Generally speaking, the so-called anti-inflammatory drugs in the general population refer to antibiotics, anti-inflammatory drugs are anti-inflammatory drugs, and anti-inflammatory drugs are antibiotics.
If it is true, there are other drugs besides antibiotics, such as glucocorticoid: dexamethasone, non-steroidal anti-inflammatory drug: paracetamol and so on. The difference is that the anti-inflammatory mechanism is different. Antibiotics directly inhibit pathogens. As long as the pathogen is sensitive to antibiotics and suppressed, the inflammatory reaction will be eliminated. Corticosteroids suppress immunity, and when the fight is not fierce, the inflammatory reaction disappears naturally, but at the expense of immunosuppression, the pathogen will be more fierce; Non-steroidal anti-inflammatory drugs inhibit the synthesis of endogenous substances that mediate inflammation, and the inflammatory response is weak without messengers. Corticosteroids, non-steroidal anti-inflammatory drugs and antibiotics are described in detail below:
glucocorticoid
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Glucocorticoid is a steroid hormone secreted by adrenal cortex, which can regulate the biosynthesis and metabolism of sugar, fat and protein, and also has anti-inflammatory effect. It is called "glucocorticoid" because its activity of regulating glucose metabolism was first recognized by people.
The basic structural features of glucocorticoids include C3 carbonyl, δ 4 and 17β ketol side chains of adrenocortical hormones, and 17α-OH and1β-oh peculiar to glucocorticoids.
At present, the concept of glucocorticoid includes not only endogenous substances with the above characteristics and activities, but also many synthetic drugs with similar structures and activities after structural optimization. At present, glucocorticoid is a widely used drug in clinic.
catalogue
[hide]
* 1 mechanism of action
* 2 Adverse reactions
* 3 development history
* 4 Clinical application
* 5 stands for drugs.
[edit]
Mechanism of action
* Physiological origin and secretion regulation
Glucocorticoid is a metabolic regulation hormone secreted by fascicular zone in the middle layer of adrenal cortex.
The secretion of glucocorticoid in the body is mainly regulated by hypothalamus-anterior pituitary-adrenal cortex axis. Corticotropin-releasing hormone (CRH) secreted by hypothalamus enters the anterior pituitary to promote the secretion of corticotropin (ACTH), which in turn can promote the secretion of cortisol. Conversely, the increase of glucocorticoid concentration in blood can inhibit the secretion of CRH and ACTH in hypothalamus and anterior pituitary, thus reducing the secretion of glucocorticoid. The increase of ACTH content can also inhibit the secretion of CRH from hypothalamus, which is a negative feedback process and ensures the balance of glucocorticoid content in the body.
The secretion of endogenous glucocorticoid has a circadian rhythm, with the lowest content at midnight and the highest content in the morning. In addition, under stress, the secretion of endogenous glucocorticoid will surge to about 10 times of the usual level.
* Physiological effects
1. Promote gluconeogenesis, reduce the uptake and utilization of glucose by peripheral tissues, increase blood sugar, and increase glycogen synthesis in liver and muscle.
2. Promote protein metabolism in extrahepatic tissues, reduce protein synthesis, and increase amino acid content and urea nitrogen excretion in serum.
3. Promote fat catabolism, reduce anabolism, increase the content of glycerol and fatty acid in blood, and increase the content of cholesterol in blood, thus activating the activity of subcutaneous lipase in limbs, decomposing subcutaneous fat in limbs and redistributing it to face, chest, abdomen, back and buttocks, resulting in centripetal obesity.
4. It has a weak mineralocorticoid-like effect, and can show the effect of potassium excretion and sodium preservation.
* pharmacological action
1. Anti-inflammatory effect: This mainly comes from
1. Increase vascular tension, reduce vascular permeability, antagonize the dilating effect of inflammatory mediators such as histamine on blood vessels, relieve local congestion, and reduce the exudation of white blood cells and body fluids.
2. Stabilize lysosomal membrane, reduce the release of cathepsin and hydrolase caused by lysosomal rupture, and reduce the release of tissue decomposition and inflammatory mediators.
3. Inhibit the recruitment of neutrophils, monocytes and macrophages to inflammatory sites.
4. Inhibit the activity of phospholipase A2, and reduce the conversion of membrane phospholipids to arachidonic acid, which is the biosynthesis precursor of prostaglandin, leukotriene, platelet activating factor and other inflammatory mediators.
5. Inhibit the synthesis and release of cytokines related to immune response such as interleukin, tumor necrosis factor and interferon.
6. Inhibit DNA synthesis and capillary proliferation of fibroblasts, hinder collagen deposition and inhibit granulation tissue formation.
2. Immunosuppressive effect: In addition to the immune system-related effects mentioned in the anti-inflammatory effect, glucocorticoid can also inhibit the transformation of B cells into plasma cells and reduce the production of antibodies; Inhibit humoral immunity and reduce the release of aggressive substances caused by antigen-antibody reaction.
3. Antitoxin effect: Although glucocorticoid has no effect on bacterial exotoxin, it has a strong anti-bacterial endotoxin effect, reduces the release of endogenous heat source substances, has a good antipyretic effect and greatly improves poisoning symptoms.
4. Anti-shock effect: This is the result of comprehensive effects of anti-inflammatory immunosuppression and anti-endotoxin. Glucocorticoid can inhibit vasoconstriction of adrenalin, norepinephrine, vasopressin, angiotensin, 5-HT and other transmitters, improve microcirculation, and its role of stabilizing lysosomes can effectively reduce the release of myocardial inhibitory factors, thus maintaining normal cardiac output and maintaining visceral blood circulation without being affected by vasoconstriction.
5. Affect the hematopoietic system: increase the production of red blood cells and hemoglobin, increase platelets and fibrinogen, increase the number of neutrophils entering the blood circulation, and reduce eosinophils and basophils of monocytes.
6. Central excitement: reduce the content of GABA in the brain, cause central excitement and produce euphoria, excitement, insomnia and other symptoms.
7. Promote gastric acid secretion
8. Inhibit the secretion of melatonin in pineal gland.
9. Reduce the intake, removal and transformation of iodine ions by thyroid.
[edit]
counteraction
It is not difficult to see from the above mechanism that the adverse reactions of glucocorticoid are as follows.
1. Iatrogenic adrenocorticosis: A series of symptoms caused by high glucocorticoid level in the body due to long-term high-dose application of glucocorticoid, including muscle atrophy (caused by long-term negative nitrogen balance), mostly occurring in the major muscles of limbs; Skin thinning; Centripetal obesity; Acne; Increased body hair; Hypertension; Hyperlipidemia; Hypokalemia (will be combined with muscle atrophy, causing muscle weakness); Increased urine sugar; Osteoporosis
2. Induce or aggravate the infection or transfer the potential infection focus in the body: This is mainly because glucocorticoid only has anti-inflammatory effect and can't really kill the pathogen causing infection, and glucocorticoid can also inhibit immunity, reduce the body's ability to resist bacterial, viral and fungal infections, and greatly increase the probability of the deterioration and spread of infection focus.
3. Cause peptic ulcer: Glucocorticoid can stimulate the secretion of gastric acid and pepsin, reduce the resistance of gastric mucosa to digestive juice, and induce or aggravate gastric or duodenal ulcer, which is called steroid-induced ulcer. Steroid-induced ulcer is characterized by superficial and multiple symptoms, which often occur in the anterior pyloric sinus, with few hidden symptoms and high rate of bleeding and perforation.
4. Induced pancreatitis and fatty liver.
5. Pregnant women can cause fetal malformation in the first three months of pregnancy, and high-dose application in the late pregnancy can inhibit fetal hypothalamus-anterior pituitary, leading to adrenal cortex atrophy and postpartum cortical insufficiency.
6. Iatrogenic adrenocortical insufficiency: Due to the negative feedback mechanism of hypothalamus-anterior pituitary-adrenocortical axis caused by long-term use, the secretion of endogenous adrenocortical hormone will be inhibited, and rebound phenomenon and drug withdrawal reactions will occur after drug withdrawal suddenly. After stopping the drug for half a year, severe stress will lead to symptoms of adrenal insufficiency, such as nausea, vomiting, loss of appetite, hypoglycemia, hypotension, shock and so on.
7. Induced schizophrenia and epilepsy
[edit]
Development history
Since 1855, people have been studying the physiological function and clinical application of adrenocortical hormone. 1927, Rogoff and Stewart used adrenal homogenate extract to keep dogs alive, which proved the existence of adrenal cortical hormone. According to this experiment, some people speculated that the biological activity of the extract was caused by a single substance, but later people separated 47 compounds from the extract, including endogenous glucocorticoid hydrocortisone and cortisone.
Early glucocorticoid drugs were all extracted from homogenate of animal organs, and the production cost was very high. Later, with the development of steroid chemistry and organic synthesis, the total synthesis of steroid hormones was realized, and any steroid hormone can be synthesized from the simplest organic compounds. However, considering the actual production cost, people generally use diosgenin as the starting material for synthesis. Diosgenin is a terpenoid glycoside extracted from the rhizome of Dioscorea opposita and Dioscorea nipponica Makino of Dioscoreaceae. Its price is low, and the use of diosgenin greatly reduces the production cost.
On the basis of hydrocortisone synthesis, people continue to study the structural optimization of glucocorticoid. Triamcinolone acetonide, a steroid compound of 16α- hydroxyl, was extracted from the urine of a patient with renal cancer. It was found that it has good glucocorticoid effect and does not cause sodium retention like hydrocortisone.
By studying the metabolic process of hydrocortisone in vivo, dexamethasone with better stability, better anti-inflammatory activity and lower sodium retention was found in 1958.
On the basis of dexamethasone, people have developed betamethasone, beclomethasone, fluoxetine and other drugs by introducing methyl and halogen structures into steroid mother rings.
[edit]
clinical application
* Clinical application
1. Treating acute or chronic adrenocortical hypofunction
2. Severe acute infection, in which toxic infection accompanied by shock or inflammatory symptoms caused by infection poses a threat to the patient's life. Glucocorticoids are used to inhibit the inflammatory symptoms and make the patient pass the critical period.
3. Anti-shock: These drugs will have beneficial effects on all kinds of shock.
4. Treat autoimmune diseases and allergic diseases. Because these drugs can inhibit immune response, they also have a good inhibitory effect on autoimmune diseases and allergic reactions. They can be used to treat rheumatoid diseases, systemic lupus erythematosus, myasthenia gravis and other diseases. In addition, these drugs can also be used to inhibit the rejection after organ transplantation to ensure the safe survival of transplanted organs.
5. Prevent the inflammation of important organs and the formation of epileptic marks: Inflammation and epileptic marks of important organs such as meninges, pleura, peritoneum, pericardium, joints and eyes will cause serious consequences, and the use of glucocorticoid in the early stage of infection can alleviate this damage.
6. Glucocorticoid can also treat blood diseases, including acute lymphoblastic leukemia, aplastic anemia, granulocytopenia, thrombocytopenia and allergic purpura.
7. The anti-inflammatory effect of glucocorticoid can be used for local treatment of some skin diseases, such as contact dermatitis, eczema and psoriasis.
* Rational use of glucocorticoid
When using glucocorticoid to treat infectious diseases, we should pay attention to rational drug use. Because glucocorticoids can quickly inhibit some inflammatory reactions in a short time and get good "curative effect", some doctors often use glucocorticoids to treat infections in order to have a good therapeutic effect, but it is actually not helpful for patients' recovery. This can be clearly seen from the mechanism of action of glucocorticoid mentioned above. Therefore, we should use glucocorticoid carefully. Only when the inflammatory reaction caused by infection is serious enough to threaten the patient's life can glucocorticoid be used in large doses for a short time to alleviate the symptoms.
Long-term use of glucocorticoids to treat chronic diseases, such as autoimmune diseases, should pay attention to rational use of the circadian rhythm of endogenous glucocorticoids secretion. Under normal circumstances, the concentration of glucocorticoids in the human body can reach four times that of the lowest in the morning. Taking glucocorticoids in the morning can synchronize the changes of exogenous and endogenous glucocorticoids in blood, reduce the influence on hypothalamus-anterior pituitary-adrenocortical axis and reduce the feedback inhibition on hypothalamus-anterior pituitary.
[edit]
Representative drugs
hydrocortisone
prednisone
dexamethasone
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Non-steroidal anti-inflammatory drugs
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Non-steroidal anti-inflammatory drugs
catalogue
[hide]
* 1 mechanism of action
* 2 Adverse reactions
* 3 development history
* 4 Clinical application
* 5 stands for drugs.
[edit]
Mechanism of action
Inflammation is an immune response of the body against infection. Prostaglandin is an important factor in mediating inflammatory response, which can dilate blood vessels, increase vascular permeability and enhance the role of other inflammatory mediators. Arachidonic acid is the precursor of prostaglandin biosynthesis, while phospholipid, which constitutes cell membrane, is the precursor of arachidonic acid biosynthesis. It is epoxidase that catalyzes the conversion of arachidonic acid into prostaglandin. At present, there are two kinds of cyclooxygenase in human body, namely cyclooxygenase 1 and cyclooxygenase-2, which are mainly distributed in blood vessels, stomach and kidneys, and cyclooxygenase-2 is mainly composed of cytokines in inflammatory environment.
Non-steroidal anti-inflammatory drugs can inhibit the activity of arachidonic acid cyclooxygenase, which is necessary for prostaglandin biosynthesis, reduce prostaglandin synthesis and inhibit inflammatory reaction. In addition, non-steroidal anti-inflammatory drugs can also inhibit the activity of phosphodiesterase, which can increase the concentration of cAMP in cells, thus stabilizing the lysosomal membrane and reducing the release of lysosomes, thus inhibiting the inflammatory reaction. This mechanism is essentially different from glucocorticoid, which is an anti-inflammatory drug with steroid structure.
The inhibitory effect of non-steroidal anti-inflammatory drugs on cyclooxygenase is reversible, and the inhibitory reaction is a balanced reaction. Its curative effect is closely related to the blood concentration, but there is one exception: acetylsalicylic acid, the famous aspirin. The acetyl group of aspirin can irreversibly combine with serine, the active center of cyclooxygenase, and irreversibly inhibit the activity of cyclooxygenase.
[edit]
counteraction
The mechanism of NSAIDs is mainly to inhibit cyclooxygenase. Because cyclooxygenase 1 is mainly distributed in blood vessels, stomach and kidney, prostaglandin catalyzed by cyclooxygenase has the function of protecting digestive tract mucosa, and the inhibition of cyclooxygenase by non-steroidal anti-inflammatory drugs will reduce the protective effect of prostaglandin on digestive tract mucosa. In addition, most non-steroidal anti-inflammatory drugs are weak acids in structure, which have a certain acidity and have a strong stimulating effect on the digestive tract. The main adverse reaction of non-steroidal anti-inflammatory drugs is digestive tract injury. Some drugs, such as piroxicam, will cause serious peptic ulcer if used for a long time.
[edit]
Development history
Long ago, people found that willow bark has certain antipyretic, analgesic and anti-inflammatory effects. 1838 Salicylic acid was extracted from willow bark, and 1860 synthesized this compound artificially. 65438-0875 found that sodium salicylate has antipyretic, analgesic and anti-inflammatory effects and is used for clinical treatment. 1853, Charles Frederic Gerard synthesized acetylsalicylic acid from salicylic acid and acetic anhydride, but it failed to attract people's attention. German chemist Hoffman, 65438-0898, worked in Bayer Pharmaceutical Factory, synthesized and used in the treatment of rheumatoid arthritis, with excellent curative effect. 1899 was introduced into clinic by Dreser and named aspirin. Aspirin is one of the most widely used drugs at present.
Another non-steroidal anti-inflammatory drug, paracetamol, which is widely used in clinic, was found in the physiological function and metabolism of aniline as a dye.
Pyrazolone non-steroidal anti-inflammatory drug is a structural modification product of quinine, an antimalarial drug. The earliest pyrazolone non-steroidal anti-inflammatory drug was antipyrine, 1884, which was used clinically, but it was gradually eliminated because of its possible adverse reactions of leukopenia and agranulocytosis. China stopped using antipyrine in 1982, but the pyrazolone NSAID developed after the structural modification of antipyrine is still active in clinic.
Aryl alkanoic acid non-steroidal anti-inflammatory drugs, including bromophenol, are a new type of non-steroidal anti-inflammatory drugs that have developed rapidly in recent years. According to the structure of serotonin, an inflammatory mediator, 196 1, indomethacin was synthesized, and its anti-inflammatory activity was five times that of cortisone.
[edit]
clinical application
* Please help to supplement.
[edit]
Representative drugs
* Aspirin
* Paracetamol
The snake stick "non-steroidal anti-inflammatory drug" symbolizing medicine and doctors is an unfinished small work related to medicine. You are welcome to actively edit or modify and expand its content.
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Page classification: small medical works | drugs
antibiotic
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catalogue
[hide]
* 1 concept
* 2 uses
* 3 Source
* 4 Classification
* 5 bactericidal action
* 6 drug resistance
* 7 See also.
[edit]
concept
Antibiotics are metabolites or synthetic analogues of microorganisms, which can inhibit the growth and survival of microorganisms in vitro without causing serious toxic and side effects to the host.
[edit]
use
* Most antibiotics inhibit the growth of pathogenic bacteria and are used to treat most bacterial infectious diseases.
* In addition to anti-infection, some antibiotics have anti-tumor activity and are used for chemotherapy of tumors.
* Some antibiotics also have immunosuppressive effects and stimulate plant growth.
Antibiotics are not only used in medical treatment, but also in agriculture, animal husbandry and food industry.
[edit]
source
* The main source of antibiotics is biosynthesis (fermentation), which can also be made by chemical synthesis and semi-synthesis.
[edit]
classify
Antibiotics can be divided into
* β -lactam antibiotic β -lactam
O penicillin
O cephalosporin
O atypical β -lactam antibiotics
* tetracycline antibiotic tetracycline
* aminoglycoside antibiotics aminoglycoside
Macrolide, a macrolide antibiotic.
* chloramphenicol antibiotic chloramphenicol
[edit]
disinfect
There are four main mechanisms for sterilization of antibiotics.
* Inhibition of bacterial cell wall synthesis: Inhibition of cell wall synthesis will lead to the rupture and death of bacterial cells. Antibacterials that work in this way include penicillin and cephalosporins. Mammalian cells have no cell walls and are not affected by these drugs.
* Interaction with cell membrane: Some antibiotics interact with cell membrane, affecting membrane permeability and being fatal to cells. Antibiotics that work in this way are polymyxin and Brevibacterium.
* Interfering with the synthesis of protein: Interfering with the synthesis of protein means that the enzymes necessary for cell survival cannot be synthesized. Antibiotics that interfere with the synthesis of protein include fosfomycin, aminoglycosides, tetracyclines and chloramphenicol.
* Inhibition of transcription and replication of nucleic acid: Inhibition of the function of nucleic acid will prevent cell division and/or synthesis of desired enzymes. Antibiotics that work in this way include nalidixic acid and dichloroacridine.
[edit]
drug resistance
There are four main mechanisms of bacterial resistance to antibiotics (including antibacterial drugs).
* decomposition or inactivation of antibiotics;
O bacteria produce a variety of active hydrolases or passivation enzymes to hydrolyze or modify antibiotics entering bacteria, making them lose their biological activity.
O β -lactamase produced by bacteria, for example, can decompose antibiotics containing β -lactam ring; Inactivate enzymes (phosphotransferase, nucleic acid transferase, acetyltransferase) produced by bacteria, and make aminoglycoside antibiotics lose antibacterial activity.
* change the target of antibacterial drugs;
O due to the mutation of bacteria itself or the modification of an enzyme produced by bacteria, the structure of the target of antibiotics (such as nucleic acid or nucleoprotein) changes, making antibacterial drugs unable to play their roles.
O For example, methicillin-resistant Staphylococcus aureus is caused by changing the protein binding site of penicillin, making bacteria insensitive to drugs.
* Changes in cell characteristics: Changes in permeability or other characteristics of bacterial cell membrane make it impossible for antibacterial drugs to enter cells.
* Drug pump produced by bacteria pumps antibiotics that enter cells out of cells: an active mode of operation produced by bacteria pumps drugs that enter cells out of cells.
[edit]
see
Classified drug list synthetic drug list drug list
Excerpted from http://zh.wikipedia.org/wiki/%E6% 8a% 97% E7% 94% 9f% E7% B4% A0.
Category: drugs