Peptic ulcer disease is caused by an imbalance between gastric acid and mucosal defenses, allowing acid to damage the stomach or duodenum lining. Helicobacter pylori infection and NSAID use are leading causes. Symptoms include abdominal pain, nausea, and vomiting. Complications include bleeding, perforation, and cancer. Treatment involves eradicating H. pylori, stopping NSAIDs, and using PPIs to reduce acid and promote healing. Endoscopic therapies can help stop bleeding.
definition
layers of the small intestine
parts of the small intestine
functions of the small intestine
types of enteritis
signs and symptoms
complications
diagnose
treatment
definition
layers of the small intestine
parts of the small intestine
functions of the small intestine
types of enteritis
signs and symptoms
complications
diagnose
treatment
Ulcerative colitis (UC) is an inflammatory bowel disease. It causes irritation, inflammation, and ulcers in the lining of your large intestine (also called your colon). There's no cure, and people usually have symptoms off and on for life
Ulcerative colitis (UC) is an inflammatory bowel disease. It causes irritation, inflammation, and ulcers in the lining of your large intestine (also called your colon). There's no cure, and people usually have symptoms off and on for life
I am a professional pharmacist. These slides provide for pharmacy department students. These slides describe pathology some topics.
Such as peptic ulcer disease, Immunity etc.
Ulcers range from small, painful sores in the mouth to bedsores and serious lesions of the stomach or interstine
Gastric ulcers :are peptic ulcers in the stomach.
Duodenal ulcers :are peptic ulcers in the duodenum
Intro to TB
epidemiology of TB
Structure of Mycobacterium TB
pathogenesis of TB
Immunosuppression by Mycobacterium TB
types of TB
Clinical manifestation
Diagnosis
Treatment
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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.
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.
Follow us on: Pinterest
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
4. Definition:
Peptic ulcer disease (PUD) is a break in the inner lining of the stomach, the
first part of the small intestine, or sometimes the lower esophagus. An ulcer
in the stomach is called a gastric ulcer, while one in the first part of the
intestines is a duodenal ulcer and the lower esophagus is esophageal ulcers
6. Under normal conditions, a physiologic balance exists between gastric acid
secretion and gastroduodenal mucosal defense. Mucosal injury and, thus,
peptic ulcer occur when the balance between the aggressive factors and
the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs,
H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal
defense by allowing back diffusion of hydrogen ions and subsequent epithelial
cell injury
8. H. pylori is a spiral or helical gram-negative rod with four to six flagella
that resides in gastric-type epithelium within or beneath the mucous layer.
This location protects the bacteria from acid and antibiotics. Its shape and
flagella aid its movement through the mucous layer, and it produces enzymes
that help it adapt to this hostile environment
Most notably, H. pylori is a potent producer of urease, which is capable of
splitting urea into ammonia and bicarbonate, creating an alkaline
microenvironment in the setting of an acidic gastric milieu
H. pylori organisms are microaerophilic and can live only in gastric
epithelium.
9. NSAIDS:
Taking nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin can
increase the risk of peptic ulcer disease by four times compared to non-
users.
The gastric mucosa protects itself from gastric acid with a layer of mucus,
the secretion of which is stimulated by certain prostaglandins. NSAIDs block
the function of cyclooxygenase 1 (COX-1), which is essential for the
production of these prostaglandins.
10. Besides this, NSAIDs also inhibit stomach mucosa cells proliferation and
mucosal blood flow, reducing bicarbonate and mucus secretion, which
reduces the integrity of the mucosa.
11. Stress:
A stress ulcer is a single or multiple mucosal defect which can become
complicated by upper gastrointestinal bleeding or physiologic stress.
Ordinary peptic ulcers are found commonly in the gastric antrum and the
duodenum whereas stress ulcers are found commonly in fundic mucosa and
can be located anywhere within the stomach and proximal duodenum.
12. Diet:
Spices Consumption
Coffee and Caffiene
Similarly, while studies have found that alcohol consumption increases risk
when associated with H. pylori infection, it does not seem to independently
increase risk.
13. Other:
Other causes of peptic ulcer disease include gastric ischaemia, drugs,
metabolic disturbances, upper abdominal radiotherapy, Crohn's disease,
and vasculitis. Gastrinomas (Zollinger–Ellison syndrome), (Gastrinomas are
neuroendocrine tumors (NETs), usually located in the duodenum or
pancreas, that secrete gastrin and cause a clinical syndrome known as
Zollinger-Ellison syndrome (ZES).) also cause multiple and difficult-to-heal
ulcers
14. Classifications:
Peptic ulcers are a form of acid–peptic disorder. Peptic ulcers can be
classified according to their location and other factors.
By location
Duodenum (called duodenal ulcer)
Esophagus (called esophageal ulcer)
Stomach (called gastric ulcer)
15. Modified Johnson
Type I: Ulcer along the body of the stomach, most often along the lesser
curve at incisura angularis along the locus minoris resistantiae. Not associated
with acid hypersecretion.
Type II: Ulcer in the body in combination with duodenal ulcers. Associated
with acid oversecretion.
Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid
oversecretion.
Type IV: Proximal gastroesophageal ulcer.
Type V: Can occur throughout the stomach. Associated with the chronic use of
NSAIDs (such as ibuprofen).
16. Signs and symptoms
Signs and symptoms of a peptic ulcer can include one or more of the
following:
abdominal pain, classically epigastric, strongly correlated with mealtimes.
In case of duodenal ulcers, the pain appears about three hours after taking
a meal and wakes the person from sleep;
Aggravating Factor in DU is Hunger in GU is Eating
17. bloating and abdominal fullness;
waterbrash (a rush of saliva after an episode of regurgitation to dilute the
acid in esophagus, although this is more associated with gastroesophageal
reflux disease);
nausea and copious vomiting;
loss of appetite and weight loss, in gastric ulcer;
18. weight gain, in duodenal ulcer, as the pain is relieved by eating;
hematemesis (vomiting of blood); this can occur due to bleeding directly
from a gastric ulcer or from damage to the esophagus from severe/continuing
vomiting.
melena (tarry, foul-smelling feces due to presence of oxidized iron from
hemoglobin);
rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to
acute peritonitis and extreme, stabbing pain, and requires immediate
surgery.
19. Complications:
Gastrointestinal bleeding is the most common complication. Sudden large
bleeding can be life-threatening. It is associated with 5% to 10% death rate.
Perforation (a hole in the wall of the gastrointestinal tract) following a
gastric ulcer often leads to catastrophic consequences if left untreated.
Erosion of the gastrointestinal wall by the ulcer leads to spillage of the
stomach or intestinal contents into the abdominal cavity, leading to an
acute chemical peritonitis. The first sign is often sudden intense abdominal
pain
20. Penetration is a form of perforation in which the hole leads to and the ulcer
continues into adjacent organs such as the liver and pancreas.
Gastric outlet obstruction(stenosis) is a narrowing of the pyloric canal by
scarring and swelling of the gastric antrum and duodenum due to peptic
ulcers. The person often presents with severe vomiting.
Cancer is included in the differential diagnosis (elucidated by biopsy),
Helicobacter pylori as the etiological factor making it 3 to 6 times more likely
to develop stomach cancer from the ulcer. The risk for developing
gastrointestinal cancer also appears to be slightly higher with gastric ulcers
23. Management:
Eradication therapy
Once the diagnosis of H. pylori is confirmed, the first-line treatment would be
a triple regimen in which pantoprazole and clarithromycin are combined
with either amoxicillin or metronidazole. This treatment regimen can be
given for 7–14 days. However, its effectiveness in eradicating H. pylori has
been reducing from 90% to 70%. However, the rate of eradication can be
increased by doubling the dosage of pantoprazole or increasing the duration
of treatment to 14 days.
Quadruple therapy (pantoprazole, clarithromycin, amoxicillin, and
metronidazole) can also be used
24. NSAIDs induced ulcers
NSAID-associated ulcers heal in 6 to 8 weeks provided the NSAIDs are
withdrawn with the introduction of proton pump inhibitors (PPI)
25. Bleeding
For those with bleeding peptic ulcers, fluid replacement with crystalloids is
sometimes given to maintain volume in the blood vessels. Maintaining
haemoglobin at greater than 7 g/dL (70 g/L) through restrictive blood
transfusion has been associated with reduced rate of death
Early endoscopic therapy can help to stop bleeding by using cautery,
endoclip, or epinephrine injection. Treatment is indicated if there is active
bleeding in the stomach, visible vessels, or an adherent clot.
For those with hypovolemic shock and ulcer size of greater than 2 cm,
there is a high chance that the endoscopic treatment would fail. Therefore,
surgery and angiographic embolism are reserved for these complicated cases