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Pharmacology

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Pharmacology

Part II: Meeting the Transporters
Host:
Let's hear from the serotonin transporter.

SERT:
My job is to remove serotonin from the synapse.

TCA:
And I stop you from doing that.

Host:
What happens then?

SERT:
Serotonin accumulates in the synaptic cleft.

TCA:
Which contributes to my antidepressant effects.

Host:
And what about norepinephrine?

NET:
I normally clear norepinephrine from the synapse.

TCA:
I inhibit you as well.

NET:
As a result, norepinephrine levels increase.

Host:
Clinical significance?

TCA:
Improved mood, increased energy, better concentration, and enhanced pain modulation.



Part III: The
Side Effects Committee

Host:
Every successful drug has critics. Let's invite the receptors responsible for your adverse effects.

Histamine H1 Receptor
H1:
I would like to file a complaint.

Host:
What happened?

H1:
The TCA blocks me.

Host:
And the consequences?

H1:
Sedation, increased appetite, and weight gain

.
TCA:
Which is why many patients take me at bedtime.
Muscarinic M1 Receptor

M1:
I also have concerns.

Host:
Please proceed.

M1:
The TCA blocks me too.

Host:
And that causes?

M1:
Dry mouth, constipation, urinary retention, blurred vision, and tachycardia.

Host:
So the famous anticholinergic effects?

M1:
Exactly.
Alpha-1 Receptor

Alpha-1:
I have a complaint as well.

Host:
Go ahead.

Alpha-1:
I maintain vascular tone when a patient stands up.

TCA:
Unfortunately, I antagonize you.

Alpha-1:
Then patients become dizzy and may develop orthostatic hypotension.

Host:
Particularly in older adults?

Alpha-1:
Precisely

.

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Pharmacology

Next meeting with Amitriptyline

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Pharmacology

👨‍⚕️🤝 Meeting with Paroxetine
“Doctor vs Paroxetine” 💊
👨‍⚕️❓ Doctor:
Please introduce yourself.
💊 Paroxetine:
Hello Doctor 👋
I am Paroxetine, an SSRI antidepressant widely used in psychiatry.
I’m approved for:
✅ Major Depressive Disorder
✅ Generalized Anxiety Disorder
✅ Panic Disorder
✅ Social Anxiety Disorder
✅ PTSD
✅ OCD
And honestly… I’m known for being one of the more “calming” SSRIs 😴🧠
👨‍⚕️❓ Doctor:
Tell me your mechanism of action.
💊 Paroxetine:
Like other SSRIs:
✅ I inhibit the serotonin transporter (SERT)
→ increasing serotonin in the synaptic cleft.
Result:
Improved mood
Reduced anxiety
Emotional stabilization
👨‍⚕️❓ Doctor:
What makes you different from other SSRIs?
💊 Paroxetine:
I have several important characteristics 👇
✅ More sedating/calming profile
✅ Strong anxiolytic effect
✅ Useful when insomnia is prominent
❌ BUT more anticholinergic effects
❌ More weight gain
❌ Worse withdrawal symptoms
👨‍⚕️ Clinical Pearl:
Among SSRIs, I’m often considered: 😴 More sedating
⚠️ Harder to discontinue
👨‍⚕️❓ Doctor:
When are you one of the BEST choices?
💊 Paroxetine:
I can be very useful in:
✅ Severe anxiety disorders
✅ Panic disorder
✅ Patients with insomnia
✅ PTSD with hyperarousal
✅ Anxiety + poor sleep
👨‍⚕️❓ Doctor:
What are your usual doses?
💊 Paroxetine:
Depression/GAD
💊 Starting dose: 20 mg daily
Panic disorder
💊 Often start lower: 10 mg daily
Then gradually increase.
Typical range: 20–50 mg/day
👨‍⚕️❓ Doctor:
How long until you work?
💊 Paroxetine:
⏳ Initial response: 1–2 weeks
⏳ Full effect: 4–8 weeks
⏳ OCD/PTSD may require longer treatment duration.
👨‍⚕️❓ Doctor:
What are your common side effects?
💊 Paroxetine:
❌ Sedation
❌ Weight gain
❌ Dry mouth
❌ Constipation
❌ Sexual dysfunction
❌ Sweating
👨‍⚕️ Clinical Pearl:
Compared with escitalopram or sertraline: ⚠️ I have more anticholinergic-type effects.
👨‍⚕️❓ Doctor:
Anticholinergic effects? Explain.
💊 Paroxetine:
I may cause:
Dry mouth
Constipation
Blurred vision
Urinary retention
Cognitive slowing
Which is especially problematic in: 👴 Elderly patients
👨‍⚕️❓ Doctor:
What serious risks should I know?
💊 Paroxetine:
⚠️ Serotonin syndrome
⚠️ Hyponatremia/SIADH
⚠️ Increased bleeding risk
⚠️ Mania activation in bipolar disorder
⚠️ Suicidal ideation in younger patients
👨‍⚕️❓ Doctor:
Which SSRI has the WORST withdrawal symptoms?
💊 Paroxetine:
Unfortunately… probably me 😅
Because: ❌ Short half-life
❌ Rapid serotonin drop after stopping
Discontinuation symptoms may include:
Dizziness
Electric shock sensations
Anxiety
Irritability
Flu-like symptoms
👨‍⚕️ Clinical Pearl: I should NEVER be stopped abruptly.
👨‍⚕️❓ Doctor:
What about drug interactions?
💊 Paroxetine:
🚫 MAOIs → contraindicated
⚠️ NSAIDs/anticoagulants → bleeding risk
⚠️ Tramadol → serotonin syndrome
⚠️ Lithium → serotonin toxicity
Also: ⚠️ I inhibit CYP2D6
Meaning:
Increased TCA levels
Metoprolol interaction
Some antipsychotic interactions
👨‍⚕️❓ Doctor:
What are your biggest disadvantages compared with other SSRIs?
💊 Paroxetine:
Compared with escitalopram/sertraline:
❌ More sedation
❌ More weight gain
❌ More withdrawal symptoms
❌ More anticholinergic effects
❌ More sexual dysfunction
👨‍⚕️❓ Doctor:
So why do psychiatrists still use you?
💊 Paroxetine:
Because clinically…
I can be VERY effective in: 😰 Severe anxiety
😴 Anxiety with insomnia
💥 Panic disorder
Some anxious patients feel calmer on me than on activating SSRIs.
👨‍⚕️❓ Doctor:
When might another SSRI be better than you?
💊 Paroxetine:
✨ Escitalopram
→ better tolerability
⚖️ Sertraline
→ better cardiac profile
⚡ Fluoxetine
→ less withdrawal + more energizing
👨‍⚕️❓ Doctor:
Final question… summarize yourself in one sentence.
💊 Paroxetine:
😴 “I’m the calming, sedating SSRI that works well for severe anxiety — but I come with more withdrawal and anticholinergic baggage.”

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Pharmacology

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Pharmacology

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Pharmacology

Esitulopram Vs Sertraline Vs Fluoxitine

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Pharmacology

Next meeting is with Ecitalopram

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Pharmacology

Exactly very useful for clinical decision which one you will prescribe

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Pharmacology

👨‍⚕️🤝 Meeting with Fluoxetine

👨‍⚕️❓ Doctor: Who are you?
💊 Fluoxetine:
I am Fluoxetine, a Selective Serotonin Reuptake Inhibitor used in major psychiatric disorders.
Approved for:
Major Depressive Disorder
Obsessive-Compulsive Disorder
Panic Disorder
Bulimia Nervosa
Premenstrual Dysphoric Disorder
👨‍⚕️❓ Doctor: What is your mechanism of action?
💊 Fluoxetine:
I inhibit the serotonin transporter (SERT), increasing serotonin levels in the synaptic cleft.
Long-term antidepressant effects involve neuroplasticity, receptor adaptation, and increased BDNF.
👨‍⚕️❓ Doctor: What makes you different from other SSRIs?
💊 Fluoxetine:
I have a very long half-life, leading to:
Lower withdrawal risk
Better adherence profile
More stable plasma levels
Mild activating effect in some patients
However, I am not more effective than other SSRIs in general—my advantage is pharmacokinetics and patient fit.
👨‍⚕️❓ Doctor: When are you the best choice?
💊 Fluoxetine:
I am preferred in:
Depression with fatigue, low energy, hypersomnia
Poor medication adherence
Concern about discontinuation syndrome
Bulimia Nervosa
Children and adolescents with depression or OCD
Patients needing an activating antidepressant
👨‍⚕️❓ Doctor: When should you be avoided?
💊 Fluoxetine:
I should be avoided or used cautiously in:
Insomnia or highly activated patients
Severe anxiety with risk of early worsening
Akathisia
Bipolar disorder (risk of mania)
Polypharmacy (CYP2D6 inhibition)
Use with Tamoxifen
Situations requiring rapid switching
👨‍⚕️❓ Doctor: What about drug interactions?
💊 Fluoxetine:
Important interactions include:
Contraindicated with Monoamine Oxidase Inhibitors
Serotonin syndrome risk with Tramadol and other serotonergic agents
Increased bleeding risk with NSAIDs and anticoagulants
CYP2D6 inhibition increasing levels of Metoprolol and TCAs
Reduced activation of Tamoxifen
👨‍⚕️❓ Doctor: What is your half-life?
💊 Fluoxetine:
Fluoxetine: 2–4 days
Norfluoxetine: 7–15 days
This explains:
Low withdrawal risk
Long persistence after stopping
Need for long washout before MAOIs (~5 weeks)
👨‍⚕️❓ Doctor: What are your side effects?
💊 Fluoxetine:
Common:
Nausea
Headache
Insomnia
Anxiety/jitteriness early
Sexual dysfunction
Sweating
Tremor
Appetite loss
Serious:
Serotonin syndrome
SIADH (hyponatremia)
Mania induction
Increased suicidal ideation in young patients
👨‍⚕️❓ Doctor: What about special populations?
💊 Fluoxetine:
Pregnancy:
Can be used if benefits outweigh risks
Possible neonatal adaptation syndrome
Lactation:
Excreted in breast milk
May cause mild infant irritability
Children/adolescents:
Strong evidence for depression and OCD
Requires monitoring for suicidality and activation
Elderly:
Start low dose due to hyponatremia risk
Renal disease:
Usually no dose adjustment
Liver disease:
Dose reduction often needed
Heart disease:
Generally safe compared to TCAs
👨‍⚕️❓ Doctor: What is your dosing and onset?
💊 Fluoxetine:
Start: 10–20 mg daily
Usual: 20–60 mg/day
Max: 80 mg/day
Onset:
1–2 weeks: early improvement
4–8 weeks: full antidepressant effect
10–12+ weeks: OCD response

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Pharmacology

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Pharmacology

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Pharmacology

Reaction: What does this mean for me? How many people read and get benefit from this? If there is no reaction, explain one thing to me: no one is interested.

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Pharmacology

👨‍⚕️🤝 Clinical Pharmacology Interview: Sertraline
💊 Sertraline – Educational Overview
👨‍⚕️❓ Doctor: Introduce yourself.
💊 Sertraline: I am Sertraline, a selective serotonin reuptake inhibitor (SSRI) used in clinical practice.
I am prescribed in the management of:
Major depressive disorder
Anxiety disorders
Obsessive-compulsive disorder (OCD)
Post-traumatic stress disorder (PTSD)
Panic disorder
Social anxiety disorder
👨‍⚕️❓ Doctor: What is your mechanism of action?
💊 Sertraline: I inhibit the serotonin transporter (SERT), leading to increased serotonin availability in the synaptic cleft.
This modulation of serotonergic neurotransmission is associated with:
Improvement in mood symptoms
Reduction in anxiety symptoms
Modulation of emotional processing
👨‍⚕️❓ Doctor: How are you used in clinical practice compared to other SSRIs?
💊 Sertraline: I am one of several SSRIs used in psychiatric practice.
Clinical selection depends on patient-specific factors such as:
Symptom profile
Comorbid conditions
Tolerability
Drug interactions
I am frequently used due to extensive clinical experience and guideline support in multiple indications.
👨‍⚕️❓ Doctor: In which conditions are you particularly studied?
💊 Sertraline: Evidence supports my use in:
Depression with comorbid anxiety symptoms
Panic disorder
PTSD
Social anxiety disorder
OCD (often requiring higher doses and longer treatment duration)
👨‍⚕️❓ Doctor: What about cardiovascular safety?
💊 Sertraline: I have a relatively favorable cardiac safety profile among SSRIs.
Low risk of QT prolongation compared with some alternatives
Often considered in patients with cardiovascular disease when SSRIs are indicated
👨‍⚕️❓ Doctor: What is the dosing approach?
💊 Sertraline: Dosing is individualized based on indication and tolerability:
Depression: typically initiated at 50 mg daily
Anxiety-related disorders: may be initiated at 25 mg daily to improve tolerability
Maximum dose: 200 mg daily
Dose adjustments are generally made gradually
👨‍⚕️❓ Doctor: What is the expected time to response?
💊 Sertraline:
Initial symptom changes: may appear within 1–2 weeks (often early tolerability or anxiety changes)
Antidepressant effect: typically 4–8 weeks
OCD: response may require 8–12 weeks or longer
👨‍⚕️❓ Doctor: What are common adverse effects?
💊 Sertraline: Commonly reported adverse effects include:
Gastrointestinal symptoms (e.g., nausea, diarrhea)
Sleep disturbances (insomnia or somnolence)
Headache
Tremor
Increased sweating
👨‍⚕️❓ Doctor: What about sexual side effects?
💊 Sertraline: Sexual dysfunction may occur with SSRIs and can include:
Reduced libido
Delayed ejaculation
Difficulty achieving orgasm
This may contribute to discontinuation in some patients.
👨‍⚕️❓ Doctor: What are important serious risks?
💊 Sertraline: Clinically important risks include:
Serotonin syndrome (especially with interacting drugs)
Hyponatremia (SIADH), particularly in older adults
Increased bleeding risk (especially with NSAIDs/anticoagulants)
Risk of manic switch in patients with bipolar disorder
Increased suicidal ideation risk in younger populations during early treatment phase
👨‍⚕️❓ Doctor: What are important drug interactions?
💊 Sertraline: Significant interactions include:
MAO inhibitors → contraindicated
Tramadol → increased serotonin syndrome risk
NSAIDs / anticoagulants → increased bleeding risk
Linezolid → risk of serotonin toxicity
Lithium → increased serotonergic effects
CYP-mediated interactions (variable clinical significance)
👨‍⚕️❓ Doctor: Can serotonin syndrome occur?
💊 Sertraline: Yes, particularly when combined with other serotonergic agents.
Symptoms may include:
Agitation
Hyperreflexia
Clonus
Autonomic instability (e.g., fever, tachycardia)
It is a potentially serious and urgent clinical condition.
👨‍⚕️❓ Doctor: What about pregnancy and breastfeeding?
💊 Sertraline:
Pregnancy: may be used when clinically indicated after risk–benefit assessment
Breastfeeding: often considered among SSRIs with lower relative infant exposure

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Pharmacology

🎙️ Neurotransmitter Talk Show 🧠
From Serotonin to the SSRI Family
Understanding the Brain Before Prescribing the Drug
📚 This content is intended for medical education only and should not replace professional psychiatric evaluation or clinical judgment.
━━━━━━━━━━━━━━━
🧠 Part 1 — Meeting Serotonin (5-HT)
👨🏻‍⚕️ Host: Good evening, everyone. Before we meet the SSRI family, we need to understand the main character of tonight’s story. Please welcome… Serotonin!
🧠 Serotonin (5-HT): Thank you for having me. My scientific name is 5-Hydroxytryptamine (5-HT), but most people call me serotonin. I’m a major neurotransmitter involved in mood regulation, anxiety, sleep, appetite, cognition, and emotional processing.
👨🏻‍⚕️ Host: Where do you come from?
🧠 Serotonin: I’m synthesized from tryptophan via a two-step pathway:
🧪 Tryptophan → 5-HTP → Serotonin (5-HT)
👨🏻‍⚕️ Host: Where are you mainly active?
🧠 Serotonin: I act in both the brain and the body.
📍 In the central nervous system, I’m produced in the raphe nuclei, regulating mood, anxiety, sleep, and cognition.
📍 About ~90% of serotonin is produced in enterochromaffin cells of the gastrointestinal tract, which explains why GI and mood effects often coexist.
👨🏻‍⚕️ Host: That explains SSRI gastrointestinal side effects?
🧠 Serotonin: Exactly.
Platelets do not synthesize serotonin but actively uptake it via SERT transporters and store it in dense granules.
Blocking SERT (as SSRIs do) reduces platelet serotonin uptake, which may increase bleeding tendency.
━━━━━━━━━━━━━━━
🧬 Part 2 — Serotonin Receptors
👨🏻‍⚕️ Host: Do all your effects occur through one receptor?
🧠 Serotonin: No. I act through multiple receptor families:
🔹 5-HT1A receptor
Associated with anxiolytic and mood-stabilizing effects. Activation promotes emotional calming.
🔹 5-HT2A receptor
Excess activation is associated with anxiety, insomnia, sexual dysfunction, and psychedelic effects in cortical regions.
🔹 5-HT2C receptor
Involved in appetite and mood regulation.
🔹 5-HT3 receptor
A ligand-gated ion channel strongly associated with nausea and vomiting.
💊 SSRI Family: That explains early SSRI-induced nausea. 5-HT3 antagonists (e.g., ondansetron) may help.
🔹 5-HT4 receptor
Mainly regulates gastrointestinal motility.
━━━━━━━━━━━━━━━
💊 Part 3 — Enter the SSRI Family
💊 SSRI Family: We are Selective Serotonin Reuptake Inhibitors.
👨🏻‍⚕️ Host: Do you produce serotonin?
💊 SSRI Family: No. We inhibit SERT transporters, increasing serotonin availability in the synaptic cleft.
👨🏻‍⚕️ Host: Why does clinical improvement take weeks?
💊 SSRI Family: Because early increased serotonin activates presynaptic 5-HT1A autoreceptors, temporarily reducing neuronal firing.
Over time, these autoreceptors desensitize, leading to sustained serotonergic transmission, neuroplastic changes, and downstream gene expression modulation.
━━━━━━━━━━━━━━━
🧠 Onset of Effect
Early improvement: 1–2 weeks
Full therapeutic effect: 4–6+ weeks
━━━━━━━━━━━━━━━
📌 Clinical Indications
💊 SSRIs are used in:
• Major Depressive Disorder
• Generalized Anxiety Disorder
• Panic Disorder
• Obsessive-Compulsive Disorder (OCD)
• Post-Traumatic Stress Disorder (PTSD)
• Social Anxiety Disorder
• Premenstrual Dysphoric Disorder (PMDD)
━━━━━━━━━━━━━━━
💊 Individual SSRIs
🧪 Fluoxetine
Long half-life → lower discontinuation risk, activating profile.
🧪 Sertraline
Broad use in depression/anxiety; GI side effects are relatively common.
🧪 Paroxetine
More sedating, higher risk of weight gain and sexual dysfunction. Significant withdrawal symptoms.
⚠️ Associated with increased risk of congenital cardiac malformations in early pregnancy; consider alternatives when possible.
🧪 Citalopram
Generally well tolerated; QT prolongation risk increases at higher doses (>40 mg/day, or >20 mg in elderly/hepatic impairment).
🧪 Escitalopram
S-enantiomer of citalopram with improved selectivity and tolerability.
🧪 Fluvoxamine
Particularly effective in OCD. Strong CYP1A2 inhibitor, leading to significant drug interactions (also affects CYP2C19).

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Pharmacology

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This mean only 0.9% of members that see the post are interesting 🤔

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Pharmacology

Meet the Tricyclic Antidepressants
An Exclusive Interview with a Legendary Drug Class

Host:
Good evening, colleagues. Today we have a special guest—a drug class that has been treating depression since the 1950s, survived the arrival of SSRIs, and still refuses to retire.
Please welcome the Tricyclic Antidepressants.

TCA:
Thank you. It is a pleasure to be here

.
Part I: Identity
Host:
Before we discuss your clinical career, could you introduce yourself?
TCA:
Certainly. I am a family of medications that includes Amitriptyline, Nortriptyline, Imipramine, and Clomipramine. Although newer antidepressants have become popular, I remain one of the most effective classes in psychiatry and pain medicine.

Host:
What makes you effective?

TCA:
My primary action is simple: I block the reuptake of serotonin and norepinephrine.

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Pharmacology

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Pharmacology

Next meeting with paroxetine

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Pharmacology

A 64-year-old man presents with:
Major depressive disorder
History of myocardial infarction 6 months ago ❤️Coronary artery disease
Currently taking:
Aspirin
Atorvastatin
Metoprolol
Complains of low mood, poor sleep, and anxiety
Which antidepressant is the MOST appropriate?
A) Fluoxetine
B) Sertraline
C) Escitalopram
D) Amitriptyline

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Pharmacology

26-year-old woman presents with:
Generalized anxiety disorder
Fear of medication side effects
History of stopping medications due to nausea
No significant medical history
Which SSRI is MOST appropriate?
A) Fluoxetine
B) Sertraline
C) Escitalopram
D) Paroxetine

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Pharmacology

👨‍⚕️🤝 Meeting with Escitalopram
“Doctor vs Escitalopram” 💊
👨‍⚕️❓ Doctor:
Please introduce yourself.
💊 Escitalopram:
Hello Doctor 👋
I am Escitalopram, an SSRI (Selective Serotonin Reuptake Inhibitor) antidepressant.
Fun fact 😎
I am the S-enantiomer of citalopram, containing the more active form responsible for most of the antidepressant effect.
I’m officially approved for:
✅ Major Depressive Disorder
✅ Generalized Anxiety Disorder
Common off-label or region-dependent uses:
✅ Panic disorder
✅ Social anxiety disorder
✅ Obsessive-Compulsive Disorder
✅ Post-Traumatic Stress Disorder
👨‍⚕️❓ Doctor:
Tell me your mechanism of action.
💊 Escitalopram:
I selectively inhibit the serotonin transporter (SERT).
Result:
✅ Increased serotonin in the synaptic cleft
✅ Improved mood
✅ Reduced anxiety
👨‍⚕️❓ Doctor:
There are many SSRIs… why should I choose YOU?
💊 Escitalopram:
Because clinicians often appreciate that I have:
✅ Very good tolerability
✅ Simple once-daily dosing
✅ Relatively fewer CYP-mediated drug interactions
✅ Strong efficacy in anxiety disorders
✅ Low rates of treatment discontinuation
👨‍⚕️📌 Clinical Pearl:
I’m commonly considered among the best-tolerated SSRIs, although individual responses vary.
👨‍⚕️❓ Doctor:
When are you one of the BEST choices?
💊 Escitalopram:
I’m commonly preferred in:
✅ Generalized Anxiety Disorder
✅ Depression with prominent anxiety symptoms
✅ First-time SSRI users
✅ Patients sensitive to side effects
✅ Long-term treatment plans
👨‍⚕️❓ Doctor:
What are your usual doses?
💊 Escitalopram:
Depression / GAD
💊 Starting dose:
10 mg daily
💊 Typical dose:
10–20 mg daily
🚫 Maximum usual dose:
20 mg/day
👨‍⚕️📌 Clinical Pearl:
Older adults and patients with liver impairment may require lower dosing.
👨‍⚕️❓ Doctor:
How long until patients feel better?
💊 Escitalopram:
⏳ Some early improvements (sleep, anxiety, energy) may appear within 1–2 weeks
⏳ Full antidepressant effect often requires 4–8 weeks
⏳ Anxiety disorders may require several weeks or longer
👨‍⚕️❓ Doctor:
What are your common side effects?
💊 Escitalopram:
❌ Nausea
❌ Headache
❌ Insomnia or somnolence
❌ Dizziness
❌ Sexual dysfunction
❌ Sweating
👨‍⚕️📌 Clinical Pearl:
Some patients experience less GI upset than with some other SSRIs such as sertraline, but individual responses differ.
👨‍⚕️❓ Doctor:
What serious risks should I know?
💊 Escitalopram:
⚠️ Serotonin syndrome
⚠️ Suicidal ideation monitoring in younger patients
⚠️ Hyponatremia / SIADH
⚠️ Increased bleeding risk
⚠️ Mania activation in susceptible patients
👨‍⚕️❓ Doctor:
Do you have important drug interactions?
💊 Escitalopram:
🚫 MAOIs → contraindicated
⚠️ Tramadol → increased serotonin syndrome risk
⚠️ NSAIDs / anticoagulants → increased bleeding risk
⚠️ Lithium → increased serotonin toxicity risk
Good news 😎
✅ Relatively fewer CYP interactions than some other SSRIs
👨‍⚕️❓ Doctor:
What are your disadvantages?
💊 Escitalopram:
❌ Sexual dysfunction
❌ Withdrawal symptoms if stopped abruptly
❌ Dose-dependent QT prolongation risk
❌ Initial anxiety or activation in some patients
👨‍⚕️📌 Clinical Pearl:
QT risk increases with:
⚠️ Higher doses
⚠️ Electrolyte abnormalities
⚠️ Other QT-prolonging drugs
QT concerns are generally more prominent with citalopram.
👨‍⚕️❓ Doctor:
What happens if patients stop you suddenly?
💊 Escitalopram:
Possible discontinuation symptoms:
❌ Dizziness
❌ Anxiety
❌ Flu-like symptoms
❌ Paresthesias ("brain zaps")
❌ Sleep disturbance
📌 Gradual tapering is generally preferred.
👨‍⚕️❓ Doctor:
When might another antidepressant be better than you?
💊 Escitalopram:
⚠️ Poor adherence expected
→ Fluoxetine may be preferred because of its longer half-life
⚠️ Major cardiac concerns
→ Sertraline is sometimes favored
⚠️ Sexual dysfunction becomes problematic
→ Bupropion may be considered

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Pharmacology

When to Prefer Fluoxetine ?

Poor adherence / missed doses: The long half-life makes it more forgiving, helping to prevent discontinuation syndrome (withdrawal) if a dose is missed.

Fatigue-dominant depression: Its activating nature can help with low-energy depression.

Bulimia nervosa: is first choice

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Pharmacology

Fluoxitine vs Sertraline

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Pharmacology

Anyone need Uptodate share to him this post
First 5 subscribe will have discount by 20 %

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Pharmacology

Nice feedback by Psychiatrist 😊

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Pharmacology

🔥ECG & ABG is Freeeeee

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Pharmacology

Sertraline Revision Note

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Pharmacology


━━━━━━━━━━━━━━━
👩🏻‍⚕️ Monitoring During SSRI Therapy
• Mood changes or suicidal ideation (early phase)
• GI symptoms
• Sleep disturbances
• Sexual dysfunction
• SIADH-related hyponatremia (especially elderly)
• Serotonin syndrome
• Mania induction in bipolar disorder
━━━━━━━━━━━━━━━
⚠️ Serious Adverse Effects
• Serotonin Syndrome
• Increased bleeding risk (platelet dysfunction)
• Hyponatremia (SIADH)
• QT prolongation (citalopram dose-dependent)
• Mania activation in bipolar disorder
🧠 Serotonin Syndrome Triad:
• Cognitive: agitation, confusion
• Autonomic: fever, diaphoresis, instability
• Neuromuscular: clonus, hyperreflexia
🚨 Medical emergency
━━━━━━━━━━━━━━━
⚠️ Drug Interactions
Avoid combinations with:
• MAO inhibitors → serotonin syndrome
• Tramadol, linezolid, triptans → serotonergic toxicity
• NSAIDs, anticoagulants → bleeding risk
• Alcohol → CNS depression
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📌 Common Clinical Mistakes
❌ Abrupt discontinuation
❌ Failure to screen for bipolar disorder
❌ Unsafe serotonergic combinations
❌ Poor counseling about delayed onset of effect
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🌐 /channel/Yaqob_Hamood

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Pharmacology

We will start by Antidepressants

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