Pharmacological terminology explained
1. Drug action Drug action The initial action between the drug and the tissue cells.
2. Pharmacological effect drug effect refers to the change in the original function of tissue cells secondary to the action of the drug.
3. Excitation where the body's original physiological and biochemical functions can be strengthened.
4. Inhibition of inhibition can weaken the body's original physiological and biochemical functions.
5. Specific specifity Most drugs produce pharmacological effects through chemical reactions, and the specificity of this chemical reaction makes the drug specific.
6. Selective selectivity drugs only have a significant effect on some tissues and organs, while have little or no effect on other tissues.
7. Therapeutic effect The results of the drug effect are conducive to changing the patient's physiological and biochemical function or pathological process, so that the diseased body returns to normal.
8. The purpose of the drug for the treatment of etiological treatment is to eliminate the primary causative factor, and the complete cure of the disease is called the cause treatment, or the cure.
9. Symptomatic treatment The purpose of symptomatic treatment is to improve the symptoms of the disease and alleviate the complications of the disease called symptomatic treatment, or to treat the symptoms.
10. Adverse reactions Adverse reactions Reactions that do not meet the purpose of medication or bring pain and harm to patients are called adverse reactions. Most adverse reactions are extensions of the drug's inherent effects.
11. Side reactions (side effects) The effect of drugs that appear at the therapeutic dose that is not related to the purpose of treatment is called side reactions, also known as side effects. Side reactions are inherent in the drug itself, caused by low drug selectivity, generally not serious, difficult to avoid.
12. Toxic reaction Toxic reaction The harmful reaction to the body occurs when the dose is too large, the medication time is too long, and the body's sensitivity is too high. It is generally more severe, but can be predicted and avoided.
13. Sequelae effect Residual effect Residual pharmacological effect when the blood drug concentration has dropped below the threshold after discontinuation of the drug.
14. Withdrawal reaction Withdrawal reaction Long-term application of certain drugs, suddenly after the drug is discontinued, the original condition is aggravated. Also known as rebound reaction
15. Allergic reaction (hypersensitive reaciton) Abnormal immune response caused by drugs in patients with allergic traits.
16. Idiosyncratic reaction a small number of patients have a bad response to certain drugs that occur differently from the usual nature. It is due to a genetic defect.
17. Dose-effect relationship Refers to the relationship between drug dose and effect. In general, within a certain dose range, the drug effect increases with the increase of the dose, and the relationship between the two is curved.
18. Dose-effectiveness curve Represents the curve of the relationship between drug dosage and effect.
19. The strength of the graded response effect of the volume response is continuously increased or decreased, which can be expressed as a specific number or the percentage of the maximum reaction.
20. The qualitative reaction quantal response effect is not a continuous change with the increase or decrease of the dose or concentration of the drug, but is manifested as a change in the nature of the reaction.
21. Minimum effective dose Minimum effective dose (threshold dose) is just the smallest dose that can cause an effect.
22. Extreme maximum effective dose refers to the maximum dose of the drug that can exert the greatest efficacy without causing a toxic reaction. In general, the dose of the drug is not allowed to exceed its extreme amount.
23. Minimum toxic dose Is just the smallest dose that can cause a toxic reaction.
24. The maximum effect that a potency efficacy drug can produce reflects the size of the drug's intrinsic activity.
25. Potency potency guides the relative dose required for the equivalent response. Reflects the size of the drug's affinity with the effector. The titer ratio of the two drugs is inversely proportional to the equivalent dose.
26. Therapeutic index Therapeutic index The ratio of half of the lethal amount of the drug to the amount of half of the effective amount. That is, TI = LD50/ED50, the larger the treatment index, the safer the drug.
27. Half of the effective dose of median effective dose ED50 can cause 50% of laboratory animals to have a positive reaction.
28. Half of the lethal dose of median lethal dose LD50 is a dose of the drug that can cause 50% of the deaths of laboratory animals.
29. Receptor receptors exist in the cell membrane, cytoplasm, and nucleus of macromolecular substances, which can recognize and bind specific ligands (drugs, transmitters, hormones, etc.) and produce biomagnification effects.
30. Agonist agonist has both affinity and intrinsic activity, can bind to the receptor, and the agonist receptor produces biological effects.
31. Antagonist antagonist has a strong affinity, but lacks intrinsic activity, can not excite the receptor and cause effect of the drug is called antagonist.
32. Competitive antagonists can compete with the same receptor reversibly with agonists, antagonists have the effect of antagonists, their binding is reversible, the effect produced when the two exist at the same time depends on the concentration of the two, and the curve can be seen on the volume-efficacy curve to shift parallel to the right, and the efficacy is unchanged.
33. Non-competitive antagonists bind firmly to the receptor, so that the number of receptors that can bind to the ligand is reduced, so that its affinity and activity are reduced. Non-competitive antagonists shift the potency curve to the right and the height (Emax) decreases.
34. Partial agonist has little intrinsic activity, and if there is no similar agonist, it can produce a weak agonistic effect, and if there is a similar agonist, it is manifested as antagonism.
35. The reverse agonist inverse agonist, after binding to the receptor, can cause the configuration of the receptor to change to the inactive state, causing the opposite effect of the agonist
36. Receptor desensitization Receptor desensitization Long-term use of agonists, so that the number of receptors, affinity, intrinsic activity decreased, the receptor sensitivity and responsiveness to agonists decreased. Divided into agonist-specific desensitization and non-specific desensitization
37. Receptor sensitization Receptor hypersensitization Long-term use of antagonists, so that the number of receptors, affinity, intrinsic activity increased, receptor sensitivity to antagonists increased.
38. Receptor upregulation or downregulation Receptor desensitization or sensitization involves only changes in receptor density.
39. The homospecific regulation ligand acts on its specific receptor, causing changes in its own receptor.
40. Heteroregulatory heterospecific regulation ligand acts on its specific receptor, producing a regulatory effect on the receptor of another ligand.
41. Passive transport of passive transport drugs depends on the concentration difference between the two sides of the membrane, from the high concentration side to the low concentration side of the transmembrane transport, when the drug concentration on both sides of the membrane reaches equilibrium, the transport is stopped.
42. Active transport of active transport drugs relies on specific vectors on cells (e.g., pumps) for transmembrane transport from the low concentration side to the high concentration side.
43. Easy diffusion facilitated diffusion A special passive transport, the drug by reversibly binding to a specific carrier on the biofilm and surplus diffusion, there is competition and saturation.
44. Transmembrane transport of filtration drug molecules through aqueous channels of cell membranes with the help of hydrostatic or osmotic pressure.
45. Simple diffusion simple diffusion fat-soluble drug cis concentration difference across cell membrane transport.
46. Membrane dynamic transport Cytosis Transport of macromolecular substances is accompanied by membrane movement.
47. Absorption of the drug The process of transmembrane transport of the drug from the site of administration into the blood circulation.
48. When the first pass elimination drug is absorbed through the gastrointestinal tract, it is partially inactivated by the metabolic enzymes of the gastrointestinal tract and hepatocytes, so that the effective amount of medicine entering the systemic circulation is reduced.
49. Distribution of drugs Distribution The process by which drugs are transported from the blood circulation to tissues and organs through transmembrane.
50. Blood-brain barrier Blood-brain barrier includes three barriers: blood-brain, blood-cerebrospinal fluid, and cerebrospinal fluid-brain, of which the blood-cerebrospinal fluid barrier is particularly important. Macromolecular, highly dissociative, high protein binding, non-fat-soluble drugs are not easily traversed through this barrier.
51. Placental barrier placental barrier Barrier barrier between placental villi and uterine blood sinuses.
52. Redistribution Intravenous injection of the anesthetic drug thiopental sodium, first distributed to the brain tissue with large blood flow plays a role, and then due to its high fat solubility, it is distributed to the fat tissue with low blood flow, so that the patient wakes up quickly. This phenomenon is called the redistribution of the drug.
53. Metabolic metabolism Biotransformation Biotransformation Drugs occur in vivo chemical structural changes.
54. Hepatic microsomal enzyme is present in the cytochrome P-450 enzyme system of hepatocyte microsomals, about 100 kinds of isoenzymes, which is the main enzyme system of drug metabolism.
55. Drug-inductor of microsomal enzyme activity Drugs that can increase the amount and activity of drug enzymes.
56. Drug inhibitor inhibitors inhibitors of microsomal enzyme activity drugs that can increase or decrease the amount and activity of drug enzymes.
57. The process of excreting secretion drugs and their metabolites is excreted by eliminating organs.
58. Hepatoenteral cycle hepatoenteral cycle drugs and metabolites enter the intestine with bile, and some drugs and metabolites can be absorbed by small intestinal epithelial cells and enter the blood circulation through the liver. This cycle between the liver, bile, and small intestine is called the hepatic and intestinal cycle.
59. Drug-time curve concentration time curve A curve in which the blood drug concentration rises and falls with time is drawn with the blood drug concentration as the ordinate coordinate and the time is the abscissa.
2021 Examination and Research Institute of Pharmacy Comprehensive 349 System Knowledge Intensive Lecture Class - Pharmacology
60. The atrioventricular model compartment model treats the human body as a system, and the interior is divided into several hypothetical atrioventricular chambers according to kinetic properties for pharmacokinetic analysis.
61. Open one-compartment model This model treats the body as an atrioventricular. Immediately after administration, the drug is evenly distributed throughout the body fluids and tissues. That is, the transport rate of the drug in various tissue parts of the body is the same or similar, and is eliminated from this chamber at a certain rate.
62. Open one compartment model This model treats the body as a central chamber and a peripheral chamber. After absorption, the drug is first distributed to tissues and organs with rich blood flow, and then to tissues and organs with less blood flow. Tissues and organs with abundant blood flow are central chambers, with small distribution volumes, and tissues and organs with less blood flow are peripheral chambers, and the distribution volume is large.
63. First-order elinimination kinetics refers to the constant proportional elimination of drugs per unit time. That is, the transport or elimination of the drug is proportional to the blood concentration.
64. Zero-order elinimination kinetics refers to the constant elimination of drugs per unit time. That is, the transport or elimination of the drug is independent of the blood drug concentration.
65. Bioavailability refers to the degree and speed of drug absorption into the body's blood circulation, bioavailability = × 100%.
66. Bioequivalence contains drugs of the same active ingredient and the same dosage, dosage form and route of administration, producing equal efficacy.
67. Apparent volume of distribution (Vd) apparent volume of distribution assumes that the drug is evenly distributed in the theoretical volume required by the body, that is, the ratio of the total amount of drug (A) in the body to the blood concentration (C) when the drug plasma and the drug distribution in the tissue reach a balance.
68. Plasma half-life t1/2 half time The time required for plasma drug concentration to drop by half.
69. Clearance clearance The body eliminates the plasma volume of the organ that clears the drug in a unit of time. That is, how many milliliters of plasma contain drugs are cleared by the body per unit time.
70. Steady state plasma concentration Css Constant ratio elimination of drugs In the process of continuous constant speed or fractional constant dose administration, the blood drug concentration will gradually increase, when the rate of administration is equal to the elimination rate, the blood concentration maintains a basically stable level. The blood concentration at this time is called the steady-state blood concentration. Every t1/2 is administered, after 5 t1/2 passes, the elimination rate is equal to the rate of administration.
71. Loading dose In order to quickly achieve the required steady-state blood concentration, a larger dose is given at the beginning of treatment. Factors that affect the action of the drug
72. Individual variation The same drug may not be able to achieve equal blood drug concentrations for different patients, and equal blood drug concentrations may not necessarily achieve the same efficacy, and this drug response that varies from person to person is called individual difference.
73. Drug interaction drug interaction Two or more drugs are combined or successively applied sequentially, causing changes in the effect and effect of the drug
74. Antagonism of the drug Antagonism combined with the effect of the drug weakened, the effect of the combination of the two drugs is less than the sum of their respective effects.
75. Compatibility contraindications incompatibility occurs in the preparation of physical and chemical changes, it makes the preparation of the drug can not be molded or affect its uniformity, stability, etc. so that it is no longer suitable for application.
76. Placebo placebo is a preparation that does not contain pharmaceutical ingredients, has no pharmacological activity, and looks like a drug,
77. Tolerance tolerance The body's sensitivity to drugs decreases, and the dose needs to be increased to maintain the original efficacy.
78. In resistance chemotherapy, pathogens or tumor cells are less sensitive to drugs.
79. Rapid tolerance tachyphylaxis develops tolerance immediately after several consecutive doses in a short period of time.
80. Cross tolerance After the body becomes resistant to one drug, the sensitivity to another drug also decreases.
81. Dependence Dependence Some drugs interact with the body, causing the body to have a psychoactive or physiological dependence and demand for this drug.
82. Habitual habituation mental dependence refers to a pleasant sense of satisfaction produced by the body after taking the drug, and the desire to take continuous medication in the spirit, the occurrence of "drug-seeking behavior", and the discontinuation of the drug does not cause serious harm to the body.
83. Addictive addiction somatic dependence physical dependence physiological dependence Repeated medication The body must have enough drugs to maintain a state of normal physiological activities, and a class of symptoms that are roughly opposite to the original pharmacological effects appear when the drug is suddenly stopped, called withdrawal symptoms.
84. Regulation of spasm Pilocarpine stimulates the ciliary muscle M receptor, the ciliary muscle contracts, causing the suspensory ligament to relax, the lens due to its own elasticity becomes convex, the diopter increases, at this time can only see the near object, it is difficult to see the far object.
85. Anticholinesterase agents anticholinesterase agents bind to cholinesterase, but the binding is firm and the hydrolysis is slower, so that the acetylcholinesterase activity is inhibited, resulting in the accumulation of acetylcholine released by cholinergic nerve endings, resulting in a choline-like effect. It is divided into reversible anticholinesterase drugs and refractory anticholinesterase drugs.
86. Atropine When rescuing organophosphorus poisoning, repeated application of large doses of atropine, the body appears skin flushing, limb warming, mydriasis, fundus vascular spasm relief, blood pressure recovery of clinical comprehensive phenomenon.
87.M choline receptor blocker muscarinic cholinoceptor blocking drgus can bind to the M receptor but can not produce choline-mimic effect, but hinder the M receptor of acetylcholine agonist, thereby antagonizing the effect of choline-like drugs.
88. Regulation of paralysis cycloplegia atropine blocks the M receptor of the ciliary muscle, the ciliary muscle relaxes, causing the suspension ligament to contract, the lens becomes concave due to its own elasticity, the diopter is reduced, at this time can only see the distant object, it is difficult to see the near object.
89. Depolarized muscle relaxants, also known as non-competitive muscle relaxants, can bind to the choline receptors of the posterior membrane of the neuromuscular junction to produce a more lasting depolarizing effect, so that the N2 receptors of the posterior membrane of the neuromuscular junction cannot respond to ACh, thereby relaxing the skeletal muscles.
90. Non-polarizing muscle relaxants, also known as competitive muscle relaxants, can compete with ACh for the N2 receptors of the posterior membrane of the neuromuscular junction, blocking the depolarization of ACh, which itself does not cause the depolarization of the postsynaptic membrane and relaxes the skeletal muscles.
91. The reversal of the vasopressor effect of epinephrine After using α receptor blockers, the vasotrophic α effect of epinephrine can be blocked, and the diastolic vascular effect β2 effect is dominant, at this time, the blood pressure given to adrenaline is not only not rising, but decreasing. Intrinsic sympathomimetic activity, some isa β receptor blockers bind to β receptors, in addition to blocking β receptors, have a partial agonist effect on β receptors.
92. Neurotransmitters Chemicals released by nerve endings that act on postsynaptic membrane receptors, causing ion channels to open and form excitatory postsynaptic potentials or inhibitory post-herniation potentials.
93. Neuromodulators can induce slow postsynaptic potentials after binding to receptors, which does not directly cause post-synaptic cell biological effects, but can modulate the release of neurotransmitters in presynaptics and the excitability of postsynaptic cells, and modulate the response of post-synaptic cells to transmitters.
94. Neurohormones The chemicals released by nerve endings enter the blood circulation and play a role in distant target organs.
95. Blood gas distribution coefficient The ratio of the concentration of inhaled anesthetic drugs in the blood to the concentration of drugs in the inhaled gas when they reach equilibrium.
Combined anesthesia combined anesthesia is an anesthesia method in which two or more anesthetic drugs or other auxiliary drugs are applied simultaneously or successively to meet the surgical requirements.
96. Isolation of anesthesia dissociative anesthesia ketamine can cause short-term memory loss and satisfactory analgesic effect, but consciousness has not completely disappeared anesthesia phenomenon.
97. Hangover reaction Symptoms such as dizziness, drowsiness, drowsiness, lack of energy and disorientation occur in the morning after taking the drug. Called a hangover reaction.
98. Artificial hibernation The use of chlorpromazine with central inhibitors (such as promethazine, piperidine, etc.) can make the body enter a deep sleep state similar to the "hibernation" of warming animals, called artificial hibernation.
99. Switching phenomenon An adverse reaction caused by long-term use of levodopa is manifested by normal or nearly normal activities of patients at the time of opening, and suddenly severe PD symptoms occur when turned off.
100. Analgesics A class of drugs that act primarily on the central nervous system and selectively eliminate or relieve pain without affecting consciousness and other sensations.
101. Opioid alkaloids Several alkaloids with analgesic effects are contained in opioids (i.e., the dried matter of the pulp that flows out of the pulp after the ripe capsules of the chestnut are scratched).
102. Morphine receptor antagonists have a large affinity with morphine receptors in the brain, but have no intrinsic activity, can completely block the binding of morphine and opioid receptors, and can compete against the effect of opioids.
103. Salicylic acid reaction When the dose of aspirin is too large (5g/day), symptoms such as headache, dizziness, nausea, vomiting, tinnitus, and decreased visual and visual power can occur, which is a manifestation of salicylate poisoning.
104. Reyes's syndrome (Reyes's syndrome) When children have toxic infectious diseases, aspirin is used to deferve, which can occasionally cause acute hepatic steatosis-encephalopathy syndrome, with liver failure and encephalopathy as the prominent manifestation, although rare, but the prognosis is poor.
105. Calcium channel blockers Selectively block calcium channel blockers, drugs that inhibit extracellular calcium ion inflow, and reduce intracellular calcium ion concentration.
The first dose of antihypertensive drugs The first dose of piperazin can cause serious orthostatic hypotension, syncope, palpitations, etc., called the first dose phenomenon. This can be avoided if the first dose is reduced to 0.5 mg and taken before bedtime.
106. Antiarrhythmic drug membrane reactivity refers to the relationship between the membrane potential level and the maximum rate of rise of the 0 phase it excites. In general, the greater the negative value of the membrane potential, the faster the rate of rise of the 0 phase, and the faster the myocardial conduction rate, that is, the greater the membrane reactivity.
107. Effective refractory period From the beginning of the depolarization to the recovery of the membrane potential to -60mV, the cell does not produce a spreadable action potential for any stimulus, that is, the effective refractive period (ERP).
108. Reentry refers to the phenomenon of impulses regurgitating back along the myocardial conduction pathway and running repeatedly.
109. Cinchona reaction Gastrointestinal reactions and central nervous system reactions with quinidine, the former including nausea, vomiting, diarrhea and loss of appetite; the latter includes tinnitus, hearing loss, dizziness, visual impairment, delirium, etc., collectively known as cinchona reaction.
110. Quinidine syncope When using quinidine, the patient suddenly has paroxysmal supraventricular tachycardia or ventricular fibrillation, causing the patient to lose consciousness, convulsions of the limbs and the reaction of respiratory arrest.
111. Inotropic drugs: drugs that can strengthen myocardial contractility, drugs used for congestive heart failure, such as cardiac glycosides.
112. Digitalization: When patients with cardiac insufficiency are treated with cardiac strengthening, they often give a sufficient amount of digitalis in the short term to make it exert sufficient effects without poisoning. Therefore, when taking drugs, the loading amount is first given within a few days (1 to 3 days) to quickly achieve a higher blood concentration, and then the maintenance amount is given to maintain the efficacy, which is the so-called digitalis yellowing.
113. Diuretics Act on the kidneys and can increase the discharge of electrolytes and water.
Osmotic diuretics Dehydration drugs After injection administration, plasma osmolality can be increased, resulting in tissue dehydration. The drug is not easy to enter the tissue through the capillaries, when the drug is filtered through the glomeruli, it is not easy to be reabsorbed by the renal tubules, thereby increasing the discharge of water and some ions, resulting in a permeable diuretic effect.
114. Hyperlipidemia The concentrations of VLDL, IDL, LDL and apoB in plasma are higher than normal.
Lipid-modulating drugs: drugs that can reduce VLDL, IDL, LDL, TG, TC and apoB, and elevate HDL and apoA.
115. Antacids A class of weak alkaline drugs, after oral administration, neutralize gastric acid, and reduce pepsin activity, play a role in relieving pain and promoting ulcer healing.
116. Laxatives can increase intestinal water, promote peristalsis, soften feces or lubricate the intestines to promote defecation.
117. Anabolic steroids are androgenic steroids that significantly promote protein synthesis.
Anti-implantation contraceptives can cause various functional and morphological changes in the endometrium and prevent the implantation of pregnant eggs.
118. First pregnancy reactions A small number of women who use contraceptives experience symptoms similar to early pregnancy reactions in the early stages of medication.
119. Iatrogenic adrenal insufficiency Long-term application of glucocorticoid drugs can feedback inhibit the secretion of ACTH in the pituitary gland, causing adrenal atrophy, decreased secretion of endogenous hormones, when the drug is suddenly stopped or the dose is reduced too quickly, adrenal insufficiency symptoms can appear, manifested as nausea, vomiting, muscle weakness, hypoglycemia, hypotension, etc., known as iatrogenic adrenal insufficiency.
120. Iatrogenic hypercorticism Large doses of exogenous glucocorticoids can cause disorders of sugar, fat, protein and water and salt metabolism in the body, and there are manifestations similar to hypercorticism: such as full moon face, buffalo back, centripetal obesity, thinning of the skin, muscle atrophy, acne, hirsutism, edema, hypokalemia, hypertension, diabetes, etc.
121. Allowing action Glucocorticoids have no direct effect on some tissue cells, but can create favorable conditions for other hormones to play a role.
122. Rebound phenomenon rebound phenomenon Recurrence or aggravation of the original disease caused by the rapid reduction or sudden discontinuation of long-term medication.
123. Alternate-day therapy Clinically, for patients who need long-term treatment with glucocorticoids, in order to minimize the inhibition of the drug on adrenal cortex function, according to the circadian rhythm of glucocorticoid secretion, the total dosage of two or one day is given once in the morning of the next day.
124. Insulin resistance is divided into acute and chronic types, the former refers to the sharp reduction in the effect of insulin due to concurrent infections, surgery, trauma, emotional agitation, etc., and the dose of insulin needs to be increased in a short period of time to hundreds or even thousands of units; it may be related to the increase in the amount of substances that antagonize insulin in the blood during stress states; the latter refers to the clinical need for more than 200U of insulin per day, and there is no complication of diabetes.
Type 125.1 diabetes Insulin-dependent diabetes mellitus is a diabetes mellitus caused by the destruction of islet B cells caused by autoimmune mechanisms and lack of insulin secretion.
126. Recombinant insulin The same high-purity formulation as natural human insulin produced by recombinant DNA technology.
127. Chemotherapeutic drugs Antimicrobials, antiparasitic drugs and anti-malignant tumor drugs are collectively referred to as chemotherapeutic drugs
128. Antibacterial drugs can inhibit or kill bacteria, drugs used to prevent and treat bacterial infections.
129. Metabolites of antibiotic microorganisms (bacteria, fungi, actinomycetes), low concentrations can inhibit or kill other pathogenic microorganisms.
130. Antibacterial spectrum Antibacterial drugs can inhibit or kill the range of bacteria.
131. Bacteriostatic drugs Only have antibacterial drugs that inhibit the growth and reproduction of bacteria without killing bacteria
132. Bactericidal drugs not only have the effect of inhibiting the growth and reproduction of bacteria, but also have the effect of killing bacteria.
133. Antibacterial activity The ability of drugs to inhibit or kill bacteria.
134.MIC drugs inhibit the lowest concentration of bacterial growth in the medium.
135. MBC drugs can kill the lowest concentration of bacteria in the medium.
136. Chemotherapy index The ratio of half of the lethal amount (LD50) of chemotherapeutic drugs to half of the effective amount (ED50) can be evaluated for the clinical application value of chemotherapeutic drugs.
137. Antibacterial after-effect postantibiotic effect After the bacteria are briefly exposed to antibacterial drugs, the antibacterial drugs in the culture medium are removed, and the bacterial reproduction cannot return to normal within a certain time frame after removing the antibacterial drugs.
138. Multi-resistant bacteria Multiple resistant bacteria are resistant to multiple antimicrobials.
139. Herxheimer reaction When penicillin G is used to treat infections such as syphilis, leptospirosis, and anthrax, symptoms may be exacerbated. Manifested by general malaise, chills, fever, sore throat, myalgia, rapid heartbeat and other symptoms, this treatment is contradictory. It may be caused by a large number of pathogens released after being killed.
140. Containment mechanism Trap mechanism (trapping mechanism) β-lactamase can be quickly and firmly bound to some enzyme-resistant β-lactam antibiotics, so that the drug stays in the extracytoplasmic space and cannot reach the target of action (PBPs) to exert antibacterial effects. Resistance to this non-enzymatic mechanism.
141. The effect of primary contact refers to the fact that when bacteria are first exposed to aminoglycoside antibiotics, they can be killed quickly, and when the unlearned bacteria are exposed to the same antibiotic again or multiple times, their bactericidal effect is significantly reduced
142. When the superinfections of double infection use broad-spectrum antibacterial drugs for a long time, the sensitive bacteria in the mouth, throat and gastrointestinal tract are inhibited by the drug, and the insensitive bacteria take the opportunity to multiply and grow in large quantities, changing from the original inferior bacteria to the dominant bacteria, resulting in new infections.
143. Gray infant syndrome gray syndrome premature infants and newborn liver glucuronate transferase deficiency, kidney excretion ability is poor, the application of large doses of chloramphenicol, easy to cause accumulation of poisoning. Symptoms such as bloating, vomiting, progressive pallor, and microcirculation disorders, called "grey baby syndrome," can die from respiratory and circulatory failure.
144. Cycle-specific drugs Drugs that only have a strong effect on cells at a certain stage of the cell proliferation cycle.
145. Cycle non-specific drugs refer to drugs that have a killing effect on cells at all stages of the cell proliferation cycle.
146. Multi-drug resistance After being exposed to an anti-malignant tumor drug, tumor cells develop resistance to a variety of other anti-malignant tumor drugs with different structures and different mechanisms of action.
147. Non-cytotoxic antineoplastic drugs A class of drugs with a rapidly developing new mechanism of action, including drugs that regulate hormone balance in vivo, monoclonal antibodies, signal transduction inhibitors, cell differentiation inducers, apoptosis inhibitors, neovascularization inhibitors, tumor gene therapy drugs and other types.