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Teicoplanin is for gram-positive bacteria only. It does not treat E.coli.
Teicoplanin is not for intraventricular use. The manufacturer strongly discourage injecting Teicoplanin into the brain.

My daughter bled into the brain. She lived for another two years and ultimately died.

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Trimipramine (Surmontil) - Dose, Side effects, Brands

Trimipramine (Surmontil) is a tricyclic antidepressant drug that is used for the symptomatic treatment of depression. It is also used as an off-label medicine for anxiety and as a sedative and hypnotic drug.

Trimipramine Uses:

Depression:
- Symptomatic relief of depression

Trimipramine dose in Adults

Trimipramine dose in the treatment of Depression:

P/O: Initial:
- one H.S. tablet containing 25 to 50 mg, or multiple doses
- In individuals who have been hospitalised, initial dosages of 100 mg per day may be recommended.
- Increase the dose to 75 to 300 mg once daily progressively based on the reaction and tolerability.
Maintenance:
- Lowest effective dose at bedtime.

Discontinuation of therapy:

Reduce withdrawal symptoms and spot re-emerging symptoms by tapering the dose gradually (e.g., over 2 to 4 weeks) when stopping antidepressant therapy after more than 3 weeks.

Reasons for a slower titration (eg, over 4 weeks) include:

High doses of antidepressants; usage of a medication with a half-life of less than 24 hours (e.g., paroxetine, venlafaxine); history of prior antidepressant withdrawal symptoms.
If uncomfortable withdrawal symptoms appear, resume the previously suggested dose and/or reduce it more gradually.
Selected patients receiving long-term care (more than 6 months) who have a history of discontinuation syndrome may benefit from tapering over a period of more than 3 months.
Ideal taper rates are not well supported by available data.

MAO inhibitor recommendations:

Switching to or from an MAO inhibitor intended to treat psychiatric disorders:

14 days should be allowed to elapse between discontinuing an MAO inhibitor intended to treat psychiatric disorders and initiation of trimipramine.
Similarly, 14 days should be allowed to elapse between discontinuing trimipramine and initiation of an MAO inhibitor intended to treat psychiatric disorders.

Trimipramine dose in Children

Trimipramine dose in the treatment of Depression:

Adolescents:
- A reduced dose of up to 50 mg daily should be used initially.
- Gradually increase the dose to 100 mg per day depending on the reaction and tolerability.
- Use the lowest effective dose for maintenance at bedtime.

Discontinuation of therapy: Refer to adult dosing.

MAO inhibitor recommendations: Refer to adult dosing.

Trimipramine pregnancy risk category: C

Negative events have been reported in animal reproduction studies.
Tricyclic antidepressants can cause irritability, convulsions, and jitteriness in neonates.
According to ACOG (2008), treatment for depression during pregnancy should be tailored to the individual and should draw on the clinical knowledge of the paediatrician, obstetrician, and mental healthcare professional.
The American Psychiatric Association states that medication treatment is not a good option for treating depression.
Women who have stopped taking antidepressant medication during pregnancy or who are at high risk of developing postpartum depression can have their medications reintroduced.
The ACOG and APA have created treatment protocols for pregnant and postpartum women who are depressed.

Dose in Kidney Disease:

Use with caution, no dosage adjustment provided in the manufacturer’s labeling.

Trimipramine dose in Liver disease:

Use with caution, no dosage adjustment provided in the manufacturer’s labeling.

Side effects of Trimipramine:

Cardiovascular:
- Cardiac Arrhythmia
- Cerebrovascular Accident
- Facial Edema
- Flushing
- Heart Block
- Hypertension
- Hypotension
- Myocardial Infarction
- Palpitations
- Tachycardia
Central Nervous System:
- Abnormal Electroencephalogram
- Agitation
- Anxiety
- Ataxia
- Confusion
- Delusions
- Disorientation
- Dizziness
- Drowsiness
- Exacerbation Of Psychosis
- Extrapyramidal Reaction
- Fatigue
- Hallucination
- Headache
- Hypomania
- Insomnia
- Nightmares
- Numbness
- Paresthesia
- Peripheral Neuropathy
- Restlessness
- Seizure
- Tingling Sensation
- Withdrawal Syndrome
Dermatologic:
- Alopecia
- Diaphoresis
- Pruritus
- Skin Photosensitivity
- Skin Rash
- Urticaria
Endocrine & Metabolic:
- Change In Libido
- Galactorrhea
- Gynecomastia
- Hyperglycemia
- Hypoglycemia
- SIADH
- Weight Gain
- Weight Loss
Gastrointestinal:
- Abdominal Cramps
- Anorexia
- Constipation
- Diarrhea
- Epigastric Distress
- Melanoglossia
- Nausea
- Paralytic Ileus
- Parotid Gland Enlargement
- Stomatitis
- Unpleasant Taste
- Vomiting
- Xerostomia
Genitourinary:
- Breast Hypertrophy
- Difficulty In Micturition
- Impotence
- Testicular Swelling
- Urinary Retention
Hematologic & Oncologic:
- Agranulocytosis
- Eosinophilia
- Petechia
- Purpura
- Thrombocytopenia
Hepatic:
- Cholestatic Jaundice
- Increased Liver Enzymes
Hypersensitivity:
- Tongue Edema
Neuromuscular & Skeletal:
- Tremor
- Weakness
Ophthalmic:
- Accommodation Disturbance
- Angle-Closure Glaucoma
- Blurred Vision
- Mydriasis
Otic:
- Tinnitus
Renal:
- Polyuria

Contraindications to Trimipramine:

Hypersensitivity to trimipramine and any other components of the formulation, or other TCAs
Usage during the early recovery stage of a MI
Psychiatric diseases are treated with MAO inhibitors. Both trimipramine and the MAO inhibitor can be administered simultaneously or within 14 days of terminating the other.
introduction of trimipramine to a patient who has taken intravenous methyleneblue along with linezolid

Warnings and precautions

Anticholinergic effects
- Anticholinergic effects may include constipation, dry and blurred vision, urinary retention, and dry mouth.
- Patients with reduced gastrointestinal motility, paralytic and ileus, urinary retentions, BPH, xerostomias, narrow-angle or other visual impairments should be cautious.
- This agent is more effective than other antidepressants in causing a high level of anticholinergic blockade.
Depression in the CNS:
- CNS depression can lead to impairment of mental or physical abilities. Patients should be cautious about driving or operating machinery that requires mental alertness.
- The level of sedation is much higher than other antidepressants.
Fractures
- Antidepressant treatment is often associated with bone fractures.
- Unexplained bone pain, tenderness, swelling or bruising in an antidepressant-treated person may indicate a fragility fracture.
Orthostatic hypotension
- Orthostatic hypotension may occur (risk is higher than other antidepressants).
- Use caution while administering this drug to patients who are more susceptible to this side effect and those who cannot tolerate transient hypotensive episodes (CVAs, cardiovascular illness, hypovolemia, or concurrent use of medications that may cause hypotension or bradycardia).
Serotonin syndrome
- Serotonin syndrome (SS), which can be life-threatening, is caused by serotonergic drugs (eg SSRIs, SNRIs), especially when combined with other serotonergic medications (eg triptans TCAs, fentanyl and buspirone, lithium, tramadol or buspirone, St John's wort. tryptophan) and agents that impair serotonin metabolism (eg MAO inhibitors to treat psychia, intravenous methyleneblue blue, intravenous methyleneblue blue, linezolid, intravenous methylene, methylene blue]
- You should keep a watchful eye out for any indications of SS in your patients, such as
  - Mental status changes (eg. agitation, hallucinations and delirium, coma).
  - Autonomic instability (eg tachycardia or labile blood pressure, diaphoresis)
  - Neuromuscular changes (eg tremors, rigidity, myoclonus, etc.)
  - GI symptoms include nausea, vomiting, diarrhea, and/or seizures.
- If you experience any of the symptoms, stop using any serotonergic medications or treatments.
Hyponatremia and inappropriate antidiuretic hormone production:
- Antidepressant medications have been associated to the onset of hyponatremia and SIADH (syndromes of inadequate antidiuretic hormone secretion).
- The elderly are the main group affected by this illness.
- Volume loss, concurrent use of diuretics, being a woman, and having a low body weight are additional risk factors.
- TCAs are less likely to cause hyponatremia than SSRIs.
Cardiovascular disease
- Patients should exercise caution if they have a history of cardiovascular illness, including stroke, MI, or conduction abnormalities.
- Compared to other antidepressants, this medication carries a higher risk of conduction problems.
- Trimipramine may act as a catalyst for underlying cardiac dysfunction, according to the American Heart Association.
Diabetes:
- It may affect glucose regulation so be careful.
Hepatic impairment
- Be careful
Hypomania and mania:
- In people with bipolar disorder, it can cause mania or hypomania.
- Bipolar patients should refrain from monotherapy
- Bipolar disorder screening should be performed on patients who have depressed symptoms. Details of past family relationships, suicide attempts, and bipolar disorder are included.
- Trimipramine has not been approved by the FDA for treatment of bipolar disorder.
Renal impairment
- Be careful.
Seizure disorder
- Patients at high risk of seizures should be treated with caution, especially those who have had seizures in the past, brain damage, head trauma or alcoholism, and patients receiving concurrent treatment with medication that could lower their seizure threshold.

Trimipramine: Drug Interaction

Risk Factor C (Monitor therapy)
Acetylcholinesterase Inhibitors	May diminish the therapeutic effect of Anticholinergic Agents. Anticholinergic Agents may diminish the therapeutic effect of Acetylcholinesterase Inhibitors.
Ajmaline	May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors).
Alcohol (Ethyl)	Alcohol's CNS depressing effect may be amplified by CNS depressants (Ethyl).
Alizapride	CNS depressants may have an enhanced CNS depressant impact.
Alpha1-Agonists	The therapeutic impact of alpha1 agonists may be enhanced by tricyclic antidepressants. The therapeutic benefit of Alpha1-Agonists may be diminished by Tricyclic Antidepressants.
Alpha2-Agonists (Ophthalmic)	The therapeutic benefit of alpha2-agonists may be diminished by tricyclic antidepressants (Ophthalmic).
Altretamine	May make tricyclic antidepressants' orthostatic hypotensive effect stronger.
Amantadine	May strengthen an anticholinergic agent's anticholinergic action.
Amezinium	Tricyclic antidepressants' harmful or hazardous effects could be increased.
Amifampridine	Amifampridine may have a stronger neuroexcitatory and/or seizure-potentiating impact when combined with substances with seizure threshold lowering potential.
Amphetamines	Tricyclic antidepressants may make amphetamines more stimulating. Tricyclic antidepressants may potentially enhance amphetamines' cardiovascular effects.
Anticholinergic Agents	Other anticholinergic agents' negative or hazardous effects might be amplified.
Antiemetics (5HT3 Antagonists)	Could make serotonin modulators' serotonergic effects stronger. Serotonin syndrome might occur from this.
Antipsychotic Agents	Serotonin modulators might make antipsychotic drugs more harmful or toxic. Serotonin modulators, in particular, may enhance dopamine blockade, potentially raising the risk for neuroleptic malignant syndrome. Serotonin modulators' serotonergic effects may be strengthened by antipsychotic drugs. Serotonin syndrome might occur from this.
Aspirin	Aspirin's antiplatelet action may be enhanced by tricyclic antidepressants (tertiary amine).
Beta2-Agonists	Tricyclic antidepressants may make beta2 agonists more harmful or poisonous.
Botulinum Toxin-Containing Products	May enhance the anticholinergic effect of Anticholinergic Agents.
Brexanolone	CNS Depressants may enhance the CNS depressant effect of Brexanolone.
Brimonidine (Topical)	May enhance the CNS depressant effect of CNS Depressants.
Cannabidiol	May enhance the CNS depressant effect of CNS Depressants.
Cannabis	May enhance the CNS depressant effect of CNS Depressants.
CarBAMazepine	May decrease the serum concentration of Tricyclic Antidepressants.
Chloral Betaine	May enhance the adverse/toxic effect of Anticholinergic Agents.
Chlorphenesin Carbamate	May enhance the adverse/toxic effect of CNS Depressants.
Cimetidine	May decrease the metabolism of Tricyclic Antidepressants.
Citalopram	Tricyclic antidepressants may improve Citalopram's serotonergic effects. Citalopram serum levels may rise in response to tricyclic antidepressants. Tricyclic Antidepressants' serum concentration may rise as a result of citalopram. Management: Keep an eye out for elevated TCA and citalopram concentrations and side effects, as well as signs and symptoms of serotonin syndrome and serotonin toxicity (such as hyperreflexia, clonus, hyperthermia, diaphoresis, tremor, autonomic instability, and changes in mental status).
CloBAZam	May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors).
CNS Depressants	May enhance the adverse/toxic effect of other CNS Depressants.
Cobicistat	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
CYP2C19 Inducers (Moderate)	May decrease the serum concentration of CYP2C19 Substrates (High risk with Inducers).
CYP2C19 Inhibitors (Moderate)	May decrease the metabolism of CYP2C19 Substrates (High risk with Inhibitors).
CYP2D6 Inhibitors (Moderate)	May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors).
Darunavir	May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors).
Desmopressin	Tricyclic antidepressants may intensify Desmopressin's harmful or hazardous effects. Tricyclic antidepressants' harmful or hazardous effects could be increased.
Dexmethylphenidate	Tricyclic Antidepressants' serum levels may rise in response to dexmethylphenidate.
Dimethindene (Topical)	CNS depressants may have an enhanced CNS depressant impact.
Doxylamine	CNS depressants may have an enhanced CNS depressant impact. Management: The producer of the pregnancy-safe drug Diclegis (doxylamine/pyridoxine) particularly advises against combining it with other CNS depressants.
Dronabinol	CNS depressants may have an enhanced CNS depressant impact.
DULoxetine	Tricyclic antidepressants' serotonergic action should be improved. Serotonin syndrome might occur from this. Tricyclic Antidepressants' metabolism may be slowed down by DULoxetine.
Escitalopram	Escitalopram's effect on the serotonergic system may be enhanced by tricyclic antidepressants. Escitalopram may make tricyclic antidepressants more concentrated in the blood. Management: If these medications are combined, keep an eye out for elevated TCA concentrations and side effects, as well as signs and symptoms of serotonin syndrome and serotonin toxicity (such as hyperreflexia, clonus, hyperthermia, diaphoresis, tremor, autonomic instability, and changes in mental status).
Esketamine	CNS depressants may have an enhanced CNS depressant impact.
FluvoxaMINE	Tricyclic antidepressants' serotonergic action should be improved. Tricyclic Antidepressants' serum levels may rise as a result of fluvoxaMINE. Management: If these medications are combined, keep an eye out for elevated TCA concentrations and side effects, as well as signs and symptoms of serotonin syndrome and serotonin toxicity (such as hyperreflexia, clonus, hyperthermia, diaphoresis, tremor, autonomic instability, and changes in mental status).
Gastrointestinal Agents (Prokinetic)	Anticholinergic Agents may diminish the therapeutic effect of Gastrointestinal Agents (Prokinetic).
Glucagon	Anticholinergic Agents may enhance the adverse/toxic effect of Glucagon. Specifically, the risk of gastrointestinal adverse effects may be increased.
Guanethidine	Tricyclic Antidepressants may diminish the therapeutic effect of Guanethidine.
HydrOXYzine	May enhance the CNS depressant effect of CNS Depressants.
Imatinib	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
Itopride	Anticholinergic Agents may diminish the therapeutic effect of Itopride.
Kava Kava	May enhance the adverse/toxic effect of CNS Depressants.
Lumacaftor	May decrease the serum concentration of CYP2C19 Substrates (High risk with Inducers).
Lumefantrine	May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors)
Magnesium Sulfate	CNS depressants may have an enhanced CNS depressant impact
Metaxalone	Could make serotonin modulators' serotonergic effects stronger. Serotonin syndrome might occur from this.
Methylphenidate	Tricyclic antidepressants' harmful or hazardous effects could be increased.
Methylphenidate	Tricyclic Antidepressants' serum levels may rise in response to methylphenidate.
MetyroSINE	Serotonin modulators' harmful or toxic effects could be exacerbated. In particular, there may be an increased risk of serotonin syndrome or serotonin poisoning.
MetyroSINE	The sedative effects of metyroSINE may be strengthened by CNS depressants.
Mianserin	Tricyclic antidepressants' harmful or hazardous effects could be increased.
Minocycline	May strengthen an anticholinergic agent's anticholinergic action.
Mirabegron	CNS depressants may have an enhanced CNS depressant impact. Anticholinergic drugs may make Mirabegron's harmful or hazardous effects worse
Mirtazapine	The CNS depressing action of mirtazapine may be enhanced by CNS depressants.
Nabilone	CNS depressants may have an enhanced CNS depressant impact.
Nicorandil	Nicorandil's hypotensive effects may be enhanced by tricyclic antidepressants.
Nitroglycerin	Nitroglycerin absorption may be decreased by anticholinergic agents. Anticholinergic medications specifically have the potential to impede or prevent the absorption of nitroglycerin by reducing the breakdown of sublingual nitroglycerin pills.
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective)	Nonsteroidal Anti-Inflammatory Drugs' (Non-steroidal) antiplatelet action may be enhanced by Tricyclic Antidepressants (Tertiary Amine) (COX-2 Selective).
Nonsteroidal Anti-Inflammatory Agents (Nonselective)	Nonsteroidal Anti-Inflammatory Drugs' (Non-steroidal) antiplatelet action may be enhanced by Tricyclic Antidepressants (Tertiary Amine) (Nonselective).
Panobinostat	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
Peginterferon Alfa-2b	May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
Perhexiline	The serum levels of perhexiline may increase when exposed to CYP2D6 Substrates (High Risk with Inhibitors). The serum concentration of CYP2D6 Substrates may rise in response to perhexiline (High risk with Inhibitors).
Piribedil	Piribedil's CNS depressing effects may be enhanced by other CNS depressants.
Pramipexole	CNS Depressants may enhance the sedative effect of Pramipexole.
Protease Inhibitors	May increase the serum concentration of Tricyclic Antidepressants.
QuiNINE	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
Ramosetron	Ramosetron's constipating effects may be enhanced by anticholinergic drugs.
ROPINIRole	The sedative effects of CNS depressants may increase those of ROPINIRole.
Rotigotine	Rotigotine's sedative effects may be boosted by CNS depressants.
Rufinamide	CNS depressants' harmful or toxic effects could be increased. Particularly, drowsiness and lightheadedness could be worsened.
Selective Serotonin Reuptake Inhibitors	Selective serotonin reuptake inhibitors may have a worsened or more hazardous effect when taken with CNS depressants. Particularly, there may be an increased risk of psychomotor impairment.
Serotonin Modulators	The negative or hazardous effects of other serotonin modulators might be increased. Serotonin syndrome may start to develop. Nicergoline and Tedizolid are exceptions.
Sertraline	Tricyclic antidepressants' serotonergic action should be improved. Tricyclic Antidepressants' serum levels may rise in response to sertraline. Management: If these medications are combined, keep an eye out for elevated TCA concentrations and side effects, as well as signs and symptoms of serotonin syndrome and serotonin toxicity (such as hyperreflexia, clonus, hyperthermia, diaphoresis, tremor, autonomic instability, and changes in mental status).
Sodium Phosphates	Tricyclic antidepressants might make sodium phosphates' harmful or hazardous effects worse. Specifically, patients with severe sodium phosphate-induced fluid/electrolyte imbalances may be at a higher risk of seizures and/or losing consciousness.
Sulfonylureas	Cyclical antidepressants might make sulfonylureas' hypoglycemia effect stronger.
Tedizolid	Could make serotonin modulators' serotonergic effects stronger. Serotonin syndrome might occur from this.
Tetrahydrocannabinol	CNS depressants may have an enhanced CNS depressant impact.
Tetrahydrocannabinol and Cannabidiol	CNS depressants may have an enhanced CNS depressant impact.
Thiazide and Thiazide-Like Diuretics	Thiazide and Thiazide-Like Diuretics' serum concentrations may be elevated by anticholinergic agents.
Thyroid Products	Tricyclic antidepressants' arrhythmogenic effects might be increased. Tricyclic Antidepressants' stimulatory action may be strengthened by thyroid products.
Topiramate	Anticholinergic drugs may intensify topiramate's harmful or toxic effects.
Trimeprazine	CNS depressants may have an enhanced CNS depressant impact.
Valproate Products	Tricyclic Antidepressants' serum levels can rise.
Vitamin K Antagonists (eg, warfarin)	The anticoagulant action of vitamin K antagonists may be increased by tricyclic antidepressants.
Yohimbine	Tricyclic antidepressants may raise the level of yohimbine in the blood.
Risk Factor D (Consider therapy modification)
Abiraterone Acetate	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity.
Alpha-/Beta-Agonists (Direct-Acting)	Tricyclic antidepressants may raise the level of yohimbine in the blood. Alpha- and beta-Agonists' vasopressor effects may be enhanced by tricyclic antidepressants (Direct-Acting). Treatment: Patients using tricyclic antidepressants should try to avoid using direct-acting alpha-/beta-agonists.
Alpha2-Agonists	Alpha2Agonists may have less of an antihypertensive effect when taken with tricyclic antidepressants. Management: Take into account avoiding this pairing. If utilised, keep an eye out for the alpha2-agonist's diminished effects. When stopping an alpha2-agonist in a patient on a TCA, proceed with extreme caution. Apraclonidine, brimonidine (ophthalmic), and lofexidine are exceptions.
Asunaprevir	May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors).
Barbiturates	May increase the metabolism of Tricyclic Antidepressants.
Blonanserin	CNS Depressants may enhance the CNS depressant effect of Blonanserin.
Buprenorphine	CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine at lower doses in patients already receiving CNS depressants.
Chlormethiazole	May enhance the CNS depressant effect of CNS Depressants. Management: Monitor closely for evidence of excessive CNS depression. The chlormethiazole labeling states that an appropriately reduced dose should be used if such a combination must be used.
Cinacalcet	Tricyclic Antidepressants' serum levels can rise. Management: When possible, look for alternatives. If these combinations are utilised, keep a close eye out for any intensified side effects, enhanced toxicity, and/or higher tricyclic antidepressant serum concentrations (where testing is possible).
CYP2C19 Inducers (Strong)	May speed up CYP2C19 substrate metabolism (High risk with Inducers). Management: Take into account a substitute for one of the interfering medications. Certain contraindications may apply to some combinations. the relevant manufacturer's label.
CYP2C19 Inhibitors (Strong)	CYP2D6 substrate metabolism may be decreased (High risk with Inhibitors).
CYP2D6 Inhibitors (Strong)	CYP2D6 substrate metabolism may be decreased (High risk with Inhibitors).
Dabrafenib	May lower the serum level of CYP2C19 substrates (High risk with Inducers). Management: Where possible, look for substitutes for the CYP2C19 substrate.
Dacomitinib	If concurrent therapy cannot be avoided, pay special attention to the substrate's clinical consequences (particularly therapeutic effects). may elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). Management: Steer clear of using dacomitinib at the same time as CYP2D6 subtrates with a limited therapeutic index.
Droperidol	CNS depressants may have an enhanced CNS depressant impact. Consider lowering the dosage of droperidol or other CNS drugs (such as opioids or barbiturates) when they are used concurrently. In separate drug interaction monographs, exceptions to this monograph are covered in more detail.
Enzalutamide	May lower the serum level of CYP2C19 substrates (High risk with Inducers). For medications that CYP2C19 activates, active metabolite concentrations may decrease instead. Treatment: Enzalutamide should not be used concurrently with CYP2C19 substrates that have a limited therapeutic index. Enzalutamide use, like with the use of any other CYP2C19 substrate, should be done with caution and under close observation
Flunitrazepam	Flunitrazepam's CNS depressing effects may be enhanced by other CNS depressants.
HYDROcodone	CNS Depressants may enhance the CNS depressant effect of HYDROcodone. Management: Avoid concomitant use of hydrocodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug.
Iohexol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iohexol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iohexol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Iomeprol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iomeprol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iomeprol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Iopamidol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iopamidol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iopamidol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Linezolid	Tricyclic antidepressants' serotonergic action should be improved. Serotonin syndrome might occur from this. Management: Whenever possible, look at alternatives to this mix. Wait at least two weeks to start taking linezolid after stopping tricyclic antidepressants (TCAs), if clinically feasible.
Linezolid	Could make serotonin modulators' serotonergic effects stronger. Serotonin syndrome might occur from this. Management: Stop using serotonin modulators two weeks before taking linezolid to reduce the chance of serotonin syndrome or serotonin poisoning. Serotonin modulators should be immediately stopped if linezolid needs to be started quickly
Lithium	Tricyclic antidepressants' neurotoxic effects might be increased. Management: Use extreme caution when using this combo. When combination treatment is therapeutically necessary, keep a vigilant eye out for any symptoms of serotonin syndrome or toxicity.
Lofexidine	The therapeutic impact of lofexidine may be diminished by tricyclic antidepressants. Management: Take into account avoiding this pairing. If utilised, keep an eye out for the alpha2-agonist's diminished effects. When stopping an alpha2-agonist in a patient on a TCA, proceed with extreme caution.
Methotrimeprazine	CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established.
Metoclopramide	Tricyclic antidepressants' harmful or hazardous effects could be increased. Management: When possible, look for substitutions for this combination. Keep an eye out for any evidence of serotonin syndrome, neuroleptic malignant syndrome, or extrapyramidal symptoms in patients taking metoclopramide along with tricyclic antidepressants.
Opioid Agonists	CNS Depressants may enhance the CNS depressant effect of Opioid Agonists. Management: Avoid concomitant use of opioid agonists and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug.
OxyCODONE	CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: Avoid concomitant use of oxycodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug.
Perampanel	May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination.
Pramlintide	May strengthen an anticholinergic agent's anticholinergic action. The Gastrointestinal tract alone is the target of these effects.
QuiNIDine	Tricyclic antidepressants may increase QuiNIDine's ability to extend QTc. Tricyclic Antidepressants' serum levels may rise in response to quiNIDine. Management: Separate drug interaction monographs go into further detail about the medications indicated as exceptions to this book.
Secretin	Anticholinergic Agents may diminish the therapeutic effect of Secretin. Management: Avoid concomitant use of anticholinergic agents and secretin. Discontinue anticholinergic agents at least 5 half-lives prior to administration of secretin.
Sodium Oxybate	May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to combined use. When combined use is needed, consider minimizing doses of one or more drugs. Use of sodium oxybate with alcohol or sedative hypnotics is contraindicated.
St John's Wort	May increase the metabolism of Tricyclic Antidepressants. The risk of serotonin syndrome may theoretically be increased.
Suvorexant	CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended.
Tapentadol	May enhance the CNS depressant effect of CNS Depressants. Management: Avoid concomitant use of tapentadol and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug.
Zolpidem	CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol.
Risk Factor X (Avoid combination)
Aclidinium	May enhance the anticholinergic effect of Anticholinergic Agents.
Azelastine (Nasal)	CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal).
Bromopride	May enhance the adverse/toxic effect of Tricyclic Antidepressants.
Bromperidol	May enhance the CNS depressant effect of CNS Depressants.
Cimetropium	Anticholinergic Agents may enhance the anticholinergic effect of Cimetropium.
Dapoxetine	May enhance the adverse/toxic effect of Serotonin Modulators.
Dronedarone	Tricyclic antidepressants may increase Dronedarone's ability to cause arrhythmias. Management: Separate drug interaction monographs go into further detail about the medications indicated as exceptions to this book.
Eluxadoline	Eluxadoline's constipating effects may be enhanced by anticholinergic drugs.
Glycopyrrolate (Oral Inhalation)	The anticholinergic effect of glycopyrrolate may be enhanced by anticholinergic agents (Oral Inhalation).
Glycopyrronium (Topical)	May strengthen an anticholinergic agent's anticholinergic action.
Iobenguane Radiopharmaceutical Products	Iobenguane radiopharmaceutical products' therapeutic effects may be reduced by tricyclic antidepressants. Treatment: Before administering iobenguane, stop taking any medications that could impede or interfere with catecholamine transport or uptake for at least five biological half-lives. After each dose of iobenguane, wait at least 7 days before administering these medications.
Ipratropium (Oral Inhalation)	May enhance the anticholinergic effect of Anticholinergic Agents.
Levosulpiride	Anticholinergic Agents may diminish the therapeutic effect of Levosulpiride.
Methylene Blue	Tricyclic antidepressants may improve Methylene Blue's serotonergic effects. Serotonin syndrome might occur from this.
Methylene Blue	Could make serotonin modulators' serotonergic effects stronger. Serotonin syndrome might occur from this.
Monoamine Oxidase Inhibitors	Tricyclic antidepressants' serotonergic action should be improved. It might result in serotonin syndrome. Although this interaction between methylene blue and linezolid is anticipated, management guidelines for this drug are different from those for other monoamine oxidase inhibitors. For more information, consult the monographs for those agents. Linezolid, Methylene Blue, and Tedizolid are exceptions.
Orphenadrine	The CNS depressing action of orphenadrine may be enhanced by CNS depressants.
Oxatomide	May enhance the anticholinergic effect of Anticholinergic Agents.
Oxomemazine	May enhance the CNS depressant effect of CNS Depressants.
Paraldehyde	CNS Depressants may enhance the CNS depressant effect of Paraldehyde.
Pitolisant	Tricyclic Antidepressants may diminish the therapeutic effect of Pitolisant.
Potassium Chloride	Anticholinergic Agents may enhance the ulcerogenic effect of Potassium Chloride. Management: Patients on drugs with substantial anticholinergic effects should avoid using any solid oral dosage form of potassium chloride.
Potassium Citrate	Anticholinergic Agents may enhance the ulcerogenic effect of Potassium Citrate.
Revefenacin	Anticholinergic Agents may enhance the anticholinergic effect of Revefenacin.
Thalidomide	CNS Depressants may enhance the CNS depressant effect of Thalidomide.
Tiotropium	Anticholinergic Agents may enhance the anticholinergic effect of Tiotropium.
Umeclidinium	May enhance the anticholinergic effect of Anticholinergic Agents.

Monitoring parameters:

Clinically indicated, serum Na+ for populations at-risk
Before and after initial therapy, blood pressure and pulse rate
Assess mental health, suicide thoughts (especially when therapy is just starting or when the doses are increasing or decreasing).
Anxiety, social functioning and panic attacks, as well as mania and mania, are all signs of unusual behavior.
Blood glucose levels
BMI and weight
ECG for patients with cardiac disease and older adults

How to administer Trimipramine?

No relation to food.
Administer the initial doses in two doses and the maintenance doses at bedtime.

Mechanism of action of Trimipramine:

Antidepressant effects are proposed to result from postsynaptic sensitization to serotonin.

Metabolism:

Hepatic with significant first-pass metabolicm

Bioavailability:

18% - 63%.

Half-life elimination:

7 - 40 hrs.

Time to peak serum concentration:

1 - 6 hrs.

Excretion:

Urinary

International Brands of Trimipramine:

Surmontil
APO-Trimipramine
NOVO-Tripramine
Apo-Trimip
Herphonal
Sapilent
Stangyl
Sumontil
Surmontil
Trimin
Tydamine

Trimipramine Brand Names in Pakistan:

No Brands Available in Pakistan.

Disclaimer Notice:

Emedz.net is not an online pharmacy:

We are not affiliated with any pharmaceutical companies:

Trimipramine (Surmontil) - Dose, Side effects, Brands

Trimipramine Uses:

Depression:

Trimipramine dose in Adults

Trimipramine dose in the treatment of Depression:

Discontinuation of therapy:

MAO inhibitor recommendations:

Trimipramine dose in Children

Trimipramine dose in the treatment of Depression:

Adolescents:

Trimipramine pregnancy risk category: C

Dose in Kidney Disease:

Trimipramine dose in Liver disease:

Side effects of Trimipramine:

Cardiovascular:

Central Nervous System:

Dermatologic:

Endocrine & Metabolic:

Gastrointestinal:

Genitourinary:

Hematologic & Oncologic:

Hepatic:

Hypersensitivity:

Neuromuscular & Skeletal:

Ophthalmic:

Otic:

Renal:

Contraindications to Trimipramine:

Warnings and precautions

Anticholinergic effects

Depression in the CNS:

Fractures

Orthostatic hypotension

Serotonin syndrome

Hyponatremia and inappropriate antidiuretic hormone production:

Cardiovascular disease

Diabetes:

Hepatic impairment

Hypomania and mania:

Renal impairment

Seizure disorder

Monitoring parameters:

How to administer Trimipramine?

Mechanism of action of Trimipramine:

International Brands of Trimipramine:

Trimipramine Brand Names in Pakistan:

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