Clinical ppt.pptx

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  • Antidotes & their MOAGROUP NO. 06CLINICAL PHARMACY (TOXICOLOGY)

  • FlumazenilASRA HAMEED12859

  • Flumazenil (GABA Modulators)Imidazobenzodiazepine derivativeAntagonizes the actions of benzodiazepines on the CNSCompetitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex

  • BenzodiazepineMechanism Of Action

    Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties.All benzodiazepines act by enhancing the actions of a natural brain chemical, GABA (gamma-aminobutyric acid). GABA is a neurotransmitter, an agent which transmits messages from one brain cell (neuron) to another. The message that GABA transmits is an inhibitory one: it tells the neurons that it contacts to slow down or stop firing. Since about 40% of the millions of neurons all over the brain respond to GABA, this means that GABA has a general quietening influence on the brain: it is in some ways the body's natural hypnotic and tranquilliser. This natural action of GABA is augmented by benzodiazepines which thus exert an extra (often excessive) inhibitory influence on neurons *

  • symptoms of BZD overdoseCentral nervous system depressionAtaxiaSlurred speechDizzinessConfusionDrowsinessBlurred visionUnresponsivenessAnxietyAgitation

    Severe symptoms include coma and respiratory depression

  • Benzodiazepine ToxicityDifferential DiagnosesAcute HypoglycemiaAlcohol ToxicityAntidepressant ToxicityEncephalitisHypernatremia (rise in serum sodium concentration by decrease in total body water)Hyponatremia [abnormally low serum Sodium

    (helps regulate the amount of water in and around cells)]Neuroleptic Agent ToxicitySedative-Hypnotic ToxicityStroke, IschemicToxicity, Antihistamine

    *

  • Tests and procedures depend on the presentation, as follows:Obtain a blood glucose level immediately if the patient has an altered mental statusObtain an arterial blood gas (ABG) if respiratory depression is presentObtain an electrocardiogram (ECG) to evaluate for co-ingestants, particularly cyclic antidepressantsObtain a chest radiograph if respiratory compromise is presentObtain a pregnancy test in women of childbearing age

    Overall, the laboratory detection of benzodiazepines (BZDs) depends upon the screening method used. Immunoassay screening techniques are performed most commonly and typically detect BZDs that are metabolized to desmethyldiazepam or oxazepam; thus, a negative screening result does not rule out the presence of a BZD. Qualitative screening of urine or blood may be performed but rarely influences treatment decisions and has no impact on immediate clinical care.*

  • In patients with an intentional overdose, measure the following:Serum electrolytesGlucoseblood urea nitrogen (BUN)Creatinine clearanceEthanolAcetaminophen level

    *

  • Approach ConsiderationsAs with any overdose, the first step is to assess the patient's airway, breathing, and circulation and to address these rapidly as needed. The cornerstone of treatment in benzodiazepine (BZD) overdoses is good supportive care and monitoring.

  • activated charcoalSingle-dose activated charcoal is not routinely recommended, as the risks far outweigh the benefit. BZD are very rarely fatal in overdoses, and the altered mental status from BZD overdose greatly increases the risk of aspiration following oral charcoal dosing.

  • FlumazenilFlumazenil is a specific antidote for BZDs, but its use in acute BZD overdose is controversial and its risks usually outweigh any possible benefit.It should be considered only in isolated iatrogenic BZD overdose in BZD-naive patients (e.g., during conscious sedation on BZD-naive patient). In long-term BZD users, flumazenil may precipitate withdrawal and seizures; in patients taking BZDs for a medical condition, flumenazil may result in exacerbation of the condition.

  • FlumazenilCommon adverse events with flumazenil include agitation and gastrointestinal symptomsSerious adverse events include supraventricular arrhythmia and convulsions

  • Vitamin C

    MECHANISM OF ACTION Necessary for collagen formation and tissue repair; plays a role in oxidation/reduction reactions as well as other metabolic pathways including synthesis of catecholamines, carnitine, and steroids; also plays a role in conversion of folic acid to folinic acid*

  • MethemoglobinemiaHemoglobin within red blood cells attaches (binds) to oxygen molecules in the lungs, which it carries through the bloodstream, then releases in tissues throughout the body. Instead of normal hemoglobin, people with methemoglobinemia, have an abnormal form called methemoglobin, which is unable to efficiently deliver oxygen to the body's tissues.

    It promote the heme iron to change from ferrous to ferric. The ferric iron cannot bind oxygen and causes cyanosis and the brown appearance of blood.

    *

  • Cyanosis is a bluish discoloration, especially of the skin and mucous membranes, due to excessive concentration of deoxyhemoglobin in the blood caused by deoxygenation.

  • Treatment andPatients with G6PD deficiencyMethylene blue is the primary emergency treatment for methemoglobinemiaMethylene blueshould not be administered to patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency, MB may not only be ineffective but it is also potentially dangerousPretreatment screening of G6PD deficiency is not usually possible in emergency. If methylene blueis contraindicated, only moderate doses of ascorbic acid Dose:300 to 1000 mg/day orally in divided doses

    Methylene blue is the primary emergency treatment for documented symptomatic methemoglobinemiaMethylene blueshould not be administered to patients with known glucose 6-phosphate dehydrogenase (G6PD) deficiency, since the reduction of methemoglobin by MB is dependent upon NADPH generated by G6PD. As a result, MB may not only be ineffective but it is also potentially dangerous, since MB has an oxidant potential that may induce hemolysis in G6PD deficient subjects.Pretreatment screening of G6PD deficiency is not usually possible in emergency. If methylene blueis contraindicated, only moderate doses of ascorbic acid (300 to 1000 mg/day orally in divided doses) should be given, as this drug may also cause oxidant hemolysis in G6PD deficient patients when given in very high doses.*

  • Repair the damaged hemoglobin

    The use of methylene blue to repair the damaged hemoglobin. That is, methylene blue, in its reduced form, is a colorless, water-solulble molecule. When it has been oxidized, it becomes blue. The blue tint that this gives to urine accounts for the last quote in Kathy Trost's article, that "I can see that old blue running out of my skin." The use of vitamin C by Dr. Deeny in Ireland achieves the same result of repairing damaged hemoglobin. However, vitamin C is colorless, so there is no excretion of blue pigment. *

  • GlucagonNEELAM SHARIF12886

    *

  • Beta Blockers and CCBs OverdoseSome beta blockers may antagonize sodium channel blockage QRS widens and some beta blockers cause efflux blockade long QT Beta blockers overdose results in bradycardia and hypotension

    CCBs prevent the opening of these voltage-gated calcium channels (myocardial cells, smooth muscle cells and -islet cells of the pancreas) and reduce calcium entry into cells during phase 2 of an action potential. In an overdose situation, receptor selectivity is lost, and effects not normally seen at therapeutic doses can occur.

    *

  • Mechanism of Action of ToxicityCalcium enters open voltage-sensitive calcium channels to promote the release of calcium from the sarcoplasmic reticulum. The released calcium combines with troponin to cause muscle contraction via actin and myosin fibers. AC catalyzes the conversion of ATP to cAMP, which activates protein kinase A (PKA), which promotes the opening of dormant calcium channels, enhances release of calcium from the sarcoplasmic reticulum, and facilitates release of calcium by troponin during diastole. Glucagon bypasses -receptors and acts directly on Gs to stimulate conversion of ATP to cAMP. Amrinone inhibits PDE(Phosphodiestrase) to prevent the degradation of cAMP. Insulin promotes the uptake and use of carbohydrates as an energy source.

  • Mechanism of action of toxicity

  • Specific features and Symptomsof Beta Blockers Overdose

  • Specific Features and Symptoms Of CCBs Overdose

  • Antidote GlucagonGlucagon is generally recognized as first-line therapy. Glucagon is a hormone secreted by the 2 cells of the pancreatic islets of Langerhans..High-dose glucagon is recommended for cardiotoxicity produced by -blocker poisoning.

  • Mechanism of antidote glucagon

  • Glucose (Dextrose 50%)AMMARAH UROOJ12852

  • MECHANISM OF INSULIN:

  • SYMPTOMS OF INSULIN TOXICITY:High doses of insulin can lead to: dyselectrolytemia.Salt and water retention hyponatremiahypoglycemia hypokalemiadizziness and mild confusionanxiety or nervousnessshakinessrapid heartbeatHungerIrritability

  • EMERGENCY TREATMENT : provide immediate attention to patient before they lead to dangerously low blood sugar. People who have low blood sugar levels are advised to consume 15 grams of a fast digesting carbohydrate, such as glucose tablets or a high-sugar food immediately. High-glucose foods include:raisins soda fruit juice honey candy

  • symptoms should improve within 15 minutes. If they dont, or if a test shows your levels are still low, repeat the above steps until your