Term
| In cholinergic transmission, ACh is found in: |
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Definition
Ganglia Postganglionic parasympathetic nerve ending Neuromuscular junction |
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Term
| Muscarinic receptors are this time of receptor: |
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Definition
| G-protein Coupled Receptor |
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Term
| These muscarinic receptors are found in the CNS, peripheral neurons, and gastric parietal cells. They are responsible for mediating the secretion of acid in the stomach. |
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Definition
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Term
| This type of muscarinic receptor is mainly found in the heart and is responsible for decreasing contractility of the heart. |
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Definition
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Term
| This type of muscarinic receptor controls glandular secretions and contraction of visceral smooth muscles. |
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Definition
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Term
| These muscarinic receptors are found centralized in the CNS |
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Definition
| M4 and M5 muscarinic receptors |
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Term
| These muscarinic receptors act through the inositol phosphate pathway. |
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Definition
| M1, M3, M5 muscarinic receptors |
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Term
| These muscarinic receptors act through inhibiting adenylate cyclase. |
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Definition
| M2 and M4 muscarinic receptors |
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Term
| Binding of ACh and this type of receptor elicits stimulation of the autonomic ganglia, stimulation of voluntary muscles, and secretion of epinephrine from the adrenal medulla. |
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Definition
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Term
| Binding of ACh with this type of receptor elicits parasympathetic stimulation. |
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Definition
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Term
| This enzyme is responsible for ACh uptake. |
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Definition
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Term
| This enzyme synthesizes ACh |
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Definition
| Choline Acetyltransferase (ChAT) |
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Term
| This transporter is responsible for loading ACh into vesicles. |
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Definition
| Vesicular Acetylcholine Transporter (VAChT) |
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Term
| This enzyme is responsible for the hydrolysis of ACh yielding choline and acetate. |
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Definition
| Acetylcholinesterase (AChE) |
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Term
| ACh release is dependent on this cation. |
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Definition
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Term
| This states that neurotransmitters are released in small elementary packets or quanta that are uniform in size. |
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Definition
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Term
This is caused by the influx of Na+ through nAChR and depolarizes the muscle fibers. |
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Definition
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Term
| This is caused by the influx of Na+ through voltage gated Na+ channels. |
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Definition
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Term
| This non-depolarizing muscle relaxant works by blocking the binding of ACh to nAChR on the post synaptic membrane of the neuromuscular junction. It is commonly used in South American poison darts. |
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Definition
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Term
This neurotoxin binds irreversibly to the nAChR, i.e. it is an irreversible antagonist for nAChR. It is a component of the venom of the Taiwanese banded krait. |
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Definition
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Term
| These neuromuscular blocking agents (muscle relaxants) are competitive reversible antagonists of nACh/nAChR. They block access of ACh to nAChR. |
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Definition
| Non-depolarizing muscle relaxants |
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Term
| These neuromuscular blocking agents (muscle relaxants) work as excessive depolarizing agonists that maintain endplate membrane depolarization. They prevent the transmission of another action potential. |
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Definition
Depolarizing muscle relaxants |
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Term
| d-tubocurarine, atracurium, and vecuronium are examples of: |
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Definition
| Non-depolarizing muscle relaxants |
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Term
| d-tubocurarine, atracurium, and vecuronium are used: |
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Definition
In conjunction with anesthesia for surgery. They help to relax tracheal muscles for endotracheal intubation. |
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Term
Succinylcholine is an example of: |
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Definition
| Depolarizing muscle relaxant |
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Term
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Definition
| With anesthesia to aid endotracheal intubation during surgery |
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Term
| Tubocurarine and pancuronium are examples of: |
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Definition
| Non-depolarizing muscle relaxants |
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Term
| These blocking agents work by blocking endplate potential thus blocking initiation of action potential in skeletal muscle. |
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Definition
| Non-depolarizing muscle relaxants |
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Term
| Non-depolarizing muscle relaxants have less side effects because: |
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Definition
| They are polar molecules that do not cross the BBB |
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Term
| These drugs are sometimes used to increase levels of ACh. |
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Definition
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Term
State the order of paralysis for non-depolarizing muscle relaxants. |
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Definition
1. Extraocular (causes double vision) 2. Extremeties: head, neck, face, hands, and feet 3. Abdomen, arms, and legs 4. Eyeblink 5. Respiratory and diaphragm (diaphragm paralysis causes death) |
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Term
State some of the side effects of non-depolarizing muscle relaxants. |
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Definition
Fall in arterial pressure (due to ganglionic blocking) Bronchospasm (due to release of histamine from mast cells) Tachycardia (due to blockade of mAChR by high drug concentrations) |
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Term
| Depolarizing blocking agents work by these two mechanisms: |
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Definition
Phase I Block Phase II Block |
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Term
| State some of the side effects of depolarizing blocking agents: |
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Definition
Bradycardia (due to direct action of succinylcholine) Hyperkalemia (especially in burn or trauma pts) Increased intraocular pressure Prolonged paralysis Malignant hyperthermia |
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Term
| Only _______ is inhibited by anticholinesterase drugs. |
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Definition
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Term
| Fasiculation, or disorganized twitching, is caused by: |
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Definition
| Depolarizing blocking agents |
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Term
| Tetanic fade is related to ________ blocking agents. |
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Definition
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Term
| ACh, carbachol, bethanechol, and pilocarpine are examples of muscarinic ________. |
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Definition
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Term
Pilocarpine, carbachol, and bethanechol are used to treat: |
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Definition
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Term
| Muscarinic agonists cause this/these effect(s) on the cardiovascular system: |
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Definition
| Decrease heart rate, decrease cardiac output |
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Term
Muscarinic agnoists cause this/these effect(s) on smooth muscle: |
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Definition
| Increase peristalic GI activity, contraction of bladder and bronchiole smooth muscle |
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Term
| Muscarinic agnoists cause this/these effect(s) on the eyes: |
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Definition
| Constrict sphincter and ciliary muscle, which decrease pupil size and accomodate near vision respectively
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Term
| Muscarinic agonists cause this/these effect(s) on CNS: |
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Definition
| If the agonist penetrates the BBB: Activate M1 receptor, cause tremor, hypothermia, increase locomotor activity |
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Term
Pilocarpine is used primarily for: |
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Definition
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Term
| Bethanechol is used primarily for: |
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Definition
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Term
| Carbachol and pilocarpine cause _____, which causes a _____. |
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Definition
| Miosis, Decrease in intraocular pressure |
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Term
| Atropine, hyoscine, ipratroprium are examples of: |
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Definition
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Term
| Tropicamide and cyclopentolate are _________ that are used for ________. |
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Definition
| Muscarinic antagonists, pupil dilation |
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Term
| Muscarinic antagonists cause this/these effect(s) on secretions: |
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Definition
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Term
| Muscarinic antagonists cause this/these effect(s) on heart rate: |
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Definition
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Term
Muscarinic antagonists cause this/these effect(s) on eyes: |
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Definition
| Pupil dilation, reduction in near vision, increase intraocular pressure |
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Term
| Muscarinic antagonists cause this/these effect(s) on GI tract: |
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Definition
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Term
| Muscarinic antagonists cause this/these effect(s) on smooth muscles: |
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Definition
| Relaxation of bronchial, ciliary, pupillary smooth muscles |
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Term
| Muscarinic antagonists cause this/these effect(s) on CNS: |
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Definition
| Excitatory effects, agitation, restlessness, disorientation |
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Term
| Atropine is clinically used for: |
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Definition
Adjunct for anesthesia to keep secretions controlled, anticholinesterase poisoning, bradycardia, GI hypermotility, cardiac arrest |
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Term
| Hyoscine is clinically used for: |
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Definition
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Term
| Atropine methonitrate is clinically used for: |
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Definition
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Term
| Ipratroprium is clinically used for: |
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Definition
| Asthma, bronchitis (antagonist for M3 mAChR) |
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Term
| Tropicamide and cyclopentolate are clinically used for: |
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Definition
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Term
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Definition
| Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis |
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Term
| Most SLUDGE effects are through which receptors? |
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Definition
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