Drug induced liver injury (DILI) and HepatotoxicityDr. Ankit Gaur
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.
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.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Drug induced liver injury (DILI) and HepatotoxicityDr. Ankit Gaur
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.
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.
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Alcoholic liver disease is a term that encompasses the hepatic manifestations of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis.
Liver Function Tests - An Approach for Primary CareJarrod Lee
This presentation is aimed at primary care physicians. It covers the fundamentals of liver function tests, including the basic principles of interpretation, and the key patterns of abnormalities. The focus is on how to approach liver function tests in a primary care setting.
Damage to the liver from years of excessive drinking causes alcohol-related liver disease (ARLD). Alcohol misuse can cause the liver to swell and become inflamed over time. Cirrhosis is a scarring condition caused by liver injury. Cirrhosis is the most advanced form of liver disease.
Medical considerations in dental treatment of patients with liver disease. Main types of liver disease, clinical manifestations, lab tests, treatment considerations.
LFT tests is also called hepatic panel.
Noninvasive methods for screening of liver dysfunction.
They reflect the synthetic function and evidence of liver damage.
These tests provide insights into several aspects of liver health,
Its ability to synthesize enzymes and protein.
Its ability to process bilirubin and secrete bile.
And the extent of liver damage.
Inorganic (non metallic) irritant Poisons by Sunil Kumar Dahasunil kumar daha
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
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Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. Introduction
• Hepatic manifestations of alcoholic over consumption.
1. Fatty liver
2. Alcoholic Hepatitis
3. Alcoholic cirrhosis
• ALD doesn’t occur below a threshold of alcohol consumption
of :-
• <14units/week in women
• <21units/week in men
• Alcoholics vs ALD
1 unit-8 gm
3. Risk factors
• Quantity of alcohol
— In men, 40–80 g/d of ethanol produces fatty liver;
in women, 20-40 g/d is enough
— 160 g/d for 10–20 years causes hepatitis or cirrhosis
• Drinking pattern: Continuous vs. intermittent
• Gender: Female twice > men
• Genetics: Monozygotic twins Vs. dizygotic
• Nutrition
• Obesity
• Malnutrition specially choline-deficient diet
• Hepatitis C infection
4.
5. Amount of alcohol in average drink
Alcohol type % alcohol
by volume
Amount Units
Beer 3.5
9
440 ml
440 ml
2
4
Wine 10
12
125 ml
750 ml
1
9
Alcopops 6 330 ml 2
Sherry 17.5 750 ml 13
Vodka/rum/gin 37.5 25 ml 1
Whisky/brandy 40 700 ml 28
Ref: Devidson’s 22nd edition
10. 1. Alcoholic fatty liver
• Accumulation of triglycerides within hepatocytes
• Can be reversed if alcohol consumption is stopped or
reduced significantly
• Has a good prognosis, disappears after 3 months of
abstinence
11. 2. Alcoholic Hepatitis
• Hepatocyte injury is characterized by-
• Mallorys Hyaline, Centrilobular necrosis, Fatty change,
Hepatocyte ballooning, PMN infiltrate, Pericellular fibrosis
• Worse prognosis than fatty liver disease
• Precursors to cirrhosis
• Potentially reversible with alcohol abstinence
12. 3. Alcoholic Liver cirrhosis
• “A condition in which there is continuing fibrosis
resulting in the subdivision of the liver into nodules of
proliferating hepatocytes surrounded by scar tissue as
the direct result of chronic alcohol abuse.”
• Irreversible condition even with abstinence
• Present in up to 50% of patients with biopsy-proven
alcoholic hepatitis
13. Contd…
Vicious circle of
Chronic inflammation
Fibrosis
Nodular regeneration
Distortion of architecture
Hepatocellular necrosis
14. Clinical syndromes of Alcoholic Liver
Diseases
Fatty Liver Alcoholic
hepatitis
Cirrhosis
• Asymptomatic
• Abnormal liver
biochemistry
• Normal or large
liver
• RUQ discomfort
• Nausea
• Rarely jaundice
• Asymptomatic
• Jaundice
• Malnutrition
• Hepatomegaly
• Features of portal
hypertension e.g.
ascites
• encephalopathy
• Stigmata of chronic
liver diseases
• Ascites/varices/enc
ephalopathy
• Large, normal or
small liver
• Hepatocellular
carcinoma
15. Investigations
• Macrocytosis in the absence of anaemia, may suggest
and support a history of alcohol misuse
• Unexplained rib fractures, particularly bilateral, on a
chest X-ray are also suggestive of alcohol misuse
• Presence of jaundice suggests alcoholic hepatitis
Test Comment
AST Increased two- to seven fold, <400 U/L, greater than ALT
ALT Increased two- to sevenfold, <400 U/L
AST/ALT Usually >1
GGTP Not specific to alcohol, easily inducible, elevated in all forms
of fatty liver
Bilirubin May be markedly increased in alcoholic hepatitis despite
modest elevation in alkaline phosphatase
PT Prolonged
Albumin Hypoalbuminemia
PMN If>5500/ml Predicts severe alcoholic hepatitis when
discriminant function > 32
16. Contd…
• We can also send for:
• Ultrasonography:
fatty infiltration and determine liver size
portal vein flow reversal, ascites, and intra-abdominal
collaterals indicates serious liver injury with less potential
for complete reversal of liver disease
• Liver Biopsy:
17. Prognosis
• Critically ill patients with alcoholic hepatitis have short-
term (30-day) mortality rates >50%
• Presence of ascites, variceal hemorrhage, deep
encephalopathy, or hepatorenal syndrome predicts a
dismal prognosis
• Pathologic stage of the injury by liver biopsy
18. Discriminant Function (DF)
• Aka ‘Maddrey score’
DF = (4.6 x increase in PT sec. )) + (serum bilirubin mg/dl)
• To assess prognosis in alcoholic hepatitis
A value over 32 implies severe liver disease with a poor
prognosis
19. Glasgow Alcoholic Hepatitis Score
Score 1 2 3
Age < 50 > 50
WCC (× 109/L) < 15 > 15 > 2.0
Urea (mmol/L) < 5 > 5 > 250
PT ratio < 1.5 1.5-2.0
Bilirubin
(μmol/L)
< 125 125-250
A score > 9 is associated with a 40% 28-day survival,
compared to 80% for patients with a score < 9
20. Model for End-stage Liver Disease
(MELD)
1-year survival (%)
MELD score No complications Complications
< 9 97 90
10-19 90 85
20-29 70 65
30-39 70 50
MELD from SI units
10 × (0.378[In serum bilirubin (μmol/L) + 1.12[In INR] + 0.957[In serum
creatinine (μmol/L)] + 0.643)
MELD from non-SI units
3.8 [In serum bilirubin (mg/dL)] + 11.2 [In INR] + 9.3 [In serum creatinine
(mg/dL)] + 6.4
21. Management
1. Alcohol Abstinence
2. Nutritional Support
3. Corticosteroid Therapy
4. Pentoxifylline
5. Liver Transplantation
* We also have to manage for :-
• Alcohol withdrawal and Wernicke's encephalopathy
• Treatment for complications of cirrhosis, such as
variceal bleeding, encephalopathy and ascites
22.
23. 1. Alcohol abstinence
• Most important treatment of all
• Effective in preventing progression of disease
• Alcohol withdrawal syndrome and Wernicke’s encephalopathy need
parallel treatment too
25. 3. Corticosteroids
• Glucocorticoids have been found to be beneficial in
patients with severe alcoholic hepatitis (Maddrey’s DF
score ≥32).
• Survival rate found to be increased in those with
Glasgow score >9
• Sepsis is the main side effect
• Should not be given to patients with active GI bleeding,
sepsis, renal failure or pancreatitis.
26. 4. Pentoxifylline
• Anti- TNF action
• Reduce incidence of hepato-renal failure
• Given in severe alcoholic hepatitis in whom
corticosteroids cannot be given
27. References
• Harrison’s Principle of Medicine,19th edition
• Davidson’s Principle and Practice of Medicine, 22nd
edition
• Kumar and Clark’s Clinical Medicine, 8th edition
Although alcohol is considered a direct hepatotoxin, only between 10 and 20%of alcoholics will develop alcoholic hepatitis.
The explanation for this apparent paradox is unclear but involves the complex interaction of
facilitating factors, such as drinking patterns, diet, obesity, and gender.
There are no diagnostic tools that can predict individual susceptibility to alcoholic liver disease.
Quantity and duration of alcohol intake are the most important risk factors involved in the development of alcoholic liver disease.
Alcohol directly affects stellate cells, transforming them into collagen producing myofibroblast cells