266 Pharmacology Pills

By Carlos Herrero Carcedo

Thanks to this book, many health care students and professionals have mastered PHARMACOLOGY.
This work consists of 266 pills of scientific knowledge of this extensive discipline organized in a practical and comfortable study for learning.

• Language: English
• Publisher: Carlos Herrero Carcedo
• Release date: Apr 5, 2020

Carlos Herrero Carcedo

Autor de dos Libros con tapa: Manual Básico de Farmacología y 200 Ideas para Mejorar la Rentabilidad de tu Farmacia, una publicación en la revista Alimentación, Equipos y Tecnología: La histamina en las distintas etapas de fabricación de conservas de atún y seis Ebooks: Disruptores Endocrinos, La Salud no es un Negocio, Obesidad Infantil. Rista. Respuesta Insuficientemente Adecuada, Vivir sin Cáncer, Ser Mayor sin Edad y Predisposición a Ser Homosexual.Posee tres licenciaturas (Farmacia, Ciencias Químicas, Ciencia y Tecnología de los Alimentos) y experiencia en los departamentos de Calidad, Producción y Ventas.

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266 PHARMACOLOGY PILLS

Carlos Herrero Carcedo

carlosherrerocarcedo.com

Index

1. The autonomic nervous system.

2. The nervous systems: sympathetic and parasympathetic.

3. Neurotransmitters.

4. Adrenergic and cholinergic impulses.

5. Cholinergic transmission.

6. Cholinergic receptors.

7. The muscarinic agonists (parasympathomimetics).

8. The muscarinic antagonists (parasympatholytics).

9. Ganglionic neurotransmission.

10. Blocking neuromuscular transmission.

11. The cholinesterase inhibitor drugs.

12. Noradrenergic transmission.

13. Adrenergic receptors.

14. The adrenergic receptor agonists.

15. The α-adrenergic receptor antagonists.

16. The β-adrenergic receptor antagonists.

17. Serotonin.

18. The treatment of migraine.

19. The mediators: adenosine, ADP and ATP.

20. The immune response.

21. Histamine.

22. Mediators of the immune and inflammatory response.

23. Non-steroidal anti-inflammatories (NSAIDs).

24. Salicylates.

25. Paracetamol.

26. Pyrazolones.

27. The propionic acid derivatives.

28. The acetic acid derivatives.

29. Oxicams.

30. Other NSAIDs.

31. H1 antihistamines.

32. Gout.

33. Rheumatoid arthritis.

34. Peptide and protein mediators.

35. Therapeutic applications of peptides and proteins.

36. Chemical mediators in the central nervous system.

37. The amino acids transmitters/excitators in the CNS.

38. The amino acids transmitters/inhibitors in the CNS.

39. Noradrenaline.

40. Dopamine.

41. 5-Hydroxytryptamine (serotonin).

42. Acetylcholine.

43. Other chemical mediators in the CNS.

44. Neuronal death.

45. Cerebrovascular accidents (strokes). 46. Alzheimer.

47. Parkinson.

48. General anesthesia.

49. General anesthetics by inhalation.

50. General intravenous anesthetics.

51. Anxiety and insomnia.

52. Benzodiazepines.

53. Other anxiolytic and hypnotic drugs.

54. Depression.

55. Types of antidepressants.

56. Tricyclic antidepressants.

57. Non-selective NA/5-HT reuptake inhibitors.

58. Selective 5-HT reuptake inhibitors.

59. Selective NA reuptake inhibitors.

60. Monoamine oxidase inhibitors (MAOI).

61. Receptor blockers, non selective-antagonists.

62. Antimaniacs.

63. Schizophrenia.

64. Antipsychotic classification.

65. Pharmacological effects of antipsychotics.

66. Adverse reactions of antipsychotics.

67. Therapeutic applications of antipsychotics.

68. Epilepsy.

69. Mechanisms of action of antiepileptics.

70. Choice of an antiepileptic.

71. Most widely used anticonvulsants.

72. The pain.

73. Morphinic drugs and opioid receptors.

74. Agonist and antagonist opiates.

75. Pharmacological actions of opiate analgesics.

76. Characteristic properties of opiate analgesics.

77. Opiate analgesics.

78. Characteristics of local anesthetics.

79. Therapeutic applications of local anesthetics.

80. Heart rate and rhythms.

81. Arrhythmias.

82. Cardiac contraction.

83. Coronary blood flow.

84. The autonomous regulation of the heart.

85. Cardiac natriuretic peptides.

86. Ischemic heart disease.

87. Mechanisms of action of antiarrhythmic drugs.

88. Class I antiarrhythmics.

89. Class II antiarrhythmics.

90. Class III antiarrhythmics. 91. Class IV antiarrhythmics.

92. Other antiarrhythmics.

93. The cardiac glycosides.

94. Digoxin mechanism of action.

95. The cardiovascular effects of digoxin.

96. Digoxin properties, poisoning and applications.

97. Other positive ionotropic drugs.

98. Antianginal drugs.

99. Organic nitrates.

100. β-adrenergic blockers.

101. Calcium antagonists.

102. Other antianginals.

103. Blood vessels.

104. The vascular endothelium.

105. The renin-angiotensin system.

106. Vasoconstrictor drugs.

107. Direct-acting vasodilator drugs.

108. Indirect-acting vasodilator drugs.

109. Heart failure.

110. Pharmacology of heart failure.

111. Treatment of heart failure.

112. Arterial hypertension.

113. Classification of antihypertensive drugs.

114. Diuretics.

115. β-adrenergic blockers.

116. α1-adrenergic blockers.

117. Angiotensin-converting enzyme inhibitors.

118. Angiotensin II receptor antagonists.

119. Calcium antagonists.

120. Central action sympathetic action inhibitors.

121. Direct vasodilators.

122. Other antihypertensive drugs.

123. Choice of antihypertensive drug.

124. Main characteristics of calcium antagonists.

125. Main characteristics of ACE inhibitors.

126. Main characteristics of beta-blockers.

127. The nephron.

128. Loop diuretics.

129. Thiazides.

130. Potassium-sparing diuretics.

131. Carbonic anhydrase inhibitors.

132. Osmotic diuretics.

133. Applications of drugs that act on the kidney.

134. Atheromatous disease.

135. Lipoproteins. 136. Statins.

137. Fibrates.

138. Lipid-lowering drugs that inhibit cholesterol absorption.

139. Nicotinic acid and derived drugs.

140. Other lipid-lowering drugs.

141. Hemostasis and thrombosis.

142. Pharmacology of platelet function.

143. Coagulation pharmacology.

144. Pharmacology of fibrinolysis.

145. Regulation of respiration.

146. Bronchial asthma.

147. Anti-asthmatic drugs.

148. β2-adrenergic receptor agonists.

149. Xanthines.

150. Anticholinergics.

151. Antagonists of cysteinyl-leukotriene receptors.

152. Antihistamines H1.

153. Glucocorticoids.

154. Chronic obstructive pulmonary disease.

155. Cough.

156. Pulmonary hypertension.

157. Pulmonary surfactants.

158. Neuronal and hormonal control of the digestive system.

159. Gastric secretion.

160. Antacids.

161. Histamine H2 receptor antagonists.

162. Proton pump inhibitors.

163. Other drugs that inhibit gastric acid secretion.

164. Helicobacter pylori infection.

165. Mucosal protective drugs.

166. Pharmacology of vomiting.

167. Prokinetics.

168. Laxative drugs.

169. Antidiarrheal drugs.

170. Chronic inflammatory bowel disease.

171. Hormones from pancreatic islets.

172. Diabetes mellitus.

173. Insulins.

174. Sulfonylureas.

175. Biguanides.

176. Thiazolidinediones.

177. Other oral antidiabetics.

178. Anterior pituitary gland.

179. Corticoliberin and corticotropin.

180. Thyroliberin and thyrotropin.

181. Somatoliberin, somatostatin and somatotropin.

182. Prolactin.

183. Posterior pituitary gland.

184. The adrenal cortex.

185. Glucocorticoids.

186. Mineralocorticoids.

187. Thyroid hormones.

188. Thyroid function abnormalities.

189. Pharmacology of hyperthyroidism.

190. Pharmacology of hypothyroidism.

191. Bone remodeling.

192. Bone structure disorders.

193. Bisphosphonates.

194. Raloxifene.

195. Parathyroid hormone.

196. Strontium ranelate.

197. Calcitonin.

198. Vitamina D preparations.

199. Calcium salts.

200. Other compounds used in bone diseases.

201. Female reproductive system.

202. Estrogens.

203. Selective modulators of estrogen receptors.

204. Progestogens.

205. Antiprogestogens.

206. Male reproductive system.

207. Androgens.

208. Antiandrogens.

209. Aromatase inhibitors.

210. Secretion with gonadal influence.

211. Oral contraceptives.

212. Uterus.

213. Erectile dysfunction.

214. Molecular basis of chemotherapy.

215. Bacterial resistance to antibiotics.

216. Biochemical mechanisms of antibiotic resistance.

217. Penicillins.

218. Cephalosporins.

219. Other β-lactam antibiotics.

220. Aminoglycosides.

221. Macrolides.

222. Glycopeptide antibiotics.

223. Other alternatives to infections by gram-positive germs.

224. Tetracyclines.

225. Cloramphenicol.

226. Lincosamides.

227. Other antibiotics.

228. Quinolones.

229. Sulfonamides.

230. Trimethoprim.

231. Cotrimoxazole.

232. Nitrofurantoin.

233. Anti-tuberculosis chemotherapy.

234. Leprosy chemotherapy.

235. Pathogenic viruses.

236. Nucleoside reverse transcriptase inhibitors.

237. Non-nucleoside reverse transcriptase inhibitors.

238. Protease inhibitors.

239. Inhibitors of viral DNA polymerase.

240. Inhibitors of HIV binding in host cells.

241. Neuraminidase inhibitors.

242. Inhibitors of viral coat dismantling.

243. Biological and immunomodulatory drugs.

244. Combined HIV treatment.

245. Fungal infections.

246. Antifungal antibiotics.

247. Synthetic antifungals.

248. The main protozoal infections.

249. Amebiasis.

250. Trypanosomiasis.

251. Leishmaniasis.

252. Other infections by flagellated protozoa.

253. Malaria.

254. Toxoplasmosis.

255. Pneumocystosis.

256. The main helminth infections.

257. Benzoimidazoles.

258. Other anthelmintics.

259. Cancer cell.

260. Alkylating drugs and related compounds.

261. Antimetabolite drugs.

262. Cytotoxic antibiotics.

263. Antineoplastic drugs derived from plants.

264. Hormones.

265. Hormonal antagonists.

266. Other antineoplastic drugs.

1. The autonomic nervous system.

The peripheral nervous system has the following elements: autonomic nervous system, somatic efferent nerves that innervate skeletal muscle and somatic and visceral afferent nerves.

The autonomic nervous system, non-consciously, regulates a large number of visceral functions: energy metabolism, contraction and relaxation of vascular and visceral smooth muscle, heartbeat, secretions, etc.

The activity of the autonomic nervous system is transmitted through the autonomic peripheral nerves, although its control and integration is carried out in the nerve centers of the central nervous system.

The autonomic nervous system is morphologically constituted by the sympathetic nervous system, the parasympathetic nervous system and the enteric nervous system.

From the nerve centers of the sympathetic nervous system, sympathetic eferences or preganglionic fibers leave to the prevertebral and paravertebral sympathetic ganglia, from which long-distance postganglionic fibers depart to innervate the target organs and tissues.

From the nerve centers of the parasympathetic nervous system, the long preganglionic efferent fibers leave towards the parasympathetic ganglia, which are usually located near or inside the effector organ innervated by postganglionic fibers.

The sympathetic nervous system and the parasympathetic nervous system also have afferent fibers that transmit the painful stimulation of the different organs.

The main difference between autonomic and somatic efferent pathways is that autonomic pathways have two neurons in series, and somatic ones only a motor neuron that connects the central nervous system with the skeletal muscle fiber.

2. The nervous systems: sympathetic and parasympathetic.

All motor fibers leaving the central nervous system, that is, all sympathetic and parasympathetic preganglionic fibers release the neurotransmitter acetylcholine, which carries out transmission by interaction with nicotinic cholinergic receptors.

All parasympathetic postganglionic fibers, and some sympathetic postganglionic fibers, release the neurotransmitter acetylcholine, which transmits, this time, by interaction with muscarinic cholinergic receptors.

Most sympathetic postganglionic fibers release noradrenaline that acts on α and β adrenergic receptors. The exception is the sweat glands, where acetylcholine acts on muscarinic cholinergic receptors.

The sympathetic and parasympathetic nervous systems exert opposite effects in the control of the heart rate, in the gastrointestinal smooth muscle, etc., but not in other situations such as the secretion of the salivary glands.

The sympathetic activity is increased in extreme cases of stress (fight, flight, etc.), increasing cardiac frequency and contractility, while parasympathetic activity predominates during rest. Both exercise a continuous physiological control of organs and metabolic processes under usual conditions.

3. Neurotransmitters.

Several neurotransmitters (cotransmission) are released in the nerve transmission and the response will be the result of the various interactions of the cotransmitters involved with their corresponding receptors.

The basis of the effector response is found in the interaction with the postsynaptic receptors, although the interaction with the presynaptic receptors is also important, which can cause a positive or negative modulation on the activity of the neuron.

Some neurotransmitters perform a modulating or regulatory function of the transmission, since they act on the release of other cotransmitters.

Neurotransmitters act directly and, in addition, can regulate presynaptic transmitter release and neuronal excitability (both actions are examples of neuromodulation where the chemical mediator increases or reduces the effectiveness of synaptic transmission without directly participating as a transmitter).

The most prominent cotransmitters are nitric oxide and vasoactive intestinal peptide (parasympathetic), ATP and neuropeptide Y (sympathetic). Besides these, there are many other substances: prostaglandins, adenosine, dopamine, GABA, 5-hydroxytryptamine, opioid peptides, endocannabinoids, etc.

The opposite effects of the sympathetic and parasympathetic systems are not only due to the opposite effects of the two transmitters but also to the inhibition of the release of acetylcholine by noradrenaline acting on the parasympathetic terminals or inhibiting the release of noradrenaline by acetylcholine.

There are drugs that selectively act as agonists or antagonists on presynaptic receptors and postsynaptic receptors of the noradrenergic system and the cholinergic system.

The antagonist drug of one of the two systems, adrenergic (sympathetic) or cholinergic (parasympathetic), will favor the expression of the other in the organ that receives the innervation of the two autonomous nervous systems with opposing actions.

Cholinergic and noradrenergic terminations respond to acetylcholine and noradrenaline, as well as other substances released as cotransmitters, synthesized and stored in the autonomic nervous system neurons that are located in the central nervous system and in the ganglia. If more than one neurotransmitter or neuromodulator is released together, each of which interacts with specific receptors, the effect obtained is a result of the actions of each of them on their presynaptic or postsynaptic receptor.

4. Adrenergic and cholinergic impulses.

Adrenergic impulses (sympathetic effect) in the sinus node of the heart cause increased heart rate (β1 receptor).

Cholinergic impulses (parasympathetic effect) in the sinus node of the heart decrease the heart rate.

Adrenergic impulses (sympathetic effect) in the atrium of the heart increase cardiac contractility (β1 receptor), while cholinergic impulses (parasympathetic effect) reduce cardiac contractility.

Adrenergic impulses (sympathetic effect) in the atrioventricular node of the heart cause increased automaticity and conduction velocity (β1 receptor), while cholinergic impulses (parasympathetic effect) decrease conduction velocity and induce atrioventricular block.

In arterioles and veins, adrenergic impulses (sympathetic effect) cause constriction (α1, α2 receptors) and dilation (β2 receptor), while cholinergic impulses (parasympathetic effect) have little effect, except for dilation in salivary glands and erectile tissue.

In the lung, adrenergic impulses (sympathetic effect) induce bronchodilation by relaxation of the tracheobronchial muscle (β2 receptor), while cholinergic impulses (parasympathetic effect) cause bronchoconstriction and increased secretion.

In the digestive tract, adrenergic impulses decrease intestinal motility and induce sphincter contraction, while cholinergic impulses increase intestinal motility, relax sphincters and stimulate secretion.

In the bladder, adrenergic impulses induce sphincter contraction or urinary retention (α1 receptor) and detrusor relaxation (β2 receptor), while cholinergic impulses cause intense detrusor contraction and sphincter relaxation.

In male sex organs, adrenergic impulses (sympathetic effect) are involved in ejaculation (α1 receptor) and cholinergic impulses (parasympathetic effect) in erection.

In the uterus, adrenergic impulses (sympathetic effect) cause intense relaxation (β2 receptor) or contraction (α1 receptor).

In the eye, adrenergic impulses (sympathetic effect) cause contraction of the radial muscle of the iris (midriasis or dilation of the pupil) and cholinergic impulses (parasympathetic effect) generate contraction of the smooth muscle of the sphincter of the iris (myosis or decrease in the size of the pupil).

In the salivary and lacrimal glands, adrenergic impulses (sympathetic effect) cause secretion (α1 receptor) and cholinergic impulses (parasympathetic effect) a much more intense secretion.

5. Cholinergic transmission.

Cholinergic neurotransmission carried out by acetylcholine in the vegetative nervous system comprises the synapses of all sympathetic and parasympathetic preganglionic fibers (acetylcholine acts on nicotinic cholinergic receptors), the neuroeffective junction of all parasympathetic postganglionic fibers (acetylcholine acts on musculoskeletal cholinergic receptors) and the transmission carried out by some sympathetic postganglionic fibers (acetylcholine also acts on muscarinic cholinergic receptors).

The muscarinic actions of acetylcholine are due to its release in postganglionic parasympathetic terminations, except in the blood vessels and in the sweat glands.

Acetylcholine reduces blood pressure, indirectly, by establishing generalized vasodilation, although most of the blood vessels lack parasympathetic innervation, because it acts on vascular endothelial cells releasing nitric oxide, the which is responsable for the relaxation of vascular smooth muscle.

Acetylcholine stimulates the secretion of sweat glands innervated by sympathetic cholinergic fibers.

The effectiveness of neurotransmission requires that the neurotransmitter be rapidly removed from the synaptic space, which is achieved thanks to cholinesteric enzymes.

The acetylcholine released in the synaptic cleft can be rapidly hydrolyzed by acetylcholinesterase in the intersynaptic space or out of the synaptic cleft and be hydrolyzed by butyrylcholinesterase or exert its action by interacting with its cholinergic receptors in the different organs.

6. Cholinergic receptors.

There are two types of cholinergic receptors: nicotinic receptors (they are part of an ionic cannel whose opening they control) and muscarinic receptors (associated with G proteins).

There are three subtypes of nicotinic receptors: the muscular (found in the motor plate membrane), the peripheral neuronal (present in the sympathetic and parasympathetic ganglion cell membrane) and the central neuronal (in various areas of the central nervous system).

There are five subtypes of muscarinic receptors: M1 (found in ganglionic neurons), M2 (present in the heart), M3 (in secretory cells, smooth muscle cells and vascular endotelial cells), M4 (found in ganglionic neurons, vas deferens and uterus) y M5 (in the brain).

Nicotine mimics the responses caused by the excitation of sympathetic and parasympathetic preganglionic fibers, while muscarine mimics the responses induced by the excitation of parasympathetic postganglionic fibers, so the receptors responsible for the first type responses were called nicotinics and the receptors that generated the second type responses muscarinics.

The muscarinic effects produced by acetylcholine (decreased conduction velocity) are canceled after the administration of a small dose of atropine (muscarinic antagonist).

A higher dose of acetylcholine, still under the influence of atropine, would induce an increase in blood pressure by stimulation of the sympathetic ganglia (vasoconstriction) followed by a secondary increase by the release of adrenaline in the adrenal gland (nicotinic effects very similar to those produced by nicotine).

7. The muscarinic agonists (parasympathomimetics).

The muscarinic agonists (parasympathomimetics) or cholinergic agonists of direct muscarinic action are: choline esters (acetylcholine, methacholine, carbachol and bethanechol), natural alkaloids (muscarine, pilocarpine and arecoline) and synthesis alkaloids (oxotremorine and xanomeline).

In the cardiovascular system, acetylcholine reduces heart rate and conduction velocity, decreases the force of cardiac contraction (atrial), reduces cardiac output and causes a marked decrease in blood pressure, as well as arteriolar dilation (effect mediated by nitric oxide).

Methacholine, carbachol, bethanechol and pilocarpine cause increased secretory and peristaltic activity of the digestive tract and sphincter relaxation (diarrheic feces and cramps appear).

Carbachol and bethanechol favor urination, selectively contracting the detrusor and relaxing the sphincter of the urinary bladder.

The muscarinic agonists (parasympathomimetics) induce a marked bronchoconstriction, an increase in secretion in the trachea and bronchial tubes, and a reduction in intraocular pressure, as they contract the smooth muscle of the iris sphincter (myosis or decrease in pupil size) and the ciliary muscle.

Pilocarpine (mainly), arecoline and muscarine cause profuse sweating, significant salivation and excessive tearing.

Bethanechol chloride is used in urinary retention (including that following surgery), gastric retention, and postoperative abdominal distention.

Pilocarpine hydrochloride would be indicated in the treatment of xerostomia (dry mouth) warning of a possible decrease in visual acuity. As a side effect causes profuse sweating. This miotic is also used in chronic and acute glaucoma.

8. The muscarinic antagonists (parasympatholytics).

The muscarinic cholinergic antagonists (parasympatholytics) are: atropine, hyoscine (scopolamine), homatropine, benzotropine, metescopolamine, butylscopolamine, ipratropium, tiotropium, trospium, otilonium, pinaverium, tropicamide, dicycloverine, tolterodine, trimebutine, pirenzepine, telenzepine, tripitamin, darifenazine and solifenazine.

The muscarinic cholinergic antagonists (parasympatholytics) inhibit the salivary, lacrimal, bronchial and sweat glands (they cause intense dry mouth) and cause pupillary dilation or mydriasis (they stop responding to light) and paralysis of the accomodation or cycloplegia due to the relaxation of the ciliary muscle, making vision difficult close.

High doses of atropine reduce gastrointestinal motility incompletely (M3 selective drugs under development), while pirenzepine inhibits gastric secretion without affecting other systems (M1 selectivity).

The muscarinic cholinergic antagonists (parasympatholytics) relax the bronchial musculature and reduce the secretion of the nasal, pharyngeal, tracheal and bronchial mucous glands. In this way, they avoid reflex bronchoconstriction (anesthesia), but not that induced by local mediators (asthma).

High doses of atropine produce excitation on the central nervous system (nerouness, irritability, disorientation, hallucinations and delirium) and, in case of intoxication, the effects are reversed with physostigmine (anticholinesterase that cancels the blockage of muscarinic cholinergic acetylcholine receptors).

Hyoscine (scopolamine) at therapeutic doses produces remarkable sedation and is used as an anticholinergic and antiemetic, as it blocks cholinergic transmission in the vestibular nuclei.

The muscarinic cholinergic antagonists (parasympatholytics) affect the extrapyramidal system reducing the side effects of many antipsychotics and applied in antiparkinsonian therapy.

Oxybutynin (transdermal sustained-release patches to avoid side reactions) and tolterodine (less side effects) are used in the treatment of overactive bladder, as well as trospium and selective M3 antagonists: darifenazine and solifenazine. On the other hand, trospium is also used in the treatment of urinary incontinence in the unstable bladder due to detrusor instability (caution in the elderly with prostatic hypertrophy, since all these drugs usually precipítate a urinary retention).

In order to produce mydriasis, cycloplegia or both effects (acute iritis, iridocyclitis, keratitis, retinal and fundus exploration), tropicamide (short action) and cyclopentolate (prolonged action) are used. In patients with predisposition can trigger an attack of acute glaucoma.

Atropine and scopolamine are used in pre-anesthetic medication to prevent vagal cardiovascular reflexes and reduce brochoconstriction and tracheobronchial, salivary and lacrimal hypersecretion.

The muscarinic cholinergic antagonists (parasympatholytics) are indicated in the spasms of the digestive smooth musculature to facilitate gastrointestinal endoscopy and radiology, as well as spasmolytics in irritable bowel síndrome or colon diverticulosis.

Atropine is useful in certain cases of atrioventricular block or bradycardia of vagal origin, as well as antidote against cholinergic agents and cholinesterase inhibitors.

9. Ganglionic neurotransmission.

The drugs that stimulate ganglionic neurotransmission (ganglionic stimulants) act selectively on nicotinic receptors and may be of natural origin, such as nicotine and lobeline (used in smoking cessation) or of synthetic origin, such as dimethylphenylpiperazinium and tetramethylammonium.

Nicotine, initially, causes stimulation of the ganglia, which generates a complex mixture of sympathetic and parasympathetic actions (increased blood pressure, increased bronchial, salivary and sweat secretions, tachycardia, tremors, breathing stimulation, nausea, etc.), although these stimulating effects, in many cases, are followed by depression.

The ganglionic blocking drugs or ganglionic blockers (hexamethonium, trimetaphan and mecamylamine) have stopped being used due to the numerous and complex effects theu produced: hypotension, inhibition of secretions, reduction of tone and gastrointestinal motility, problems in urination, etc.

10. Blocking neuromuscular transmission.

The non-depolarizing neuromuscular blockers (tubocurarine, alcuronium, atracurium, cisatracurium, mivacurium, doxacurium, pancuronium, vecuronium, rocuronium, pipecuronium and rapacuronium) act as competitive antagonists since the neuromuscular blockade they produce can be reversed after the increased in acetylcholine in the plate motor (though the direct addition of acetylcholine or, indirectly, with the administration of anticholinesterase agents).

The non-depolarizing neuromuscular blockers are used in anesthesia for the induction of long-lasting muscle relaxation, in seizures present in tetanus or when it is required to facilitate mechanical ventilation. Initially, the extrinsic muscles of the eye and facials are paralyzed; those of limbs, neck, trunk, intercostal muscles and diaphragm then follow, the respiratory muscles being the first to recover.

Cisatracurium, doxacurium, pipecuronium and vecuronium lack cardiovascular effects and do not increase the release of hystamine, while pancuronium, rapacuronium and rocuronium produce tachycardia.

The depolarizing neuromuscular blockers (decamethonium and suxamethonium) act as agonists on the nicotinic receptors of the terminal motor plate, in the same way as acetylcholine, although the difference is that decamethonium (in disuse due to its prolonged effect) and suxamethonium (succinylcholine) are not metabolized by acetylcholinesterase and remain on the endplate long enough for sustained depolarization to induce a loss of electrical excitability and neuromuscular blockage occurs.

Suxamethonium (succinylcholine) produces intense relaxation of 3-5 minutes duration and spontaneous recovery, and is used in endotracheal intubation, short-term procedures (dislocations), drug-induced seizures and electroconvulsive therapy.

The depolarizing neuromuscular blockers cause bradycardia, loss of muscle potassium that induces hyperkalemia (increased extracelular potassium can cause cardiac arrest in situations of liver disease, burns and injuries with muscle denervation), increased intraocular pressure and prolonged paralysis in patients with plasma cholinesterase deficiency or who are using anticholinesterase agents.

The co-administration of suxamethonium and halothane (inhalation anesthetic) can cause malignant hyperthermia (idiosyncratic disorder characterized by intense muscle spasm with high increase in body temperatura that can cause death), which is fought with the dantrolene drug, as it inhibits muscle contraction by preventing calcium from the sarcoplasmic reticulum.

Neuromuscular transmission can be blocked with presynaptic drugs that interfere with the synthesis of acetylcholine (hemicolinium and triethylcholine) or that inhibit the release of acetylcholine (botulinum toxin: used in the treatment of blepharospam, hemifacial spasm, strabismus and spasmodic torticollis, vesamicol, β-bungarotoxin and tetanus toxin).

11. The cholinesterase inhibitor drugs.

The cholinesterase inhibitor drugs or anticholinesterase agents (edrophonium, ambenonium, physostigmine, neostigmine, pyridostigmine, rivastigmine, diflos, parathion, ecotiopathe, galantamine and donepezil) favor cholinergic transmission, since they prevent the inactivation of acetylcholine by inhibiting the action of the two types of cholinesterase that hydrolyse acetylcholine (acetylcholinesterase and butyrylcholinesterase).

Anticholinesterase drugs increase and prolong the action of acetylcholine released in motor terminations, which allows repeated binding of the neurotransmitter with nicotinic receptors and the restoration of synaptic transmission when the receptors are blocked by a competitive antagonist or by antibodies (myasthenia gravis).

The cholinesterase inhibitor drugs or anticholinesterase agents cause myosis and contraction of the ciliary muscle (blockage of accommodation and difficulty focusing on near visión), increased peristaltic activity and stimulation of gastric secretion, bradycardia and arterial hypotension, increased bronchiole tone and tracheobronchial hypersecretion.

Edrophonium is an anticholinesterase drug with rapid action (seconds) and a short duration (less than 15 minutes). It is used in the diagnosis of myasthenia gravis, a disease characterized by pronounced weakness of the striated muscle (in the case that it were, the improvement would be sudden), and to resolve the doubt between myasthenic crisis or cholinergic crisis (it will resolve one and briefly worsen the second).

Myasthenia gravis is treated with neostigmine, pyridostigmine or ambenonium.

Some anticholinesterase drugs that cross the blood brain barrier (donepezil, rivastigmine and galantamine) are used in the treatment of Alzheimer’s disease, since they increase cholinergic activity and improve cognitive function.

12. Noradrenergic transmission.

In the noradrenergic transmission three natural catecholamines participate: dopamine, noradrenaline and adrenaline, which form three links followed in the synthesis of catecholamines (requires the activity of four enzymes that are not always found together in all cells).

The synaptic vesicles contained in the varicosities of the peripheral noradrenergic neurons (sympathetic postganglionic) are the place of synthesis, storage and release of noradrenaline, and coliberation of other mediators such as ATP and neuropeptide Y.

The concentration of noradrenaline in the vesicles is very high and is maintained thanks to the vesicular monoamine transporter and the formation of the noradrenaline-ATP-chromogranin A complex that prevents its exist. Th enerve stimulation causes the depolarization of the nerve termination membrane, opening its calcium channels, so that, as a consequence of calcium entry, the release of noradrenaline, dopamine-β-hydroxylase, ATP and chromogranin A.

The first two enzymes that metabolize catecholamines, are located intracellularly (reuptake into the cell is necessary for degradation), are well distributed throughout the body, including the brain, and are catechol-O-methyltransferase (COMT) and monoaminoxidase (MAO).

The neurotransmitter cell uptake can be: neuronal (the nerve endings capture 75% of the newly released noradrenaline, recycling it and can be released again by the nerve stimulus) and extraneuronal (important for adrenaline, where non-neuronal neighboring cells they capture catecholamines that are not stored, but are subsequently metabolized by the MAO or by the COMT).

13. Adrenergic receptors.

Adrenergic receptors are selective molecular structures of catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine). Depending on the response obtained, in various organs, to natural catecholamienes and synthetic isoprenaline (isoproterenol), adrenergic receptors are classified into two clases, α and β, with two subtypes α1, α2 (each with three additional subtypes) and three subtypes β1, β2 and β3, classified according to the order of potency of the agonists or the existence of selective antagonists.

The α1-adrenergic receptors (NA> A >> ISO) acuse vasoconstriction, increase in blood pressure, contraction of the radial iris muscle (mydriasis) and digestive and bladder sphincters, glycogenolysis (hyperglycemia) and secretion of salivary glands and sweaty.

The α2-adrenergic receptors (A> NA >> ISO) produce inhibition of neurotransmitter release (hypotension), platelet aggregation and inhibition of insulin secretion (hyperglycemia).

The β1-adrenergic receptors (ISO> NA> A) induce increase in cardiac frequency and contractility, increase in automaticity and driving speed.

The β2-adrenergic receptors (ISO> A> NA) produce bronchodilation, vasodilation, relaxation of the visceral smooth muscle (digestive, uterus, bladder detrusor, etc.), muscular tremor and hepatic glycogenolysis.

The β3-adrenergic