#selegiline

[seagullcharmer]

besties for the resties

[knifedog]

Sally got prescribed selegiline which should help with the sundowning. it's a liquid i have to squirt into her mouth every morning and it'll be a week before we see a change.

its something she'll have to be on for the rest of her life but if it helps her it's worth the hassle. i just want her to be comfortable.

oh and she also got her rabies vaccine so she can go fight raccoons

[kingsofeverything]

Hi Lauren I just read your post on Rufus and I just wanted to let you know that I'm going through the same thing with my baby boy. I have a Morkie named Lucky he is 13yrs old and my poor baby was recently diagnosed with Dementia and Glaucoma/Cataracts. He has also been dealing with Diabetes for a few years now. My Lucky is blind and can't hear as well as he used to so getting around has been rough. He sleeps a lot throughout the day but he does still sleep at night however more frequently he gets up to either walk around or just stare at the wall. I'm just trying to make him as comfortable as I can. This is all new to me as well and sometimes I wonder if he doesn't go naturally to heaven will I be able to make that final decision. I honestly don't know but I pray for guidance and strength. I'm praying for you as well.. I hope you have a great night.

i'm sorry to hear about lucky! sending you guys love.

it's been rough around here. rufus is taking a lot of meds for his anxiety and sleep and it's helping for now. we've already had to add/adjust because what worked at first stopped working after a few weeks. my vet's main concern (and mine) is that rufus is happy and comfortable. i know we'll wind up having him put to sleep just because from what i've learned about ccd is that once their minds reach a certain point, they're afraid all the time. right now rufus takes selegiline in the morning, then around 3pm i give him 300mg of gabapentin. at 8:30ish he gets another 300mg of gabapentin and 10mg melatonin. that's what's working for now.

he's still eating and drinking and he's remembering to go outside to go to the bathroom, so i'm thankful. once he stops doing any of those, we'll have to reevaluate. but it's end of life care at this point.

[iikciim]

Anti-Parkinson's

Anatomy, Physiology, and Pathophysiology Overview

Parkinson’s disease is a chronic, progressive, neurodegenerative disorder causing the degeneration of dopamine-producing neurons in the brain. Patients with this disease also have elevated acetylcholine levels and lowered dopamine levels.

Dopamine is an inhibitory neurotransmitter and acetylcholine is an excitatory neurotransmitter in this area of the brain. Parkinson’s disease results from an imbalance in these two neurotransmitters in the basal ganglia.

Parkinson’s disease affects at least 1 million Americans and 4 million people worldwide. Over 60,000 patients are diagnosed each year in the United States. It is the second most common neurodegenerative disease after Alzheimer’s disease.

There are no readily available laboratory tests that can detect or confirm Parkinson’s disease. The diagnosis is usually made on the basis of the classic symptoms and physical findings.

The classic symptoms of Parkinson’s disease include bradykinesia, postural instability, rigidity, and tremors (TRAP [tremor, rigidity, akinesia, postural instability] with akinesia really manifesting as bradykinesia).

Symptoms of Parkinson’s disease do not appear until approximately 80% of the dopamine stored in the substantia nigra has been deleted; thus, by the time the disease is diagnosed, only approximately 20% of the patient’s original dopaminergic terminals are functioning normally.

Rapid swings in the response to levodopa, called the on-off phenomenon, result in the worsening of the disease with too little dopamine or dyskinesias with too much.

In contrast, the wearing-off phenomenon occurs when anti–Parkinson’s disease medications begin to lose their effectiveness, despite maximal dosing, as the disease progresses.

Dyskinesia is the difficulty in performing voluntary movements and is commonly seen in the disease. Most frequent are chorea (irregular, spasmodic, involuntary movements of the limbs or facial muscles) and dystonia (abnormal muscle tone leading to impaired or abnormal movements). Dystonia commonly involves the head, neck, or feet and is a symptom common to patients with Parkinson’s disease.

Dyskinesias also occur as an adverse effect of some of the anti-Parkinson's drugs.

These motor complications make Parkinson’s disease a prominent cause of disability. Dementia may also result and is referred to as Parkinson’s disease-associated dementia.

Up to 40% of patients with Parkinson’s disease will experience psychosis and hallucinations. In 2016, a new drug, pimavanserin (Nuplazid), was approved for the treatment of hallucinations and delusions associated with Parkinson’s disease psychosis. Pimavanserin is a selective serotonin 5-HT2A inverse agonist and has no effect on dopaminergic receptors.

Treatment of the disease centers around drug therapy, but many experts believe that physical activity is as important as any drug therapy, and together these greatly improve mobility. For severe cases, the surgical technique of deep brain stimulation may be used.

Drug therapy is aimed at increasing the levels of dopamine and/or antagonizing the effects of acetylcholine. Drug therapy is used to slow the progression of symptoms.

Drugs used in the treatment of Parkinson’s disease include amantadine, benztropine, bromocriptine, carbidopa-levodopa, entacapone, ropinirole, and selegiline. They have a variety of mechanisms of action and many adverse effects, drug interactions, and dosing concerns.

As long as there are functioning nerve terminals that can take up dopamine, the symptoms of Parkinson’s disease can be at least partially controlled.

https://bb-csuohio.blackboard.com/bbcswebdav/pid-7116320-dt-content-rid-80385680_1/xid-80385680_1

Pharmacology Overview

Indirect-Acting Dopaminergic Drugs

Monoamine Oxidase Inhibitors

The primary role of monoamine oxidase (MAO) enzymes is the breakdown of catecholamines, such as dopamine, norepinephrine, and epinephrine, as well as serotonin.

Giving an MAO-B inhibitor such as selegiline or rasagiline causes an increase in the levels of dopaminergic stimulation in the central nervous system (CNS), helping to counter the dopaminergic deficiency.

Selegiline and rasagiline are adjunctive drugs currently approved for use in combination with carbidopa-levodopa when the response to levodopa is fluctuating; they may also be beneficial as prophylactic drugs to delay reduction in a patient’s response to levodopa. As Parkinson’s disease progresses, it becomes more difficult to manage it with levodopa, and ultimately the patient is seriously debilitated, generally 5 to 10 years after the start of therapy.

The newest drugs approved for “off” episodes include istradefyllins, (Nourianz) which is an adenosine receptor antagonist, and opicapone, which is a COMT inhibitor.

Dopamine Modulator

Only one drug—amantadine (Symmetrel)—is currently known to function as a dopamine modulator for the management of Parkinson’s disease.

Amantadine appears to work by causing the release of dopamine and other catecholamines from their storage sites and also blocks the reuptake of dopamine into the nerve fibers.

Because amantadine does not directly stimulate dopaminergic receptors, it is considered to be indirect acting. Amantadine also has some anticholinergic properties.

Amantadine is generally indicated in the early stages of Parkinson’s disease while there are still some intact neurons. It can be used in the moderate to advanced stages to help control symptoms of tremors but is usually effective for only 6 to 12 months.

Common adverse effects include dizziness, insomnia, and nausea. Amantadine causes increased anticholinergic adverse effects when given with anticholinergic drugs.

Catechol Ortho-Methyltransferase Inhibitors

Drugs in this category include entacapone (Comtan), tolcapone (Tasmar), and, most recently, opicapone (Ongentys), approved specifically as adjunctive treatment of "Off" episodes. 

Tolcapone acts both centrally and peripherally, whereas entacapone cannot cross the blood-brain barrier and therefore can act only peripherally. They prolong the duration of action of levodopa, especially when levodopa is given with carbidopa, resulting in the reduction of the wearing-off phenomenon.

Both catechol ortho-methyltransferase (COMT) inhibitors (tolcapone and entacapone) are contraindicated in cases of known drug allergy. Tolcapone is also contraindicated in cases of liver failure.

Tolcapone has been associated with severe liver failure and carries a black box warning related to hepatotoxicity.

Commonly reported adverse effects with both COMT inhibitors include gastrointestinal (GI) upset and urine discoloration. In addition, they also can worsen dyskinesia.

Neither tolcapone nor entacapone are to be taken with nonselective MAO inhibitors because of cardiovascular risk due to reduced catecholamine metabolism. However, the selective MAO-B inhibitor selegiline may be safely taken concurrently with COMT inhibitors.

https://bb-csuohio.blackboard.com/bbcswebdav/pid-7116320-dt-content-rid-80385677_1/xid-80385677_1

Direct-Acting Dopamine Receptor Agonists

Direct-acting dopamine receptor agonists are drugs used to treat Parkinson’s disease, often as first-line agents used on diagnosis. These drugs include two subclasses: nondopamine dopamine receptor agonists (NDDRAs) and dopamine replacement drugs.

All NDDRAs work by direct stimulation of presynaptic and/or postsynaptic dopamine receptors in the brain. They may be used in the early or late stages of the disease.

The traditional role of the NDDRAs bromocriptine, pramipexole, ropinirole, and rotigotine has been as adjuncts to levodopa for the management of motor fluctuations; however, they are now often used as first-line therapy.

Known allergy is a contraindication to dopaminergic drug therapy. These drugs are not to be used concurrently with catecholamines due to the cardiovascular risks.

The traditional cornerstone of therapy for Parkinson’s disease has been the drug levodopa, the biological precursor of dopamine. Dopamine must be administered orally as levodopa because exogenously administered dopamine cannot pass through the blood-brain barrier. Levodopa cannot be used by itself in the brain and must be combined with another substance, carbidopa. The combination product carbidopa-levodopa provides exogenous sources of dopamine and is the drug of choice in the later stages of Parkinson’s disease.

Large doses result in high peripheral levels of dopamine and lead to many unwanted adverse effects, including confusion, involuntary movements, GI distress, hypotension, and even cardiac dysrhythmias. These problems are avoided when levodopa is given with carbidopa.

Levodopa and carbidopa are both contraindicated in cases of angle-closure glaucoma because they can raise intraocular pressure, but they may be used cautiously in open-angle glaucoma. Neither drug is to be used in patients with any undiagnosed skin condition, because both drugs can activate malignant melanoma.

Adverse effects of dopamine replacement drugs include cardiac dysrhythmias, hypotension, chorea, muscle cramps, and GI distress.

https://bb-csuohio.blackboard.com/bbcswebdav/pid-7116320-dt-content-rid-80385678_1/xid-80385678_1

Anticholinergic Drugs

Anticholinergic drugs block the effects of the neurotransmitter acetylcholine at cholinergic receptors in the brain as well as in the rest of the body. They are used as adjunct drug therapy in Parkinson’s disease due to their antitremor properties.

Anticholinergic drugs can cause dry mouth or decreased salivation, urinary retention, decreased GI motility (constipation), dilated pupils (mydriasis), and smooth muscle relaxation.

Anticholinergics must be used cautiously in older adults because of significant potential adverse effects, such as confusion, urinary retention, visual blurring, palpitations, and increased intraocular pressure.

https://bb-csuohio.blackboard.com/bbcswebdav/pid-7116320-dt-content-rid-80385679_1/xid-80385679_1

Nursing Process

After patients are confronted with the diagnosis of Parkinson’s disease, they will soon learn that their quality of life depends on drug therapy and nondrug measures.

Before medications for Parkinson’s disease are given, assess and document vital signs and ABCs (airway, breathing, and circulation). Obtain a complete nursing history with a thorough physical assessment, including compiling a comprehensive medication profile.

With indirect-acting dopamine receptor agonists, such as amantadine, and direct-acting dopamine receptor agonists, such as carbidopa-levodopa, include supine and standing blood pressures (because of drug-related postural hypotension), height, weight, medication, and medical and nursing history. Include family, significant others, and caregivers in the assessment and data collection process.

Assess motor skills, including abilities and deficiencies, and for the presence of akinesia, bradykinesia, postural instability, rigidity, tremors, staggering gait, or drooling.

It is important to understand the gynecologic history of the patient and to know if the patient is pregnant and/or lactating. Some dopamine replacement drugs cross into the placenta and into breast milk and have unknown actions in the pediatric patient.

When anticholinergic drugs are prescribed, assess the patient carefully to determine the gross level of organ functioning—especially in those systems most affected by Parkinson’s disease, including the GI, genitourinary, visual, cardiac, and neurologic systems.

Pay close attention to any present or past changes in mental status as well as the presence of confusion, disorientation, or psychotic-like behavior. This is important to consider in elderly patients because of a decline in liver function, a subsequent higher risk for adverse effects and possible toxicity, and an overall increased sensitivity to drugs.

With indirect-acting dopamine receptor agonists, cardiac status is important to assess and document because of the adverse effects of hypotension/hypertension and chest pain.

Encourage patients, family, or caregivers to begin keeping a daily drug calendar or journal including the drugs prescribed, dosage, frequency/timing, and therapeutic and adverse changes.

During the start of dopaminergic drug therapy, the patient will most likely need assistance when walking because of the dizziness and possibly syncope caused by these drugs.

With anticholinergic drugs, patients need to take the medication as prescribed, after meals or at bedtime, and not at the same time as with other medications.

Be cautious with the sound-alike drugs: selegiline is an MAOI, whereas Salagen is an oral form of pilocarpine used to manage dry mouth in patients with Sjögren’s syndrome or in those receiving radiation therapy.

Nutritional concerns include making sure the patient is taking adequate fiber, vegetables, and fruits, as well as an increase in fluid intake, if not contraindicated. Additional concerns include the distribution of protein intake over the course of the day if taking levodopa/carbidopa. The drug is to be taken one-half hour before eating a protein-containing meal or one hour after.

Be aware of all other forms of therapies that may be beneficial, such as support groups, water aerobics, and occupational and physical therapy.

Aerobic exercise may have a positive effect on the patient while improving quality of life and socialization. Although it has not been proven that exercise can slow the progression of this disease, it can help patients feel better mentally and physically.

Tai Chi may be one option of exercise that has been shown to improve balance, flexibility, and strength in a variety of individuals.

Simple stretching and strengthening exercises are important to consider in those with Parkinson’s disease. All exercises must be approved by the patient’s health care provider.

Prevention of falls is important—reduce risk by installing shower or tub grab-bars, adequate lighting in the house especially at night, and removing or securing loose rugs that may increase the risk of tripping.

Therapeutic responses to the antiparkinson drugs include an improved sense of well-being, improved mental status, increased appetite, ability to perform activities of daily living, improved concentration and ability to think more clearly, and a decrease in the intensity of Parkinsonian symptoms.

Monitor for adverse effects such as dizziness; nausea; syncope; insomnia; GI upset (associated with indirect-acting dopamine receptor agonists such as selegiline, amantadine, entacapone, and tolcapone); ataxia; depression (associated with direct-acting dopamine receptor agonists such as bromocriptine); palpitations; hypotension; urinary retention; and depression (associated with dopamine replacement drugs such as levodopa and carbidopa).

Patient considerations include providing individual and family support along with options for care of the family member with Parkinson’s disease. The disease is long-term and lifelong, as well as debilitating. A holistic approach in which all aspects of the patient and family are considered and respected is the key to quality nursing care.

[darkmaga-returns]

Story at-a-glance

Dopamine and progesterone have therapeutic effects against cancer, while estrogen and serotonin promote cancer growth and spread

Selegiline, an antidepressant that belongs to a class of drugs called monoamine oxidase (MAO) inhibitors, might be effective as an anticancer therapeutic for breast cancer

Selegiline works by inhibiting monoamine oxidase B (MAO-B), which increases dopamine levels in the brain

Lifestyle factors like exercise, sleep, diet and stress management naturally increase dopamine levels

Reducing exposure to the known human carcinogen estrogen and lowering your estrogen load are also important anticancer strategies

[zayashr]

ما هو علاج مرض باركنسون؟

علاج مرض باركنسون يشمل مجموعة من الاستراتيجيات تهدف إلى تخفيف الأعراض وتحسين جودة الحياة. لا يوجد علاج نهائي للمرض، ولكن هناك عدة خيارات علاجية يمكن أن تساعد في إدارة

جراحات مرض باركنسون تُستخدم عادةً لعلاج الأعراض عندما لا تكون الأدوية كافية أو عندما تسبب الأدوية آثارًا جانبية غير مقبولة. هناك عدة أنواع من الجراحات التي يمكن استخدامها لعلاج مرض باركنسون:

الأعراض بشكل فعال.

1. الأدوية:

ليفودوبا/كاربيدوبا (Levodopa/Carbidopa): يعتبر العلاج الأكثر فعالية. ليفودوبا يتحول إلى دوبامين في الدماغ، مما يساعد على تخفيف الأعراض الحركية. كاربيدوبا يساعد على منع تحلل ليفودوبا قبل وصوله إلى الدماغ.

ناهضات الدوبامين (Dopamine Agonists): مثل براميبكسول (Pramipexole) وروبينيرول (Ropinirole)، تحاكي عمل الدوبامين في الدماغ.

مثبطات مونوامين أوكسيداز ب (MAO-B Inhibitors): مثل سيليجيلين (Selegiline) ورازاجيلين (Rasagiline)، تساعد على الحفاظ على مستوى الدوبامين في الدماغ.

مثبطات ناقلة الكاتيكول-أو-مثيل ترانسفيراز (COMT Inhibitors): مثل إنتاكابون (Entacapone)، تساعد على زيادة فعالية ليفودوبا.

الأدوية المضادة للكولين (Anticholinergics): تستخدم لتقليل الرعاش وتحسين التوازن.

أمانتادين (Amantadine): يمكن أن يساعد في التحكم في الحركات غير الطوعية (dyskinesia) الناتجة عن استخدام ليفودوبا.

2. الجراحة:

التحفيز العميق للدماغ (Deep Brain Stimulation - DBS): يتضمن زرع أقطاب كهربائية في مناطق محددة من الدماغ. جهاز مولد النبضات الكهربائية المزروع تحت جلد الصدر يرسل إشارات كهربائية لتنظيم نشاط الدماغ.

الاستئصال الجراحي (Lesioning): يشمل تدمير مناطق معينة من الدماغ مثل الكرة الشاحبة أو المهاد لتخفيف الأعراض.

3. العلاج الطبيعي والتأهيل:

العلاج الطبيعي: يساعد على تحسين القوة، التوازن، والمرونة.

العلاج الوظيفي: يساعد المرضى على تحسين قدراتهم في أداء الأنشطة اليومية.

العلاج بالكلام: يساعد في تحسين مشاكل النطق والبلع.

4. الدعم النفسي والاجتماعي:

العلاج النفسي: يمكن أن يساعد في التعامل مع الاكتئاب، القلق، والتغيرات المزاجية المرتبطة بالمرض.

مجموعات الدعم: توفر الدعم العاطفي والاجتماعي للمرضى وعائلاتهم.

5. العلاجات التكميلية:

التغذية السليمة: النظام الغذائي المتوازن يمكن أن يساعد في الحفاظ على الصحة العامة.

العلاج بالموسيقى، العلاج بالفن، والعلاج بالحيوانات: يمكن أن تساعد في تحسين الحالة النفسية وتقليل التوتر.

6. الإدارة الذاتية:

التمارين الرياضية: ممارسة التمارين بانتظام يمكن أن تساعد في تحسين الحركة واللياقة البدنية.

التثقيف المستمر: معرفة المزيد عن المرض وكيفية التعامل معه يمكن أن يساعد المرضى وأسرهم في إدارة الحالة بشكل أفضل.

العوامل المؤثرة في اختيار العلاج:

مرحلة المرض: تختلف العلاجات باختلاف مراحل المرض.

الأعراض السائدة: يحدد نوع الأعراض وشدتها الخيارات العلاجية الأنسب.

الحالة الصحية العامة: يؤثر وجود حالات طبية أخرى على اختيار العلاج.

المتابعة والرعاية:

الزيارات المنتظمة للطبيب: لتقييم تقدم العلاج وتعديل الخطة العلاجية إذا لزم الأمر.

الفحوصات الدورية: للتحقق من الآثار الجانبية ومراقبة الصحة العامة.

تحتاج إدارة مرض باركنسون إلى نهج متعدد التخصصات يشمل الأطباء والمختصين في العلاج الطبيعي والوظيفي والنفسي لتقديم الرعاية الشاملة والدعم المستمر للمرضى.

[teachingrounds]

Q. There are 5 second-line medications for migraine prophylaxis. What are they?

.

.

.

A. Monoamine oxidase inhibitors (e.g. selegiline / Emsam*), botulinum toxin A (Botox), calcitonin gene-related peptide (CGRP) inhibitors, cyproheptadine (Periactin), and gabapentin (Neurontin).

Pro-Tip: Of these, cyproheptadine and gabapentin have unproven efficacy.

Source for this week is Jasvinder Chawla’s “Migraine Headache Treatment & Management” article on Medscape.

Picture of selegiline / Emsam

[seagullcharmer]

does that [let's take ibuprofen together!] meme again but it's selegiline holding out a tiny vicodyn

[johnmark0404]

Adderall and Methylphenidate Difference and Potency: Choose Your Option for ADHD

Adderall and Methylphenidate medicines are used to treat attention deficit Hyperactivity disorder Composition: Adderall formulation of amphetamine salts, including dextroamphetamine and levoamphetamine. Belongs to the group of phenethylamine class Methylphenidate is a phenethylamine derivative. and belongs to the piperidine class. Side effects: Adderall can increase heart rate and blood pressure not suitable for people with heart deseaseProlonged use can lead to dependence. Methylphenidate: it can cause loss of appetite, sleep difficulty, dry mouth, nausea, stomach ache, and dizziness can also cause anxiety, and irritability Both are available in immediate and extended-release formulations. Prescribed extended-release versions of Adderall are Adderall XR and Mydayis

While Methylphenidate, popular extended-release forms Concerta and Ritalin LA Adderal works negatively with MAO inhibitors.

Avoid using MAO inhibitors like isocarboxazid, linezolid, metaxalone, methylene blue, safinamide, selegiline, and tranylcypromine when using Adderall. While with Methylphenidate stop taking MAO like moclobemide, phenelzine, procarbazine, and rasagiline. Dexmethylphenidate and methylphenidate and drugs which have dexmethylphenidate. 

[biomedres]

Ligand-Based Virtual Screening for the Inhibitors of Monoamine Oxidase B

Ligand-Based Virtual Screening for the Inhibitors of Monoamine Oxidase B in Biomedical Journal of Scientific & Technical Research

https://biomedres.us/fulltexts/BJSTR.MS.ID.006029.php

The inhibition of monoamine oxidase enzyme suggests the significant target for the regulation of depression and Parkinson’s disease. The current studies were based on the identification of potent scaffold from several known inhibitors of monoamine oxidase and marketed inhibitors of MAO-B namely selegiline, rasagiline and safinamide were retrieved from Zinc database and database was prepared. Based upon the pharmacophore, screening of potential inhibitors of MAO-B downloaded from databases were done. Different similarity searching on the basis of structures of rasagiline and safinamide assembled a total of 456 compounds from Zinc database. Out of these 456, 37 compounds were chosen, and filter was applied for the generation of pharmacophore method. The resultant binding interactions and binding energies inside the active pocket were monitored and reported. The lowest binding energy and highest binding interactions were established for ZINC ID 89775104 as -12.43. ADME properties of all the 37 compounds were also performed. These findings may help for future studies in order to design the potent and selective inhibitors of MAO-B. Furthermore, the current studies suggested new findings for MAO-B inhibitors, especially for aging based neurodegenerative diseases. The searched and screened compounds emerge to be promising scaffold and may be used for the drug design and development for the targeted neurodegenerative diseases.

For more articles in Journals on Biomedical Sciences click here bjstr

Follow on Twitter : https://twitter.com/Biomedres01 Follow on Blogger :https://biomedres01.blogspot.com/ Like Our Pins On :https://www.pinterest.com/biomedres/

[seagullcharmer]

also since my friend lin has been drawing + talking abt dnd characters i need to sit down and draw ref sheets of my dnd characters so i can commission them

[thahxa]

thankfully at therapeutic doses selegiline and rasagiline don't require any diet modifications! because they only inhibit maob and not maoa they aren't subject to cheese effect

People taking MAOIs generally need to change their diets to limit or avoid foods and beverages containing tyramine.[23] If large amounts of tyramine are consumed, they may develop a hypertensive crisis, which can be fatal.[24] Examples of foods and beverages with potentially high levels of tyramine include cheese, Chianti wine, and pickled fish.[25]

well guess that one's out of the running