Applied Pharmacology Flashcards
Define the difference between a drug and a medicine.
A drug is a chemical substance that can have a positive or negative biological effect on the body, where as a medicine can contain more than one drug/substance and the intention is to have a positive/therapeutic effect.
Outline the mechanism and unwanted side effects of an NSAID such as aspirin.
Bind to and block COX1 enzymes to halt the production of prostanoids and provide gastric protection, blood flow (thinning) and platelet aggregation but side effects include aspirin-induced asthma and gastritis, reduce renal filtration.
Outline the mechanism of action and unwanted side effects of a strong opioid such as morphine.
Morphine will act as an agonist and bind to G-protein coupled receptors. This causes cellular hyperpolarisation, decreasing neuronal/nerve cell excitability and sensitivity, reducing nociception, and elicit analgesia effects. Side effects include constipation, depression of cough reflex, nausea, and respiratory depression.
Outline the mechanism and unwanted side effects of paracetamol.
Although not anti-inflammatory, paracetamol targets COX2 enzyme and can reduce prostaglandin production or activate cannabinoid receptors, which produces analgesic and antipyretic effects. Side effects include skin reactions, nausea, loss of appetite and stomach cramps.
Describe the WHO analgesic ladder and explain why is has been increasingly been brought into question.
- Mild pain = non-opioid NSAIDs
- Moderate pain = mild opioids with or without NSAIDs
- Severe pain = strong opioids with or without steps 1 and 2
The key concept of the ladder is that it is essential to have adequate knowledge about pain, to assess its degree in a patient through proper evaluation, and to prescribe appropriate medications and improve quality of life by treating acute pain.
Describe the physiological mechanism behind aspirin induced asthma.
Because aspirin targets COX1 enzymes and halts production of prostaglandins, the chain completely moves the other way and over produces leukotrienes, which are bronchoconstrictors and therefore, promote asthma symptoms.
What does NSAIDs stand for?
Non-steroidal anti-inflammatory drugs.
Describe the arachidonic acid cascade.
First produced by phospholipase A2, then converted into many compound molecules. COX is a pivotal enzyme that is made which produce tissue specific molecules and are converted into prostanoids. There are direct links to nociception, activation and sensitisation of free nerve endings and this is what NSAIDs block.
Describe the properties of COX1 enzymes.
They are in most tissues and cells, but mainly lie in the endoplasmic reticulum. The effects they have are gastric protection, blood flow and platelet aggregation.
Describe the properties of COX2 enzymes.
They are in mast cells, fibroblasts, macrophages, endothelial cells and mainly lie in the nuclear membrane. The effects they have are inflammation, pain and fever.
What are the 4 main therapeutic effects of NSAIDs.
Anti-inflammatory, analgesic, antipyretic, platelet aggregation.
Outline the anti-inflammatory effects of NSAIDs.
COX2 derived prostaglandins inhibition, which are vasodilators and release other vasodilators (substance P and histamine) which leads to:
- Reduced vasodilation, oedema, swelling, redness, neurogenic inflammation
Outline the analgesic effects of NSAIDs.
Inhibition of COX2 derived prostaglandins in dorsal horn which leads to reduced central and peripheral sensitisation of free nerve endings and reduced rate of nociception/pain.
Outline the antipyretic effects of NSAIDs.
Binding to COX2 enzymes reduces PGE2 production which inhibits temperature sensitive neurons in the hypothalamus, this resets the homeostatic point in the body and wide fever is reduced.
Outline the platelet aggregation effects of NSAIDs.
COX1 inhibition reduced thromboxane A2 production which reduces the creating network of fibrin and platelets that create blood clots. Acts as blood thinners and new platelet production is required.
