BIOL122 Lecture Notes - Lecture 2: Ascites, Ultimate Tensile Strength, Competitive Inhibition
Inflammation and NSAIDS:
Mediators of inflammation:
Inflammation is the body’s response to injury; injurious agents activate many
chemical factors from either:
i) Cells:
- Histamine
ii) Plasma
-complement cascade (they launch the inflammatory response)
Phases of inflammation:
Vascular phase: changes in vascular calibre and flow
1) Vasoconstriction (lasting only seconds)
2) Vasodilation: increased blood flow, redness and warmth
3) Increased vascular permeability: Pores enlarge- leaky capillaries, swelling
(oedema)
• Exudate
• Transudate
Cellular phase: emigration of WBC
• Leukocytes are recruited from blood
- Neutrophils
- Monocytes- macrophages
• Leukocytes migrate to site of injury via chemotaxis
• Leukocytes activated to perform function- phagocytes
Repair phase: repair cannot occur until injurious agent is removed
• By mitosis and scar formation
• Inflammation is essential for healing
Cardinal signs of inflammation:
- Redness
- Warmth
- Swelling
- Pain
- Loss of
function
Chronic inflammation
• Persistent due too:
+ failure to remove offending pathogen
+ autoimmune disease
+ persistent presence of irritant
• Lasts 2 weeks or longer
• WBC involved are typically macrophages and lymphocytes
• Tissue destruction
Systemic effects of inflammation
• Fever
• Malaise- general feeling of discomfort
• Anorexia- loss of appetite
• Accelerated degeneration of skeletal muscle proteins
• Hepatic protein synthesis
• Leucocytosis- above normal range of WBC
Pharmacology:
Anti- inflammatory drugs (2 main groups)
1) Glucorticoids (steroid drugs)
- Cortisone, cortisol, prednisolone
2) Non-steroidal anti-inflammatory drugs (NSAIDS)
- Aspirin, ibuprofen
Glucorticoids:
• Pharmacodynamics: prevent formation of key chemicals that mediate
inflammation
• Pharmacokinetics: varied
• Pharmacological effects:
- Anti- inflammatory effects: blocking formation of pro- inflammatory
cytokines whilst promoting pro- inflammatory cytokines
- Immunosuppressant effects: decrease lymphocyte number and
function
• Indications: autoimmune disease, allergies, asthma
Glucocorticoids:
• Adverse effects:
- Supress body’s response to injury or infection
- Prolong wound healing
- Supress body’s capacity to synthesise glucorticoids- adrenal shock
• Drug interactions
• Contraindications
Non- steroidal anti- inflammatory drugs (NSAIDS)
• Pharmacodynamics: competitive inhibition of COX-1 and COX- 2 enzymes
• Pharmacokinetics
• Pharmacological effects
• Indications
Document Summary
Inflammation is the body"s response to injury; injurious agents activate many chemical factors from either: Vascular phase: changes in vascular calibre and flow: vasoconstriction (lasting only seconds, vasodilation: increased blood flow, redness and warmth, increased vascular permeability: pores enlarge- leaky capillaries, swelling (oedema, exudate, transudate. Cellular phase: emigration of wbc: leukocytes are recruited from blood. Monocytes- macrophages: leukocytes migrate to site of injury via chemotaxis, leukocytes activated to perform function- phagocytes. Repair phase: repair cannot occur until injurious agent is removed: by mitosis and scar formation. + persistent presence of irritant: lasts 2 weeks or longer, wbc involved are typically macrophages and lymphocytes, tissue destruction. Systemic effects of inflammation: fever, malaise- general feeling of discomfort, anorexia- loss of appetite, accelerated degeneration of skeletal muscle proteins, hepatic protein synthesis, leucocytosis- above normal range of wbc. Anti- inflammatory drugs (2 main groups: glucorticoids (steroid drugs) Cortisone, cortisol, prednisolone: non-steroidal anti-inflammatory drugs (nsaids)
