藥學(xué)英語(yǔ)重點(diǎn).doc

Parkinsons disease Etiology:PD is caused by the death of the nerve cells in the substantia nigra,which produce the neurotransmitter dopamine.without dopamine,the brain is unable to transmit messages between nerve cells,resulting in a decrease in muscle function.when 80% of dopamine producing cells are damaged the symptoms of PD start to appear.Benzodiazepine Mechanism of action 1 GABAa receptor composition varies in different regious. 2 BNZs bind to receptors with a&r subunits 3 BNZ binding enhances the effect of GABA on the Cl- current 4 BNZs-increase the frequency of Cl- channel openings in presence of GABA 5 BNZs exert on effect in the absence of GABA 6 The effects & binding of BNZ was blocked bu flumezenil (BNZ antagonist) 7 Not all BNZs are identical.BNZs-high doses commonly produce anterograde amnesia.Barbiturates Multiple mechanism: Bind to GABAa receptors at different site.dont compere for BNZ binding & are not blocked by flumazenil;increase the duration of Cl- channel openings 1 increase GABA effect 2 directly activate GABAa channels at high concentrations. 3 block effects of glutamate NT. 4 block Na+ channels. Diazepan Given iv,is used for status epilepticus in adults.it is also effective against all other types of seizures,particularly petit mal and other minor seizures Antipsychotic mechanism: Primarily dopamine antagonists.of the many contemporary theories of schizophrenia,the most enduring has been the dopamine hypothesis.increased baseline occupancy of D2 receptors by dopamine in schizophrenia.act at D2 D3 and D4 receptors.Phenothiazines pharmacologic effectsCNS effects:1 the antiphychotic effect are believed to be due to antagonism of dopaminergic neurotransmission by blocking D2 receptors in the limbic,nigrostriatal and hypothalamic systems. 2 extrapyramidal symptons occur most often with chronic administration.they can be treated by lowering the dose or by using an anticholinergic antiparkinsonian drug such as benztropine mesylate 3 phenothiazines having the greatest antihistaminic and anticholinergic properties will exhibit the fewest entrapyramidal effects 4 most phenothiazines are antiemetic.they antagonize apomorphine,which stimulate the CTZ.in high dose,phenothiazine may directly depress the medullary vomiting center. 5 phenothiazines are capable of altering temperature-regulating mechanisms.normally,they produce hypothermia however,in a hot climate they can cause hyperthermia,because of failure to lase body heat. 6 since phenothiazines depress the hypothalamus,endocrime alterations may occur,weight gain and increased appetite are seen with phenothiazine use.Peripheral effects:1 an -adrenergic blocking activity result in orthostatic hypotension,especially with the chlorpromazine. 2 anticholinergic effects can result in blurned vision,decreased sweating and urinary retention. 3 chlorprom azine is a potent local anesthetic. Glucocorticoids Introduction The adrenal cortex secretes several steroid hormones into the bloodstream.these are classified by their action into 2 main classes-glucocorticoids and mineralocorticoids. Glucocorticoids physiological effects 1 carbohydrate metabolism 2 protein metabolism 3 fat metabolism 4 water and salt metabolism 5 nucleic acid metabolismSeizure - brief episode of abormal electrical activity in the nerve cells of the brain.Convulsion - involuntary spasmodic contractions of any or all voluntary muscles throughout the body.Epilepsy - chronic recurrent pattern of seizuresPhenytoin indications-grand mal epilepsyEthosuximide Ethosuximide is the optimal choice in the treatment of petit mal epilepsyWhat is pain? 1 pain can be defined as a somatic sensation of acute discomfort,a symptom of some physical hurt or disorder,or even emotional distress. 2 it is a common human experience,therefore the idea of pain and pain managemgnt appear throughout history. 3 pain is a crucial aspect of the bodys defense mechanisms. 4 pain is a part of a rapid warning relay instruction to the motor neurons of the central nervous system to minimize detected physical harm. 5 pain can be classified into 2 types.The opioid receptors There are 4 main opioid receptors,the mu receptor,the delta receptor,the kappa receptor,and the ORL-1 receptor.The k-receptor 1 the kappa receptor is very different from the mu-receptor in the fact thar there are not many significant agonist of the kappa receptor known. 2 the kappa receptor is associated directly with analgesia and sedation but with none of the undesired side effects associated with the mu receptor. 3 because of this,it is an area of focus in current research and shows promise in the development of a safer analgesic. 4 when agonist or ligand binds to the kappa receptor,it induces a conformational change that results directly in the closing of the calcium ion channels in the terminal of the neuron and the neuron can not relay pain messages. 5 another difference between the kappa and mu-receptors is that the kappa receptors only affect nerves that relaypain produced by nonthermal stimuli .and mu-receptor inhibit all pain signals. 6 there are 3 subtypes of the kappa receptor however the difference between these subtypes is not clearly known.Future 1 kappa receptor 2 another