimulation of receptors that respond to heat, vibration, stretch and chemical stimuli released from damaged cells

Question 9

Non-nociceptive

Answer 9

From within peripheral and CNS, no specific receptors but nerve cell dysfunction

Question 10

To treat somatic/ visceral pain (nocicpetive)

Answer 10

NSAIDs, weak and strong opioids

Question 11

To treat neuropathic pain (non-nociceptive)

Answer 11

Anti-depressants, anti-convulsants, anti-arrhythmics

Question 12

What happens when tissues are damaged?

Answer 12

Release of chemical mediators e.g. bradykinin, histamine, 5-HT
Activation of C fibres
Inflammation- moving plasma and leucocytes from blood into injured tissues, results in swelling, heat and pain

Question 13

Prostaglandins

Answer 13

Chemical messengers made from fatty acids that play a role in influencing pain signals, and regulation of inflammation
Transmission of pain information to the brain
Modulation of the hypothalamic thermostat
Inflammation

Question 14

Cyclo-oxygenase

Answer 14

Enzyme responsible for formation of prostaglandins
Two known forms:
COX 1- always present in most cells
COX 2- induced in inflammatory cells
COX turns arachidonic acid into prostaglandins and thromboxanes

Question 15

Inflammatory pathway

Answer 15

COX 1 enzyme (physiological)-
TxA2- control of platelet aggregation
PGI2- protection of gastric mucosa
PGE2- control of renal blood flow

COX 2 enzyme (induced)-
Prostaglandins- inflammation

Question 16

Vascular events of acute inflammation

Answer 16

COX > histamine, PGI2, PGE2 > dilatation of the small arterioles > increased blood flow > stasis of the blood > increase in permeability of postcapillary venules > exudation of fluid (plasma and leukocytes into damaged area) > activation of the complement system, fibriolytic system, coagulation system and kinin system

Question 17

NSAIDs

Answer 17

Most have three major types of effect:
Anti-inflammatory effect
Analgesic effect- decrease production of the prostaglandins that sensitise nociceptors to inflammatory mediators
Antipyretic effect- NSAIDs reset the thermostat by inhibition of E-type prostaglandin production in the hypothalamus

Question 18

Anti-inflammatory effects of NSAIDs

Answer 18

Mainly reduce vasodilation, oedema (indirectly- the vasodilation facilitates the action of mediators such as histamine which increase permeability of post capillary venules), and decrease pain

Question 19

Primary action of NSAIDs

Answer 19

The primary action of NSAIDs is the inhibition of COX

Most NSAIDs inhibit both isoenzymes but vary in the degree of inhibition of each

Question 20

COX selectivity

Answer 20

Most COX 1 specific:
Aspirin, Sulindac, Ibuprofen, Flurbiprofen, Diclofenac, Naproxen, Celcoxib, Rofecoxib
Most COX 2 specific

Question 21

Common unwanted effects of NSAIDs

Answer 21

GI disturbance, dyspepsia, nausea and vomiting (due to effects of gastric mucosa), skin reactions e.g. rash, reversible renal insufficiency, can trigger asthma attacks
NSAIDs should be avoided in the elderly because this group of patients already suffer mild renal dysfunction

Question 22

Mild to moderate pain

Answer 22

Paracetamol- 15-20 mg/kg orally or rectally, max 1g
or
Ibuprofen- 10mg/kg, max 400mg, contraindicated if severe asthma, surgery in the last 2 weeks, GI bleeding/ulcer

Question 23

Moderate pain

Answer 23

Intranasal Fentanyl 1.5mcg/kg, max 100mcg
and
Paracetamol and or ibuprofen
+/- tramadol, morphine (orally), codeine

Question 24

Severe pain

Answer 24

Morphine IV 0.1mg/kg (0.05mg/kg if less than one year old/prior opiate)
Consider N2O or IN fentanyl prior to IV insertion depending on severity or the requirement for other therapy

Question 25

Aspirin

Answer 25

Non-selective and irreversibly inhibits both COX1 and COX2
Inhibits prostaglandins to combat inflammation and pain (300-900mg every 4-6 hours)
Blocks the formation of thromboxane in platelets, producing an inhibitory effect on platelet aggregation
Anticoagulant property makes aspirin useful for reducing the incidence of heart attacks

Question 26

Ibuprofen

Answer 26

Non selective COX inhibitor (200-400mg 3 x per day)
Milder antiplatelet effect
The analgesic, antipyretic and anti-inflammatory activity of NSAIDs is achieved mainly through inhibition of COX 2
Inhibition of COX 1 would be responsible for unwanted effects on platelet aggregation and the GI tract

Question 27

Paracetamol

Answer 27

COX-3, found in the brain and spinal cord is selectively inhibited by paracetamol > relieving pain and reducing fever without having unwanted GI side effects
Very effective tolerable analgesic, underused, safe for the majority
First step on WHO analgesic ladder
Should be used regularly in chronic pain alongside additional analgesia if needed
Can cause fatal hepatoxicity, but is safe when dosage kept within therapeutic guidelines
Be aware of the contents and effects of combination products

Question 28

Anti-pyretic effect of paracetamol

Answer 28

A centre in the hypothalamus regulates temperature, fever occurs when there is a disturbance of this thermostat, causing sweating and dilation of superficial blood vessels
Paracetamol works as a thermoregulator in the hypothalamus