Pharmacology Flashcards
NSAIDs
MOA - All inhibit COX 1 and 2 enzymes, preventing conversion of arachdoinc acid to prostaglandins, reducing inflammation
Used for - Mild pain, swelling etc
SE: GI irritation/peptic ulcers, decreased renal BF, cardiovascular risk (heart failure, MI) and bleeding risk due to inhibition of PGI2, PGE2 and TXA2 (bleeding risk) respectively
E.g. Ibuprofen, high dose aspirin, naproxen,
COX 1 enzyme function
- Generates prostaglandins
Protects stomach from HCl (PGI2), involved in platelet aggregation (TXA2) and renal blood flow (PGE2)
- Found in BV, smooth muscles, mesothelial cells
High dose aspirin, ibuprofen, naproxen
NSAIDs
COX 2 enzyme function
Generates prostaglandins - Induce inflammatory cells E.g. macrophages
Paracetamol
MOA - Inhibits prostaglandin synthesis via inhibition of COX 3 enzyme and or PGE2 in CNS - helps regulate prostaglandin synthesis in the hypothalamus, resetting thermostat)
- Used as an analgesic and antipyretic (NOT an NSAID as it doesn’t reduce inflammation)
Used for - mild pain without inflammation
SE - rare at normal doses, possible allergic reactions, rarely depletion of gluthoine causing acidosis
CI - Caution given those to with liver impairment as its metabolised by the liver and can lead to liver damage due to accumulation if not metabolised
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Methotrexate, hydroxycloroquine, Sulfasalazine
DMARDs
Prednisolone, hydrocortisone/cortisol
Glucocorticoids
Opioids
- Moderate or strong analgesic effect
MOA - Bind to opioid receptors located widely on nerve cells in the CNS, Inhibiting the release of neurotransmitters blocking pain message being sent to CNS.
SE - common - sedation, drowsiness, apathy, cognitive impairment, tranquility
Severe - depression of respiration from overdose (GF), suppress cough centre of the brain, pupillary constriction, nausea and vomiting (chemoreceptor trigger zone activated), relieve diarrhoea, can cause itching and reactions via histamine release
CI - Impaired pulmonary function, hepatic/renal dysfunction (can’t process), hypothyroidism and head injuries that can impair cognition
E.g. Mild - codeine, dihyrocodiene, tramadol,
Strong - morphine, oxycodone, methadone,
Opioid receptors
Mu 1 (G protein) - most common, main analgesic affect responsible for central interpretation of pain
Mu 2 (G protein) - Respiratory depression, spinal analgesia, physical dependance, euphoria
Kappa (G protein) - Vasodilation, provide analgesic effect, euphoria and dysphoria
Delta (G protein)- Analgesic affect causing a reduction in gastric mobility
- Nalaxone is a competitive antagonist for the Mu receptors
Oxycodone, methadone, morphine
Strong opioids
Bisphosphates
- Knock out osteoclasts to prevent bone weakening
- Used in osteoporosis
E.g. Alendronic acid, risedronate and alendronate
SE - Heart burn, GI irritation, osteonecrosis of jaw and atypical femoral fracture
DMARDs (disease modifying anti rheumatic drugs)
Used for delaying progression of rheumatoid arthritis (more long term and contrast to NSAIDs and steroids
E.g. Methotrexate - Inhibits dihydrofolate reductase (folic acid) and suppresses immune system (don’t give during pregnancy)
SE - GI irritation, renal and liver toxicity, oral sores, hypersensitivity reactions, blood disorders
*Folic acid reduces risk of bone marrow suppression
Others include - Hydroxycloroquine and sulfasalazine,
Codiene, dihydrocodiene, tramadol
Mild opioids
Alendronic acid, risedronate, alendronate
Osteoblast drugs
Glucocorticoids
Mediate stress, control homeostasis and are used to dampen down immune system and reduce inflammation such as inflammatory cytokines E.g. Carpel tunnel syndrome to reduce inflammation
MOA - Inhibit phospholipase A2 from converting membrane phospholipids into arachidonic acid, reducing prostaglandin and leukotriene (allergic response) levels
- Inhibits insulin by binding to receptor widely expressed in cytoplasm leading to increased blood glucose levels (energy is needed during stress), - - -
SE - Can induce type 2, weight gain…
E.g. Prednisolone and hydrocortisone/cortisol
