SRT Live Lecture A on Anti-Inflammatory Drugs Flashcards
(30 cards)
What are the three major modes of cell communication?
- Neural: neurotransmitters via nerves (e.g., autonomic nervous system)
- Endocrine: hormones via bloodstream
- Local mediators: paracrine signals for nearby cells (e.g., histamine, prostaglandins)
Why is inflammation essential despite its potential for harm?
- Facilitates healing
- Responds to tissue injury and infection
- Alerts body to damage (e.g., pain, redness, swelling)
What are local mediators and their typical characteristics?
- Act in a confined area
- Chemically unstable (labile)
- Rapidly degraded or diluted
- Include histamine, prostaglandins, leukotrienes, nitric oxide
Where are mast cells typically found in the body?
- Skin
- Gut
- Airways (sites of environmental contact)
What activates mast cells in allergic reactions?
- Allergen binds to IgE antibodies
- Cross-linking of IgE on FcεRI receptors
- Degranulation and histamine release
What is histamine’s role in inflammation?
- Vasodilation (redness)
- Increased vascular permeability (swelling)
- Stimulates sensory neurons (itching and flare)
What is the “triple response” of histamine?
- Redness (vasodilation)
- Swelling (vascular leak)
- Flare (neural stimulation causing wider redness)
What are H₁ receptor antagonists and their main use?
- Antihistamines
- Block histamine at H₁ receptors
- Used to treat allergies (e.g., hay fever, urticaria)
What differentiates first- and second-generation antihistamines?
First-gen: Cross blood-brain barrier → sedative
Second-gen: Minimal brain penetration → less drowsy (e.g., cetirizine, loratadine)
What caused the 2016 thunderstorm asthma event in Melbourne?
- High grass pollen + storm
- Pollen particles broken down into smaller fragments
- Deep inhalation triggered widespread mast cell activation in lungs
What are eicosanoids and their major classes?
- Eicosanoids are lipid-derived mediators.
- Major classes: prostaglandins, thromboxanes, and leukotrienes.
What is the precursor of prostaglandins and leukotrienes?
- Arachidonic acid
- Released from membrane phospholipids by phospholipase A₂
What is the rate-limiting step in prostanoid synthesis?
- Activation of phospholipase A₂
- Frees arachidonic acid from membrane
Which enzymes convert arachidonic acid into prostanoids?
- Cyclooxygenase (COX) → PGG₂ → PGH₂
- Tissue-specific synthases convert PGH₂ into bioactive prostaglandins and thromboxanes
What does lipoxygenase do?
- Converts arachidonic acid to leukotrienes
- Especially cysteinyl leukotrienes (important in asthma)
What biological effects are mediated by prostanoids?
- Vascular tone (vasodilation/constriction)
- Platelet aggregation (promotion or inhibition)
- Gastric protection (mucus secretion, acid suppression)
- Kidney perfusion
- Pain and fever enhancement
How do prostanoids enhance pain responses?
- Act synergistically with mediators like bradykinin
- Amplify pain signal and duration
What is the mechanism of prostanoid action?
- Bind to specific G protein-coupled receptors (GPCRs)
- Activate intracellular signaling pathways
What is the origin of aspirin (acetylsalicylic acid)?
- Derived from salicylic acid in willow bark and spirea
- Modified to reduce GI irritation
What are the three main actions of NSAIDs?
- Anti-inflammatory
- Analgesic
- Antipyretic
How do NSAIDs exert their pharmacological effects?
- Inhibit cyclooxygenase (COX)
- Prevent prostanoid synthesis
What are COX-1 and COX-2?
- COX-1: Constitutive; involved in physiological functions
- COX-2: Inducible during inflammation
How do NSAIDs differ from corticosteroids?
- NSAIDs: Inhibit COX → reduce prostanoid synthesis
- Corticosteroids: Broader anti-inflammatory effects → gene expression modulation
Which common over-the-counter drugs are NSAIDs?
- Aspirin
- Ibuprofen
- Naproxen
