This document discusses alcoholic liver disease (ALD). It begins by defining ALD and its stages - fatty liver, alcoholic hepatitis, and cirrhosis. It then discusses risk factors like gender, genetics, and drinking patterns. Symptoms for each stage are provided. The pathophysiology of steatosis, hepatitis, and cirrhosis are explained. Diagnostic tests including blood tests, imaging, and biopsy are outlined. Management of ALD focuses on abstinence, nutrition, medications to prevent complications, and potentially transplantation for late-stage disease.
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.
Peptic ulcers are sores that develop in the lining of the stomach, lower esophagus, or small intestine. They're usually formed as a result of inflammation caused by the bacteria H. pylori, as well as from erosion from stomach acids. Peptic ulcers are a fairly common health problem.
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.
Peptic ulcers are sores that develop in the lining of the stomach, lower esophagus, or small intestine. They're usually formed as a result of inflammation caused by the bacteria H. pylori, as well as from erosion from stomach acids. Peptic ulcers are a fairly common health problem.
Heart failure (HF) is a common cardiovascular condition with increasing incidence and prevalence. Unlike western countries where heart failure is predominantly a disease of elderly, in India it affects younger age group. Heart failure is a chronic condition in which the heart cannot pump enough blood and oxygen to support other organs in your body.
Heart failure (HF) is a common cardiovascular condition with increasing incidence and prevalence. Unlike western countries where heart failure is predominantly a disease of elderly, in India it affects younger age group. Heart failure is a chronic condition in which the heart cannot pump enough blood and oxygen to support other organs in your body.
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism. ... As cirrhosis progresses, more and more scar tissue forms, making it difficult for the liver to function (decompensated cirrhosis)
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Correlation liver disfunction and infection disease (dengue typhoid fever)01mataharitimoer MT
Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever)
Dr Erwin, SpPD, FINASIM
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
2. ALD, the term that encompasses the liver manifestations of alcohol
overconsumption, including fatty liver, alcoholic hepatitis, and
chronic hepatitis with liver fibrosis or cirrhosis.
It may well represent the oldest form of liver injury known to
humankind.
Many people with alcoholic liver disease experience no symptoms
in the early stage of the disease.
3. Consumption of 60–80g per day (about 75–100 ml/day) for 20
years or more in men.
Consumption of 20g/day (about 25 ml/day) for women
significantly increases the risk of liver damage.
Women have double the risk of getting ALD when compared
to men
4.
5. 80% of alcohol passes through the liver to be detoxified.
Chronic consumption of alcohol results in the secretion of pro-
inflammatory cytokines (TNF-alpha, Interleukin 6 [IL6] and
Interleukin 8 [IL8]), oxidative stress, lipid peroxidation, and
acetaldehyde toxicity.
6.
7. Quantity of alcohol taken:Consumption of 60–80g per day
(about 75–100 mL/day) for 20 years or more in men, or
20g/day (about 25 mL/day) for women significantly increases
the risk of hepatitis and fibrosis by 7 to 47%.
Pattern of drinking: Drinking outside of meal times
increases up to 3 times the risk of alcoholic liver disease.
Gender: Women are twice as susceptible to alcohol-related
liver disease, and may develop alcoholic liver disease with
shorter durations and doses of chronic consumption.
Hepatitis C infection: A concomitant hepatitis C infection
significantly accelerates the process of liver injury.
Genetic factors: Genetic factors predispose both to
alcoholism and to alcoholic liver disease. Polymorphisms in
the enzymes.
8. Iron overload (Hemochromatosis)
Diet: Malnutrition, particularly vitamin A and E deficiencies,
can worsen alcohol-induced liver damage by preventing
regeneration of hepatocytes.
9. Symptoms vary, based on how bad the disease is. You may not
have symptoms in the early stages. Symptoms tend to be
worse after a period of heavy drinking.
Digestive symptoms include:
Pain and swelling in the abdomen
Decreased appetite and weight loss
Nausea and vomiting
Fatigue
Dry mouth and increased thirst
Bleeding from enlarged veins in the walls of the lower part of
the esophagus.
10. Skin problems such as:
Yellow colour in the skin, mucus membranes, or eyes
(jaundice)
Small, red spider-like veins on the skin
Very dark or pale skin
Redness on the feet or hands
Itching
Brain and nervous system symptoms include:
Problems with thinking, memory, and mood
Fainting and light headedness
Numbness in legs and feet
11.
12.
13. Fatty change, or steatosis is the accumulation of fatty acids in
liver cells.
Alcoholism causes development of large fatty globules (macro
vesicular steatosis) throughout the liver and can begin to occur
after a few days of heavy drinking.
Alcohol is metabolized by alcohol dehydrogenase (ADH) into
acetaldehyde
Aldehyde dehydrogenase (ALDH) into acetic acid, which is
finally oxidized into carbon dioxide (CO2) and water ( H2O).
A higher NADH concentration induces fatty acid synthesis
while a decreased NAD level results in decreased fatty acid
oxidation.
triglycerides accumulate, resulting in fatty liver
14. Weakness
Nausea
Abdominal pain
Loss of appetite
Malaise(generally feeling unwell)
15.
16. Alcoholic hepatitis is characterized by the inflammation of
hepatocytes. Between 10% and 35% of heavy drinkers develop
alcoholic hepatitis (NIAAA, 1993).
Development of hepatitis is not directly related to the dose of
alcohol, some people seem more prone to this reaction than
others. This is called alcoholic steato necrosis and the
inflammation appears to predispose to liver fibrosis.
Inflammatory cytokines (TNF-alpha, IL6 and IL8) are thought
to be essential in the initiation and perpetuation liver injury
by inducing apoptosis and necrosis.
Symptoms may include pain or tenderness in the abdomen,
jaundice , spider like veins appear on the skin, malaise, fever,
nausea and loss of appetite.
End stage there will be hair loss, dark urine, black or pale
stools, dizziness, fatigue, loss of libido, bleeding gums or
nose, edema, vomiting, muscle cramps, weight loss
17. Cirrhosis is a late stage of serious liver disease marked by
inflammation (swelling), fibrosis (cellular hardening) and
damaged membranes preventing detoxification of chemicals in the
body, ending in scarring and necrosis(cell death).
Between 10% to 20% of heavy drinkers will develop cirrhosis of
the liver (NIAAA, 1993).
Acetaldehyde may be responsible for alcohol-induced fibrosis by
stimulating collagen deposition by hepatic stellate cells.
Symptoms include jaundice (yellowing), hepatomegaly, pain and
tenderness from the structural changes in damaged liver
architecture.
18.
19. LIVER FUNCTION TESTS:
These are simple, inexpensive and easy to perform but
cannot be used in alone to make diagnosis which include ;
• Serum albumin levels and prothrombin time indicates hepatic
protein synthesis,
• bilirubin is a marker of whole liver function, transaminase
levels indicate hepatocellular injury and death.
• alkaline phosphatase levels estimate the impedance of bile
flow.
20. Imaging tests:
An ultrasound scan , CT scan or a MRI scan also be
carried. These scans produce detailed images of liver.
Imaging studies do not confirm the presence of alcoholic liver
disease .
Can be used to assess for hepatic parenchymal changes.
Ultrasound, CT scan, and MRI can be used to diagnose fatty
change, cirrhosis, or neoplastic diseases of the liver.
21. Liver biopsy:
A fine needle is inserted into body and a small sample of liver
cell is taken under local anaesthesia and is examined under
microscope.
Biopsy may be indicated in:
Any patient with serum aminotransferases elevations that persist
for >6 months, even if the patient is asymptomatic.
Patients who have evidence of liver failure (eg, abnormal
prothrombin time, hypoalbuminemia) in addition to elevated
aminotransferases.
If a coagulopathy is present, transjugular biopsy is usually safer than
percutaneous biopsy.
Patients in whom the diagnosis of alcoholic hepatitis is uncertain
based upon clinical and laboratory findings.
22. Patients who may have more than one type of liver disease (such
as alcohol and hepatitis C) in whom a liver biopsy may help
determine the relative contribution of these factors .
Patients in whom a more detailed understanding of prognosis is
desired.
Endoscopy:
An endoscope is a thin long flexible tube with a light and video
camera at one end this tube is passed into oesophagus and
stomach and examine for varices
23. Portal hypertension is a common complication of cirrhosis.
When the liver becomes severely scarred it is harder for blood to
move through it. This leads to an increase in blood pressure.
The blood must also find a new way to return to your heart. It does
this by opening up new blood vessels, usually along the lining of
your stomach or oesophagus (the long tube that carries food from the
throat to the stomach).
These new blood vessels are known as varices.
If the blood pressure rises to a certain level, it can become too high
for the varices to cope with, causing the walls of the varices to split
and bleed.
This can cause long-term bleeding, which can lead to anaemia .
24. Symptoms of portal hypertension ;
Ascites
Hepatic encephalopathy
Pancytopenia
Spleenomegaly
Bloody vomiting
melena
Symptoms of varices ;
Black ,tarry stools
Bloody stools
Light headedness
Paleness
vomiting
26. Primary prevention of bleeding episode
1-Beta-Blockers
Propranolol ; 40mg initially increasing every 3-7days,maintenance
80-240mg/8-12hrly,not exceed60mg/day
Nadolol ;10-30mg/12hrly p/o
Timolol ;10-30 mg/12hrly p/o, maintenance 20-40 mg /day
2-Isosorbide mononitrate
30-60 mg once a day in the morning.
27. • Accumultion of fluid in the peritoneal cavity . The medical
condition is also known as peritoneal cavity fluid,peritoneal
fluid excess, hydroperitoneum
• A low salt diet may be enough to facilitate the elimination of
ascites and delay reaccumulation of fluid.(60-90mEq/day).
• Mild ascites is hard to notice, but severe ascites generally
lead to abdominal distension
• Amounts of upto 35 liters are possible.
• Symptoms of ascites;
Abdominal distension with fullness in the flanks
Abdominal and back pain
Gateroesophageal reflux
28.
29. Management of cirrhotic ascites
Bed rest and sodium restriction[60-90meq/day to
1500-2000mg of salt/day]
Spironolactone : 100-400 mg/day
Furosemide : 40-160mg/day
Hydrochlorothiazide : 50mg/day
30. A high level of toxins in the blood due to liver damage is
known as hepatic encephalopathy.
Symptoms of hepatic encephalopathy include:
agitation
confusion
disorientation
muscle stiffness
muscle tremors
difficulty speaking
in very serious cases, coma
31. Lactulose:
15-30ml orally 2-4 times per day.
Antibiotics:
Metronidazole:
250mg orally 3 times daily .
Neomycin:
0.5-1g orally every 6-12 hrs for 7 days.
Rifaximin:
400mg orally 3 times daily.
LOLA:
L-ornithine L-aspartate 9g orally 3 times daily
MANAGEMENT
33. Abstinence is the most important therapeutic intervention for
patients with ALD .
Abstinence has been shown to improve the outcome and
histological features of hepatic injury, to reduce portal
pressure and decrease progression to cirrhosis, and to improve
survival at all stages in patients with ALD
◦ Less than 20 % of patients will demonstrate progression of
liver disease after abstinence .
◦ 5 year survival improves from 34 % to 60 % for those with
decompensated liver disease
34. ◦ Alcoholism is associated with nutritional deficiencies .
◦ The presence of significant protein calorie malnutrition is a
common finding in alcoholics, as are deficiencies in a
number of vitamins and trace minerals, including vitamins
A, D, thiamine, folate, pyridoxine, and zinc .
35. ALCOHOLIC HEPATITIS
Prednisolone :
40mg orally daily for 4 weeks; then taper the dose.
FOLIC ACID DEFICIENCY :
Folic acid :
1mg orally daily in conjugation with improved dietary intake
until repletion occurs.
THIAMINE DEFICIENCY :
THIAMINE:
100mg orally or subcutaneously daily for 2 weeks or until
repleted.
36. VITAMIN D DEFICIENCY:
Ergocalciferol:
12,000 to 50,000 international units orally daily; reassess
vitamin D serum levels in 2 to 3 months.
VITAMIN E DEFICIENCY :
Vitamin E
400 IU orally daily
VITAMIN A DEFICIENCY :
25,000 TO 50,000 IU orally 3 times weekly.
37. Silymarin
Antioxidative and antifibrotic properties.
Believed to enhance liver regeneration and protect
hapetocytes from toxicity
• Recommended dose is 140mg 2-3 times /day
38. Liver transplantation remains the only definitive
therapy.
Alcoholic hepatitis has been considered an absolute
contraindication to liver transplantation.
Editor's Notes
Alcohol Hepatitis- Liver inflammation caused by drinking too much alcohol
Fatty liver- accumulation of fats or triglycerides in liver caused by alcoholic cirrhosis.
Liver fibrosis(scarring liver) is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases.
An explanation of alcohol related liver disease
NIAAA- National institute on alcohol abuse and alcoholism.
Greek work askites baglike
American college of gastroenterology and american association for the study of liver disease guidlines recommend 1.2-1.5g/kg of protein and 35-40kcal/kg of body weight per day in patient with ALD.