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  1. 1. 1 College of pharmacy Inflamation Prepared by *Miran Mustafa *Niga Taymoor *Frishta Ahmad Hawar Ezzat Nigar Mohammed Karmand Salih Group {C}
  2. 2. 2 Inflamation Is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, The classical signs of acute inflammation are pain, heat, redness, swelling, and loss of function. Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection. Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen. However, inflammation is a stereotyped response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen… Causes Burns Chemical irritants Frostbite Toxins Infection by pathogens Physical injury, blunt or penetrating Immune reactions due to hypersensitivity Ionizing radiation Foreign bodies, including splinters, dirt and debris Stress Trauma Alcohol Type of Inflamation 1-Acute inflammation is a short-term process, usually appearing within a few minutes or hours and ceasing upon the removal of the injurious stimulus.
  3. 3. 3 It is characterized by five cardinal signs : 1-Dolor (pain) 2- Calor (heat) 3-Rubor (redness) 4- Tumor (swelling) (loss of function)of function)Functio laesa-5 2-Chronic Inflamation If the condition causing acute inflammation is not resolved, the inflammation may pass to a longer term chronic phase. Also, some pathogies by their nature tend to directly provoke chronic rather than acute inflammation. Many of the features of acute inflammation continue as the inflammation becomes chronic, including increased blood flow and increased capillary permeability. Accumulation of white blood cells also continues, but the composition of the cells changes. inflammatory mediators Molecules that are released by immune cells during times when harmful agents invade our body.
  4. 4. 4 Procedure: 1- injection of anti-inflammatory drug. ( unknown 4 ) 2- wait 30 mins. 3- measure the thichness of the paw. ( 0.3 cm ) 4- injection of albumine. ( 1 unit ) 5- wait 30 mins. (20 mins ) 6- measure the thickness of the paw. ( 0.4 cm ) 7- wait 30 mins. (20 mins ) 8- measure the thickness of the paw. ( 0.32 cm ) Results: G1 / 0.15 → 0.5 Acetaminophen G2 /0.3 → 0.4 → 0.3 ASA ( Acetyl Salicylic Acid ) G3 /0.3 → 0.5 → 0.3 Dexamethasone G4 /0.3 → 0.4 → 0.32 Piroxicam
  5. 5. 5 Discussion The aim of this experiment is to Know the effect of {Dexamethasone ,piroxicam , ASA , Acetaminophen} in inflamation & to determin which one of them is more potent. We inject those drug to the paw of the rat and as the drug become more potent the paw of the rat become thinner acording to that the potensy of drug in which we use it is like that Dexamethasone piroxicam ASA Acetaminophen Dexamethasoneis a potent synthetic member of the glucocorticoid class of steroid drugs. It acts as an anti-inflammatory andimmunosuppressant, When injected in to the paw of the rat the sickness of paw was (0.3)& after (30 min.) the sickness was (0.5)& after another (20min.) the sickness of paw was (0.3) ,In comparision with other NSAIDs in wich we use it Dexamethason was the most potent . Mechanism of action Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. This complex binds to DNA elements (glucocorticoid response elements) which results in a modification of transcription and, hence, protein synthesis in order to achieve inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of dexamethasone are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. *Piroxicamis a non-steroidal anti-inflammatory drug of the oxicam class used to relieve the symptoms of rheumatoid and osteoarthritis,
  6. 6. 6 primary dysmenorrhoea, postoperative pain; and act as an analgesic, especially where there is an inflammatory component, When injected in to the paw of the rat the sickness of paw was (0.3)& after (30 min.) the sickness was (0.4)& after another (20min.) the sickness of paw was (0.32), It is less potent than Dexomethasone. Mechanism of action is a non-selective COX inhibitor possessing both analgesic and antipyretic properties. It undergoes enterohepatic circulation. *Acetyl Salicylic Acid (Asprin) is a salicylate drug, often used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. When injected in to the paw of the rat the sickness of paw was (0.3)& after (30 min.) the sickness was (0.4)& after another (20min.) the sickness of paw was (0.3). It is less potent than Dexomethasone & Paroxicam,The result Here is error this is may be because of the unaccuracy of measuring the thickness of the paw of the rat. Mechanism of action Aspirin's effects and respective mechanisms of action vary with dose: *Low doses (typically 75 to 81 mg/day) are sufficient to irreversibly acetylate serine 530 of cyclooxygenase (COX)-1, This effect inhibits platelet generation of thromboxane A2, resulting in an antithrombotic effect. *Intermediate doses (650 mg to 4 g/day) inhibit cyclooxygenase (COX)- 1 and COX-2, blocking prostaglandin (PG) production, and have analgesic and antipyretic effects.
  7. 7. 7 *High doses (between 4 and 8 g/day) are effective as antiinflammatory agents in rheumatic disorders; the mechanism(s) of action at these high doses may include both PG-dependent (particularly COX-2 dependent PGE2) and independent effects ,However, the usefulness of aspirin at these high doses is limited by toxicity, including tinnitus, hearing loss, and gastric intolerance.. *Acetaminophen: is a widely used over-the-counter analgesic and antipyretic ,Paracetamol is classified as a mild analgesic. It is commonly used for the relief of headaches and other minor aches and pains. When injected in to the paw of the rat the sickness of paw was (0.15)& after (30 min.) the sickness was (0.5)& after another (20min.) the sickness of paw was (0.5) Because has no anti-inflamatory effect so the sickness of paw was not change.. Mechanism of action Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX- 2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation
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