In this presentation I have tried to explain the defination, Mechanism of drug induced liver injury (DILI) and hepatotoxicity with the help of few examples.
Definition, Patterns/types and mechanisms of drug induced liver disorders, assessment of drug induced liver disorders and its treatment (pharmacotherapeutics-3)
Definition, Patterns/types and mechanisms of drug induced liver disorders, assessment of drug induced liver disorders and its treatment (pharmacotherapeutics-3)
DILI is possible consequence of ingestion of OTC drugs like PCM.
so it require careful clinical knowledge before taking drugs without doctors prescriptions...
In this presentation i have tried to thoroughly discuss about the concept of Drug induced kidney disease or injury, the mechanism behind it, its classification and how to access it.
Drug induced hematological disorders @rxvichu!!!RxVichuZ
This is my 35th powerpoint..published here in Google Slideshare...
And I wish to thank everyone who have supported me in my 2 year long journey......
This ppt is regarding DRUG INDUCED HEMATOLOGICAL DISORDERS, covering the definitions, causative drugs, pathophysiological mechanisms, manifestations,and management of 5 blood disorders.
Do go through this ppt, and send me ur reviews!!
Regards,
Vishnu.R.Nair.
DILI is possible consequence of ingestion of OTC drugs like PCM.
so it require careful clinical knowledge before taking drugs without doctors prescriptions...
In this presentation i have tried to thoroughly discuss about the concept of Drug induced kidney disease or injury, the mechanism behind it, its classification and how to access it.
Drug induced hematological disorders @rxvichu!!!RxVichuZ
This is my 35th powerpoint..published here in Google Slideshare...
And I wish to thank everyone who have supported me in my 2 year long journey......
This ppt is regarding DRUG INDUCED HEMATOLOGICAL DISORDERS, covering the definitions, causative drugs, pathophysiological mechanisms, manifestations,and management of 5 blood disorders.
Do go through this ppt, and send me ur reviews!!
Regards,
Vishnu.R.Nair.
The liver plays a key role in detoxifying harmful substances that you may eat, drink, inhale or rub on your skin. Toxic hepatitis is liver inflammation that occurs when your liver is damaged by toxic chemicals, drugs or certain poisonous mushrooms.
The Emerging Role of Pharmacists in Public Health.pptxDr. Ankit Gaur
The Emerging Role of Pharmacists in Public Health: Opportunities and Challenges
General system theory, steven's system model, Pharmacists in india, Disaster management and emergency care, rational use of medicine, RNTCP programme. National Aids Control Programme.
This presentation is about Stress and its impact on health. I have tried to cover everything related to it, stressors, coping mechanisms, tools, types etc.
Gastro esophageal Reflux Disease (GERD) and its managementDr. Ankit Gaur
In this presentation I have tried to explain in brief about gastro esophageal Reflux Disease (GERD), its etiology, risk factors, diagnosis, and its management via pharmacotherapy.
In this presentation I have tried to discuss in brief about obsessive compulsive disorder and its treatment both pharmacological and non pharmacological.
In this presentation I have tried to explain in brief about pain management, different types of pain, its diagnostic criteria, its physiology, and its treatment approaches both pharmacological and non pharmacological
Respiratory Tract Infections- A Pharmacotherapeutic ApproachDr. Ankit Gaur
In this presentation I have tried to explain the types, etiology, pathophysiology of respiratory tract infections such as bronchitis, pnemonia, otitis media, sinusitis, pharyngitis, and their treatment
In this presentation I have tried to explain in brief about the dosage adjustment in renal disorders, how to carry out this process and the important formulae which are used in it.
In this presentation i have tried to explain in brief about nomograms and their applications, the general approach to individualise doage regimen by using pharmacokinetic data
In this presentation I have tried to explain in detail about tablets, their different types, ingredients which are used to prepare them, and the procedure to prepare them as well. This presentation is very useful for pharmacy students.
In this presentation i have tried to explain in details about the Total Parenteral Nutrition (TPN) , what is it, who needs it, and how to prepare it and the necessary procedure with instructions. It is very useful for the individuals from Nutrition, Nursing, Pharmacists, and Medical background.
in this presentation i have tried to briefly discuss about diuretics (water pills), their classification, mechanism of action, pharmacokinetics and pharmacodynamics of these drugs
In this presentation i have tried to explain in brief about CPR, how and when it has to be done and the important things to be kept in mind while doing it. This ppt is very helpful for every individual who is looking for the info regarding CPR.
In this presentation i have tried to explain in detail about the nux vomica and khurchi bark. This presentation is useful for the individuals who are looking for information on this topic especially for those students who are studying Pharmacognosy.
In this presentation i have tried to explain in detail about the measurements of the outcomes which are used in epidemiology such as prevalence, incidence, fatality rate, crude death rate etc.
In this presentation i tried to explain in detail about cohort studies, their types, how to conduct them, their outcomes, and how to calculate sample size of these studies.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. LIVERPHYSIOLOGIC FUNCTION
Formation and
secretion of bile
Nutrient and
vitamin
metabolism
(amino acid, lipid,
glucose)
Detoxification &
inactivation of
various
substances (toxin,
drug)
Synthesis of
plasma proteins
(albumin, clotting
factor)
Immune system
kupffer cells.
2
3. HEPATOTOXICITY
Hepatotoxicity refers to liver damage. Certain
medicinal agents, when taken in overdoses
and sometimes even when introduced
within therapeutic ranges, may injure the
organ.
Other chemical agents, such as those used in
laboratories and industries, natural chemicals
e.g., microcystins and herbal remedies can
also induce hepatotoxicity.
Chemicals that cause liver injury are called
hepatotoxin.
4. DRUG-INDUCED LIVER INJURY / DISEASE (DILI)
Liver injury may be produced by a large
variety of chemical substances
The type and degree of injury produced is
extremely varied, and may mimic the entire
spectrum of hepatobiliary disorders.
The central role played by the liver in the
clearance and biotransformation of
chemical susceptibility to drug-induced
injury.
Drugs can initiate progressive chronic liver
disease and are the single leading cause of
acute liver failure.
6. Intrinsic hepatotoxicity is regarded as dose-
dependent and predictable above an
approximate threshold dose.
Whereas idiosyncratic hepatotoxicity occurs
without obvious dose-dependency and in an
unpredictable fashion.
Allergic idiosyncratic hepatotoxicity is
characterized by the presence of typical
symptoms and signs of adaptive immune
reactions, including fever, skin reactions,
eosinophilia, formation of autoantibodies, and
a short latency time particularly after re-
exposure. 6
7. RISK FACTORS OF LIVER INJURY
Pharmacokinetic
s – Metabolism
Specific immune
system
Initial liver injury
Progression of liver
injury
Cytokine,
TNF, ROS
Acute
liver
failure
Chronic
liver failure
Enviromental Risk
Factor
Genetic Risk Factor
8. 8
FORMS OF LIVER TOXICITY:-
Zonal Necrosis- This is the most common type of
drug induced liver cell necrosis where the injury is
largely confined to a particular zone of the liver
lobule.
Hepatitis- Disease of the liver causing
inflammation.
Cholestasis- Cholestasis is a condition where
bile cannot flow from the liver to the duodenum.
Steatosis- Steatosis is a condition characterised
by the build up of fat within the liver, sometimes
triggering inflammation of the liver
9. 9
• Granuloma- A granuloma is one of a number of
forms of localized nodular inflammation found in
tissues.
• Vascular lesions- They result from injury to the
vascular endothelium.
• Neoplasm- Neoplasm or tumor, tissue composed
of cells that grow in an abnormal way.
11. 1.Initial Mechanisms of Toxicity: Direct Cell Stress,
Direct Mitochondrial Impairment, and Specific
Immune Reactions
2. Direct and Death Receptor-Mediated Pathways
Leading to Mitochondrial Permeability Transition
3. Apoptosis and Necrosis 11
13. 13
SIGNS AND SYMPTOMS:-
Yellowing of the skin and whites of the eyes
(jaundice)
Fatigue
Loss of appetite
Nausea and vomiting
Weight loss
Dark or tea-colored urine
14. PRACTICAL GUIDELINE FOR DIAGNOSIS &
EARLY MANAGEMENT OF DILI
Preplanned LFT,
evaluation of drug
Careful history taking/rule out other
etiologies, evualate the type of liver injury
DILI is unlikely DILI is suspected
Diagnosis of
DILI
Hepatocellular type
or mixed
Discontinue the
suspected drug
Cholestatic type
Careful
monitoring
ALT > 8 x ULN at any
one time or
ALT > 5 x ULN for
more than 2 wk or
ALT > 3 x ULN, and
total bilirubin > 2 x
ULN or PT-INR > 1.5
x UNL
Symptoms
related to liver
injury such as
jaundice or
Total bilirubin > 3
x ULN or
PT-INR > 1.5 x
ULN
When a drug is initiated
When liver dysfunction is
recognized
20. DRUGS CAUSING LIVER DAMAGE
Acetaminophen:-(Paracetamol, also known by the
brand name Tylenol and Panadol) is usually well
tolerated in prescribed dose but overdose is the
most common cause of drug induced liver disease
and acute liver failure worldwide.
20
Nonsteroidal anti-inflammatory drugs- Aspirin,
phenylbutazone, ibuprofen, sulindac,
phenylbutazone, piroxicam, diclofenac and
indomethacin.
20
21. Glucocorticoids- Glucocorticoids are so named
due to their effect on carbohydrate mechanism.
they promote glycogen storage in liver. The
classical effect of prolonged use both in adult
and paediatric population is steatosis.
Isoniazid- Isoniazide (INH) is one of the most
commonly used drug for tuberculosis; it is
associated with mild elevation of liver enzymes
in up to 20% of patients and severe
hepatotoxicity in 1-2% of patients
22. Natural products- Amanita mushroom, particularly
the destroying angels, aflatoxins.
Industrial toxin- Arsenic, Carbon tetraChloride, Vinyl
Chloride.
Herbal and alternative remedies- Ackee fruit,
Camphor, Pyrrolizidine alkaloids, Horse chestnut
leaf, Valerian, Comfrey (often used in herbal tea).
2
2
23. 1- CARBON TETRA CHLORIDE
Carbon tetrachloride was widely used as a
cleaning solvent, fire extinguisher agent, and
anthelmintics.
Because of its liver toxicity and known
carcinogenicity in animals, its role has become
limited; it is now used mainly as an intermediate
in chemical manufacturing.
24. MECHANISM OF TOXICITY
Carbon tetrachloride is a potent hepatic and renal
toxin. The mechanism is thought to be a result of a
toxic free-radical intermediate of metabolism.
(CCl4) undergoes hepatic reductive metabolism to
CCl3 and CCl3OO free radicals toxic intermediates
which may initiate hepatocellular damage..
Chronic use of metabolic enzyme inducers such as
phenobarbital and ethanol increase the toxicity of
carbon tetrachloride. Carbon tetrachloride is a
known animal and suspected human carcinogen.
26. MANAGEMENT
Remove the subject from exposure area.
Maintain normobaric or hyperbaric oxygen.
In case of ingestion administer activated charcoal.
Ipecac induced vomiting may be useful for initial
treatment.
N-acetylcysteine may minimize hepatic and renal
toxicity by providing a scavenger for the toxic
intermediate.
27. 2- ACETAMINOPHEN
Acetaminophen is a widely used drug found in many
over the counter and prescription analgesics
medication.
In adults, toxicity may occur by ingestion of greater
than 7.5-10g (24 regular strength or 15 extra
strength caplets or tablets) over a period of 8 hours
or less.
28. MECHANISM OF TOXICITY
Acetaminophen is metabolized in the liver by
conjugation to non-toxic glutathione. The
conjugated product is eliminated in the urine. But in
an acute overdose, the liver's normal glutathione
reserves are depleted; the excess acetaminophen
is then metabolized to highly toxic metabolite: N-
acetyl-p-benzoquinone (NABQI). NABQI is very
reactive causing hepatocellular death and
subsequent massive liver cell necrosis.
29. MECHANISM OF ACETAMINOPHEN-INDUCED HEPATOTOXICTY
At usual therapeutic dosages, acetaminophen is metabolized conjugation reactions. The capacity
becomes saturated at higher dosages diversion of the drug to the P-450-mediated pathway
generates reactive electrophile N-acetyl-p-benzoquinone imine (NAPQI) undergoes phase 2
conjugation with glutathione glutathione depletion allowing the electrophile to exert damaging
effects within the cell via covalent binding.
31. MANAGEMENT
Ipecac Syrup
Activated Charcoal
N-Acetyl Cysteine (loading dose is 150mg/kg in
200ml of 5% dextrose infused over 15-60
minutes).
Methionine can also be given.
32. 3- ETHANOL
Commercial beer, wine, and liquors contain various
amounts of ethanol. Ethanol is also found in a variety of
perfumes, mouthwashes, many food flavorings (eg,
vanilla, almond, and lemon extracts), pharmaceutical
preparations (eg, elixirs), and many other products.
Ethanol is frequently ingested recreationally and is the
most common co-ingestant with other drugs in suicide
attempts. Ethanol may also serve as an antidote in the
emergency treatment of methanol and ethylene glycol
poisonings.
33. MECHANISM OF TOXICITY
Ethanol is also oxidized in liver by an ethanol-inducible
cytochrome P-450 enzyme that converted the contents
to toxic radicals. Induction also results in energy
wastage and increased production of acetaldehyde
that results in injury to cells and mitochondria with a
striking impairment of oxygen utilization.
Acetaldehyde also causes glutathione depletion and
lipid peroxidation, and stimulates hepatic collagen
synthesis, thereby promoting fibrosis and cell damage.
34. SIGN & SYMPTOMS
Euphoria
Impairment of balance & muscle coordination
Nausea
Vomiting
Hypoglycemia
Ketoacidosis
Respiratory Depression
Pale, bluish, cold and clammy skin due to insufficient
oxygen
Coma
35. MANAGEMENT
Protect the airway and provide supportive treatment.
Don’t induce vomiting or activated charcoal
Give glucose & thiamine to treat alcoholic ketoacidosis
Correct hypothermia with gradual rewarming
No specific antidote available
Perform hemodylasis for efficient ethanol removal.
36. 4- AFLATOXINS
The aflatoxins are a group of structurally related toxic
compounds produced by certain strains of the fungi
Aspergillus flavus and A. parasiticus.
Aflatoxicosis is poisoning that results from ingestion of
aflatoxins in contaminated food. Among 18 different
types of aflatoxins identified, major members are
aflatoxin B1, B2, G1 and G2. Aflatoxin B1 is the most
toxic and most prevalent among this family.
37. MECHANISM OF TOXICITY
The major target for the toxicity of aflatoxins is the
liver. Oxidation by cytochrome P450, aflatoxins then
bind to DNA or proteins and impair their functions.
Aflatoxins produce necrosis of liver cells, damage
to mitochondria, and proliferation of bile ducts.
Aflatoxin also suppress the immune system of the
body.
39. MANAGEMENT
The FDA’s goal for aflatoxins has been to minimize
contamination by the cause.
Provide supportive treatment.
There is no specific antidote for toxicity of aflatoxins.
Timely administration of methionine (200 mg/kg) and
sodium thiosulfate (50 mg/kg), at eight hour intervals,
is proven to be of therapeutic value.
40. PHENYTOIN-INDUCED HEPATOTOXICITY
The interval between the initiation of phenytoin therapy and
the onset of clinical abnormalities ranges from 1 to 6
weeks in the vast majority of patients.
Presenting symptoms fever, rash and lymph-
adenopathy, Jaundice and hepato-splenomegaly.
Biochemical features abnormal serum bilirubin,
transaminases, and ALP levels
The morphologic and pathologic abnormalities are non-
specific primary hepatocellular degeneration and/or
necrosis.
40