MindMap Gallery Egressive nervous system-choline chemoline drug
In Chapter 6, we deeply explored the classification and application of cholinesterase drugs and their mechanism of action, especially the classification and application of anticholinesterase drugs. These drugs inhibit AchE activity and accumulate Ach in large quantities, thereby agonizing M receptors and N receptors, producing M-like and N-like effects. Drugs such as marcosin and neosidine have significant effects in the treatment of glaucoma and irisitis. However, excessive use may lead to a "cholinergic crisis", so you should pay attention to compressing the inner canthus during use to avoid systemic reactions. Understanding the pharmacological effects, contraindications and adverse reactions of these drugs is crucial for safe and effective application.
Edited at 2025-03-10 15:16:04Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Chapter 6. Choline-like drugs
Directly acting on choline receptors
Complete choline pseudo-
acetylcholine
Ach for medicinal use is artificially synthesized, but has few clinical applications and is mainly used in pharmacological research.
Pharmacological effects
Agitated M and N receptors
M-sample effect
Cardiovascular
Inhibition→Slow heart rate, weakened myocardial contraction, vasodilation, BP↓
smooth muscle
(Bronchial, gastrointestinal tract, uterus, urinary tract) contraction
Reduce the pupil and regulate spasm (distinct objects are unclear)
Gland secretion↑
Sweat glands, bronchial glands, digestive glands
N-like effects
When the Ach dose is slightly larger, N receptors can be activated, showing the excitation of N1 and N2 receptors.
N1 excitement
Gangular excitation → manifests as symptoms of sympathetic and parasympathetic excitation → manifestations for each organ depend on the manifestations of stimulation that are dominated by the usual dominant nerve excitation
e.g. The smooth muscle of the gastrointestinal tract is mainly innervated by the parasympathetic nerve → contraction; the blood vessels are mainly innervated by the sympathetic nerve → contraction; the blood vessels are mainly innervated by the sympathetic nerve → contraction
N2 excitement
Skeletal muscle contraction
Carbaccholine
Similar to Ach, but with high toxicity
Chrysanthesia
Pharmacological effects
A certain selectivity: Directly agonize the M receptor and produce an M-like effect
Opposite the eyes
Reduce pupils
Pupil sphincter contraction
Reduce intraocular pressure
When the pupil is reduced, the iris contracts, opens the anterior chamber angle to clear the circulation of the aquatic abdomen
Regulate spasm
When the pupil is shrinking, the ciliary muscle also contracts → the suspension ligament is relaxed → the lens is more convex → the distant object is unclear
To the glands
Increase gland secretion
Salivary glands and sweat glands are the most obvious
application
glaucoma
Glaucoma is a headache caused by increased intraocular pressure and unclear vision.
Irisitis
Must be used interactively with the mydriatic atropine → Prevent and treat adhesion with lens
Things to note
When dropping the eyes, press the inner canthus to avoid entering the nasal mucosa through the nasal lacrimal duct and absorbing blood, thereby causing systemic reactions.
Anticholinesterase drugs
Inhibiting AchE activity, preventing Ach from being hydrolyzed and accumulates in large quantities, thereby agonizing M receptors and N receptors, producing M-like and N-like effects.
Classification
Easy to reverse type
Refers to the easy recovery of AchE activity
New Side
Quaternary ammonium drugs → high polarity → not easy to pass through the blood-brain barrier and cornea
Mechanism of action
Inhibiting cholinesterase activity →Ach destruction ↓ →Ach↑ →M and N-like effects
Pharmacological effects
Gastrointestinal tract and bladder smooth muscles have obvious effects
The skeletal muscles have obvious excitation effects
application
Myasthenia gravis
Suppress AchE
Directly arouse N2 receptor
Promote the release of Ach by motor nerve endings
Excessive dose can cause a "cholinergic crisis"
Abdominal bloating and urinary retention after surgery
After the operation, the intestine is stimulated, and peristalsis is slowed down → bloating
Anesthetics, etc., relax the bladder detrusor muscle → urinary retention
Mechanism of action: Strengthening the contraction of the gastrointestinal tract and bladder smooth muscle
Toxicosis of muscle relaxation overdose
Atropine poisoning
Atropine: M receptor blocker
Adverse reactions
Enhance gastrointestinal peristalsis → abdominal pain, nausea and vomiting
neostigmine is lighter
Contraindications
Mechanical intestinal obstruction, urinary tract obstruction, bronchial asthma
Pyridostigmine and ambenonium have similar effects as neostigmine. But the former is weaker, the latter is stronger
Tyraniline
Ammonium tertiary drugs → weak polarity → easy to pass the center and cornea
Opposite the eyes
effect
Reduce pupils
Reduce eye pressure
Regulating spasm-difficulty in seeing distant objects
Things to note
Strong effect on ciliary muscles
What's different from pilocarpine
Can cause headaches, eye pain and blurred vision
Compress the inner canthus when the eyes are dripped to avoid systemic symptoms
N2 receptors can also be aroused at large doses
Skeletal muscle tremor
It can also promote gland secretion, but mainly acts on the eyes
Difficult to reverse type
It means that the activity of AchE is not easy to recover