This document presents information on parasympathomimetics, which are drugs that mimic the effects of parasympathetic nervous system stimulation. It discusses how parasympathomimetics can directly activate cholinergic receptors through agonists like acetylcholine, muscarine, and pilocarpine. It also describes how anticholinesterase drugs inhibit the acetylcholinesterase enzyme, increasing the availability of acetylcholine at cholinergic synapses. Specific parasympathomimetic drugs discussed include bethanechol, carbachol, pilocarpine, and echothiophate. The document provides details on the mechanisms of action and therapeutic uses of these cholinergic drugs.
drug relative to eyes with their meiotic and mydriatic effect.
In the presentation discus about spasm of accommodation and cycloplegic action on eye . pharmacological action , dosage also discussed of condition developed on eye i.e. Glaucoma
Local anesthesia and how to block the face was discussed. The presentation covered the historical perspective of local anesthetics from cocaine to modern agents like lidocaine. It described the mechanism of action as blocking sodium channels, preventing nerve impulse transmission. Relevant anatomy for nerve blocks and types of local anesthetics were presented. EMLA cream and dosages were also mentioned.
Pilocarpine is an eye drop medication used to treat glaucoma by reducing the pressure inside the eye. It works by stimulating muscarinic receptors in the eye, causing the iris sphincter muscle and ciliary muscle to contract. This contraction allows fluid to drain from the eye more easily, thereby lowering intraocular pressure. Pilocarpine should not be used by patients with uveitis or pupillary block glaucoma, or those with an allergy to pilocarpine. Common side effects include blurred vision, eye pain, headaches, and nausea.
Skeletal muscle relaxants are drugs that act peripherally at neuromuscular junction/ muscle fibre itself or centrally in the cerebrospinal axis to reduce muscle tone and/or cause paralysis. • A muscle relaxants is a drug that affects skeletal muscle function and decreases the muscle tone
This document is a lecture on sedative-hypnotic and anxiolytic drugs given by Dr. Marc Imhotep Cray. The learning objectives cover the GABAA receptor structure and drug binding sites, pharmacokinetics of benzodiazepines, similarities and differences among benzodiazepines and between benzodiazepines and barbiturates, factors in drug selection, and abuse potential of sedative-hypnotics. The lecture discusses mechanisms of action, side effects, clinical uses including treatment of anxiety and insomnia, and specifics of benzodiazepines, barbiturates, and other agents.
This document provides information on antiepileptic drugs (AEDs). It defines epilepsy and different types including generalized and partial seizures. It discusses the classification and mechanisms of action of AEDs including effects on sodium channels, GABA neurotransmission, and calcium channels. Specific AEDs described in detail include phenytoin, carbamazepine, oxcarbazepine, and eslicarbazepine. Their indications, mechanisms, adverse effects, drug interactions and important notes are summarized. Carbamazepine is also described as the drug of choice for treating trigeminal neuralgia.
The document provides guidance on how to prepare a case report presentation. It discusses including key elements like the chief complaint, history of present illness, past medical history, family history, social history, medications, allergies, review of systems, physical exam, lab results, ECG findings, assessment, and questions. It emphasizes focusing on clinically relevant information and interpreting exam and lab findings rather than just reporting values. The document also discusses using a "SOAP" format for case discussions with a pharmacist perspective rather than just copying the physician's notes.
Barbiturates were once commonly used as sedatives and hypnotics but have been replaced by benzodiazepines and newer drugs due to risk of addiction. They act by potentiating the inhibitory neurotransmitter GABA at GABA-A receptors. While no longer recommended for insomnia, barbiturates are still used for seizures, especially in neonates, when other drugs fail. Adverse effects include respiratory depression, hypotension, and development of tolerance with repeated use.
This document discusses adrenergic agonists and antagonists. It describes the synthesis, storage, release, and degradation of catecholamines like norepinephrine. It outlines the different subtypes of alpha and beta adrenergic receptors, their locations, and the effects of agonist binding. Key adrenergic drugs like epinephrine, norepinephrine, dopamine, and dobutamine are explained in terms of their mechanisms of action, therapeutic uses, dosages, and adverse effects. Interactions between adrenergic drugs and other medications are also noted.
Migraine is a central nervous system disorder with a genetic basis. People with migraines have a hyperexcitable brain that is more sensitive to triggers. During migraine attacks, there is a wave of reduced blood flow called cortical spreading depression that starts in the occipital cortex and progresses forward. Repeated attacks can lead to changes in brain structures involved in pain processing like the periaqueductal gray, and an increased risk of white matter lesions. Preventive treatments aim to reduce central nervous system excitability underlying migraine while acute treatments target trigeminal pain pathways activated during attacks.
This document presents information on parasympathomimetics, which are drugs that mimic the effects of parasympathetic nervous system stimulation. It discusses how parasympathomimetics can directly activate cholinergic receptors through agonists like acetylcholine, muscarine, and pilocarpine. It also describes how anticholinesterase drugs inhibit the acetylcholinesterase enzyme, increasing the availability of acetylcholine at cholinergic synapses. Specific parasympathomimetic drugs discussed include bethanechol, carbachol, pilocarpine, and echothiophate. The document provides details on the mechanisms of action and therapeutic uses of these cholinergic drugs.
drug relative to eyes with their meiotic and mydriatic effect.
In the presentation discus about spasm of accommodation and cycloplegic action on eye . pharmacological action , dosage also discussed of condition developed on eye i.e. Glaucoma
Local anesthesia and how to block the face was discussed. The presentation covered the historical perspective of local anesthetics from cocaine to modern agents like lidocaine. It described the mechanism of action as blocking sodium channels, preventing nerve impulse transmission. Relevant anatomy for nerve blocks and types of local anesthetics were presented. EMLA cream and dosages were also mentioned.
Pilocarpine is an eye drop medication used to treat glaucoma by reducing the pressure inside the eye. It works by stimulating muscarinic receptors in the eye, causing the iris sphincter muscle and ciliary muscle to contract. This contraction allows fluid to drain from the eye more easily, thereby lowering intraocular pressure. Pilocarpine should not be used by patients with uveitis or pupillary block glaucoma, or those with an allergy to pilocarpine. Common side effects include blurred vision, eye pain, headaches, and nausea.
Skeletal muscle relaxants are drugs that act peripherally at neuromuscular junction/ muscle fibre itself or centrally in the cerebrospinal axis to reduce muscle tone and/or cause paralysis. • A muscle relaxants is a drug that affects skeletal muscle function and decreases the muscle tone
This document is a lecture on sedative-hypnotic and anxiolytic drugs given by Dr. Marc Imhotep Cray. The learning objectives cover the GABAA receptor structure and drug binding sites, pharmacokinetics of benzodiazepines, similarities and differences among benzodiazepines and between benzodiazepines and barbiturates, factors in drug selection, and abuse potential of sedative-hypnotics. The lecture discusses mechanisms of action, side effects, clinical uses including treatment of anxiety and insomnia, and specifics of benzodiazepines, barbiturates, and other agents.
This document provides information on antiepileptic drugs (AEDs). It defines epilepsy and different types including generalized and partial seizures. It discusses the classification and mechanisms of action of AEDs including effects on sodium channels, GABA neurotransmission, and calcium channels. Specific AEDs described in detail include phenytoin, carbamazepine, oxcarbazepine, and eslicarbazepine. Their indications, mechanisms, adverse effects, drug interactions and important notes are summarized. Carbamazepine is also described as the drug of choice for treating trigeminal neuralgia.
The document provides guidance on how to prepare a case report presentation. It discusses including key elements like the chief complaint, history of present illness, past medical history, family history, social history, medications, allergies, review of systems, physical exam, lab results, ECG findings, assessment, and questions. It emphasizes focusing on clinically relevant information and interpreting exam and lab findings rather than just reporting values. The document also discusses using a "SOAP" format for case discussions with a pharmacist perspective rather than just copying the physician's notes.
Barbiturates were once commonly used as sedatives and hypnotics but have been replaced by benzodiazepines and newer drugs due to risk of addiction. They act by potentiating the inhibitory neurotransmitter GABA at GABA-A receptors. While no longer recommended for insomnia, barbiturates are still used for seizures, especially in neonates, when other drugs fail. Adverse effects include respiratory depression, hypotension, and development of tolerance with repeated use.
This document discusses adrenergic agonists and antagonists. It describes the synthesis, storage, release, and degradation of catecholamines like norepinephrine. It outlines the different subtypes of alpha and beta adrenergic receptors, their locations, and the effects of agonist binding. Key adrenergic drugs like epinephrine, norepinephrine, dopamine, and dobutamine are explained in terms of their mechanisms of action, therapeutic uses, dosages, and adverse effects. Interactions between adrenergic drugs and other medications are also noted.
Migraine is a central nervous system disorder with a genetic basis. People with migraines have a hyperexcitable brain that is more sensitive to triggers. During migraine attacks, there is a wave of reduced blood flow called cortical spreading depression that starts in the occipital cortex and progresses forward. Repeated attacks can lead to changes in brain structures involved in pain processing like the periaqueductal gray, and an increased risk of white matter lesions. Preventive treatments aim to reduce central nervous system excitability underlying migraine while acute treatments target trigeminal pain pathways activated during attacks.
