Communication workshop OTC advice Flashcards
How to choose the correct product
Patient charcateristics Indication and contra-indications Formulation Dose Patient preference Red flag symptoms Evidence base Licensing considerations Referral criteria (conditional vs unconditional)
What information should you provide?
If a product is recommended: 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- be assertive
Pain perception
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)
Acute pain
Usually rapid in onset usually identifiable cause Limited duration Tends to get better Biological significance
Chronic pain
Not necessarily an identifiable cause Large emotional component Unpredictable duration Does not get better None or negative meaning
Pain is transmitted through three different levels:
Nociception: peripheral activation and release of pain mediators
Travel through primary nociceptors, C and Ad fibres
Pain gating: dorsal horn of the spinal cord
Travels through ascending and descending secondary fibres
Pain perception: The brain (thalamus, limbic and cortical systems)
Nociceptive pain
Stimulation of receptors that respond to heat, vibration, stretch and chemical stimuli released from damaged cells
Non-nociceptive pain
From within peripheral and CNS, no specific receptors, but nerve cells dysfunction
Treatment of somatic pain
NSAIDs, weak and strong opioids
Treatment of visceral pain
NSAIDs, weak and strong opioids
Treatment of neuropathic pain
Anti-depressants, anti-convulsants, anti-arrhythmics
What happens when tissues are damaged?
Release of chemical mediators e.g. bradykinin, histamine, 5-HT and inflammatory mediators e.g. prostaglandins
Activation of C fibres
Inflammation- a protective mechanism, moving plasma and leucocytes from blood into injured tissues, results is swelling, heat and pain, no beneficial function
Prostaglandins
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
Cyclooxygenase (COX)
Enzyme responsible for formation of prostaglandins
COX 1- always present in most cells
COX 2- induced in inflammatory cells
Vascular events of acute inflammation
Prostaglandins and histamine cause dilatation of the small arterioles
Causes increased blood flow
Causes stasis of the blood
Causes increase in permeability of postcapillary venules
Exudation of fluid- plasma and leukocytes into damaged area
Causes activation of the complement system, fibriolytic system, coagulation system and kinin system
NSAIDs
Most have three major types of effect:
Anti-inflammatory effects
Analgesic effect- decrease production of the prostaglandins that sensitise noiciceptors to inflammatory mediators such as bradykinin
Antipyretic effect- NSAIDs reset the thermostat by inhibition of E-type prostaglandin production in the hypothalamus
he primary action of NSAIDs is the inhibition of COX, most NSAIDs inhibit both isoenzymes but vary in he degree of inhibition of each
Anti-inflammatory effects of NSAIDs
NSAIDs reduce mainly those components of the inflammatory and immune response in which products of COX II action play a significant part, namely:
Decrease vasodilation
Decrease oedema (indirectly, the vasodilatation facilitates the action of mediators such as histamine which increase permeability of postcapillary venules)
Decreases pain
Common unwanted effects
Gastrointestinal disturbance, dyspepsia, nausea and vomiting due to effects on 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
Aspirin
Non-selective and irreversibly inhibits both COX 1 and COX 2
Inhibits prostaglandins, to combat inflammation and pain (300-900mg every 4-6h)
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 (75mg)
Ibuprofen
Non-selective COX inhibitor (200/400mg-400mg 3x per day)
Milder antiplatelet effect
The analgesic, antipyretic, and anti-inflammatory activity of NSADs is achieved mainly through inhibition of COX-2
Inhibition of COX-1 would be responsible for unwanted effects on platelet aggregation and the gastrointestinal tract
Paracetamol
COX-3, found in the brain and spinal cord is selectively inhibited by paracetamol, relieving pain and reducing fever without having unwanted gastrointestinal side effects
Anti-pyretic effect- a centre in the hypothalamus regulates temperature, fever occurs when there is a disturbance of this thermostat, causing sweating and dilatation of superficial blood vessels»_space; paracetamol works as a thermoregulator in the hypothalamus
First step on WHO analgesic ladder
Can cause fatal hepatoxicity, but is safe when dosage kept within therapeutic guidelines
