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Farmakologi Racun & Antidot

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Farmakologi Racun & Antidot Departemen Farmakologi Fakultas Kedokteran UNISSULA POISONS, VENOMS & TOXINS Every natural or synthetic chemical can cause injury if the dose is high enough. Poisons are chemicals that can injure or impair body functions. Toxins are mostly described as substances produced by microorganisms. Venoms are substances injected by one species into another. Venoms and toxins are mostly proteins or polypeptides. Many of toxins and poisons are alkaloids (drugs of plant origin). KLASIFIKASI KERACUNAN MENURUT CARA TERJADINYA 1. Self poisoning • Minum obat dengan dosis >> tapi dengan pengetahuan dosis ini tidak berbahaya • Hanya untuk menarik perhatian, tidak untuk bunuh diri, sering insektisida 2. Attempted suicide Ada maksud untuk bunuh diri, sering barbiturat & hipnotik-sedatif 3. Accidental poisoning Jelas kecelakaan, tanpa faktor kesengajaan, sering terjadi pada anak usia <5 tahun 4. Homicidal poisoning Tindakan kriminal KLASIFIKASI KERACUNAN MENURUT MULA WAKTU TERJADINYA 1. Keracunan akut Terjadi mendadak diagnosa lebih mudah ditegakkan Sering mengenai banyak orang Gejala sering menyerupai sindrom penyakit (toxidrom) 2. Keracunan kronik Gejala timbul perlahan & lama sesudah pajanan diagnosis sulit ditegakkan Ciri khas : zat penyebab diekskresi >24 jam, t1/2 panjang akumulasi Manifestasi kronik pada organ tertentu oleh zat kimia dg t1/2 pendek akibat akumulasi (ex : nekrosis papila ginjal akibat analgesik) Route of exposure : Direct contact Ingestion Inhalation Toxicokinetics Toxicodynamics Toksikokinetik & Toksikodinamik Toksikokinetik: ADME suatu toxin (racun) Volume of distribution Volume semu suatu senyawa didistribusi ke seluruh tubuh Large Vd (>5 L/kg), co., antidepresan, opioid, verapamil, propranolol, antipsikotik, antimalaria Small Vd (<1 L/kg), co., salisilat, etanol, litium, fenitoin Klirens Volume plasma yang dibersihkan dari obat per satuan waktu Klirens total = klirens ginjal + klirens hepar + klirens organ lain Pasien keracunan Obat melukai epitel barier saluran cerna ↑ absorpsi obat Kapasitas hepar untuk memetabolisme obat terbatas ↑ obat di sirkulasi Kapasitas ikatan protein plasma terbatas ↑ obat bebas dalam sirkulasi TOXICOKINETICS & TOXICODYNAMICS Toxicokinetics, which is analogous to pharmacokinetics, is the study of the absorption, distribution, metabolism, and excretion of a xenobiotic under circumstances that produce toxicity or excessive exposure. Toxicodynamics,which is analogous to pharmacodynamics, is the study of the relationship of toxic concentrations of xenobiotics to clinical effect. Xenobiotics are all substances that are foreign to the body. ABSORPTION Absorption is the process by which a xenobiotic enters the body. Both the rate (ka) and extent of absorption (F) are measurable and important determinants of toxicity. The rate of absorption often predicts the onset of action, whereas the extent of absorption (bioavailability) often predicts the intensity of the effect and depends, in part, on first-pass effects. A xenobiotic must diffuse through a number of membranes before it can reach its site of action. Absorpsi adalah proses di mana xenobiotik memasuki tubuh. Baik laju (ka) dan tingkat penyerapan (F) merupakan penentu toksisitas yang terukur dan penting. Tingkat penyerapan sering memprediksi onset aksi, sedangkan tingkat penyerapan (bioavailabilitas) sering memprediksi intensitas efek dan tergantung, sebagian, pada efek first-pass. Xenobiotik harus berdifusi melalui sejumlah membran sebelum dapat mencapai tempat kerjanya. DISTRIBUTION Volume of distribution (Vd) is the proportionality term used to relate the dose of the xenobiotic the individual receives to the resultant plasma concentration. Measure of how much drug is located inside & outside of the plasma compartment. Once bound to plasma protein, a xenobiotic with high binding affinity will remain largely confined to the plasma until elimination occurs. Most plasma measurements of xenobiotic concentration reflect total drug (bound plus unbound). Only the unbound drug is free to diffuse through membranes for distribution or for elimination. Volume distribusi (Vd) adalah istilah proporsionalitas yang digunakan untuk menghubungkan dosis xenobiotik yang diterima individu dengan konsentrasi plasma yang dihasilkan. Ukur berapa banyak obat yang terletak di dalam & di luar kompartemen plasma. Setelah terikat dengan protein plasma, xenobiotik dengan afinitas pengikatan yang tinggi akan tetap terbatas pada plasma sampai eliminasi terjadi. Sebagian besar pengukuran plasma konsentrasi xenobiotik mencerminkan total obat (terikat plus tidak terikat). Hanya obat tanpa batas yang bebas difusi melalui membran untuk distribusi atau untuk eliminasi. DISTRIBUTION Large Vd (>5 L/kg) : antidepressant, opioid, verapamil, propranolol, antipsychotic, antimalaria. Small Vd (<1 L/kg), co., salicylate, ethanol, litium, phenytoin. If the Vd is large (>1 L/kg), it is unlikely that hemodialysis, hemoperfusion, or exchange transfusion would be effective because most of the xenobiotic is outside of the plasma compartment. Specific therapeutic maneuvers in the overdose : alter xenobiotic distribution by inactivating and/or enhancing elimination to limit toxicity (a) manipulation of serum or urine pH (salicylates); (b) use of chelators (lead); and (c) the use of antibodies or antibody fragments (digoxin). Vd besar (> 5 L / kg): antidepresan, opioid, verapamil, propranolol, antipsikotik, antimalaria. Vd kecil (<1 L / kg), co., Salisilat, etanol, litium, fenitoin. Jika Vd besar (> 1 L / kg), tidak mungkin hemodialisis, hemoperfusi, atau transfusi tukar akan efektif karena sebagian besar xenobiotik berada di luar kompartemen plasma. Manuver terapeutik spesifik dalam overdosis: mengubah distribusi xenobiotik dengan menonaktifkan dan / atau meningkatkan eliminasi untuk membatasi toksisitas (a) manipulasi pH serum atau urin (salisilat); (b) penggunaan chelators (timbal); dan (c) penggunaan antibodi atau fragmen antibodi (digoxin). ELIMINATION Removal of a parent compound from the body (elimination) begins as soon as the xenobiotic is delivered to clearance organs such as the liver, kidneys, and lungs. As expected, the functional integrity of the major organ systems (cardiovascular, lungs, renal, hepatic) are major determinants of the efficiency of xenobiotic removal and of therapeutically administered antidotes. Penghapusan senyawa induk dari tubuh (eliminasi) dimulai segera setelah xenobiotik dikirimkan ke organ pembersihan seperti hati, ginjal, dan paru-paru. Seperti yang diharapkan, integritas fungsional sistem organ utama (kardiovaskular, paru-paru, ginjal, hati) adalah penentu utama dari efisiensi penghapusan xenobiotik dan penangkal terapeutik yang diberikan secara terapeutik. ELIMINATION Elimination can be accomplished by biotransformation to one or more metabolites, or by excretion from the body of unchanged xenobiotic. Lipophilic (nonpolar) xenobiotics are usually metabolized in the liver to hydrophilic metabolites, which are then excreted by the kidneys. Metabolic reactions, catalyzed by enzymes, categorized as either phase I or phase II, generally result in pharmacologically inactive metabolites; active metabolites may have different toxicities than the parent compounds. Eliminasi dapat dicapai dengan biotransformasi menjadi satu atau lebih metabolit, atau dengan ekskresi dari tubuh xenobiotik yang tidak berubah. Lipofilik (nonpolar) xenobiotik biasanya dimetabolisme di hati menjadi metabolit hidrofilik, yang kemudian diekskresikan oleh ginjal. Reaksi metabolik, dikatalisasi oleh enzim, dikategorikan sebagai fase I atau fase II, umumnya menghasilkan metabolit yang tidak aktif secara farmakologi; metabolit aktif mungkin memiliki toksisitas yang berbeda dari senyawa induknya. DRUG METABOLISM Active Drug to Inactive Metabolite hydroxylation Phenobarbital Hydroxyphenobarbital Active Drug to Active Metabolite acetylation Procainamide N-acetylprocainamide Inactive Drug (prodrug) to Active Metabolite converted hydrolisis Clopidogrel 2-oxo-clopidogrel Active metabolite Active Drug to Reactive Metabolite Acetaminophen Reactive metabolite Toksidrom Racun Suhu HR RR TD Status mental Pupil Kulit Contoh Opioids Euforia, Morfin, somnolens, heroin, koma oksikodon Simpato Agitasi, delirium, diafore Kokain, mimetik psikosis, kejang, sis amfetamin, halusinasi teofilin, kafein, efedrin Antikoli Delirium, Flushin Ipratropium, nergik psikosis, kejang, g, antihistamin halusinasi, koma, kering , TCA, atropin Organof Confusion, Diafore Malation, osfat fasikulasi, koma sis paration, ekotiofat, soman Barbitur Somnolens, Benzodiazep at, ataksia, koma in, alkohol, hipnotik barbiturat -sedatif TOXICANTS THAT AFFECT TEMPERATURE Hyperthermia & Hypothermia TOXICANTS THAT AFFECT RESPIRATION Bradypnea & Tachypnea TOXICANTS THAT CAUSE HEMOLYSIS Immune & Nonimmune Mediated TOXICANTS THAT AFFECT THE CARDIOVASCULAR SYSTEM Vascular tone, heart conduction, pulse Hypertension Hypotension Conduction abnormalities & heart block Bradycardia Tachydysrhythmia Pulse TOXICANTS THAT AFFECT THE AUTONOMIC NERVOUS SYSTEM Toxicants that Act as Cholinergic Blockers Anticholinergic-Synonyms Cholinergic blockers / Antimuscarinic / Antiparasympathetic / Cholinolytic / Parasympatholytic / Antispasmodic / Spasmolytic / Cholinergic neurons : Include all sympathetic and parasympathetic preganglionic neurons and nerve supply to the adrenal medulla. Parasympathetic postganglionic neurons (autonomic effector sites). Sympathetic postganglionic neurons which innervate
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