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Description - A non-depolarizing neuromuscular blocking agent with short duration of
action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.
Indication - For use, as an adjunct to general anesthesia, to facilitate endotracheal intubation
and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
Pharmacodynamics - Atracurium is a nondepolarizing skeletal muscle relaxant.
Atracurium can be used most advantageously if muscle twitch response to peripheral nerve stimulation is monitored to assess degree of muscle relaxation. The duration of neuromuscular block produced by Atracurium is approximately one third to one half the duration of block by d-tubocurarine, metocurine, and pancuronium at initially equipotent doses. As with other nondepolarizing neuromuscular blockers, the time to onset of paralysis decreases and the duration of maximum effect increases with increasing doses of Atracurium. Repeated administration of maintenance doses of Atracurium has no cumulative effect on the duration of neuromuscular block if recovery is allowed to begin prior to repeat dosing. Moreover, the time needed to recover from repeat doses does not change with additional doses. Repeat doses can therefore be administered at relatively regular intervals with predictable results.
Mechanism of action - Atracurium antagonizes the neurotransmitter action of
acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate. This antagonism is inhibited, and neuromuscular block reversed, by acetylcholinesterase inhibitors such as neostigmine, edrophonium, and pyridostigmine.
Half life - The elimination half-life is approximately 20 minutes. Toxicity - Excessive doses can be expected to produce enhanced pharmacological effects.
Overdosage may increase the risk of histamine release and cardiovascular effects, especially hypotension.
Indication - For induction and maintenance of general anesthesia. Pharmacodynamics - Isoflurane is a general inhalation anesthetic used for induction and
maintenance of general anesthesia. It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cellcell coupling and altering the activity of the channels that underlie the action potential.
Mechanism of action - Isoflurane induces a reduction in junctional conductance by
decreasing gap junction channel opening times and increasing gap junction channel closing times. Isoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Isoflurane also binds to the GABA receptor, the large conductance Ca2+ activated potassium channel, the glutamate receptor and the glycine receptor.
Indication -For the treatment of cancer patients with severe pain that breaks through their
regular narcotic therapy.
Pharmacodynamics - Fentanyl is an opioid analgesic. Fentanyl interacts predominately
with the opioid mu-receptor but also binds to kappa and delta-type opioid receptors. These mubinding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, Fentanyl exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Fentanyl may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Fentanyl depresses the respiratory centers, depresses the cough reflex, and constricts the pupils.
Mechanism of action - Opiate receptors are coupled with G-protein receptors and function
as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the Gprotein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Fentanyl's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. Half life - 7 (range 3-12) hours
Indication - Used for the promotion of diuresis before irreversible renal failure becomes
established, the reduction of intracranial pressure, the treatment of cerebral edema, and the promotion of urinary excretion of toxic substances.
Pharmacodynamics - Chemically, mannitol is an alcohol and a sugar, or a polyol; it is
similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this reason, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is commonly used to increase urine production (diuretic). It is also used to treat or prevent medical conditions that are caused by an increase in body fluids/water (e.g., cerebral edema, glaucoma, kidney failure). Mannitol is frequently given along with other diuretics (e.g., furosemide, chlorothiazide) and/or IV fluid replacement.
Mechanism of action - Mannitol is an osmotic diuretic that is metabolically inert in
humans and occurs naturally, as a sugar or sugar alcohol, in fruits and vegetables. Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma. As a result, cerebral edema, elevated intracranial pressure, and cerebrospinal fluid volume and pressure may be reduced. As a diurectic mannitol induces diuresis because it is not reabsorbed in the renal tubule, thereby increasing the osmolality of the glomerular filtrate, facilitating excretion of water, and inhibiting the renal tubular reabsorption of sodium, chloride, and other solutes. Mannitol promotes the urinary excretion of toxic materials and protects against nephrotoxicity by preventing the concentration of toxic substances in the tubular fluid. As an Antiglaucoma agent mannitol levates blood plasma osmolarity, resulting in enhanced flow of water from the eye into plasma and a consequent reduction in intraocular pressure. As a renal function diagnostic aid mannitol is freely filtered by the glomeruli with less than 10% tubular reabsorption. Therefore, its urinary excretion rate may serve as a measurement of glomerular filtration rate (GFR). Half life - 100 minutes
Indication - Neostigmine is used for the symptomatic treatment of myasthenia gravis by
improving muscle tone.
Pharmacodynamics - Neostigmine is a cholinesterase inhibitor used in the treatment of
myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction.
Mechanism of action - Neostigmine is a parasympathomimetic, specifically, a reversible
cholinesterase inhibitor. The drug inhibits acetylcholinesterase which is responsible for the degredation of acetylcholine. So, with acetylcholinesterase inhibited, more acetylcholine is
present By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors which are involved in muscle contraction.. It does not cross the blood-brain barrier.
Absorption - Neostigmine bromide is poorly absorbed from the gastrointestinal tract
following oral administration
Indication - For use as a preoperative antimuscarinic to reduce salivary, tracheobronchial,
and pharyngeal secretions, to reduce the volume and free acidity of gastric secretions and to block cardiac vagal inhibitory reflexes during induction of anesthesia and intubation.
Pharmacodynamics - Glycopyrrolate decreases acid secretion in the stomach. Hence it can
be used for treating ulcers in the stomach and small intestine, in combination with other medications. In anesthesia, glycopyrrolate injection serves as a preoperative antimuscarinic operation that reduces salivary, tracheobronchial, and pharyngeal secretions, as well as decreases the acidity of gastric secretions blocks cardiac vagal inhibitory reflexes during intubation
Mechanism of action - Glycopyrrolate binds competitively to the muscarinic acetylcholine
receptor. Like other anticholinergic (antimuscarinic) agents, it inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and bronchial secretions.
Absorption - Rapidly absorbed (1-2 minutes) after intravenous injection
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