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Anticholinergics

Anticholinergics

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Anticholinergics

  1. 1. ANTICHOLINERGICS Dr.Amudhan Arvind
  2. 2. An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system they inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells
  3. 3. Anticholinergic drugs Antinicotinic drugs Ganglionic blockers Neuromuscular blockers Antimuscarinic drugs
  4. 4. ANTIMUSCARINIC DRUGS Antimuscarinic drugs Naturally occurring antimuscarinic Semisynthetic Derivatives Synthetic antimuscarinics
  5. 5. Antimuscarinic Agents Natural Alkaloids Atropine Hyoscine (scopolamine) Extract of Belladona Semisynthetic Homatropine Encatropine Methylatropine Methscopoline Synthetic Tropicamide Glycopyrrolate Pirenzeline
  6. 6. STRUCTURE  Atropine is a product resulted from esterification of tropic and tropine base  In scopolamine, there is an oxygen bridging (epoxide)  In homatropine, hydroxymethyl of atropine is replaced by an OH-radical (tertiary)
  7. 7. PHARMACOKINETIC  Tertiary group:  lipid soluble  distribution is wide  absorption from gut and across conjunctiva is good  absorption across skin in suitable vehicle is good.  Significant concentration is reached within 0.5-1h (eg. scopolamine)  Quaternary group:  not very lipid soluble  distribution is confined to peripheral tissues (no central toxicity)  absorption from the site of application is poor
  8. 8.  Metabolism:  1/2 is metabolized by hepatic esterase (atropinase)  1/3 is excreted unchanged in the urine  80% excreted in the urine with an half-life of 2h  the effects on the eye persist 40-72h
  9. 9. PHARMACODYNAMIC  Interaction with muscarinic receptors: reversible, competitive  Receptor selectivity:  Atropine: -selective for muscarinic receptors  non-selective for muscarinic receptor subtypes  But, pirenzepine a selective antagonist for m1- receptors(stomach parietal cells)  Quaternary group:  not very selective for muscarinic receptors  can also antagonize Nicotinic-receptors in autonomic ganglia
  10. 10.  Tissue selectivity:  Tissues more sensitive to:  Atropine: salivary, sweat and bronchial glands  Pirenzepine (telenzepine, more effective): acid secretion from parietal cells (stomach)  Scopolamine: more effective on vestibular disturbances (eg. Motion sickness)
  11. 11. SOURCE  Atropine  - From Atropa belladonnea Datura stromonium  Occurs as l-form, not stable  racemizes to dl-form rapidly  commercial products contain dl-form  l-form is 100-times as potent as d- or dl-forms  -Scopolamine  From Hyosciamus niger  Occurs as l-form  its l- form is stable
  12. 12.  Muscarinic antagonists prevent the effects of ACh by blocking its binding to muscarinic receptors on effector cells at parasympathetic neuroeffector junctions, in peripheral ganglia, and in the CNS.  In general, muscarinic antagonists cause little blockade of nicotinic receptors.  The quaternary ammonium antagonists generally exhibit a greater degree of nicotinic blocking activity and therefore are more likely to interfere with ganglionic or neuromuscular transmission.
  13. 13.  Most clinically available muscarinic antagonists are nonselective and their actions differ little from those of atropine, the prototype of the group.  No subtypeselective antagonist, including pirenzepine, is completely selective
  14. 14. STRUCTURE-ACTIVITY RELATIONSHIPS  An intact ester of tropine and tropic acid is essential for antimuscarinic action,  The presence of a free OH group in the acyl portion of the ester also is important for activity.  When given parenterally, quaternary ammonium derivatives more potent than their parent compounds in both muscarinic and ganglionic (nicotinic) blocking activities.  The quaternary derivatives, when given orally, are poorly and unreliably absorbed.
  15. 15. MECHANISM OF ACTION.  Atropine and related compounds compete with ACh and other muscarinic agonists for a common binding site on the muscarinic receptor.  Since antagonism by atropine is competitive, it can be overcome if the concentration of ACh at muscarinic receptors of the effector organ is increased sufficiently.  Muscarinic receptor antagonists inhibit responses to postganglionic cholinergic nerve stimulation less effectively than they inhibit responses to injected choline esters.
  16. 16. EFFECTS OF ATROPINE IN RELATION TO DOSE
  17. 17. PHARMACOLOGICAL EFFECTS OF MUSCARINIC ANTAGONISTS CNS  In clinical dose:  - With atropine:  - a long lasting sedation with slow onset  - stimulation of vagal nuclei in the brain stem  With scopolamine:  - sedative effect is more powerful (drowsiness, amnesia)
  18. 18.  In toxic dose: (both atropine and scopolamine)  Excitement  Agitation  Hallucination  Coma  Disorientation  Delerium
  19. 19.  EYE  Mydriasis  Paralysis of ciliary muscle (cycloplegia):  Loss of accommodation  Adjustment of eye for far vision  Photophobia  Blurred vision  Lasts for 7-10 days  Acute glaucoma attack in patient with narrow irido- corneal angle due to impairment of drainage  Reduction of lacrimal secretion leading dry sandy eye
  20. 20. CARDIOVASCULAR SYSTEM  Low dose central vagal stimulation  initial bradycardia  followed by tachycardia resulting from peripheral anticholinergic efffec and thus unopposed sympathetic activity  Moderate dose tachycardia due to unopposed sympathetic activity  Atroventricular conduction:  accelereted due to unopposed sympathetic activity  PR shortening in ECG  in toxic doses, conduction block
  21. 21.  At toxic doses:  suppression of thermoregulatory sweating cutaneous vasodilatation at Release of hiatamine by blush areas (face, neck, ear)  The net CV effects:  Tachycardia  Slight elevation in blood pressure due to vasomotor centre stimulation
  22. 22. RESPIRATORY SYSTEM  Some bronchodilatation  Inhibition of bronchial secretion  Premedication in anaesthesiology: Used before inhalant anesthetics to reduce  -Bronchial secretions  -laryngospasm  -risk of airway obstructions  -postoperative pneumonia
  23. 23. GASTROINTESTINAL TRACT  Inhibition of saliva secretion → Dry mouth  Gastric secretion:  Blocked to lesser extent by atropine.  But, is blocked by pirenzepine and telenzepine  Volume of secretion and amount of acid, pepsin and mucine are all reduced  Large doses of atropine are necessary to reduce gastric secretions
  24. 24.  Motility of gut is more powerfully depressed by atropine than gastrointestinal secretions  Smooth musles of gut wall are paralysed  Propulsive movements are diminished  Sphincter muscles are not able to relax,constipation  Gastric emptying time prolonged  Intestinal transit time is lengthened  Some antimuscarinics have direct spasmolytic effect as well
  25. 25. GENITO-URINARY TRACT  Smooth muscles of ureter and bladder wall are relaxed  This is useful in the treatment of spastic pain due to mild urinary inflammations  Sphincter muscles of bladder become unable to relax.  urinary retention  may be hazardous in elder with prostate hypertrophy  Helpful in increasing bladder capacity  Controls detrusor hypereflexia in neurogenic bladder
  26. 26.  EFFECTS ON SWEAT GLAND  Thermoregulatory sweating is depressed by atropine  In adults, large doses of atropine can increase body temperature  In infants and children, even ordinary doses may cause atropine fever
  27. 27.  Other actions:  Markedly decreases salivary,lacrimal and tracheobronchial secretion  Decrease secretion of acid,pepsin and mucus of stomach  Mild local anaesthetic action on cornea
  28. 28. ATROPINE SUBSTITUTES  Most of semisynthgetic belladona alkaloid derivatives and synthetic compounds are atropine sucbstitutes  Differs only slightly from atropine
  29. 29. USES  Respiratory system:  Ipratropium and tiotropium .  Used in Asthma and COPD  These agents often are used with inhaled long-acting β2 adrenergic receptor agonists,  Ipratropium is administered four times daily via a metered-dose inhaler ornebulizer;  tiotropium is administered once daily via a dry powder inhaler.  Ipratropium also is FDA-approved for use in nasal inhalers for the treatment of the rhinorrhea associated with the common cold or with allergic or nonallergicperennial rhinitis..
  30. 30. GENITOURINARY TRACT.  Overactive urinary bladder can be successfully treated with muscarinic receptor antagonists.  These agents can lower intravesicular pressure, increase capacity, and reduce the frequency of contractions by antagonizing parasympathetic control of the bladder; they also may alter bladder sensation during filling  Muscarinic antagonists can be used to treat enuresis in children  In overactive bladder  oxybutynin  tolterodine  trospium chloride  Darifenacin ,  Solifenacin , and  Fesoterodine  Flavoxate
  31. 31.  The most important adverse reactions are consequences of muscarinic receptor blockade and include xerostomia, blurred vision, and GI side effects such as constipation and dyspepsia.  CNS-related antimuscarinic effects, including drowsiness, dizziness, and confusion, can occur and are particularly problematic in elderly patients.  CNS effects appear to be less likely with trospium, a quaternary amine, and with darifenacin and solifenacin;  The latter agents are relatively selective for M3 receptors and therefore have minimal effects on M1 receptors in the CNS, which appear to play an important role in memory and cognition
  32. 32. GI TRACT  As antisecretory.  In Peptic ulcer.  Pirenzepine  Telenzepine.  In reducing spasticity or motility of the GI tract (e.g., atropine,hyoscyamine and scopolamine) alone or in combination with sedatives or antianxiety agents(e.g., chlordiazepoxide
  33. 33.  Reduce tone and motility  M3-selective antagonists might achieve more selectivity  Glycopyrrolate also is used to reduce GI tone and motility.  Diarrhea associated with irritation of the lower bowel, may respond to atropine-like drugs, an effect that likely involves actions on ion transport as well as motility.  Dicyclomine is a weak muscarinic receptor antagonist that also has nonspecific direct spasmolytic effects on smooth muscle of the GI tract.  It is occasionally used in the treatment of diarrhea- predominant irritable bowel syndrome.
  34. 34. EYE.  Produce mydriasis and cycloplegia.  For breaking or preventing the development of adhesions between the iris and the lens.  Complete cycloplegia may be necessary in the treatment of iridocyclitis and choroiditis and for accurate measurement of refractive errors.  Homatropine hydrobromide  Cyclopentolate hydrochloride  Tropicamide
  35. 35. CARDIOVASCULAR SYSTEM.  Atropine may be considered in the initial treatment of patients with acute myocardial infarction in whom excessive vagal tone causes sinus bradycardia or AV nodal block.  Doses that are too low can cause a paradoxical bradycardia , while excessive doses will cause tachycardia that may extend the infarct by increasing the demand for oxygen.  It has little effect on most ventricular rhythms.  Eliminate premature ventricular contractions associated with a very slow atrial rate.  Reduce the degree of AV block when increased vagal tone is a major factor in the conduction defect, such as the second- degree AV block that can be produced by digitalis.  Selective M2 receptor antagonists would be of potential utility in blocking ACh-mediated bradycardia or AV block.
  36. 36. CENTRAL NERVOUS SYSTEM.  In prevention of motion sickness.  Scopolamine is the most effective agent  A transdermal preparation of scopolamine is used prophylactically for the prevention of motion sickness.  In the treatment of Parkinson disease.  Benztropine  Trihexyphenidyl  Biperiden  Selective M1 and M4 muscarinic antagonists may be efficacious for the treatment of Parkinson disease  While selective M3 antagonists may be useful in the treatment of obesity and associated metabolic abnormalities.
  37. 37.  Uses in Anesthesia.  Atropine commonly is given to block responses to vagal reflexes induced by surgical manipulation of visceral organs.  Atropine or glycopyrrolate is used with neostigmine to block its parasympathomimetic effects  Serious cardiac arrhythmias have occasionally occurred, perhaps because of the initial bradycardia produced by atropine combined with the cholinomimetic effects of neostigmine.
  38. 38. ANTICHOLINESTERASE POISONING  Atropine is not an actual antidote for organophosphate poisoning.  By blocking the action of acetylcholine at Muscarinic receptors, atropine also serves as a treatment for poisoning by organophosphate insecticides  Atropine is often used in conjunction with oximes  Atropine is given as a treatment for SLUDGE syndrome (salivation, lacrimation, urination, diaphoresi s, gastrointestinal motility, emesis) symptoms caused by organophosphate poisoning.
  39. 39.  Other Therapeutic Uses of Muscarinic Antagonists.  Methscopolamine –In temporary relief of symptoms of allergic rhinitis, sinusitis, and the common cold.  Homatropine potent as a ganglionic blocking agent,primarily used with hydrocodone as an antitussive combination
  40. 40.  MUSHROOM INTOXICATION  I) Intoxications with rapid onset (eg. within 2 hours)  II) Intoxications with slow onset (eg. within 2 to 6 hours)
  41. 41.  Rapid acting mushroom intoxications  1. -Mushrooms: Inocybe, Clitocybe  -posses high amount of muscarine  -cause severe parasympathomimetic effects  -onset of intoxication symptoms: within 15-30mins  -antidote: Atropine  2. -Mushrooms: Psilocibe, Copelandin, Pancoulus, Gymnopilus species  -posses psychoactive alkaloids such as psilocybin and psilocin  -cause delirium, euphoria, hallucination  -induce no sleep  - symptoms last 2-4 hours  -Treatment: Diazepam, phenothiazines
  42. 42.  3. -Mushrooms: A. muscaria, A. pantherina, A. cothurnate, A. gemmata  -posses GABA antagonists such as ibotenic acid and mushimol  -cause delirium, euphoria, hallucination  -but do induce sleep and coma  -symptoms resemble those of atropine, but not responsive physostigmine  -symptoms last 2-9 hours  - no antidote available  4. -Mushroom: Coprinus atramentarius  -contain coprin which inhibits aldehyde dehydrogenase  -cause disulfiram-like effects (aldehyde reaction!)  -toxic effects appear, when alcohol is drunken 2-3h after ingestion of mushrooms
  43. 43.  Slow acting mushroom intoxications  Amanita phalloides group  -Mushrooms: A. phalloides, A. verna, A. virosa  -Toxins: Phalloidin and α-Amanitin  α-Amanitin Inhibition of Depression of mRNA RNA- polymerase-II protein synthesis  - hepatotoxicity Tissue necrosis  - nephrotoxicity  - CNS toxicity
  44. 44.  Intoxications have 3 phases  1sth phase:  - resembles muscarine intoxication  - symptoms appear 8-12h after mushroom ingestion  2nd phase:  - symptoms in the first phase lessen and disappear within 24- 48h  - patient becomes asymptomatic in appearance  - but, biochemical hepatic changes continue developing  eg. - increase in transaminase activity  - elevation of biliuribin levels  - prolongation of prothrombin time  - lasts 2-6 days  -the patient may be discharged from the hospital considering healed
  45. 45.  3rd phase:  - begins abruptly with signs and symptoms of hepatotoxicity and nephrotoxicity: -  jaundice  - encephalopathy  - coagulopathy  - hypoglycemia  - acute renal insufficiency  1/3th of patients die within a week or so
  46. 46. ATROPINE POISONING  In overdoses, atropine is poisonous.  Atropine is incapacitating at doses of 10 to 20 mg per person.  Its LD50 is estimated to be 453 mg per person  The antidote to atropine is physostigmine or pilocarpine  These associations reflect the specific changes of warm, dry skin from decreased sweating, blurry vision, decreased sweating/lacrimation, vasodilation  This set of symptoms is known as anticholinergic toxidrome "hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter".
  47. 47.  ADVERSE EFFECTS OF ANTIMUSCARINICS  -Mydriasis and cycloplegia, when used against gut disorders  -Blockade of all parasympathetic functions:  -dry mouth, sandy eye  -mydriasis  -tachycardia, hot and flushed skin  -agitation, delirium, hallucination  -elevation of body temperature (children)
  48. 48.  -Treatment of adverse effects:  -due to overdose of atropine and its tertiary congeners  Physostigmine:  - 1-4mg, iv. in adults  - 0.5-1mg iv. in children  - Severe hyperthermia: - cooling blanket  - Seizures: -iv. diazepam
  49. 49.  CONTRAINDICATIONS OF ANTIMUSCARINICS  - Glaucoma (angle closure)  - Prostatic hypertrophy (elderly)  - Peptic ulcer (slowing of gastric emptying)  Exception: Pirenzepine, Telenzepine
  50. 50.  Central antimuscarinics used against Parkinson’s disease  Trihexyphenidyl 6-20mg  Procyclidine 7.5-30mg  Orphenanrine 150-400mg  Ethopropazine 150-300mg  Chlorphenoxamine 150-460mg  Biperiden 2-12mg  Benzotropine mesylate
  51. 51.  Ganglion-blocking agents competitively block the action of acetylcholine and similar agonists at nicotinic (Nn) receptors of both parasympathetic and sympathetic autonomic ganglia.
  52. 52.  Ganglionic blockers  Hexamethonium : acts mainly by channel blocker  Decamethonium  Quaternary -Tetraethyl ammonium:  short acting  -Pentolinium  -Chlorizondamine  -Trimetaphan:  very short acting  -Mecamylamine  Secondary -Pempidine
  53. 53.  Mechanism of ganglionic block:  1) Depolarizing block, eg. by sustained depolarization: Ach, nicotine, carbamoylcholine  2) Nondepolarizing competitive antagonism of Ni receptors  3) Channel block: Hexamethonium
  54. 54.  Results of ganglion blockade  CNS:  - Quaternary group is devoid of such effects  - Secondary group readily enters CNS: sedation, tremor, choreiform movements,mental disturbances  EYE:  - Moderate mydriasis (since p.sympathetic influence on iris is dominant)  - Cycloplegia with loss of accommodation
  55. 55.  CVS:  - Sympathetic CV reflexes are depressed  - Sympathetic influence on arteriols and veins are diminished, PVR and venous return are reduced, vasodilatation, hypotension (orthostatic), tachycardia  GUT:  - Secretions and motility are inhibited  - Some degree of constipation  Urinary system:  - Urination is blocked  - Urine retention in a man with prostate hypertrophy  Thermoregulatory sweating is blocked.
  56. 56. THERAPEUTIC USES:  1) Hypertension:  - rapid tolerance development and orthostatic hypotension  -now more effective agents are available  2) Acute hypertensive crisis in a patient with dissecting aortic aneurism.  Trimetaphan: 0.5-3mg/min by iv infusion  Disadvantage: tolerance development within 48h  3) Production of controlled hypotension to minimize haemorrhage at the operative field.  Trimetaphan: 1-4mg/min by iv infusion  4) Autonomic hyperreflexia (or reflex sympathetic dystrophy)
  57. 57.  Side effects:  The most serious one is orthostatic hypotension
  58. 58. NEUROMUSCULAR BLOCKERS  Block synaptic transmission at the neuromuscular junction  Affect synaptic transmission only at skeletal muscle  Does not affect nerve transmission, action potential generation  Act at nicotinic acetylcholine receptor NM
  59. 59. Classification: Neuromuscular blocking agents:- 1) Depolarizing muscle relaxants. 2) Non-depolarizing muscle relaxants
  60. 60. Depolarizing Muscle relaxants:  Succinylcholine (short acting) Non-depolarizing Muscle relaxants: Short acting:  Mivacurium Intermediate –acting:  Atracurium,  Cisatracurium,  Vecuronium,  Rocuronium Long acting :  Doxacurium  Pancuronium  Pipecuronium
  61. 61. MECHANISM OF ACTION SUXAMETHONIUM: • Block transmission by causing prolonged depolarization of endplate at neuromuscular junction. • Manifestation by initial series of muscle twitches (fasciculation) followed by flaccid paralysis. • It immediately metabolize in plasma by Pseudo- cholinesterase which is synthesized by liver so to prevent its metabolism in plasma it should be given at faster rate.
  62. 62. SYSTEMIC EFFECTS  Cardiovascular: Produces muscarinic effects as acetylcholine , therefore causes bradycardia ( but when given high doses causes tachycardia because of stimulation of nicotinic receptors at sympathetic ganglions.)  Hyperkalemia: Occurs due to excessive muscle fasciculations. Ventricular fibrillation can occur due to hyperkalemia.  CNS: Increases intracranial tension ( due to contraction of neck vessels)  Eye: Increases intraocular pressure.
  63. 63.  GIT: Increases intra-gastric pressure , salivation, peristalsis.  Muscle pains ( myalgia): This is a very common problem in post operative period. These are due to excessive muscle contractions.  Malignant hyperthermia  Severe Anaphylaxis  Masseter Spasm : Sch can cause masseter spasm especially in children & patients susceptible for malignant hyperthermia. Doesnot require reversal rather cholinesterase inhibitors (neostigmine) can prolong the depolarizing block (because these agents also inhibits the pseudocholinesterase)
  64. 64. NON-DEPOLARIZING MUSCLE RELAXANTS: Mechanism of action: • It blocks nicotinic receptors competitively resulting in inhibition of sodium channels and excitatory post- synaptic potential. • It binds at the same site at which acetylcholine binds. • All NDMR are quarternary ammonium compounds & highly water soluble i.e. hydrophilic. So, they do not cross blood brain barrier & placenta except Gallamine.
  65. 65. BROAD CLASSIFICATION  These are broadly divided into steroidal compounds and benzylisoquinoline (BZIQ) compunds.  STEROIDAL COMPOUNS: (vagolytic properties) It includes PANCURONIUM,VECURONIUM , PIPECURONIUM,ROCURONIUM, RAPACURONIUM,DOXACURIUM  BZIQ(Benzylisoquinoline): (hystamine realease) It includes d-Tubocurare, Metocurine, Doxacurium, Atracurium, Mivacurium, Cisatracurium  OTHERS includes Gallamine, Alcuronium
  66. 66. DIFFERENCES BETWEEN DEPOLARIZING & NON- DEPOLARIZING BLOCK Depolarizing Nondepolarizing Also called Phase I block - Block preceded by muscle fasciculations No fasciculations Depolarizing blocking drugs are called Leptocurare Called pachycurare Does not require reversal rather cholinesterase inhibitors (Neostigmine) can prolong the depolarizing block ( because these agents also inhibit the pseudocholinesterase). Reversed by cholinesterase inhibitors like Neostigmine.
  67. 67. NDMR ARE USED IN ANAESTHESIA FOR:  Maintenance of anaesthesia.  For intubation where succinylcholine is contraindicated ( Rocuronium is of choice)  For precurarization to prevent postoperative myalgias by succinylcholine.
  68. 68. STEROIDAL COMPOUNDS Pancuronium  Very commonly used as it is inexpensive.  It releases noradrenaline & can cause tachycardia & hypertension. Because of this there are increased chances of arrhythmia with halothane Pipercuronium  It is a pancuronium derivative with no vagolytic activity, so cardiovascular stable, slightly more potent Vercuronium  It is very commonly used now a days. It is cardiovascular stable. Shorter duration of action.  It is the muscle relaxant of choice in cardiac patient. Rocuronium  8 times more potent than vecuronium and it also has earlier onset of action  Because of onset comparable to succinylcholine it is suitable for rapid sequence intubation as an alternative to succinylcholine.
  69. 69. BENZYLISOQUINOLINE COMPOUNDS  D- Tubocurare  It is named so because it was carried in bamboo tubes & used as arrow poison for hunting by Amazon people.  It has highest propensity to release histamine  It causes maximum ganglion blockade. Because of ganglion blocking & histamine releasing property it can produce severe hypotension.  Due to histamine release it can produce severe bronchospasm.
  70. 70. REVERSAL OF BLOCK  Drugs used for reversal of block are cholinesterase inhibitors (anticholinesterases).  Reversal should be given only after some evidence of spontaneous recovery appear. Mechanism of Action  It inactivate the enzyme acetylcholinesterase which is responsible for break down of actetylcholine, thus increasing the amount of acetylcholine available for competition with non depolarizing agent thereby re-establishing neuromuscular transmission.  Anticholinesterases used for reversal are:  Neostigmine  Pyridostigmine  Edrophonium  Physostigmine
  71. 71. FACTORS PROLONGING THE NEUROMUSCULAR BLOCAKDE  Neonates  Old age  Obesity  Hepatic disease (both depolarizer & NMDR)  Renal disease ( only NDMR)  Inhalational agents : Prolong the block by both depolarizers & NDMR. Inhalational agents decrease the requirement of relaxant .The maximum relaxation is by ether followed by desflurane  Antibiotics: Both depolarizers & NMDR  Aminoglycosides.  Tetracyclines.
  72. 72.  Local Anaesthetics : Except procaine local anaesthetics prolong the action by stabilizing post synaptic membrane.  Hypothermia : Decreases metabolism of muscle relaxants.  Hypocalcemia: Calcium is required for producing action potential. Action of NDMR is enhanced.  Hypokalemia : NMDR block is enhanced.  Acid base imbalances especially acidosis.  Calcium channel blockers  Dantrolene  Neuromuscular disease  Hypermagnesemia.
  73. 73. DRUGS WHICH ANTAGONISE NEUROMUSCULAR BLOCKADE  They reverse the block by NDMR only  Phenytoin  Carbamazepine  Calcium  Cholinesterase inhibitors  Azathioprine  Steroids.
  74. 74. SUGAMMADEX  An agent for reversal of neuromuscular blockade by the agent rocuronium in general anaesthesia.  It is the first selective relaxant binding agent (SRBA) .  Sugammadex is a modified γ-cyclodextrin  The rocuronium molecule bound within sugammadex's lipophilic core, is rendered unavailable to bind to the acetylcholine receptor at the neuromuscular junction.  No need to rely on anticholinesterase
  75. 75. DRUGS WITH ANTICHOLNERGIC ACTION  ANTIHISTAMINES (H-1 BLOCKERS)  Chlorpheniramine  Cyproheptadine  Diphenhydramine  Hydroxyzine  CARDIOVASCULAR MEDICATIONS  Furosemide  Digoxin  Nifedipine  Disopyramide  ANTIDEPRESSANTS  Amoxapine  Amitriptyline  Clomipramine  Desipramine  Doxepin  Imipramine  Nortriptyline  Protriptyline  Paroxetine
  76. 76.  GASTROINTESTINAL MEDICATIONS  Antidiarrheal Medications  Diphenoxylate  Atropine  Antispasmodic Medications  Belladonna  Clidinium  Chlordiazepoxide  Dicyclomine  Hyoscyamine  Propantheline  Antiulcer Medications  Cimetidine  Ranitidine  ANTIPSYCHOTIC MEDICATIONS  Chlorpromazine  Clozapine  Olanzapine  Thioridazine
  77. 77.  MUSCLE RELAXANTS  Cyclobenzaprine  Dantrolene  Orphenadrine URINARY INCONTINENCE  Oxybutynin  Probantheline  Solifenacin  Tolterodine  Trospium  ANTIVERTIGO MEDICATIONS  Meclizine  Scopolamine PHENOTHIAZINE ANTIEMETICS  Prochlorperazine  Promethazine
  78. 78. NEWER ANTICHOLINERGICS  Umeclinidium bromide:  An anticholinergic drug approved for use in combination with vilanterol (as umeclidinium bromide/vilanterol) for the treatment of COPD  Aclinidium  An anticholinergic for the long-term management of chronic obstructive pulmonary disease (COPD). It has a much higher propensity to bind to muscarinic receptors than nicotinic receptors.  FDA approved on July 24, 2012.
  79. 79. DARIFENACIN  Darifenacin is a medication used to treat urinary incontinence.  Darifenacin works by blocking the M3 muscarinic acetylcholine receptor, which is primarily responsible for bladder muscle contractions.  It thereby decreases the urgency to urinate. It should not be used in people with urinary retention.  98% bound to plasma proteins  Hepatic metabolism. Primarily mediated by the cytochrome P450 enzymes CYP2D6 and CYP3A4.
  80. 80. SOLIFENACIN  Solifenacin is a competitive cholinergic receptor antagonist.  The binding of acetylcholine to these receptors, particularly the M3 receptor subtype, plays a critical role in the contraction of smooth muscle.  By preventing the binding of acetylcholine to these receptors, solifenacin reduces smooth muscle tone in the bladder, allowing the bladder to retain larger volumes of urine and reducing the number of micturition, urgency and incontinence episodes.  Because of a long elimination half life, a once-a-day dose can offer 24 hour control of the urinary bladder smooth muscle tone.

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Anticholinergics

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