This document discusses hair dye poisoning from paraphenyl diamine (PPD). Key points include:
- PPD poisoning commonly causes suicide attempts and presents with cervicofacial edema, dysphagia, rhabdomyolysis and acute renal failure.
- PPD can cause cardiac complications like myocarditis and ventricular arrhythmias.
- Treatment involves gastric lavage, steroids, diuretics, bicarbonate and dialysis. Preventing renal failure and managing hemodynamic disturbances are important goals.
- Intravenous methylprednisolone showed rapid reduction in edema and clinical improvement.
This document summarizes information about hair dye poisoning. It discusses how hair dye, particularly cheap stone hair dye containing high concentrations of paraphenylenediamine (PPD), has become a common means of suicide. The key symptoms of hair dye poisoning are stridor and upper airway edema, rhabdomyolysis evidenced by brown urine, and acute renal failure. Treatment involves securing the airway through intubation or tracheostomy, managing cardiac arrhythmias, using alkaline diuresis and dialysis to prevent renal failure, and supportive care. The mortality rate remains high, around 12-24%, primarily due to airway edema and renal failure, but early intervention can help reduce deaths.
The document discusses hair dye poisoning, which is emerging as a common means of suicide, especially among females in India. Hair dyes contain toxic ingredients like paraphenylenediamine (PPD) and resorcinol. Poisoning symptoms include angioedema, rhabdomyolysis, myocarditis, and renal failure. Treatment focuses on airway protection, fluid resuscitation, dialysis, and managing complications to prevent death. Raising awareness about hair dye poisoning can help reduce mortality through early intervention.
Paraphenylenediamine (PPD) is a hair dye ingredient that can cause toxicity when ingested. PPD poisoning leads to angioedema, rhabdomyolysis, myoglobinuria, hepatic necrosis, and hypotension. Patients may require tracheostomy, ventilation, ICU care, and have high mortality. Labs will show elevated white blood cell count, CPK, liver enzymes, and creatinine. Management involves airway support, ventilation if needed, IV fluids, gastric lavage, diuresis, treating complications like hyperkalemia, and monitoring for acute renal failure.
Hair dye (super vasmol-33) poisoning – A case reportHair dye (super vasmol 33...pharmaindexing
- The author reports a case of a 28-year-old woman who intentionally consumed 150 mL of the hair dye Super Vasmol-33, which contains the toxic chemical paraphenylenediamine (PPD).
- She was brought to the emergency room and found to have severe cervicofacial edema requiring an emergency tracheostomy. Laboratory findings showed rhabdomyolysis and elevated creatine kinase levels.
- She was treated supportively and recovered fully without requiring dialysis. Intentional ingestion of hair dyes containing PPD is an increasing means of suicide in rural India due to easy availability, and requires prompt supportive care.
Super-vasmol hair dye poisoning is a major cause of suicidal poisoning in India, as its main toxic ingredient, paraphenylene diamine (PPD), is cheap and readily available. PPD poisoning can cause multi-organ dysfunction and failure through two phases - an initial acute presentation with angioedema and airway obstruction within 4-6 hours, followed by a subacute phase involving rhabdomyolysis, acute renal failure, hepatitis, and metabolic acidosis. Aggressive management is focused on airway protection, steroids to reduce angioedema, fluid resuscitation to prevent renal failure, and dialysis as needed.
The document discusses various types of arrhythmias including bradycardia, tachycardia, ventricular tachycardia, atrial flutter and atrial fibrillation. It then describes the causes and mechanisms of arrhythmias. It discusses several classes of antiarrhythmic drugs like membrane stabilizing agents, beta blockers, drugs causing repolarization and calcium channel blockers. It provides details about specific drugs like lidocaine, phenytoin, mexilitine, procainamide and quinidine including their mechanisms of action, indications, contraindications, side effects and dosages.
Methanol is a colorless, volatile, flammable liquid that is rapidly absorbed through the gastrointestinal tract and distributed throughout the body. It is metabolized into formaldehyde by alcohol dehydrogenase and further into toxic formic acid. Formic acid inhibits cytochrome c oxidase in mitochondria, preventing ATP production and ultimately causing cell death if enough accumulates. Symptoms of methanol poisoning include nausea, blindness, respiratory failure, and death. Treatment involves inhibiting methanol metabolism with ethanol or fomepizole, removing formic acid through hemodialysis, correcting acidosis, and administering folinic acid and sodium bicarbonate.
This document provides an overview of haemostatic agents for medical students. It defines key terms related to haemostasis and classifies haemostatic agents into categories including coagulants, local haemostatics, and antifibrinolytics. Vitamin K and its role in coagulation factor synthesis is described in detail. Specific agents are explained within each category, along with their mechanisms of action, indications for use, and important adverse effects.
This document summarizes information about hair dye poisoning. It discusses how hair dye, particularly cheap stone hair dye containing high concentrations of paraphenylenediamine (PPD), has become a common means of suicide. The key symptoms of hair dye poisoning are stridor and upper airway edema, rhabdomyolysis evidenced by brown urine, and acute renal failure. Treatment involves securing the airway through intubation or tracheostomy, managing cardiac arrhythmias, using alkaline diuresis and dialysis to prevent renal failure, and supportive care. The mortality rate remains high, around 12-24%, primarily due to airway edema and renal failure, but early intervention can help reduce deaths.
The document discusses hair dye poisoning, which is emerging as a common means of suicide, especially among females in India. Hair dyes contain toxic ingredients like paraphenylenediamine (PPD) and resorcinol. Poisoning symptoms include angioedema, rhabdomyolysis, myocarditis, and renal failure. Treatment focuses on airway protection, fluid resuscitation, dialysis, and managing complications to prevent death. Raising awareness about hair dye poisoning can help reduce mortality through early intervention.
Paraphenylenediamine (PPD) is a hair dye ingredient that can cause toxicity when ingested. PPD poisoning leads to angioedema, rhabdomyolysis, myoglobinuria, hepatic necrosis, and hypotension. Patients may require tracheostomy, ventilation, ICU care, and have high mortality. Labs will show elevated white blood cell count, CPK, liver enzymes, and creatinine. Management involves airway support, ventilation if needed, IV fluids, gastric lavage, diuresis, treating complications like hyperkalemia, and monitoring for acute renal failure.
Hair dye (super vasmol-33) poisoning – A case reportHair dye (super vasmol 33...pharmaindexing
- The author reports a case of a 28-year-old woman who intentionally consumed 150 mL of the hair dye Super Vasmol-33, which contains the toxic chemical paraphenylenediamine (PPD).
- She was brought to the emergency room and found to have severe cervicofacial edema requiring an emergency tracheostomy. Laboratory findings showed rhabdomyolysis and elevated creatine kinase levels.
- She was treated supportively and recovered fully without requiring dialysis. Intentional ingestion of hair dyes containing PPD is an increasing means of suicide in rural India due to easy availability, and requires prompt supportive care.
Super-vasmol hair dye poisoning is a major cause of suicidal poisoning in India, as its main toxic ingredient, paraphenylene diamine (PPD), is cheap and readily available. PPD poisoning can cause multi-organ dysfunction and failure through two phases - an initial acute presentation with angioedema and airway obstruction within 4-6 hours, followed by a subacute phase involving rhabdomyolysis, acute renal failure, hepatitis, and metabolic acidosis. Aggressive management is focused on airway protection, steroids to reduce angioedema, fluid resuscitation to prevent renal failure, and dialysis as needed.
The document discusses various types of arrhythmias including bradycardia, tachycardia, ventricular tachycardia, atrial flutter and atrial fibrillation. It then describes the causes and mechanisms of arrhythmias. It discusses several classes of antiarrhythmic drugs like membrane stabilizing agents, beta blockers, drugs causing repolarization and calcium channel blockers. It provides details about specific drugs like lidocaine, phenytoin, mexilitine, procainamide and quinidine including their mechanisms of action, indications, contraindications, side effects and dosages.
Methanol is a colorless, volatile, flammable liquid that is rapidly absorbed through the gastrointestinal tract and distributed throughout the body. It is metabolized into formaldehyde by alcohol dehydrogenase and further into toxic formic acid. Formic acid inhibits cytochrome c oxidase in mitochondria, preventing ATP production and ultimately causing cell death if enough accumulates. Symptoms of methanol poisoning include nausea, blindness, respiratory failure, and death. Treatment involves inhibiting methanol metabolism with ethanol or fomepizole, removing formic acid through hemodialysis, correcting acidosis, and administering folinic acid and sodium bicarbonate.
This document provides an overview of haemostatic agents for medical students. It defines key terms related to haemostasis and classifies haemostatic agents into categories including coagulants, local haemostatics, and antifibrinolytics. Vitamin K and its role in coagulation factor synthesis is described in detail. Specific agents are explained within each category, along with their mechanisms of action, indications for use, and important adverse effects.
Amiodarone is a class III antiarrhythmic drug that is effective for treating atrial fibrillation and flutter as well as ventricular arrhythmias. It works by blocking potassium channels, sodium channels, and adrenergic receptors. Amiodarone has a large volume of distribution, long half-life, and is associated with various adverse effects involving the heart, thyroid, lungs, skin and other organs. It can cause interactions with many other drugs due to its effects on hepatic enzymes and drug transporters.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
I. Drugs that improve capillary function, called capillarotonics, reduce capillary fragility and permeability. They act as antioxidants and prevent damage to blood vessel walls. Some examples are bioflavonoids like diosmin and rutin, semisynthetic flavonoids like troxerutin, and saponins from horse chestnut. They are used for various hemorrhagic, skin, and retinal conditions.
II. Venotonic drugs improve blood flow in veins and reduce swelling. Examples are Detralex (diosmin/hesperidine), Endotelon from grape seeds, and troxerutin which is also used locally for wounds. They are used for chronic venous
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, and side effects. The main classes covered are:
1. Salidiuretics (thiazides) such as hydrochlorothiazide which increase sodium and chloride excretion in the distal renal tubules.
2. Loop diuretics such as furosemide which act on the ascending limb of Henle's loop to increase excretion of sodium, chloride, magnesium and calcium.
3. Carbonic anhydrase inhibitors like acetazolamide which inhibit the enzyme carbonic anhydrase in the kidneys and other tissues.
4. Potassium-sparing diuretics including sp
The document discusses drugs that affect blood and their mechanisms of action. It describes how drugs like heparin and warfarin are used as anticoagulants to prevent thrombosis by inhibiting platelet activation and coagulation factors. It also discusses how thrombolytic drugs like streptokinase work by converting plasminogen to plasmin to lyse thrombi. The document outlines how other drugs like aspirin inhibit platelet aggregation for conditions like heart attacks.
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
Methanol toxicity is summarized in 3 sentences:
Methanol is a toxic alcohol that is metabolized in the body to formaldehyde and formic acid, causing metabolic acidosis, vision loss and neurological effects. Common sources of methanol exposure include fuels, solvents, antifreeze and windshield washer fluid. The antidotes ethanol and fomepizole work by competitively inhibiting the enzyme alcohol dehydrogenase and preventing methanol from being metabolized.
The document discusses various hematologic drugs used to treat conditions related to blood circulation. It covers the mechanisms, indications, contraindications, side effects and nursing considerations for different classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics.
This document discusses drugs used to treat deep vein thrombosis (DVT). It outlines platelet aggregation inhibitors, anticoagulants, and thrombolytic drugs - their mechanisms of action, uses, and adverse effects. Platelet aggregation inhibitors work by inhibiting cyclooxygenase-1 or blocking platelet receptors. Anticoagulants like heparin and warfarin prevent clotting by suppressing clotting factors. Thrombolytic drugs dissolve blood clots by activating plasminogen to form plasmin, which breaks down fibrin in clots. While these drugs can effectively treat DVT, they may increase bleeding risk as a side effect.
Hydrazide (Hydrochlorothiazide Tablets) is used in the management of hypertension (high blood pressure) either as the sole therapeutic agent, or in combination with other antihypertensives. It is also used to treat swelling due to fluid build up.
This document discusses anticoagulants, including heparin. It defines anticoagulants as drugs used to reduce blood coagulability and classifies them into those used in vivo and in vitro. It provides details on heparin, including its discovery, chemistry, mechanisms of action, pharmacokinetics, dosage, adverse effects, contraindications, and uses.
1) Methanol is toxic to humans when ingested and is sometimes used as an ethanol substitute by alcoholics. It is metabolized to formaldehyde and formic acid which cause metabolic acidosis, blindness, and can be fatal.
2) The toxic effects of methanol occur after a latent period of 30 hours as it is slowly metabolized. Symptoms include vision loss, seizures, coma and death. Treatment focuses on preventing further metabolism using fomepizole or ethanol and enhancing excretion through hemodialysis.
3) Diagnosis is based on history of ingestion and laboratory findings showing a large osmolar or anion gap metabolic acidosis. Levels of methanol, formate or a
This document discusses coagulants and anticoagulants. It describes the four factors involved in blood clotting and the coagulation process. Anticoagulants prevent blood clotting in blood vessels and are classified as in vitro or in vivo. Common anticoagulants include heparin, warfarin, anisindione, and clopidogrel. Anticoagulants interfere with vitamin K dependent clotting factor synthesis in the liver by inhibiting the gamma-carboxylation of certain clotting factors, which is essential for their coagulation function.
Heparin is an anticoagulant used to prevent and treat blood clots. It works by interacting with antithrombin to accelerate the inhibition of enzymes involved in clot formation. Heparin can be unfractionated or low molecular weight and is derived from animal tissues, administered intravenously or subcutaneously, and has a short half-life of 1.5 hours. Its indications include treating and preventing deep vein thrombosis, pulmonary embolism, and arterial clots. Common adverse effects include bleeding risks and hematologic issues.
Drugs acting on blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document discusses various anti-hemorrhagic drugs including anti-thrombotics, thrombolytic drugs, and anticoagulants. Anti-thrombotics include anti-platelet drugs like aspirin and clopidogrel. Thrombolytics break up blood clots and include drugs like streptokinase. Anticoagulants prevent clotting and include heparin, vitamin K antagonists, and calcium sequesters like citrate and EDTA used for blood collection and testing.
The document discusses drugs affecting blood and their mechanisms of action. It describes agents that stimulate or inhibit erythropoiesis, such as iron supplements or vitamin B12/folic acid deficiencies respectively. It also covers platelet aggregation inhibitors like aspirin, anticoagulants like heparin, and thrombolytic drugs like streptokinase used to treat thrombosis. Growth factors that stimulate leukopoiesis and chemotherapy drugs that inhibit it are also mentioned.
This document discusses various treatments and medications for bleeding and anticoagulation. It describes different classes of anticoagulant drugs that prevent blood clotting, including coumarins (vitamin K antagonists) like warfarin, heparin, and newer direct factor Xa and thrombin inhibitors. It provides details on specific medications within each class, their mechanisms of action, uses, advantages, disadvantages, and adverse effects. Alternative anticoagulants explored include antithrombin protein therapeutics and substances from snake venoms or leeches.
Diabetes insipidus is caused by a lack of antidiuretic hormone (ADH), also known as vasopressin, which is normally released by the pituitary gland. ADH helps regulate water balance in the body by increasing water reabsorption in the kidneys. Two case studies are presented: a young male diagnosed with a brain tumor after initially being treated for psychogenic polydipsia, and an older female found to have a craniopharyngioma after presenting with severe polydipsia and polyuria. Investigations including blood tests, imaging, and water deprivation tests can help diagnose the underlying cause, and treatment involves replacing ADH with desmopressin.
The document discusses hair dye poisoning, which is emerging as a common means of suicide, especially among females in India. Hair dyes contain toxic ingredients like paraphenylenediamine (PPD) and resorcinol. Poisoning symptoms include angioedema, rhabdomyolysis, myocarditis, and renal failure. Treatment focuses on airway protection, fluid resuscitation, dialysis, and managing complications to prevent death. Raising awareness about hair dye poisoning can help reduce mortality through early intervention.
Amiodarone is a class III antiarrhythmic drug that is effective for treating atrial fibrillation and flutter as well as ventricular arrhythmias. It works by blocking potassium channels, sodium channels, and adrenergic receptors. Amiodarone has a large volume of distribution, long half-life, and is associated with various adverse effects involving the heart, thyroid, lungs, skin and other organs. It can cause interactions with many other drugs due to its effects on hepatic enzymes and drug transporters.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
I. Drugs that improve capillary function, called capillarotonics, reduce capillary fragility and permeability. They act as antioxidants and prevent damage to blood vessel walls. Some examples are bioflavonoids like diosmin and rutin, semisynthetic flavonoids like troxerutin, and saponins from horse chestnut. They are used for various hemorrhagic, skin, and retinal conditions.
II. Venotonic drugs improve blood flow in veins and reduce swelling. Examples are Detralex (diosmin/hesperidine), Endotelon from grape seeds, and troxerutin which is also used locally for wounds. They are used for chronic venous
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, and side effects. The main classes covered are:
1. Salidiuretics (thiazides) such as hydrochlorothiazide which increase sodium and chloride excretion in the distal renal tubules.
2. Loop diuretics such as furosemide which act on the ascending limb of Henle's loop to increase excretion of sodium, chloride, magnesium and calcium.
3. Carbonic anhydrase inhibitors like acetazolamide which inhibit the enzyme carbonic anhydrase in the kidneys and other tissues.
4. Potassium-sparing diuretics including sp
The document discusses drugs that affect blood and their mechanisms of action. It describes how drugs like heparin and warfarin are used as anticoagulants to prevent thrombosis by inhibiting platelet activation and coagulation factors. It also discusses how thrombolytic drugs like streptokinase work by converting plasminogen to plasmin to lyse thrombi. The document outlines how other drugs like aspirin inhibit platelet aggregation for conditions like heart attacks.
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
Methanol toxicity is summarized in 3 sentences:
Methanol is a toxic alcohol that is metabolized in the body to formaldehyde and formic acid, causing metabolic acidosis, vision loss and neurological effects. Common sources of methanol exposure include fuels, solvents, antifreeze and windshield washer fluid. The antidotes ethanol and fomepizole work by competitively inhibiting the enzyme alcohol dehydrogenase and preventing methanol from being metabolized.
The document discusses various hematologic drugs used to treat conditions related to blood circulation. It covers the mechanisms, indications, contraindications, side effects and nursing considerations for different classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics.
This document discusses drugs used to treat deep vein thrombosis (DVT). It outlines platelet aggregation inhibitors, anticoagulants, and thrombolytic drugs - their mechanisms of action, uses, and adverse effects. Platelet aggregation inhibitors work by inhibiting cyclooxygenase-1 or blocking platelet receptors. Anticoagulants like heparin and warfarin prevent clotting by suppressing clotting factors. Thrombolytic drugs dissolve blood clots by activating plasminogen to form plasmin, which breaks down fibrin in clots. While these drugs can effectively treat DVT, they may increase bleeding risk as a side effect.
Hydrazide (Hydrochlorothiazide Tablets) is used in the management of hypertension (high blood pressure) either as the sole therapeutic agent, or in combination with other antihypertensives. It is also used to treat swelling due to fluid build up.
This document discusses anticoagulants, including heparin. It defines anticoagulants as drugs used to reduce blood coagulability and classifies them into those used in vivo and in vitro. It provides details on heparin, including its discovery, chemistry, mechanisms of action, pharmacokinetics, dosage, adverse effects, contraindications, and uses.
1) Methanol is toxic to humans when ingested and is sometimes used as an ethanol substitute by alcoholics. It is metabolized to formaldehyde and formic acid which cause metabolic acidosis, blindness, and can be fatal.
2) The toxic effects of methanol occur after a latent period of 30 hours as it is slowly metabolized. Symptoms include vision loss, seizures, coma and death. Treatment focuses on preventing further metabolism using fomepizole or ethanol and enhancing excretion through hemodialysis.
3) Diagnosis is based on history of ingestion and laboratory findings showing a large osmolar or anion gap metabolic acidosis. Levels of methanol, formate or a
This document discusses coagulants and anticoagulants. It describes the four factors involved in blood clotting and the coagulation process. Anticoagulants prevent blood clotting in blood vessels and are classified as in vitro or in vivo. Common anticoagulants include heparin, warfarin, anisindione, and clopidogrel. Anticoagulants interfere with vitamin K dependent clotting factor synthesis in the liver by inhibiting the gamma-carboxylation of certain clotting factors, which is essential for their coagulation function.
Heparin is an anticoagulant used to prevent and treat blood clots. It works by interacting with antithrombin to accelerate the inhibition of enzymes involved in clot formation. Heparin can be unfractionated or low molecular weight and is derived from animal tissues, administered intravenously or subcutaneously, and has a short half-life of 1.5 hours. Its indications include treating and preventing deep vein thrombosis, pulmonary embolism, and arterial clots. Common adverse effects include bleeding risks and hematologic issues.
Drugs acting on blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document discusses various anti-hemorrhagic drugs including anti-thrombotics, thrombolytic drugs, and anticoagulants. Anti-thrombotics include anti-platelet drugs like aspirin and clopidogrel. Thrombolytics break up blood clots and include drugs like streptokinase. Anticoagulants prevent clotting and include heparin, vitamin K antagonists, and calcium sequesters like citrate and EDTA used for blood collection and testing.
The document discusses drugs affecting blood and their mechanisms of action. It describes agents that stimulate or inhibit erythropoiesis, such as iron supplements or vitamin B12/folic acid deficiencies respectively. It also covers platelet aggregation inhibitors like aspirin, anticoagulants like heparin, and thrombolytic drugs like streptokinase used to treat thrombosis. Growth factors that stimulate leukopoiesis and chemotherapy drugs that inhibit it are also mentioned.
This document discusses various treatments and medications for bleeding and anticoagulation. It describes different classes of anticoagulant drugs that prevent blood clotting, including coumarins (vitamin K antagonists) like warfarin, heparin, and newer direct factor Xa and thrombin inhibitors. It provides details on specific medications within each class, their mechanisms of action, uses, advantages, disadvantages, and adverse effects. Alternative anticoagulants explored include antithrombin protein therapeutics and substances from snake venoms or leeches.
Diabetes insipidus is caused by a lack of antidiuretic hormone (ADH), also known as vasopressin, which is normally released by the pituitary gland. ADH helps regulate water balance in the body by increasing water reabsorption in the kidneys. Two case studies are presented: a young male diagnosed with a brain tumor after initially being treated for psychogenic polydipsia, and an older female found to have a craniopharyngioma after presenting with severe polydipsia and polyuria. Investigations including blood tests, imaging, and water deprivation tests can help diagnose the underlying cause, and treatment involves replacing ADH with desmopressin.
The document discusses hair dye poisoning, which is emerging as a common means of suicide, especially among females in India. Hair dyes contain toxic ingredients like paraphenylenediamine (PPD) and resorcinol. Poisoning symptoms include angioedema, rhabdomyolysis, myocarditis, and renal failure. Treatment focuses on airway protection, fluid resuscitation, dialysis, and managing complications to prevent death. Raising awareness about hair dye poisoning can help reduce mortality through early intervention.
This document provides information on the clinical features and management of methanol, aluminium phosphide, benzodiazepine, and cocaine poisoning. It describes the mechanisms of toxicity, signs and symptoms, toxic dose thresholds, diagnostic tests, and treatment approaches for each type of poisoning including gastric lavage, activated charcoal, antidotes like ethanol, flumazenil and supportive care. Complications involve the central nervous system, eyes, gastrointestinal tract, cardiovascular system and mortality is high for aluminium phosphide poisoning.
Intravenous fluids and parenteral nutritions slides Dr sarfarazSarfaraz Ahmad
The document discusses various types of parenteral fluids used in intravenous therapy, including crystalloids, colloids, blood products, and miscellaneous fluids. It provides details on the composition, properties, indications, and considerations of commonly used crystalloids like saline, dextrose, lactated ringer's, sodium bicarbonate and colloids like albumin, hetastarch, dextran, and mannitol. Whole blood components like packed red blood cells and fresh frozen plasma are also summarized.
Hyponatremia is the most common electrolyte abnormality seen in hospitalized patients. It is caused by an imbalance of water in the body, resulting in a dilution of sodium concentration. The document discusses the various types of hyponatremia (hypovolemic, euvolemic, hypervolemic) based on extracellular fluid volume status and their underlying causes such as SIADH, heart failure, liver cirrhosis. It also covers the diagnostic evaluation, management principles, and treatment approaches for acute symptomatic and chronic hyponatremia which involves slow correction of sodium levels to avoid osmotic demyelination syndrome.
Hypertension also known as high blood pressure is an effect of fast paced life. This presentation discusses various medicines used to cure hypertension.
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses a case of a 56-year-old female patient presenting with bilateral lower leg cellulitis and hyponatremia. She has a history of epilepsy, intellectual disability, and is on multiple medications including Moduretic. Initial workup found sodium of 118 mmol/L. She was started on IV saline and diuretics. Carbamazepine was identified as a potential cause of drug-induced hyponatremia and was replaced with levetiracetam. She was discharged on frequent sodium monitoring. The document then reviews hyponatremia causes, presentation, evaluation, and treatment considerations including the risk of rapid correction.
1. Drowning is defined as respiratory impairment from submersion in a liquid medium and is a major cause of accidental death, especially in children ages 1-14.
2. Management of drowning victims involves resuscitation, treatment of hypoxic-ischemic encephalopathy, and prevention of complications.
3. Prevention strategies focus on supervision during water activities, swimming lessons, CPR training, and safety measures around pools.
Approach to a patient with hyponatremia (2) (1)Mohit Aggarwal
The document discusses hyponatremia, which refers to a low serum sodium level. It begins by defining hyponatremia and providing normal sodium levels. It then covers the frequency, age and sex predispositions, physiology/pathophysiology, types and causes. The types include hypovolemic, euvolemic, hypervolemic, redistributive, and pseudohyponatremia. Common causes are discussed like SIADH, heart failure, cirrhosis. The clinical approach involves assessing volume status, labs like sodium, osmolality, urine sodium. Management depends on the type and involves restricting free water intake or using hypertonic saline in severe cases to slowly correct the
1. Dialysis patients are at high risk for infections like hepatitis B, hepatitis C, and bloodstream infections due to their weakened immune systems and frequent use of catheters and needles for dialysis access.
2. Hepatitis B and C infections are bloodborne viruses that can cause chronic liver inflammation, while bloodstream infections enter through vascular access sites like catheters.
3. Patients should watch for signs of infection like fever, swelling or redness at the access site, pus, or severe pain and report these promptly to reduce risk of serious complications. Frequent hospitalization and procedures also increase infection risk for these vulnerable patients
This document provides an overview of osmotic demyelination syndrome (ODS), also known as central pontine myelinolysis. It discusses the history, controversies in nomenclature, pathology, epidemiology, pathophysiology, clinical features, diagnosis, management including prevention, re-lowering sodium levels, supportive care and investigational therapies, prognosis, and key references. The document is intended as an educational resource for physicians on ODS.
The document discusses disorders of the parathyroid glands, which regulate calcium, phosphate, and magnesium levels. It covers primary hyperparathyroidism, caused by excessive PTH from hyperfunctioning parathyroid glands, and secondary hyperparathyroidism, which is an adaptive response to low calcium levels. It also discusses hypoparathyroidism, caused by PTH deficiency, and the resulting hypocalcemia and its neuromuscular symptoms. Diagnosis and treatment options are provided for each disorder.
- Disorders of the parathyroid glands can lead to abnormalities in calcium homeostasis. The main hormones involved are parathyroid hormone (PTH) and calcitonin, which work in opposition to maintain normal calcium levels.
- Primary hyperparathyroidism is caused by excessive PTH from overactive parathyroid glands. This disrupts the normal feedback inhibition and leads to hypercalcemia. It is usually treated with surgical removal of the affected gland(s).
- Medical treatments for hypercalcemia aim to increase calcium excretion and inhibit bone resorption through hydration, diuretics, calcitonin, bisphosphosphonates, and glucocorticoids in some cases
This document discusses thyroid and parathyroid disorders. It covers hyperthyroidism and hypothyroidism, their causes, symptoms, and treatment options. Hyperthyroidism is often caused by Graves' disease and results in excess thyroid hormones. Hypothyroidism is often caused by Hashimoto's disease and results in reduced thyroid hormones. Hyperparathyroidism is caused by excess parathyroid hormone from tumors on the parathyroid glands, leading to high blood calcium. Hypoparathyroidism is caused by low parathyroid hormone, leading to low blood calcium. Both conditions are typically treated through diet, supplements, and surgery if needed.
This document discusses thyroid and parathyroid disorders. It covers hyperthyroidism and hypothyroidism, their causes, symptoms, and treatment options. Hyperthyroidism is often caused by Graves' disease and results in excess thyroid hormones. Hypothyroidism is often caused by Hashimoto's disease and results in low thyroid hormones. Hyperparathyroidism is caused by excess parathyroid hormone from tumors on the parathyroid glands, leading to high blood calcium. Hypoparathyroidism is caused by low parathyroid hormone, leading to low blood calcium. Both conditions are treated through diet, supplements, and sometimes surgery.
Hypoparathyroidism is a rare condition where the parathyroid glands do not produce enough parathyroid hormone, resulting in low blood calcium and high blood phosphorus levels. The parathyroid glands regulate calcium and phosphorus levels. Without enough parathyroid hormone, individuals experience hypocalcemia and associated symptoms like muscle spasms. Treatment involves calcium and vitamin D supplementation to raise calcium levels and prevent complications.
This document provides information on disorders of the parathyroid glands. It discusses the anatomy and function of the parathyroid glands, including their role in calcium regulation and production of parathyroid hormone (PTH). It describes primary hyperparathyroidism, which results from excessive PTH production, and its clinical features. The document also covers hypoparathyroidism, which is a deficiency of PTH, and its signs, symptoms and treatment with calcium and vitamin D supplementation. In summary, the document outlines key endocrine disorders of the parathyroid glands, their effects on calcium levels, and management approaches for hyperparathyroidism and hypoparathyroidism.
3. Hair dye poisoning has been emerging as one of the
important causes of intentional self harm in the developing
world.
Branded hair dyes like ‘Godrej’, supervasmol Kesh
kala,Colourmate etc. are available in powder or liquid
forms.
The concentration of active substance i.e. paraphenyl
diamine varies from 70-90 % in Stone Hair Dye and 2-10%
in branded dyes which are used for giving black colour to
hair.
The Stone Hair Dye is extremely cheap and freely
available, making it an attractive option for suicidal intent.
4. The chemical used in Hair Dye is a derivative of
paranitroaniline and is called paraphenyl-diamine (PPD).
It is brownish to black coloured solid which is partially
soluble in water and easily soluble in hydrogen peroxide
(H2O2).
PPD is a good hydrogen donor and is metabolized by
electron oxidation to an active radical by cytochrome P450
peroxidase to form a reactive benzoquinone diamine.
This is further oxidized to a trimer known as
Brandowaski’s base, a compound reported to cause
anaphylaxis as well as being strongly mutagenic.
5. The characteristic features are severe angioneurotic
edema, rhabdomyolysis and intravascular hemolysis
with hemoglobinuria culminating in acute renal
failure.
PPD can bring about rhabdomyolysis by promoting
calcium release and leakage of calcium ions from the
smooth endoplasmic reticulum, followed by
continuous contraction and irreversible change in the
muscle's structure. Rhabdomyolysis is the main cause
of acute renal failure.
6. Propylene glycol, one another potential nephrotoxin is
a viscous, colorless liquid commonly used as a solvent
in hair dyes. It is associated with hyperosmolality,
raised anion gap metabolic acidosis, central nervous
system depression, arrhythmias and renal dysfunction.
Resorcinol found in hair dyes is a phenol derivative,
which may also contribute to renal toxicity. In
addition, a few hair dyes also contain lead acetate and
Bismuth sulfate, which can cause chronic kidney
disease or acute interstitial nephritis respectively.
7. The characteristic triad of features encountered are
early angioneurotic edema with
stridor, rhabdomyolysis with chocolate colored urine
and acute renal failure. When ever this combination
occurs in poisoning, hair dye is a strong suspect.
8. The study comprised of 1383 cases.
67 cases were brought dead .
83 cases died within first 5 hrs. of admission after
gastric lavage, drugs and I/V fluid therapy .
Out of 1233 remaining cases 167 cases of dye ingestion
did not have any feature of toxicity and were
discharged or absconded in the first 12 hrs.
41 cases of stone hair dye who had relatively mild
disease did not opt for investigations and were treated
with I/V fluids and drugs were excluded from this
study. 3 cases of known cardiac and 2 cases of known
renal diseases were excluded from the study.
9. Finally study comprised of 1020 cases who were
thoroughly investigated and treated.
In 631 cases out of 1020 cases ECG was done at 1st hour
after admission and then cardiac monitoring was done
in ICU.
It was realized later in the study that cases of stone
hair dye who died suddenly, were developing
ventricular tachyarrhythmias.
Therefore in the latter half of the study after admission
in emergency ward cases were immediately shifted and
managed in intensive care unit with cardiac
monitoring.
10. The data was analysed from the following points:-
1. Demographic profile
2. Clinical profile
3. Morbidity and mortality pattern
4. Outcome with different management strategy given in
the hospital.
11. PPD can be detected in urine by thin layer
chromatography on silica gel; solvent system benzene;
ethyl acetate (50:50) or hexane;acetone (90:60) and
sprayed with 0.2% solution of potassium dichromate
as a chromogenic reagent to give a pinkish brown spot.
Elevated levels of creatine phosphokinase and aldolase
in the serum
On the basis of clinical features.
Ecg changes.
12. ECG changes were tachycardia, T wave inversion, ST
segment elevation or depression, Bundle branch
blocks, intraventricular conduction defects , atrial and
ventricular premature complexes, atrial fibrillation
and the cases subsequently developed ventricular
tachyarrhythmia. Confirmed with troponin-T.
13. The treatment was based on the following principles-
1.Since no antidote is available against PPD management was
basically supportive.
2.Gastric lavage was followed by intravenous
methylprednisolone 1 gm/day for 5 days or hydrocortisone
100 mg 8 hourly for 7 days.
3.Oxygen was administered for Hypoxic cases
4.Sodium bicarbonate was administered to prevent
myoglobin precipitation in kidney (average dosage was 1
ampoule containing 22.5 meq. in 500 ml normal saline
every 8 hourly) along with loop diuretics (furosemide or
torsemide) to maintain adequate urine volume.(cont..
14. 5.Chlorpheniramine maleate one ampoule IV every 8
hrly till cervicofacial edema subsided (average 3-5
days).
6.Calcium gluconate was given to counteract
hypocalcemia. (10% calcium gluconate 10 ml every 8
hourly till hypocalcaemia subsided).
7.Vasopressors (intravenous Dopamine and/or
noradrenaline) were used if hypotension persisted
despite adequate fluid therapy.(cont…
15. 8.Dialysis- Hemodialysis or Peritoneal dialysis was used
for cases with renal shut down and resistant
hyperkalemia.
9.Intravenous amiodarone and defibrillation for
ventricular tachyarrhythmia management.
16. A total of 1020 cases were studied. 734 were female and
286 were male cases .
The reason for ingesting drug was mainly suicidal 998
cases (97.84 %). The remaining were accidental 19
cases (1.86%) and homicidal 3 (0.29%).
Symptomatology was directly related to the dose of
PPD ingested.
On transthoracic echocardiography,the findings were
regional wall motionabnormality and decreased left
ventricular ejections fraction (LVEF≤35%) in 126 cases
on day 2 to day 5 which subsequently improved on
follow up in cases survived.
17. Symptoms / Sign No. of cases Percentage
Severe edema of 745 73.03
face and neck
Dysphagia 726 71.17
Chocolate brown 549 53.82
colour urine
Pain /rigidity of 480 47.05
limb
Respiratory 229 22.45
difficulty
Tachycardia 229 22.45
Hypotension 149 14.61
Chest pain 141 13.82
18. Symptoms/signs No of cases percentage
Palpitation 139 13.63
Decreased urine output 130 12.75
Rise in blood pressure 80 7.84
Nasal twang of voice 59 5.78
Presyncope / Syncope 47 4.61
Nasal regurgitation 25 2.45
Convulsion 23 2.25
19.
20.
21.
22. PPD poisoning is common in females and in younger
age group with maximum number of suicidal intent.
Route of poisoning was ingestional in all cases.
Clinical features were typical cerviofacial
edema, dysphagia,chocolate brown color urine, pain
and / or rigidity of limbs,respiratory
difficulty, hypotension, decreased urine output.
Commonly seen abnormal laboratory investigation
were raised liver enzymes, myoglobinuria, raised
CPK, hypocalcemia,albuminuria, raised serum
creatinine, hyperkalemia, hyperbilirubinemia, derange
d PT and aPTT and acute tubular necrosis on renal
23. Cardiac complications were in the form of suspected
myocarditis leading to ventricular tachyarrhythmia.
Late mortality was mainly due to renal failure and its
related complications.
Preventing renal failure with abundant fluid
infusion, alkalinization of urine and the correction of
hemodynamic disturbances was a very important goal.
Results of hemodialysis were found to be better than
peritoneal dialysis though the toxin is not removed by
dialysis.
Intravenous methyl prednisolone given in high doses
showed rapid reduction of cervicofacial edema and
symptomatic improvement.
24. It is important that medical
fraternity should be aware of this
poison because the poison is
available quite freely and used
extensively.