This document discusses ulcerative lesions of the intestines, including peptic ulcer disease, infectious causes like typhoid and tuberculosis, and inflammatory bowel disease like ulcerative colitis and Crohn's disease. It provides details on the definition, sites, epidemiology, etiology, pathogenesis, clinical features, investigations, management and complications of these conditions. Peptic ulcer disease is most commonly caused by H. pylori infection or NSAID use. Typhoid causes circumscribed ulcers in the ileum due to Salmonella typhi infection. Tuberculosis can cause ulcers in the ileocecal region. Ulcerative colitis causes continuous ulcers in the colon, while Crohn's disease causes transm
Gastric Cancer - Deifinition , epidemiology , histological types and molecular genetics and WHO update
Reference - WHO Classificiation of tumors of Digestive system
Rosai and Ackermann
Gastric Cancer - Deifinition , epidemiology , histological types and molecular genetics and WHO update
Reference - WHO Classificiation of tumors of Digestive system
Rosai and Ackermann
IT INCLUDES ANATOMY, PHYSIOLOGY AND PATHOLOGY OF LIVER .
THE SOURCES ARE:-
THE MEDICAL TEXT BOOK OF ROBBIN'S PATHOLOGY
AND OTHERS
IMAGES SOURCE :- ATLAS BOOKS AND INTERNET
This is a powerpoint slideshow discussing some of the commonest disorders of colon; namely Hirschsprung's disease, Diverticular diseases of colon, ulcerative colitis, pseudomembranous colitis and ischemic colitis.
IT INCLUDES ANATOMY, PHYSIOLOGY AND PATHOLOGY OF LIVER .
THE SOURCES ARE:-
THE MEDICAL TEXT BOOK OF ROBBIN'S PATHOLOGY
AND OTHERS
IMAGES SOURCE :- ATLAS BOOKS AND INTERNET
This is a powerpoint slideshow discussing some of the commonest disorders of colon; namely Hirschsprung's disease, Diverticular diseases of colon, ulcerative colitis, pseudomembranous colitis and ischemic colitis.
Principles of Virtual Reality In Surgical Training - Review by Sanjoy SanyalSanjoy Sanyal
This PPT was presented in 10th National Medical Dental Conference in Seychelles in February 2007. It has been reproduced on 'as is' basis. It was also presented in faculty and students's symposium in a medical school in Seychelles. Presenter is Dr Sanjoy Sanyal, (then) Associate Professor and Masters candidate in Royal College of Surgeons of Edinburgh / University of Bath
Typhoid enteric perforation: A febrile killer!KETAN VAGHOLKAR
Typhoid enteric perforation still happens to be the most lethal complication of typhoid fever. Even in urban settings the condition is misdiagnosed causing death. A careful history followed by aproper clinical examination can still help in proper and pronpt diagnosis of this condition.
Ulcerative colitis explanation, management and therapyYuliaDjatiwardani2
A chronic, inflammatory bowel disease that causes inflammation in the digestive tract.
Ulcerative colitis is usually only in the innermost lining of the large intestine (colon) and rectum. Forms range from mild to severe. Having ulcerative colitis puts a patient at increased risk of developing colon cancer.
Symptoms include rectal bleeding, bloody diarrhoea, abdominal cramps and pain.
Treatment includes medication and surgery.
Abdominal TB can involve any part of GIT from mouth to anus, the peritoneum and pancreato-billiary system.
Total EP TB accounts for about 10-12% of total no. of TB cases, out of which 11-16% are abdominal koch.
Sixth most frequent EP TB after lymphatics, genitourinary, bone & joint, milliary & meningeal TB.
Caused by M. tuberculosis, M. bovis & NTM.
Age group 20-40 most commonly affected & slight female preponderance has been described.
Before era of HIV infection > 80% TB was confined to lung
Extrapulmonary TB increases with HIV
40 –60% TB in HIV+ pt are extrapulmonary
Globally, proportion of co-infected pt > 8 %
~ 0.4 million people in India are co-infected.
In one study, 16.6% abdominal TB pt in Bombay was HIV +.
Mechanisms by which M. tuberculosis reach the GIT:
Hematogenous spread from primary lung focus
Ingestion of bacilli in sputum from active pulmonary focus.
Direct spread from adjacent organs.
Via lymph channels from infected LN
Rare Mechanism:
Contiguous spread of infection from a fallopian tube
TB peritonitis as complication of peritoneal dialysis
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
More than one site may be involved
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
More than one site may be involved
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
More than one site may be involved
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.
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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
3. PEPTIC ULCER DISEASE
DEFINITION
A circumscribed ulceration of the
gastrointestinal mucosa occurring in areas
exposed to acid and pepsin.
Sites:
Duodenum
Stomach
Oesophagus
Gastro-enterostomy stoma
Related to ectopic gastric mucosa (e.g. in Meckel’s
diverticulum)
4.
5. Epidemiology of PUD
Prevalence about 5-10%
Higher prevalence in low socioeconomic classes and
with certain diseases
Duodenal ulcer M/F: 3:1
Gastric ulcer equal in both sexes but increases with
age
Family history: 3-4 increased risk .
Cigarette smoking: ulceration increased
Emotional disturbances and Stress: increase gastric
acid secretion
6. Etiopathogenesis
•
•
•
•
•
•
H. Pylori: 70% of all cases.
Other causes include
NSAIDS
Alcohol
Gastritis
Socioeconomic status
Genetic factors
Stress –shock, sepsis or severe trauma
Burns(curling ulcer)
Head trauma (cushing ulcer)
7.
8. Helicobacter factors in
pathogenesis
Some strains are more pathogenic than others. The Cag
A (cytotoxic) antigen is one important virulence factor
Human variability also plays a part (e.g. individuals who
produce high levels of IL-1 in inflammation get pan
gastritis and Gastric ulcer, lower levels associated with
antral gastritis and Duodenal ulcer)
9. Duodenal Ulcers
duodenal sites are 4x as common as gastric sites
most common in middle age
peak 30-50 years
Male to female ratio—4:1
Genetic link: 3x more common in 1st degree relatives
more common in patients with blood group O
associated with increased serum pepsinogen
H. pylori infection common
up to 95%
smoking is twice as common
10. Gastric Ulcers
common in late middle age
incidence increases with age
Male to female ratio—2:1
More common in patients with blood group A
Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer
Less related to H. pylori than duodenal ulcers – about
80%
10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
11.
Symptoms of duodenal ulcer
disease:
epigastric pain 2 hours after meal or on a empty
stomach or during night
pyrosis
good nutrition
obstipation
seasonal dependence (spring, autumn)
12.
Symptoms of gastric ulcer disease:
epigastric pain after meal or during meal
upper dyspeptic syndrome – loss of appetite, nauzea,
vomiting, flatulence
vomitting brings relief
reduced nutrition
loss of weight
14. Diagnosis
Stool for fecal occult blood
Labs: CBC , liver function test, amylase and lipase.
Upper GI Endoscopy: Any pt >50 yrs with new onset of
symptoms or those with alarm markings including anemia,
weight loss, or GI bleeding.
15. Helicobacter pylori detection
Invasive( through
endoscopy)
Gastric biopsy and
staining
culture of Bx specimen
Tests using urease
enzyme in Bx
specimens
Bacterial DNA detection
by PCR
Non-invasive:
Urea breath test
H.pylori antibodies
Stool antigen
Salivary antigen
16. Staining methods of Helicobacter pylori
Warthin–Starry stain- The Warthin Starry stain (WS) is
a silver nitrate based staining method
Leung stain- It is a novel Alcian yellow-toluidine blue
(Leung) stain for H.pylori.
Methylene blue
17.
18.
19. Biopsy of peptic ulcer:
Biopsy is necessary to distinguish between benign and
malignant ulcers.
Biopsy should be taken from the ulcer edge, at least
from each quadrant.
Upto 10-12 biopsies may be taken to exclude cancer.
Repeat endoscopy may be necessary if biopsies are
negative and there is high index of suspicion.
20. Morphology of peptic ulcers
Clean, non-elevated
edge
Granulation tissue
base (floor)
Underlying fibrosis
24. Microscopic features
Thickening of vessels caused by subendothelial fibrous
proliferation.
Hypertrophy of nerve bundles.
Mucosa surrounding the ulcer is pyloric type.
Necrotic surface shows superimposed infection by
candida albicans.
In case of H. pylori infection following features are
noted
at the ulcer edge : loss of apical portion of cells,
dropout of epithelial cells,
erosion, cellular tufts.
25. Healing process
Regenerating epithelium grows over the surface.
Intestinal metaplasia
May contain chief and parietal cells (ulcer in the
fundus area)
Gastritis remains after ulcer has healed.
Cellular atypia may be present.
27. Differential Diagnosis
Neoplasm of the stomach
Pancreatitis
Pancreatic cancer
Diverticulitis
Nonulcer dyspepsia (also called functional dyspepsia)
Cholecystitis
Gastritis
GERD
MI—not to be missed if having chest pain
28. Natural history of PUD
PUD is a chronic episodic disease with relapses and
remissions.
If left untreated, 30-40 % of ulcers heal within 8
weeks.
Recurrence rate without treatment is 70% during first
year and 90% within 2 years.
Complications develop in 20% of PUD
29. Infectious causes
1. TYPHOID
Acute enteric infectious disease
caused by Salmonella typhi (S.Typhi).
Clinical features : prolonged fever, Relative bradycardia,
apathetic facial expressions, roseola, splenomegaly,
hepatomegaly, leukopenia.
Can lead to intestinal perforation, intestinal hemorrhage
31.
Pathogenesis
The amount of bacilli infection (>105bacteria)
Bacteria ingested orally
Stomach barrier (some Eliminated)
Enters the small intestine
Penetrate the mucus layer
Enter mononuclear phagocytes of ileal peyer's patches and
mesenteric lymph nodes
Proliferate in mononuclear phagocytes
spread to blood causing primary bacteremia (Incubation period).
32.
enter spleen, liver and bone marrow (reticulo-endothelial
system)
further proliferation occurs
A lot of bacteria enter blood again causing secondary
bacteremia.
Recovery
33. PATHOLOGY
Proliferation of RES (reticuloendothelial system )
Specific changes in lymphoid tissues and mesenteric
lymph nodes."typhoid nodules―
Most characteristic lesion:
Ulceration of mucosa in the region of the Peyer’s patches of
the small intestine
35. Major findings in lower ileum
Hyperplasia stage(1st week):
swelling lymphoid tissue and proliferation of macrophages.
Necrosis stage(2nd week):
necrosis of swelling lymph nodes or solitary follicles.
Ulceration stage(3rd week):
Oval ulcer with its long axis parallel to the small intestine , this results
from sloughing and shedding of necrotic lymphoid tissue in the
peyers patches leading to intestinal hemorrhage, perforation .
Stage of healing (from 4th week):
healing of ulcer, no cicatrices and no contraction
36. 2. Gastrointestinal Tuberculosis
•
•
•
Abdominal tuberculosis is usually secondary to pulmonary
tuberculosis
Sites:
The ileocecal region is the most common area of involvement in
the gastrointestinal tract due to the abundance of lymphoid
tissue.
The natural course of gastrointestinal tuberculosis may be
Ulcerative
hypertrophic or
ulcer hypertrophic.
37. Clinical presentation
Abdominal pain mimicking peptic ulcer disease with
stomach or duodenal infection;
Malabsorption with infection of the small intestine;
Pain, diarrhea, or hematochezia with infection of the
colon.
40.
3. AMOEBIC ULCER
The causative organism is parasitic protozoan, called
Entamoeba histolytica.
Site: It usually involves caecum and ascending
colon followed by sigmoid colon, rectum, and appendix.
In severe cases the entire colon is involved.
The spectrum of colitis in amoebiasis ranges from
mucosal thickening, to multiple cyst formation, to diffuse
Inflammation / oedema, to necrosis and perforation of
colonic wall.
41. Life cycle
Mouth - Cyst ingested
Excyst to trophozoite
Passed in stool
Amoebic disease
Cyst
Trophozoite
Invades gut mucosa – cyst formation
42. Clinical presentation
•
•
•
•
•
•
Gradual onset of bloody diarrhoea
Abdominal pain and tenderness.
Leucocytes and pus may be present in stool.
Fever present in <40% of patients.
Weight loss and anorexia can be present.
Local inflammatory masses, amoebomas, may cause
obstructive symptoms
43.
Gross features:
Begin as small foci of necrosis that progress to ulcers.
In the early stages the colonic ulcers have a narrow neck
and thus appear as small nodules
As the ulcers enlarge they always retain their undermined
base but the ulcerated area of the mucosa becomes
larger.
The base of the ulcer is covered by grey - white exudate.
There is always undenuded mucosa between the ulcers.
44.
Microscopic features:
The ulcer is typically 'flask- shaped' and the broad base is
composed of fibrin and cellular debris.
A sharp line divides the necrotic and viable mucosa
Trophozoites are found on the surface of the ulcers, in the
exudate and in the crater.
They are frequently found in the submucosa, muscularis
propria, serosa.
45.
46.
47. ― IBD is a set of
chronic
inflammatory
conditions resulting
from inappropriate
and persistent
activation of the
mucosal immune
system ,driven by
the presence of
normal intestinal
flora.‖
48. HISTORY
ULCERATIVE COLITIS
•
First officially described by Wilks and Moxon in 1875.
• Before this discovery , all the diarrheal diseases were
believed to be caused by infectious agents and bacteria.
49. Crohn’s disease
•
In 1913 Dr Dalziel described transmural intestinal
inflammation in 13 autopsied patients.
•
In 1930 Burril Crohn described TERMINAL
ILEITIS first .
50. Epidemiology of IBD
Ulcerative colitis Crohn’s disease
Incidence (US)
11/100 000
7/100 000
Age of onset
15-30 & 60-80
15-30 & 60-80
Male:female ratio
Smoking
1:1
May prevent
disease
1.1-1.8:1
May cause disease
Oral contraceptive No increased risk Relative risk
Appendectomy
Not protective
Monozygotic twins 8% concordance
Protective
67% concordance
52. GENETIC
•
Genome wide scanning with microsatellite DNA markers
has identified several genetic sites as being potentially
associated with UC or CD.
•
Significant linkages have been reported on
chromosomes 1, 3, 6, 7, 12, 14, 16, and 19.
•
One of the clearest linkages is for IBD-1, a susceptibility
locus in the pericentromeric region of chromosome 16.
53. •
Detailed analysis has resulted in the identification of the
nucleotide-binding oligomerization domain 2 (NOD2)
gene and protein.
•
NOD2 is also known as caspase activation and
recruitment domain 15 (CARD15).
•
This is a polymorphic gene, the product of which is
involved in the innate immune system.
54. NOD2 PROTEIN
EXPRESSED IN macrophages / monocytes
FUNCTION AS AN INTRACELLULAR RECEPTOR
MICROBES
TRIGGER NF- kB pathway
NOD2 gene
mutation
CYTOKINES AND OTHER PROTEINS
INNATE IMMUNE DEFENSE MECHANISM
DOWN REGULATION OF INNATE IMMUNITY
LEADS TO INFLAMMATORY BOWEL
55. Abnormal host immunoreactivity
IBD is characterized by immunoregulatory defects in the
mucosa, which appear to be associated with microbial
exposure.
A number of theories have been advanced concerning the
pathogenesis of this process:
- dysfunctional immune host response to
normal
luminal component
- infection with a specific pathogen
- defective mucosal barrier to luminal antigens.
56. •
•
It is hypothesized that exposure to commensal bacteria
down-regulates the inflammatory genes and blocks
activation of the NF-kB pathway, thus inhibiting the
inflammatory immune response of the gut to the
microbes and food antigens to which it is constantly
exposed.
58.
Defective barrier function
IBD is associated with increased permeability of
the epithelial lining of the gut resulting in continuous
stimulation of the mucosal immune system.
Luminal bacteria appear to intensify the
permeability defect further, establishing a self-sustaining
cycle of mucosal inflammation that allows for uptake and
translocation of bacteria.
59. Ulcerative colitis
Is an inflammatory disease involving only the large
intestine.
The inner lining or mucosa of the intestine becomes
inflamed and develops ulcers.
Always starts in rectum and is continuous until some
proximal part of the colon.
Involves the mucosa and submucosa
60. sites
40-50% of patients have disease limited to the rectum
and rectosigmoid
30-40% of patients have disease extending beyond the
sigmoid
20% of patients have a total colitis
Proximal spread occurs in continuity without areas of
uninvolved mucosa
61. Ulcerative colitis – clinical presentation
The major symptoms of UC are:
- diarrhea
- rectal bleeding
- tenesmus
- passage of mucus
- crampy abdominal pain
62. Ulcerative colitis – macroscopic
features
Mucosa is :
- erythematous, has a granular surface that looks like a
sand paper
In more severe diseases:
- hemorrhagic, edematous and ulcerated
In fulminant disease a toxic colitis or a toxic megacolon
may develop ( wall become very thin and mucosa is
severly ulcerated)
64. Ulcerative colitis – microscopic
features
Process is limited to the mucosa and submucosa with
deeper layer unaffected
Two major histologic features:
- the crypt architecture of the colon is distorted
- some patients have basal plasma cells and multiple
basal lymphoid aggregates
70. Ulcerative colitis - complications
Hemorrhage
Perforation
Stricture
Toxic megacolon (transverse colon with a diameter of
more than 5 to 6 cm with loss of haustration)
72. Crohn’s disease (CD)
Also referred to as granulomatous or regional
enteritis, granulomatous ileitis, ileocolitis
Can have non-continuous pattern-‖skip lesions‖, with
areas of severe inflammation with intervening
normal mucosa
Most frequently affects distal third of small intestine
and the colon
Affects all layers of the affected bowel
73. sites
Can affect any part of GI tract from the mouth to the
anus
30-40% of patients have small bowel disease alone
40-55% of patients have both small and large intestines
disease
15-25% of patients have colitis alone
In 75% of patients with small intestinal disease the
terminal ileum in involved in 90%
74. Crohn’s disease – sign and
symptoms
Ileocolitis
- right lower quadrant pain and diarhhea
- palpable mass, fever and leucocytosis
- pain is colickly and relieved by defecation
Jejunoileitis
- inflammatory disease is associated with loss of digestive
and absorptive surface
75. Crohn’s disease – sign and
symptoms
Colitis and perianal disease
- low grade fever, malaise, diarrhea, crampy abdominal
pain, sometimes hematochezia
- pain is caused by passage of fecal material through
narrowed and inflamed segments of large bowel
Gastroduodenal disease
- nausea, vomiting, epigastric pain
- second portion of duodenum is more commonly involved
than the bulb
76. Crohn’s disease – macroscopic
features
CD is a transmural process
CD is segmental with skip areas in the midst of diseased
intestine
In one –third of patients with CD perirectal fistulas,
fissures, abscesses, anal stenosis are present
78. Crohn’s disease – macroscopic
features
mild disease is characterized by:
aphtous or small superficial ulcerations
In more active disease:
stellate ulcerations fuse longitudinally and transversely to
demarcate island of mucosa that are histologically
normal
Cobblestone appearance is characteristic of CD
82. M/E :
Mucosal inflammation
Mucosa normal and retain mucus.
Well-defined focus of inflammatory cells
surrounded by non inflammed and normal mucosa
As the disease establish , neutrophils infiltrate isolated
crypts – abscess – ultimate destruction.
86. A - Mucosal
Granuloma
eroding a crypt of
lieberkhun and
initiating crypt
abscess
formation.
B - Crypt
obliterated by
Granuloma
formation
87. •
Non Caseating Granuloma-in ½ cases , Sarcoid
Granuloma in all tissue layers.
Others:
•
In diseased segments muscularis mucosa exhibits
reduplication ,
strictures.
thickening, irregularity's leads to
like,
90. Complications of Crohn's Disease:
Perianal fistulas
Perianal skin ulceration
Increased incidence of gall and kidney stones (due to
malabsorption of fats and bile salts)
92. Risk of Malignancy in IBD
In Crohn’s disease, increased risk of cancer of the
affected areas is seen
In ulcerative colitis, 8-10 years after initial
diagnosis, there is a steady, significant increased
risk of developing cancer
Prognostic factors increasing malignancy risk in
UC:
• Duration of disease 10 yrs or more
• Pancolonic involvement
• Continuous progressive disease
• Severe initial onset
• Associated liver disease
93. Gross :
Thick mucosa with finely nodular or velvety surface
configuration.
Lesion polypoid , elevated , nodular or villous formation.
94. M/E :
Adenocarcinoma with varying degree of
differentiation .
Always accompanied by dysplastic changes .
95. Evaluation of Dysplasia
1 - Negative for Dysplasia.
2 - Indefinite for Dysplasia,probably Negative.
3 - Indefinite for Dysplasia, Unknown.
4 - Indefinite for Dysplasia,probably Positive.
5 - Positive for Dysplasia,Low Grade.
6 - Positive for Dysplasia,High Grade.
96.
97.
98.
99. Lab Findings in IBD
CBC’s:
Anemia is common due to blood loss or
malabsorption
Leukocytosis & thrombocytosis also common
ESR typically elevated; monitors disease activity
Abnormal LFTs may represent pericholangitis or
sclerosing cholangitis
Low serum albumin (protein-losing enteropathy)
suggests extensive colitis
100. Features
UC
CD
Rectal Bleeding
Common
Inconspicuous
Abdominal mass
Practically never
10-15%
Abdominal pain
Left sided
Right sided
Sigmoidoscopy
Abnormal 95%
Abnormal <50%
Free perforation
12%
04%
Colon CA
2%
Rare
Anal complications
Minor
75%, fissures, fistulas,
ulceration
Response to steroid
75%
25%
Result of surgery
Good
Fair
Clinical
101. Features
UC
CD
Sparing of rectum
Exceptional
90%
Involvement of ileum
Rare
Common
Strictures
Absent
Present
Skip areas
Absent
Common
Internal fistula
Absent
May be present
Longitudinal and transverse
ulcers
Exceptional
Common
Fissuring
Absent
Common
Radiographic
102. Features
UC
CD
Distribution of involvement
Diffuse
Focal
Mucosal atrophy
Marked
Minimal
Cytoplasmic Mucin
Diminished
Preserved
Lymphoid aggregates
Rare
Common
Edema
Minimal
Marked
Hyperemia
May be extreme
Minimal
Granulomas
Absent
Present in 60%
Fissuring
Absent
Present
Crypt abscesses
Common
Rare
Rectal involvement
Practically always
50%
Morphologic
The most important contributing factors are H pylori, NSAIDs, acid, and pepsin. Additional aggressive factors include smoking, ethanol, bile acids, aspirin, steroids, and stress.Important protective factors are mucus, bicarbonate, mucosal blood flow, prostaglandins, hydrophobic layer, and epithelial renewal. When an imbalance occurs, Peptic ulcer ds might develop
--H Pylori Causes intense inflammatory and immune response. (Inter leukinL-1, IL-6, TNF, IL-8).it Enhance gastric acid secretion and impairs duodenal bicarbonate production
--------Rapid urease tests are considered the endoscopic diagnostic test of choice. The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori are present, bacterial urease converts urea to ammonia, which changes pH and produces a color change
Picture shows Clusters of bacteria on Warthin–Starry staining. WS stains organisms dark brown to black, and the background light golden brown/golden yellow.
The 1st figure shows Hpylori with leung stain…2nd figure shows rod shaped bacilli satained with methylene blue in the gastric pit.
--PETIC ulcer are 4x more common in proximal duodenum then in stomach.they are solitary in more then 80% of patient.classic peptic ulcer is round to oval sharpely punched out defect.this is endoscopic view of peptic ulcer showing….
This is a gross view of a chronic gastric ulcer showingruggae. There is “punched-out” defect with sharp, overhanging margins
Picture shows duodenal peptic ulcer located in first portion of duodenum
Picture shows cross-section of a duodenal ulcer crater with an acute inflammatory exudate
This is picture showing pathogenesis of typhoid fever…
Picture shows circumfential ulceration which is characteristic of intestinal TB
Entamoebahistolytica has a biphasic life cycle, existing in two forms; as an infectious cyst and an amoeboid trophozoite. Transmission is by feco-oral route.
-----------In more severe cases fulminant amoebic colitis develops. Liver involvement is more common in these cases,
-----------------------Muscle coat of the large intestine form a barrier to the penetrating trophozoites which fan out laterally producing a flask-shaped ulcer with narrow neck and broad base.
--------There is little inflammatory response in the early ulcers.
Picture showing amebic colitis,multiple undermined ulcers are present in cecum and ascending colon.
Picture shows Histological cross section of classical flask shaped amoebic ulcer in colonic mucosa
-----------It Refers to two chronic diseases that cause inflammation of the intestines:ulcerative colitis and Crohn's disease.
UC- chemicals in tobacco especially nicotine has a protective effect by increasing the mucus production in the colon and rectum. It also suppresses the immune system and prevents inflammation. But in CD- such chemicals like nicotine, CO, free radicals acts as immunosuppressants on macrophages thus many harmful bacteria cannot be cleared from the gut, they may also lead to restricion in blood flow inside the gut walls thus making intestine more susceptible to develop crohnsds.
The NOD2 gene is expressed mainly in monocyte/macrophage cell lines, where it has a role in host-signaling pathways. One effect is the activation of nuclear factor (NF)-kB Activation leads to production of a wide variety of nonspecific mediators of inflammation like cytokines, growth factors, and metabolites of arachidonic acid and reactive oxygen ultimately lead to tissue destruction
------Inibd Exposure to luminal micro flora triggers an inflammatory response by the cells lining the mucosa, leading to a chronic, destructive immune response.
------------------------ A number of reports suggest a link between Crohnds and early measles infection.
Picture showing
Picture shows chronic form of ulcerative colitis with mucosal ulceration and residual foci of elevated and hyperimic mucosa.
The luminal border is irregular; the colonic crypts have lost their parallel arrangement, and they are branched and budded. The muscularismucosae is hypertrophied.
The luminal border is irregular. Increased inflammatory cells are present within the lamina propria.
Picture showing toxic megacolon.it is complication of ulcerative colitis..
This slide shows a segment of intestine with Crohn’s disease. This disease does NOT involve bowel in a uniform manner, i.e., there are skip areas. It is a disease, however, in which the affected segments are involved in their entire thickness: mucosa, submucosa, muscularis, and serosa –a transmural involvement
Picture shoeing Cobblestone lesions" usually in terminal ileum and "skip lesions" which are discontinuous areas of inflammation, edema and fibrosis
Crohn colitis demonstrating the "focal active colitis" pattern of injury showing infiltration of chronic inflammatory cells in the lamina propria.
this is a picture showing chronic crohns colitis..the branched crypt is feature of chronicity..
This is a picture showing noncaseatinggranuloma is present in the lamina propria of an uninvolved region of colonic mucosa
This diagram shows Lymphocytic inflitration and the formation of non-caseatinggranuloma.
Picture showing low grade dysplasia with chronic ulcerative colitis.
Cbc-complete blood count
This slide shows differentiating features between ulcerative colitis and crohns ds.1st clinical feature
This diagram shows distribution of lesions in inflammatory bowel disease.the distinction between crohnds and ulcerative colitis is primarily based on morphology.Incrohnds there are skip lesions but in ulcerative colitis there is continuos colon involvement.incrohns ulceration and fissure are seen and in ulcerative there is pseudopolyp are characteristic.