MindMap Gallery Pharmacological antipsychotic drugs thought guide
Mind map on pharmacological antipsychotic drugs, including antischizophrenia drugs, antimanic drugs, antidepressants, etc.
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antipsychotic drugs
antischizophrenia drugs
Schizophrenia
definition
A group of the most common schizophrenia characterized by incoordination between thinking, emotion, and behavior, and separation between mental activity and reality.
Classification
Type one
Positive symptoms: hallucinations and delusions
Type II
Negative symptoms: apathy, lack of initiative
Drug Classification
Classic antischizophrenia drugs
Phenothiazines
Chlorpromazine
Basic function
Blocks multiple receptors, including dopamine receptors, M-choline receptors, alpha-adrenergic receptors, and 5-HT receptors
Pharmacological effects
Effects on the central nervous system
Anti-schizophrenia effect
Features
It has a strong inhibitory effect on the central nervous system, and increasing the dose will not cause anesthesia.
Normal people can become quieter and less active after taking a therapeutic dose orally.
Patients with schizophrenia have good anti-schizophrenia effects after taking it, and can quickly control the state of excitement and restlessness.
mechanism
Antagonizes D2-like receptors in the mesolimbic and mesocortical systems (but has a higher incidence of extrapyramidal reactions)
Antiemetic effect
Small doses can antagonize the vomiting caused by the dopamine receptor agonist apomorphine by antagonizing the D2-like receptors in the emetic chemoreceptor area in the floor of the fourth ventricle of the medulla.
Large doses can directly inhibit the vomiting center
It is effective against intractable hiccups, mainly by inhibiting the central regulatory parts of hiccups near the medulla oblongata and emetic chemoreceptor areas.
Inability to combat vomiting caused by vestibular stimulation
thermoregulatory effect
Inhibits hypothalamic thermoregulation
Reduce the body temperature of febrile and normal bodies
The cooling effect changes with the temperature of the external environment and is applied simultaneously with physical cooling to have a synergistic cooling effect.
Effect on autonomic nervous system
Antagonizes α-adrenergic receptors, causing blood vessels to dilate and lower blood pressure, but is not suitable for the treatment of hypertension
Antagonizes M choline receptors, causing dry mouth, constipation, and blurred vision
Effect on endocrine
Activates D2 subtype receptors in the nodule infundibulum system
Promote the release of prolactin, inhibit the release of gonadotropins and glucocorticoids, and inhibit the secretion of pituitary growth hormone (for the treatment of gigantism)
Clinical application
Schizophrenia
Significant relief of positive symptoms
The treatment effect is good for acute patients, but the effect is poor for chronic patients.
Ineffective for patients with type 2 schizophrenia or even worsen their condition
It is effective for organic schizophrenia and symptomatic schizophrenia, but the dose must be small and the drug must be stopped immediately after the symptoms are controlled.
Vomiting and persistent hiccups
It has a significant anti-emetic effect on vomiting caused by drugs (digitalis, morphine, tetracycline) and diseases (uremia, malignant tumors)
Effective for stubborn hiccups
Not effective against motion sickness
Hypothermic anesthesia and artificial hibernation
Physical cooling combined with chlorpromazine can be used for hypothermic anesthesia
Chlorpromazine combined with pethidine, promethazine can be used for artificial hibernation
Artificial hibernation is mostly used for severe trauma. Adjuvant treatment for septic shock, febrile convulsions, central hyperthermia, and thyroid storm
adverse symptoms
Common adverse reactions
Central depression symptoms
Lethargy, apathy, weakness
M receptor antagonist symptoms
Blurred vision, dry mouth, no sweat, constipation, elevated intraocular pressure
a receptor antagonism
Nasal congestion, decreased blood pressure, orthostatic hypotension, radiation palpitations
Chlorpromazine-induced decrease in blood pressure cannot be treated with epinephrine (reversal effect of epinephrine) and must be treated with norepinephrine
extrapyramidal reaction
parkinsonism
Increased muscle tone, dull face, slow movements, muscle tremors, and salivation
akathisia
Restless, wandering repeatedly
acute dystonia
Muscle spasm of the tongue, face, neck, and back causes patients to have forced mouth opening, tongue protrusion, torticollis, respiratory movement disorders, and dysphagia.
tardive dyskinesia
A special and persistent movement disorder caused by long-term use of chlorpromazine. Involuntary stereotyped movements of the mouth and face, generalized choreathetosis, which do not disappear for a long time after drug withdrawal.
Mechanism: Dopamine receptors are antagonized for a long time, and receptor sensitivity increases or feedback promotes increased release of dopamine receptors in the presynaptic membrane.
Anticholinergic drugs worsen symptoms, anti-DA drugs reduce reactions
mental disorder
Convulsions and epilepsy
allergic reaction
Cardiovascular and endocrine system responses
hyperprolactinemia
acute poisoning
After taking a large amount at one time, drowsiness occurs, blood pressure drops to shock levels, and myocardial damage occurs.
Symptomatic treatment
Contraindications
Lowers the convulsion threshold and induces epilepsy, so it is contraindicated in people with a history of epilepsy and convulsions.
Increases intraocular pressure, contraindicated in patients with glaucoma
Causes hyperlactosis, mammary gland hyperplasia and breast cancer patients.
Causes arrhythmias, so use with caution in patients with coronary heart disease
medicine interactions
Enhance the central depressant effect of other drugs: such as ethanol, sedative-hypnotics, antihistamines, and analgesics.
Thiaxanthenes
Chlorprothixol
Flupentixol
Butyrophenones
haloperidol
droperidol
pimozide
other
Penfluridol
Sulpiride
Atypical antischizophrenia drugs
clozapine
Broad spectrum neuroleptics
Weak affinity to D2 receptors, blocking D4 receptors and 5-HT2 receptors
No extrapyramidal reactions
For patients who are ineffective with other antischizophrenia drugs or have excessive extrapyramidal reactions
Risperidone
Affinity for 5-HT receptors is greater than D2 receptors
For the treatment of first-episode acute or chronic patients
Mechanism
Phenothiazines
Blocks dopamine receptors in mesolimbic pathways and mesocortical pathways
Atypical antischizophrenia drugs
Clozapine, risperidone block serotonin receptors
antimanic drugs
mania
Elevated mood, irritability, excessive activity, and loss of control over thinking and speech
drug
antischizophrenia drugs
Lithium carbonate
mechanism
Reduce cell excitability: The physical and chemical properties are similar to those of sodium ions. Through displacement, it inhibits the generation of action potential by sodium ions.
Inhibits the release of central neurotransmitters NA and DA, promotes reuptake, and increases fire suppression
Attenuate the effect of NA stimulating a1 receptor and inhibit the reaction mediated by adenylyl cyclase and phospholipase C
Effect
Effective for acute mania and hypomania, mainly used for anti-mania
Treat manic depression,
Bidirectional cycle of mania and depression
Adverse reactions
There are many adverse reactions and the safe range is narrow. The optimal concentration is 0.8-1.5mmol/l. If the concentration is greater than 2, poisoning symptoms will appear. When the blood concentration is greater than 1.6, the drug should be stopped immediately.
rescue
No special antagonists, only symptomatic treatment
Antidepressants
Mechanism
Non-selective inhibition of NA and 5-HT reuptake, such as imipramine
Selectively inhibit NA reuptake, such as desipramine
Selective inhibition of 5-HT reuptake, such as fluoxetine
Inhibit monoamine oxidase, such as moclobemide
Block presynaptic membrane pre-a2 adrenergic receptors and increase NA release, such as mirtazapine
Classification
tricyclic antidepressants
Non-selective monoamine uptake inhibitors
Imipramine
Pharmacological effects
Central Nervous System
Blocks the reuptake of NS and 5-HT in nerve terminals, increases the transmitter concentration in the synaptic gap, and promotes synaptic transmission function.
antidepressant effect
autonomic nervous system
Blocks M choline receptors, manifesting as blurred vision, dry mouth, constipation, and urinary retention
Cardiovascular system effects
Blocks a1 receptors, lowers blood pressure, and causes arrhythmias, among which tachycardia is more common.
Clinical application
Treat depression
Treat enuresis
block a1 receptor
Anxiety and Phobias
Taboo
It can easily cause urinary retention, so it is contraindicated for prostatic hypertrophy.
Increases intraocular pressure, so it is contraindicated in glaucoma
medicine interactions
Concomitant use with monoamine oxidase inhibitors and central nervous system depressants may enhance their function.
NA reuptake inhibitors
Desipramine
Pharmacological effects
Strong NA reuptake inhibitor drugs can also inhibit the reuptake of 5-HT and antagonize H1 receptors.
Effective for mild and moderate depression
Mainly used for depression due to lack of NA in the brain
Clinical application
Treat depression
5-HT reuptake inhibitors
Fluoxetine
Pharmacological effects
Potent 5-HT reuptake inhibitor
Clinical application
Treat depression
Treating Bulimia Nervosa
Monoamine oxidase inhibitors
Moclobemide
Mechanism
Reversibly inhibits type A monoamine oxidase in the brain, inhibits the degradation of catecholamines in vesicles in the presynaptic membrane or in the synaptic cleft, thereby increasing the levels of norepinephrine, dopamine, and 5-HT in the brain.
Features
works fast
Monoamine oxidase activity recovers quickly after drug withdrawal
Taboo
It is prohibited to combine with other antidepressants to avoid causing "serotonin syndrome"
anti-anxiety medication
Benzodiazepines