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Anti-epileptic and anticonvulsive drugs
Revealing the secrets of anti-epileptics and anti-convulsants: Secret weapons to protect brain health Epilepsy is a chronic central nervous system disease where sudden abnormal discharges of brain neurons lead to transient dysfunction. Antiepileptics and anticonvulsants are at the heart of treatment, such as phenytoin, carbamazepine, etc., which can control systemic or localized seizures. Long-term medication use requires regular monitoring of blood signs and liver function to avoid toxic reactions. Magnesium sulfate is often used to control ejaculation, while IV calcium agent is used to rescue poisoning. Remember not to stop the medicine suddenly to avoid rebound. Understanding these drugs is the key to protecting the health of epilepsy patients!
Edited at 2025-03-10 15:20:57- Rumi 10 spiritual high-dimensional awakenings
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.
- Pathophysiology - Heart failure
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.
- Pathophysiology - ischemia - reperfusion injury
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.
Anti-epileptic and anticonvulsive drugs
- Rumi 10 spiritual high-dimensional awakenings
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.
- Pathophysiology - Heart failure
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.
- Pathophysiology - ischemia - reperfusion injury
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.
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Chapter 15 Anti-epileptics and anticonvulsive drugs
Anti-epileptic drugs
epilepsy
A chronic central nervous system disease
Unclear cause
Clinical manifestations
It is a chronic disease that causes sudden abnormal discharge of brain neurons, leading to temporary brain dysfunction.
Classification
Localized seizures
Simple
Local limb movement/perception abnormality
Short duration
Generally <1min
Comprehensive
That is, "psychomotor attack"
Clinical symptoms are mainly manifested as consciousness disorders, which can also manifest as mental symptoms and autonomic symptoms. A few can develop systemic attacks.
Shorter duration
Tens of seconds-minutes
Systemic attacks
Absent episode
That is, "small attack"
More common in children
symptom
It manifests as a brief loss of consciousness, suddenly beginning and ending
Short duration
seconds-ten seconds
Myoclonus seizure
Classification
Infant myoclonus
Children's myoclonic
Post-pubertal myoclonus
symptom
Sudden short tremor-like contraction
Short duration
A few seconds
Tonic-clonic seizure
That is, "major attack"
Attacks are not divided into time and place → very harmful
symptom
Sudden loss of consciousness
Toxicclonic twitching throughout the body
Cyanosis
Respiratory distress or even stop
Lip bite
Close your eyes or turn them up
Severe people with incontinence, etc.
"State of Epilepsy"
concept
During continuous epilepsy, consciousness has not fully recovered and has frequent recurrences or has been on the rise for more than 30 minutes.
Status of epilepsy in systemic seizures are often accompanied by varying degrees of consciousness and motor dysfunction, and in severe cases, there are symptoms of cerebral edema and increased cranial pressure.
Treatment drugs
Phentoin/Dalun Dine
Mechanism of action
Membrane stabilization
Treatment dosage
Block the excitability of Na channels, ↓ membranes
Significant frequency dependence—the Na channel blocking effect on neurons with abnormal discharges of high-frequency
Inhibiting the rapid inactivated (T-type) Ca2 channel →Ca2 inflow↓, membrane excitability↓
Also has frequency dependency
Larger dose
Suppress K outflow
Extend the action potential duration APD and effective refractory ERP
Cell autonomy↓
Enhanced GABA functionality
Inhibit the uptake of GABA by nerve endings in high concentrations → GABA concentration in synaptic cleft↑→Cl-influence↑→ membrane potential hyperpolarization, inhibiting the occurrence and diffusion of high-frequency discharge
In vivo process
absorb
Weak acid, difficult to dissolve in water → Made into sodium salt → Strong alkaline, high irritation → Intramuscular injection will produce local precipitation → Generally, muscle and subcutaneous injection are not selected
Oral absorption is slow and irregular
Generally, the blood volume can reach its peak 3-12 hours after a single dose oral dose
Bioavailability F
Different preparations are different
There are also big differences in individuals
distributed
High plasma protein binding rate
About 90%
Pay attention to their mutual influence when taken with other drugs that bind more to plasma proteins
eliminate
Hepatic drug enzyme metabolism as inactive products and excretes them out of the body
And it is a liver enzyme inducer
It can increase liver enzyme activity
Combined with other medicines can speed up its metabolism
The elimination method is related to blood drug concentration
＜10μg/ml
First-order dynamic elimination
The elimination rate remains unchanged, but the elimination amount changes
Has a half-life
＞10μg/ml
Level 0 dynamic elimination
The elimination amount remains unchanged, the elimination rate changes
No half-life
application
Anti-epileptic
Treatment of major and localized attacks
Ineffective for minor attacks
Membrane stabilization → Treatment of peripheral neuralgia
Trigeminal neuralgia, glossopharyngeal neuralgia, etc.
Reduce cell autonomy → Anti-arrhythmia
Adverse reactions
Symptoms of gastrointestinal irritation
Nausea, vomiting, etc.
Exclusive - gingival hyperplasia
Incidence rate 20%
More common in teenagers
Allergic reactions
Itchy skin, rash
Granulocyte deficiency, thrombocytopenia, aplastic anemia
Liver toxicity, etc.
Patients with epilepsy who have been taking phenytoin for a long time should regularly check blood signs and liver function.
Teratogenic reaction
Occasional teratogenesis in early pregnancy
Dosage-related toxic reactions
iV is too fast
Arrhythmia
BP↓
Generally, iV is only used to rescue patients with continuous epilepsy seizures
Oral overdose
Influences cerebellum and vestibular function
＞40μg/ml
Insanity
＞50μg/ml
coma
Carbamazepine/amideimidazine
Mechanism of action
The mechanism is similar to phenytoin, and the therapeutic dose blocks Na channels and inhibits neuronal discharge
application
It is one of the first choice for epilepsy and localized seizures
Anti-depression, anti-convulsion
The treatment of peripheral neuralgia is better than phenytoin
In vivo process
absorb
Good absorption after oral administration
distributed
Low plasma protein binding rate
75%
eliminate
Metabolites in the liver are active (epoxides)
The active metabolite has a long half-life, about 35 hours
Continuous medication may accumulate
It is also a liver enzyme inducer →
Repeated administration can accelerate your metabolism
The half-life can be shortened by 50% after 3-4 weeks of continuous use.
Adverse reactions
Dizziness, blurred vision, nausea and vomiting, ataxia
Thrombocytopenia, water and sodium retention
Temporary liver function abnormality, occasional regenerative disorder anemia
You should also check blood signs and liver function regularly
Phenobarbital/Lumina
Treatment of epilepsy, status epilepsy, localized seizures
Palmidone/deoxyphenitol
The same as phenobarbital
Usually used in combination with phenytoin or carbamazepine, but not meaningful when used in combination with phenobarbital.
Can enhance the efficacy
Ethexuxamide
Clinical application
Treatment of epilepsy seizures
Mechanism of action
Abnormal discharge of 3HZ plays an important role in epilepsy patients with epilepsy → Ethsumin can block T-type Ca2 → Inhibit 3HZ discharge
Adverse reactions
Low toxicity, common symptoms of gastrointestinal irritation
Drowsiness, dizziness, etc.
Use with psychiatric history with caution
Prone to mental behavior abnormalities
Sodium valproate
Broad-spectrum antiepileptic drugs
It has certain therapeutic effects on all types of epilepsy
Mechanism of action
Increase the GABA content in the brain
Improve glutamate decarboxylase activity → GABA synthesis ↑
Inhibiting the activity of GABA aminotransferase and succinate semialdehyde dehydrogenase → GABA decomposition↓
→Central suppression
Block Na channels
Blocks T-type Ca2 channel and inhibits 3HZ discharge
Theoretical basis for the treatment of epilepsy
Clinical application
Mainly combined with other antiepileptic drugs
Adverse reactions
Lighter
Occasionally liver damage
BDZs
Diazepam, lorazepam
For status epilepsy
Clonazepam
For minor attacks
Lamotriazine
Pharmacological effects and characteristics are similar to phenytoin and carbamazepine
Generally used to treat refractory epilepsy
Clinical application attention
Pay attention to its toxic reactions when taking medication for a long time
Regular blood signs and liver function checks
Do not stop or change medicine suddenly
To avoid bounce (the bounce phenomenon is very serious)
Anticonvulsant
Magnesium sulfate
Pharmacological effects
By route of administration
oral
Mg2 does not absorb
catharsis
Gay
injection
Systemic effect
Inhibit CNS and relax skeletal muscles
Dilate blood vessels and lower blood pressure
Systemic action mechanism
Extracellular fluid Mg2 ↑, chemical properties similar to Ca2 → antagonize Ca2 action →
Motor nerve ending Ach release ↓→Skeletal muscle relaxation
Intracellular Ca2 ↓→Vascular dilation
Mg2 excessive inhibition of myocardial muscle
Clinical application
Control ejaculation attacks
Anticonvulsive-relaxation skeletal muscles
Sedation-Inhibition of CNS
Dilate blood vessels - lower blood pressure
Adverse reactions
excess
Inhibiting respiration (respiratory muscle relaxation)
BP↓→Death
Rescue by poisoning
iV calcium agent
Calcium chloride
Calcium granule, etc.