135 - NSAIDS, Anti-inflammatories Flashcards
(24 cards)
List the effects of COX-1 (GOOD) enzyme stimulation:
Always present in body
Stimulated by usual wear and tear of body, results in normal repair
List the effects of COX-2 (BAD) enzyme stimulation:
Produces prostaglandins associated with inflammation and in kidney for normal renal function
Responds to injury and results in inflammation
Not always present in body
List the actions / effects of prostaglandins in the inflammatory process:
Areas of inflammation – vasodilation, pain, swelling, impaired cellular function
List the actions / effects of thromboxanes in the inflammatory process:
Vasoconstriction, platelet aggregation
List the actions / effects of leukotrienes in the inflammatory process:
Inflammatory mediators and respond to allergy and inflammation, bronchoconstriction, vascular permability
Discuss the anti-inflammatory effects of NSAIDs:
Decrease inflammation antipyretic
Analgesia anticancer
Platelet aggregation inhibition
Discuss the inhibition of platelet aggregation effects of NSAIDs:
Inhibits thromboxane production
What is the mechanism of action for NSAIDs:
Inhibits cyclooxygenase
May decrease prostaglandin activity
Decrease phagocytic function of neutrophils
List the side effects of NSAIDs:
GI irritation GI ulcers
Anorexia diarrhea
Decrease renal blood flow hepatotoxicity
Define analgesia.
Inability to feel pain
Define inflammation as to causes and components:
Occurs as response to sub lethal injury to cells
Components consist of increased blood flow to area, increased capillary permeability, pain, chemotaxis leads to phagocytosis, coagulation and fibrinolytic pathways activated
List some of the damage that the inflammatory processes can do:
Allergy shock edema proud flesh
List the cardinal signs of inflammation:
Heat Edema Erythema Pain Loss of function
List the general categories of activity of the glucocorticosteroids:
Anti-inflammatory anti-shock
Antipruritic immunosuppressive
Metabolism influence on CHO, fat, protein
Explain how glucocorticoids work to produce an anti-inflammatory effect:
Stabilize cell membranes, stabilize lysosomal membranes, disrupt histamine synthesis, inhibit interleukin synthesis, reduce exudative process
List the possible uses for glucocorticoids:
Decrease swelling, pain after inury
Decrease pruritis, hypersensitivity and allergic reactions of skin and mucous membranes
Alter immune response in autoimmune disorders, aplastic anemia
Rupture lymphocytes in neoplasia’s
Shock reversal
Diagnostics
Replacements
List some drawbacks to the use of glucocorticosteroids:
Overuse in medicine, no pain or fever relief
List the common side effects of glucocorticosteroids:
Polyuria polydipsia
Polyphagia weight gain
GI ulcers bleeding
Depressed healing infection susceptibility
Muscle weakness thin, dry, coarse fur
Behavior changes iatrogenic Cushings or Addisons Dz
K+ loss Na, H20 retention > edema, ascites
Abortion
Discuss why glucocorticosteroids are tapered off after therapeutically using them for more than two days.
After administration, the body ceases manufacture of cortisol; the body can not recover fast enough to prevent problems from this
Explain the role of histamines in inflammation:
Chemical inflammatory mediator and responsible for hypersensitive reactions
List the effects of histamine on the body:
Histamine causes vessel dilation, capillary permeability, smooth muscle spasm, glandular secretion increase, bronchiole constriction
Explain how antihistamines function – mechanism of action:
They prevent histamine from attaching to receptor sites
State the effect of H1 receptor / histamine 1 receptor stimulation:
Capillary vasodilation, increased capillary permeability, results in flushing of face, headache and tends to lower arterial pressure. Contraction of smooth muscles, such as bronchial and digestive.
State the effect of H2 receptor / histamine 2 receptor stimulation:
increase of gastric secretion of HCl, the main H2 effect, cardiac stimulation, vasodilation: stimulation of H2 receptors induces vasodilation, but the H2 vasodilator effect of slower onset and more durable than that of H1, small bronchodilator effect.
