The document discusses peptic ulcer disease, summarizing key points in 3 sentences:
Peptic ulcers are caused by an imbalance between aggressive and protective factors in the stomach and duodenum, most notably infection with Helicobacter pylori bacteria. Common symptoms of duodenal ulcers include abdominal pain relieved by food and potential complications of bleeding, perforation, and obstruction. Gastric ulcers can occur anywhere in the stomach and may be difficult to distinguish from gastric cancer, with bleeding and perforation being major risks.
surgeries involved in gastroenterology: gastrointestinal surgery, conditions treated with gastrointestinal surgeries,procedure and side effects of these surgeries, open gastrointestinal surgeries and minimally invasive gastrointestinal surgeries
Gastric Perforation From Peptic Ulcer Disease - A Review of the Surgical Trea...Joseph A. Di Como MD
A PowerPoint presentation reviewing gastric perforation for peptic ulcer disease and a review of the surgical treatment options. Intended for medical professionals and students.
surgeries involved in gastroenterology: gastrointestinal surgery, conditions treated with gastrointestinal surgeries,procedure and side effects of these surgeries, open gastrointestinal surgeries and minimally invasive gastrointestinal surgeries
Gastric Perforation From Peptic Ulcer Disease - A Review of the Surgical Trea...Joseph A. Di Como MD
A PowerPoint presentation reviewing gastric perforation for peptic ulcer disease and a review of the surgical treatment options. Intended for medical professionals and students.
5 Nursing Care Plans and Test Taking Skills1nurses
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5 Nursing Care Plans and Test Taking Skills1nurses
http://1nurses.com Grab this Exclusive report on 5 Surgeries namely Appendectomy,Cholecystectomy,Gastrectomy,Thyroidectomy and Cesarean Operation. Learn Test Taking Skills for your Nclex Exams.
This topic helps you , how to approach a patient having peptic ulcer disease and how to diagnose finally how to end up with treatment. Peptic ulcer disease a chronic disease of stomach and duodenum where the protective layer of stomach and duodenum weakens by many factors most common is H Pylori infection. Infection of H Pylori cause ulcer over time.
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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
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
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.
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
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.
3. Embryology
• Appear as fusiform dilatation of foregut
in the 4th week.
• Rotates 90* clockwise in longitudinal
axis
• Posterior wall elongates faster than
anterior wall- Greater and lesser
curvatures.
• Rotates in anteroposterior axis – caudal
or pyloric end towards right
4. Topography and relations
• Mobile
• Only fixed point of reference-
GEJ – left of midline behind 7th
costal cartilage @ T10 level
8. Lymphatics
• 4 zones:
• Zone I (inferior gastric) drains into the
subpyloric and omental nodes
• Zone II (splenic) drains into the
pancreaticosplenic nodes
• Zone III (superior gastric) drains into the
superior gastric nodes
• Zone IV (hepatic) drains into the suprapyloric
nodes
12. Regulation of gastric secretion
• Neural- Sympathetic or
parasympathetic
• Hormonal- Gastric peptides or
amines
13.
14. • Vagal control of gastric acid secretion
and potentiation by histamine and
gastrin.
15. Gastrin
• Produced by G cells – gastric antrum
• G-34 (big gastrin), G-17 (little gastrin), and G-14 (minigastrin)
• Pentapeptide sequence at the carboxyl terminus - is the biologically active component
• Release - stimulated by food - protein
• Major hormonal regulator of the gastric phase of acid secretion after a meal
16. • Has considerable trophic effects on the parietal cells and gastric ECL cells
• Prolonged hypergastrinemia leads to
• mucosal hyperplasia
• an increase in the number of ECL cells
• under some circumstances, is associated with the development of gastric carcinoid
tumors
19. Gastric Motility
• Regulated by extrinsic and intrinsic neural mechanisms and by myogenic control
• Fasting Gastric Motility
• Gastric pacemaker cells of cajal
• Slow waves travel at 3 cycles/minute in a circumferential and antegrade fashion
toward the pylorus
• Cyclical pattern of electrical activity - slow waves and electrical spikes, which has
been termed the Myoelectric Migrating Complex.
20. • Postprandial Gastric Motility
• Ingestion of a meal results in
• Decrease in the resting tone of the proximal stomach - receptive relaxation and
Fundus- gastric accommodation, respectively
• Repetitive forceful contractions of the midportion and antral portion of the stomach
• Food particles to be propelled against a closed pylorus, with subsequent retropulsion
of solids and liquids.
21. Gastric Barrier Function
• Gastric Mucus and Bicarbonate
• Gelatinous layer containing
• proteins, glycoproteins, mucopolysaccharide, and bicarbonate,
• Lines the superficial gastric epithelium
• Form a barrier between luminal contents and gastric mucosal cells.
• Neutralizes intraluminal acid - more physiologic pH at the mucosal surface
• maintains a steep pH gradient across it, which ranges from a pH of 2 on the luminal
side to a pH of 7 on the epithelial side
• Inhibitors of cyclooxygenase (COX), such as aspirin or nonsteroidal anti-inflammatory
drugs (NSAIDs) – inhibit mucus production
22. • Blood flow
• Reduced by more than 75%, marked mucosal injury results
• Injury exacerbated in the presence of luminal acid
• Restitution or reconstitution
• injured surface epithelial cells are replaced rapidly by the migration of surface
mucous cells located along the basement membranes.
• It occurs within minutes and does not require cell division
23. Peptic ulcer disease
• Epidemiology
• Pathogenesis
• Duodenal ulcers
• Gastric ulcers
• Both types tend to occur near mucosal junctions.
• Duodenal ulcers – duodenal-pyloric junction
• Gastric ulcers – oxynticantral junction, the antral-pyloric junction, or the
esophagogastric junction
24. Epidemiology
• defined as erosions in the gastric or duodenal mucosa that extend
through the muscularis mucosae
• Surgical treatment has declined since the advent of different acid
suppression strategies and eradication of H. pylori
• Complications – Bleeding, perforation and obstruction
• Perforation carries the highest mortality risk - upto 30%
25. Pathogenesis
• Peptic ulcers are caused by increased aggressive factors, decreased defensive factors, or
both.
• Damaging factors
• Hydrochloric acid secretion,
• Pepsins,
• Ethanol ingestion,
• Smoking,
• Duodenal reflux of bile,
• Ischemia,
• NSAIDs,
• Hypoxia,
• Most notably, H. pylori infection
26. Helicobacter pylori
• 80% to 95% of duodenal ulcers and
• Approximately 75% of gastric ulcers
• Primary causative factor in the pathogenesis of PUD
• Spiral or helical gram-negative rod with 4-6 flagella
that resides
• Resides in gastric-type epithelium within or beneath
the mucous layer
• Infection was associated with a twofold
• Increased risk of developing gastric cancer
Immunohistochemical staining
of H. pylori (brown) from a gastric biopsy
27. • Potent producer of urease
• Creates an alkaline microenvironment
• Splits urea into ammonia and bicarbonate, which is capable of splitting, in the setting
of an acidic gastric milieu microaerophilic
• Can live only in gastric epithelium
• Can also be found in heterotopic gastric mucosa
• In the proximal esophagus, in barrett esophagus,
• In gastric metaplasia in the duodenum,
• Within a meckel’s diverticulum, and
• In heterotopic gastric mucosa in the rectum
28. • Mechanisms responsible for H. pylori–induced GI injury
1. Production of toxic products that cause local tissue injury
• Ammonia, cytotoxins, mucinase, phospholipases
2. Induction of a local mucosal immune response
3. Increased gastrin levels with a resultant increase in acid secretion
• Basal and stimulated gastrin level increased – reduced antral D cells
4. Gastric metaplasia occurring in the duodenum
29. NSAIDs
• Risk for bleeding and ulceration is proportional to the daily dosage of NSAIDs
• Absorbed through the stomach and small intestine
• As systemic inhibitors of the cyclooxygenase enzymes
• Rate-limiting step of prostaglandin synthesis in the GI tract.
• Prostaglandins promote gastric and duodenal mucosal protection via numerous
mechanisms,
• Including increasing mucin and bicarbonate secretion
• And increasing blood flow to the mucosal endothelium
30. • a 2-fold to 10-fold increased risk for GI complications
• The risk for mucosal injury or ulceration is roughly proportional to the anti-inflammatory
effect associated with each NSAID
• H. pylori ulcers, - duodenum,
• NSAID-induced ulcers - stomach.
• H. pylori ulcers - chronic active gastritis,
• Whereas gastritis is not frequently found with NSAID-induced ulcers, occurring only
approximately 25% of the time.
• When NSAID use is discontinued, the ulcers usually do not recur.
31. • Acid
• Important but likely noncausative role
• In duodenal ulcers, there is a large overlap of acid levels between patients with ulcers
and normal subjects.
• Almost 70% of patients with duodenal ulcers have an acid output within the normal
range.
• For types I and IV gastric ulcers, which are not associated with excessive acid secretion,
acid acts as an important cofactor, exacerbating the underlying ulcer damage and
attenuating the ability of the stomach to heal.
• For patients with type II or III gastric ulcers, gastric acid hypersecretion seems to be more
common, and consequently these ulcers behave more like duodenal ulcers
32. Duodenal ulcers
• Requirements are acid and pepsin secretion in combination with infection by H. pylori or
ingestion of NSAIDs more common
• Secretory abnormalities relate to
• Decreased bicarbonate secretion,
• Increased nocturnal acid secretion,
• Increased duodenal acid load, and
• Increased daytime acid secretion
33. Gastric ulcers
• Occur anywhere in the stomach,
usually present on the lesser curvature
• Peak incidence of gastric ulcers
occurrence is between 55 and 65 years
of age
• Presence of acid appears to be
essential
• Rapid healing follows
• Antacid therapy,
• Antisecretory therapy, or
• Vagotomy,
• Even when the lesion-bearing portion of
the stomach is left intact
34. Clinical Manifestations
• Duodenal Ulcers
• Abdominal Pain
• most common symptom
• well-localized mid-epigastric
• Frequently relieved by food
• presence of constant pain suggests
• deeper penetration of the ulcer
• and referral of pain to the back – penetration into the pancreas
• Diffuse peritoneal irritation - free perforation.
35. • Perforation
• About 5%
• Penetrate through the duodenum into the free peritoneal cavity
• Elicit a chemical peritonitis
• Patient can typically recall the exact time of onset of abdominal pain
• Frequently accompanied by fever, tachycardia, dehydration, and ileus.
• Abdominal examination- exquisite tenderness, rigidity, and rebound
• Demonstration of free air underneath the diaphragm on an upright chest
radiograph.
36. • Bleeding
• Most common cause of death in patients
• Gastroduodenal artery
• Bleeding duodenal ulcers account for about 25% of all upper GI bleeding
patients.
37. • Obstruction.
• Acute inflammation of the duodenum - functional gastric outlet obstruction
• Manifested by
• Delayed gastric emptying, anorexia, or nausea accompanied by vomiting.
• Chronic inflammation of the duodenum - recurrent episodes of healing followed
by repair and scarring with, ultimately, fibrosis and stenosis of the duodenal
lumen
• Painless vomiting of large volumes of gastric contents with similar metabolic
abnormalities as seen in the acute situation.
• The stomach can become massively dilated in this setting and it rapidly loses its
muscular tone.
• Marked weight loss and malnutrition are also common in this situation.
38. • Gastric ulcer
• Clinical challenge in that it is often impossible to differentiate between gastric
carcinoma and benign ulcers
• Recurrent episodes
• Surgical intervention is required in 8% to 20%
• Most frequent - perforation
• along the anterior aspect of the lesser curvature.
• larger ulcers are associated with more morbidity and higher mortality rates
• Hemorrhage - 35% to 40% - at some point during the course of gastric ulceration
• Hemorrhage and Gastric Outlet Obstruction- type 2 and type 3 gastric ulcers