Anti-Parkinsonian Drugs | MAO-B and COMT Inhibitors скачать в хорошем качестве

Anti-Parkinsonian Drugs | MAO-B and COMT Inhibitors

Welcome to sqadia.com where we are covering subject-specific topics. We have landed on pharmacology, and you will be seeing more subjects on sqadia.com so stick around. Today we will be talking about Antiparkinsonian Drugs and their actions in the body. ▬ 📌 Parkinson’s Disease Parkinson’s disease is a disease of the basal ganglia and is characterized by a poverty of movement, rigidity, and tremor. It is progressive and leads to increasing disability unless effective treatment is given. In the early 1960s, analysis of the brains of patients dying with Parkinson’s disease revealed greatly decreased levels of dopamine in the basal ganglia that include: 🔹Caudate Nucleus 🔹Putamen 🔹Globus Pallidus Parkinson’s disease thus became the first disease to be associated with a specific transmitter abnormality in the brain. 👉 Etiology The cause of Parkinson’s disease is unknown, and no endogenous or environmental neurotoxin has been discovered. However, the possibility that such a chemical exists has been suggested dramatically by the discovery in Californian drug addicts (who were trying to make pethidine) that 1‐methyl‐4‐phenyl‐1,2,3,6‐ tetrahydropyridine (MPTP) causes degeneration of the nigrostriatal tract and Parkinson’s disease. MPTP acts indirectly via a metabolite, 1‐methyl‐4‐phenylpyridine (or MPP positive), which is formed by the action of MAO-B. It is not certain how MPP positive kills dopaminergic nerve cells, but free radicals generated during its formation by Monoamine oxidase-B may poison mitochondria and damage the cell membrane by peroxidation. 👉 Secondary Parkinsonism Drugs such as phenothiazines and haloperidol, whose major pharmacologic action is the blockade of dopamine receptors in the brain, may produce Parkinsonian symptoms (also called pseudoparkinsonism). These drugs should be used with caution in patients with Parkinson’s disease. ▬ 📌 Anti-Parkinsonian Drugs Anti-Parkinson’s drugs classification is as follows: 🔹Levodopa in combination with Carbidopa 🔹Dopamine Agonists 🔹Monoamine Oxidase B Inhibitors 🔹COMT Inhibitors 🔹Antimuscarinics Watch the video for details on the classification os anti Parkinson's drugs 👉 Levodopa in combination with Carbidopa Levodopa is the immediate precursor of dopamine and can penetrate the brain, where it is converted to dopamine. The site of this de-carboxylation in the Parkinsonian brain is uncertain, but as dopa decarboxylase is not rate limiting, there may be sufficient enzymes in the remaining dopaminergic nerve terminals. Another possibility is that the conversion occurs in neither adrenergic nor serotonergic terminals because the de-carboxylase activity in these neurons is not specific. In any event, the release of dopamine replaced in the brain by levodopa therapy must be very abnormal, and it is remarkable that most patients with Parkinson’s disease benefit, often dramatically, from its administration. Watch this video for the antiparkinson drugs mechanism of action. 👉 Dopamine Agonists Dopamine agonists include ergot derivatives, for example, bromocriptine, and newer non‐ergot drugs, for example, ropinirole. The ergot derivatives may cause fibrotic changes leading to restrictive valvular heart disease. This was thought to be rare, but in one study, pergolide was associated with valvular effects in 30 percent of patients. Dopamine agonists have no advantage over levodopa and the adverse effects are similar commonly: 🔹Nausea 🔹Psychiatric Symptoms 🔹Postural Hypotension 🔹Daytime Somnolence 🔹Impulse Control Disorders, Like Gambling and Hyper-Sexuality 👉 Monoamine oxidase B inhibitors Selegiline and Rasagiline selectively inhibit MAO-B present in the brain, for which dopamine, but neither norepinephrine nor serotonin, is a substrate. They reduce the metabolism of dopamine in the brain and potentiate the actions of levodopa, the dose of which can be reduced by up to one‐third. 👉 COMT Inhibitors Entacapone inhibits COMT or Catechol-o-Methyl Transferase. It slows the elimination of levodopa and prolongs the duration of a single dose. It has no antiparkinsonian action alone, but it augments the action of levodopa and reduces the ‘off’ time in late disease. 👉 Antimuscarinics Blockage of cholinergic transmission produces effects like augmentation of dopaminergic transmission since it helps to correct the imbalance in the dopamine-acetyl-choline ratio. These agents can induce mood changes and produce xerostomia (dryness of the mouth), constipation, and visual problems typical of muscarinic blockers. They interfere with gastrointestinal peristalsis and are contraindicated in patients with: 🔹Glaucoma 🔹Prostatic Hyperplasia 🔹Pyloric Stenosis So that was all! ▬ 🎬 5500+ sqadia.com Medical Videos ▬▬▬▬▬▬▬▬▬▬ 👩🏻‍⚕️ Accessible Medical Student Education 24/7/365 💡 Simplifying Medical Learning 💪 Study Hard, Dream Big, Achieve More