Communication- OTC advice Flashcards Preview

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Flashcards in Communication- OTC advice Deck (28):

How to choose the correct product

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


What info should you provide?

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


The sensation of pain is increased by:

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


The sensation of pain is decreased by:

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


Features of acute pain

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


Features of chronic pain

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


Pain is transmitted through 3 different levels:

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



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



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


To treat somatic/ visceral pain (nocicpetive)

NSAIDs, weak and strong opioids


To treat neuropathic pain (non-nociceptive)

Anti-depressants, anti-convulsants, anti-arrhythmics


What happens when tissues are damaged?

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



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



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


Inflammatory pathway

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


Vascular events of acute inflammation

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



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


Anti-inflammatory effects of NSAIDs

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


Primary action of NSAIDs

The primary action of NSAIDs is the inhibition of COX
Most NSAIDs inhibit both isoenzymes but vary in the degree of inhibition of each


COX selectivity

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


Common unwanted effects of NSAIDs

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


Mild to moderate pain

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


Moderate pain

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


Severe pain

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



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



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



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


Anti-pyretic effect of paracetamol

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