Crohn's disease is a type of inflammatory bowel disease that can affect any part of the gastrointestinal tract. It is characterized by patchy areas of inflammation that can involve both the small intestine and colon. Common symptoms include abdominal pain, diarrhea, and weight loss. Microscopically, Crohn's disease shows non-caseating granulomas in 35% of cases. It has variable presentation and a course of flare-ups and remissions. Smoking increases the risk of developing Crohn's disease.
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease. The immune system attacks the body’s cell and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but most often harms the heart, joints, skin, lungs, blood vessels, liver, kidney and nervous system.
Over 40 different genes predispose to SLE.
Characterized by remission and exacerbation.
inflammatory bowel disease is a diagnosis of exclusion and it has two form known as crohn's disease which can affect all GI tract from ''gum to bum'' with skip lesion and the formation of cobblestones. ulcerative colitis affect only the colon and also causes proctitis and toxic megacolon. both of the disease has extraGI symptoms like sclerosing cholangitis, uveitis, ankylosing spondylitis,conjunctivitis, liver cirrhosis, pyoderma gangrenosum, arthropathy and althralgia, etc .
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease. The immune system attacks the body’s cell and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but most often harms the heart, joints, skin, lungs, blood vessels, liver, kidney and nervous system.
Over 40 different genes predispose to SLE.
Characterized by remission and exacerbation.
inflammatory bowel disease is a diagnosis of exclusion and it has two form known as crohn's disease which can affect all GI tract from ''gum to bum'' with skip lesion and the formation of cobblestones. ulcerative colitis affect only the colon and also causes proctitis and toxic megacolon. both of the disease has extraGI symptoms like sclerosing cholangitis, uveitis, ankylosing spondylitis,conjunctivitis, liver cirrhosis, pyoderma gangrenosum, arthropathy and althralgia, etc .
It discusses investigations useful in diagnosis of inflammatory bowel disease and their important findings e.g Barium enema, histopathology, a word about indeterminate colitis and followed by discussion of possible etiologies to be ruled out before diagnosing IBD
Join us for a lecture on inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. Roger S. Klein, MD, FACP, will highlight the latest in diagnostic technologies and treatment approaches for IBD. He also will discuss the importance of comprehensive care to help prevent IBD-associated health problems.
A brief introduction to the IBD and its classification. Mainly dealing here with the Imaging techniques used in the diagnosis of the IBD.
Inflammatory bowel disease (IBD) is an idiopathic disease caused by a dysregulated immune response to host intestinal microflora. The two major types of inflammatory bowel disease are ulcerative colitis (UC), which is limited to the colon, and Crohn disease (CD), which can affect any segment of the gastrointestinal tract from the mouth to the anus, involves "skip lesions," and is transmural. There is a genetic predisposition for IBD, and patients with this condition are more prone to the development of malignancy.
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.
This is a presentation detailing facts about abdominal tuberculosis. Intended for healthcare professionals and medical students
Dr Manoj K Ghoda
Gujarat Gastro Group
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
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.
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.
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.
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
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.
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.
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
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.
3. Introduction
• Crohn’s Disease is an idiopathic, chronic, transmural
inflammatory process of the bowel that can affect
any part of the gastro intestinal tract from the mouth
to the anus.
• Most cases involve the small bowel, particularly the
terminal ileum.
4. Crohn’s Disease
• Crohn's disease seems to run in some families. It can
occur in people of all age groups but is most often
diagnosed in young adults.
5. Burrill Bernard Crohn
BBC
(June 13, 1884 – July 29, 1983) was an
American gastroenterologist
and one of the first to describe the disease for
which he is known, Crohn's diseas .
7. Prevalence
• Higher number of cases of Crohn’s disease found in
western industrialized nations.
• Males and females are equally affected.
• Smokers are three times more likely to develop
Crohn's disease.
• Crohn's disease tends to present initially in the teens
and twenties.
8. Classification of CD
On the area of the gastrointestinal tract which it
affects:
• Ileocolic Crohn's disease: Affects both the ileum
and the large intestine (50%)
• Crohn's ileitis: Affects the ileum only (30%)
• Crohn's colitis: Affects the large intestine,
accounts for the remaining twenty percent of
cases.
9. Classification of CD
On the behavior of disease as it progresses:
• Stricturing disease causes narrowing of the bowel
which may lead to bowel obstruction or changes in the
caliber of the feces.
Stricturing
10. Classification of CD
• Penetrating disease creates abnormal passage ways between
the bowel and other structures such as the skin.
• Inflammatory disease causes inflammation without causing
strictures or fistulae.
Inflammatory Penetrating
11. Morphology
Crohn disease may occur in any area of the GI
tract, but the most common sites involved at
presentation are the terminal ileum,
ileocecal valve, and cecum.
12. Disease is limited to the small intestine alone
in about 40% of cases; the small intestine
and colon are both involved in 30% of
patients; and the remainder have only
colonic involvement.
13. • The presence of multiple, separate, sharply
delineated areas of disease, resulting in skip
lesions, is characteristic of Crohn disease and
may help in the differentiation from
ulcerative colitis. Strictures are common.
14. • The earliest Crohn disease lesion, the
aphthous ulcer, may progress, and multiple
lesions often coalesce into elongated,
serpentine ulcers oriented along the axis of
the bowel. Edema and loss of the normal
mucosal texture are common.
15. • Sparing of interspersed mucosa, a result of
the patchy distribution of Crohn disease,
results in a coarsely textured, cobblestone
appearance in which diseased tissue is
depressed below the level of normal mucosa
16. Fissures frequently develop between mucosal folds
and may extend deeply to become fistula tracts or
sites of perforation.
17. The intestinal wall is thickened and rubbery as
a consequence of transmural edema,
inflammation, submucosal fibrosis, and
hypertrophy of the muscularis propria, all of
which contribute to stricture formation.
18. • In cases with extensive transmural disease,
mesenteric fat frequently extends around the
serosal surface (creeping fat) .
19. • The microscopic features of active Crohn
disease include abundant neutrophils that
infiltrate and damage crypt epithelium.
Clusters of neutrophils within a crypt are
referred to as crypt abscesses and
are often associated with crypt destruction.
20. • Ulceration is common in Crohn disease, and
there may be an abrupt transition between
ulcerated and adjacent normal mucosa. Even
in areas where gross examination suggests
diffuse disease, microscopic pathology can
appear patchy.
21. • Repeated cycles of crypt destruction and
regeneration lead to distortion of mucosal
architecture; the normally straight and
parallel crypts take on bizarre branching
shapes and unusual orientations to one
another.
22. • Epithelial metaplasia, another consequence of
chronic relapsing injury, often takes the form of
gastric antral-appearing glands, and is called
pseudopyloric metaplasia. Paneth cell
metaplasia may also occur in the left colon,
where Paneth cells are normally absent. These
architectural and metaplastic changes may
persist even when active inflammation has
resolved. Mucosal atrophy, with loss of crypts,
may occur after years of disease.
23. • Noncaseating granulomas, a hallmark of Crohn
disease, are found in approximately 35% of
cases and may occur in areas of active disease
or uninvolved regions in any layer of the
intestinal wall. Granulomas may also be present
in mesenteric lymph nodes. Cutaneous
granulomas form nodules that are referred to
as metastatic Crohn disease. The absence of
granulomas does not preclude a diagnosis of
Crohn disease.
24. Gross pathology of Crohn disease. A, Small-intestinal stricture. B, Linear mucosal
ulcers and thickened intestinal wall. C, Perforation and associated serositis. D,
Creeping fat.
25. Microscopic pathology of Crohn disease. A, Haphazard crypt organization results
from repeated injury and regeneration. B, Noncaseating granuloma. C, Transmural
Crohn disease with submucosal and serosal granulomas (arrows).
26. Symptoms
• Onset of Crohn's disease is between 15-30
years of age.
• People with Crohn's disease will go through
periods of flare-ups and remission.
27. Common symptoms of Crohn's disease:
• abdominal pain
• diarrhoea
• weight loss
Less common symptoms include:
• poor appetite
• fever, night sweats
• rectal pain/rectal bleeding
Some patients with Crohn's disease also develop symptoms outside of
the gastrointestinal tract; these symptoms include:
• arthritis
• skin rash
• inflammation of the iris of the eye.
Symptoms
28. Clinical Features
• The clinical manifestations of Crohn disease
are extremely variable. In most patients
disease begins with intermittent attacks of
relatively mild diarrhea, fever, and
abdominal pain.
29. • Approximately 20% of patients present
acutely with right lower quadrant pain, fever,
and bloody diarrhea that may mimic acute
appendicitis or bowel perforation. Periods of
active disease are typically interrupted by
asymptomatic periods that last for weeks to
many months.
30. • Disease re-activation can be associated with
a variety of external triggers, including
physical or emotional stress,
• specific dietary items, and
• cigarette smoking.
31. • Smocking is a strong exogenous risk factor
for development of Crohn disease and, in
some cases, disease onset is associated with
initiation of smoking. Unfortunately, smoking
cessation does not result in disease
remission.
32. • Iron-deficiency anemia may develop in
individuals with colonic disease, while
extensive small bowel disease may result in
serum protein loss and hypoalbuminemia,
generalized nutrient malabsorption, or
malabsorption of vitamin B12 and bile salts.
Fibrosing strictures, particularly of the
terminal ileum, are common and require
surgical resection.
33. • Disease often recurs at the site of
anastamosis, and as many as 40% of patients
require additional resections within 10 years.
Fistulae develop between loops of bowel and
may also involve the urinary bladder, vagina,
and abdominal or perianal skin. Perforations
and peritoneal abscesses are common.
34. Extra-intestinal manifestations of
Crohn disease
uveitis,
migratory polyarthritis,
sacroiliitis,
ankylosing spondylitis,
erythema nodosum, and
clubbing of the fingertips, any of which may
develop before intestinal disease is
recognized.
35. Pericholangitis and primary sclerosing
cholangitis occur in Crohn disease but are
more common in ulcerative colitis. Risk of
colonic adenocarcinoma is increased in
patients with long-standing colonic disease.
36. Comparisons of various factors in Crohn's disease and ulcerative
colitis
Crohn's DiseaseCrohn's Disease Ulcerative ColitisUlcerative Colitis
Involves terminal ileumInvolves terminal ileum CommonlyCommonly SeldomSeldom
Involves colon?Involves colon?
Involves rectum?Involves rectum?
UsuallyUsually
SeldomSeldom
AlwaysAlways
UsuallyUsually
Peri-anal involvementPeri-anal involvement CommonlCommonl SeldomSeldom
Bile duct involvement?Bile duct involvement? Not associatedNot associated Higher rate of PrimaryHigher rate of Primary
sclerosing cholangitissclerosing cholangitis
Distribution of DiseaseDistribution of Disease Patchy areas ofPatchy areas of
inflammationinflammation
Continuous area ofContinuous area of
inflammationinflammation
EndoscopyEndoscopy Linear and serpiginousLinear and serpiginous
(snake-like) ulcers(snake-like) ulcers
Continuous ulcerContinuous ulcer
Depth of inflammationDepth of inflammation May be transmural, deepMay be transmural, deep
into tissuesinto tissues
Shallow, mucosalShallow, mucosal
37. Fistulae, abnormalFistulae, abnormal
passageways betweenpassageways between
organsorgans
CommonlyCommonly SeldomSeldom
BiopsyBiopsy Can have granulomataCan have granulomata Crypt abscesses andCrypt abscesses and
cryptitiscryptitis
Surgical cure ?Surgical cure ?
SmokingSmoking
Often returns followingOften returns following
removal of affectedremoval of affected
partpart
Higher risk for smokersHigher risk for smokers
Usually cured byUsually cured by
removal of colon, canremoval of colon, can
be followed bybe followed by
po uchitispo uchitis
Lower risk for smokersLower risk for smokers
Autoimmune diseaseAutoimmune disease Generally regarded asGenerally regarded as
an autoimmunean autoimmune
diseasedisease
No consensusNo consensus
Cancer risk?Cancer risk? Lower than ulcerativeLower than ulcerative
colitiscolitis
Higher than Crohn'sHigher than Crohn's
Comparisons of various factors in Crohn's disease and UC (Cont.)
38. Features UC CD
Morphologic
Distribution Diffuse,mucosal
&submucosal,
left sided
Focal, trans-
mural, right
sided
Mucosal atrophy Marked Minimal
Cytoplasmic mucin ↓ Preserved
Lymphoid aggregate Rare Common
Edema Minimal marked
41. Ulcerative Colitis
• Ulcerative colitis is a disease that causes ulcers in the
lining of the rectum and colon. Ulcers form where
inflammation has killed the cells that usually line the
colon.
• Ulcerative colitis can happen at any age, but it
usually starts between the ages of 15 and 30. It tends
to run in families.
42.
43.
44. Symptoms
Common symptoms of ulcerative colitis include:
• rectal bleeding and diarrhoea
• Variability of symptoms reflects differences in the extent of
disease (the amount of the colon and rectum that are
inflamed) and the intensity of inflammation.
• Generally, patients with inflammation confined to the rectum
and a short segment of the colon adjacent to the rectum have
milder symptoms and a better prognosis than patients with
more widespread inflammation of the colon.
45. Ulcerative Colitis
• Ulcerative proctitis refers to inflammation that is limited to the rectum. In
many patients with ulcerative proctitis, mild intermittent rectal bleeding
may be the only symptom. Other patients with more severe rectal
inflammation may, in addition, experience rectal pain, urgency (sudden
feeling of having to defecate and a need to rush to the bathroom for fear
of soiling), and tenesmus (ineffective, painful urge to move one's bowels).
• Proctosigmoiditis involves inflammation of the rectum and the sigmoid
colon (a short segment of the colon contiguous to the rectum). Symptoms
of proctosigmoiditis, like that of proctitis, include rectal bleeding, urgency,
and tenesmus. Some patients with proctosigmoiditis also develop bloody
diarrhea and cramps.
46. Ulcerative Colitis
• Left-sided colitis involves inflammation that starts at the rectum and extends up
the left colon (sigmoid colon and the descending colon). Symptoms of left-sided
colitis include bloody diarrhoea, abdominal cramps, weight loss, and left-sided
abdominal pain.
• Pancolitis or universal colitis refers to inflammation affecting the entire colon
(right colon, left colon, transverse colon and the rectum). Symptoms of pancolitis
include bloody diarrhoea, abdominal pain and cramps, weight loss, fatigue, fever,
and night sweats.
• Fulminant colitis is a rare but severe form of pancolitis. Patients with fulminant
colitis are extremely ill with dehydration, severe abdominal pain, protracted
diarrhea with bleeding, and even shock. They are at risk of developing toxic
megacolon (marked dilatation of the colon due to severe inflammation) and colon
rupture (perforation).