Crohn's disease and ulcerative colitis are the two main forms of inflammatory bowel disease. Crohn's can affect any part of the gastrointestinal tract and is characterized by transmural inflammation and granulomas. Ulcerative colitis only affects the colon and causes superficial ulcers. Both conditions are diagnosed based on symptoms, endoscopic findings, and histology. Treatment involves medications to induce and maintain remission as well as surgery for complications.
UC is an idiopathic IBD that affects the colonic mucosa.
Hallmark of UC is bloody diarrhea often with prominent symptoms of rectal urgency and tenesmus.
The clinical course is marked by exacerbations and remissions.
The diagnosis of UC is suspected on clinical grounds and supported by the appropriate findings on
Proctosigmoidoscopy or colonoscopy
Biopsy
By negative stool examination for infectious causes
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
UC is an idiopathic IBD that affects the colonic mucosa.
Hallmark of UC is bloody diarrhea often with prominent symptoms of rectal urgency and tenesmus.
The clinical course is marked by exacerbations and remissions.
The diagnosis of UC is suspected on clinical grounds and supported by the appropriate findings on
Proctosigmoidoscopy or colonoscopy
Biopsy
By negative stool examination for infectious causes
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
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.
LOWER GI HEMORRHAGE- PLAYLIST OF 6 VIDEOS
Dear Viewers,
Greetings from “Surgical Educator”.
I have made a playlist for Lower GI Hemorrhage which consists of six videos on various causes of Lower GI Hemorrhage. They are Introduction, diverticular disease, haemorrhoids, fissure-in-ano, colorectal carcinoma and inflammatory bowel disease. If you watch all these videos together you will become confident to tackle the clinical problem of Lower GI Hemorrhage. You can watch these videos in the following link: https://www.youtube.com/playlist…
Thank you for watching the videos.
Ulcerative colitis is a diffuse non- specific inflammatory disease of the large intestine of unknown cause, primarily affecting the mucosa, characterized by erosions and/or ulcerations. The disease is characterized by repeated cycles of relapses and remissions, occasionally accompanied by extra-intestinal manifestations.
A variety of immunologic changes have been documented in UC. T cells accumulate in the lamina propria of the diseased colonic segment. these T cells are cytotoxic to colonic epithelium. This change is accompanied by an increase in the population of B cells and plasma cells, with increased production of immunoglobulin G (IgG) and immunoglobulin E (IgE).
Ant colonic antibodies have been detected in patients with UC. A small proportion of patients with ulcerative colitis have smooth muscle and ant cytoskeletal antibodies.
Microscopically, acute and chronic inflammatory infiltrate of the lamina propria, crypt branching, and villous atrophy are present in ulcerative colitis. Microscopic changes also include inflammation of the crypts of Lieberkühn and abscesses. These findings are accompanied by a discharge of mucus from the goblet cells, the number of which is reduced as the disease progresses. The ulcerated areas are soon covered by granulation tissue. Excessive fibrosis is not a feature of the disease. The undermining of mucosa and an excess of granulation tissue lead to the formation of pseudo polyps.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
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
2. Introduction
Inflammatory bowel disease or IBD is a chronic,
relapsing inflammation of bowel possibly due to
abnormal immune response to enteric flora.
The two major forms of IBD are recognized as:-
Crohn’s disease (CD) which affect any part of the GI
tract from “gum to bum”.
Ulcerative colitis (UC) which affect only the colon.
3. There is a degree of overlap between these two
conditions, in there clinical features, histological and
radiological abnormalities. In 10% of cases of IBD
causing colitis a definitive diagnosis is either UC or CD
is not possible and the diagnosis is term as colitis of
undetermined type and etiology (CUTE).
Its clinical useful to distinguished between these two
conditions because of differences in their
management, although in reality they may represent
two aspect of the same disease.
4. Epidemiology
The incidence and prevalence of IBD are highest in
westernized nations, the incidence of CD varies from
country to country but is approximately 4-10 per
100000 annually with the prevalence 25-100 per
100000.The incidence of UC is stable at 6-15/10000
annually with a prevalence of 80-150/100000. The
disease is more prevalent in the west, particularly
Caucasian and eastern European Jews.
5. Etiology
Genetic factors
Smoking
NSAIDs
Hygiene
Nutritional factors
Appendectomy
The intestinal microbiota
The intestinal immune system
6. CROHN’S
Crohn’s disease is a chronic inflammatory condition
that affect any part of the GI tract from mouth to anus
but has the tendency to affect the ileum and ascending
colon (ileocolonic disease).
The disease can involve one small areas with relatively
normal bowel in between (skip lesion). It may also
involve the whole of the colon (total colitis) sometimes
without macroscopic small bowel involvement.
7.
8. Macroscopic features of CD
The involved bowel is usually thickened and is
narrowed. Deep ulcers and fissures in mucosa produce
a cobblestones appearance. Fistula and abscesses
maybe seen which reflect penetrating disease.
9. An early features is aphthoid ulceration, usually seen
at colonoscopy; later larger and deeper ulcers appears
in a patchy distribution again producing a cobblestone
appearance.
10. Microscopic features of CD
The earliest lesions are aphthoid ulceration and focal
crypt abscesses with loose aggregations of
macrophages, which form non-caseating granulomas
in all layers of the bowel wall. Granulomas can be seen
in lymph node, mesentery, peritoneum, liver and
pancreas. Although granulomas are a pathognomic
features of CD, there are rarely found on mucosal
biopsies.
11. Sign and Symptoms of CD
MAJOR SYMPTOMS:-
Watery Diarrhea
Abdominal pain
Weight loss
CONSTITUTIONAL SYMPTOMS:-
Malaise, lethargy, anorexia, nausea, vomiting, and low
great fever maybe present and 15% no gastrointestinal
symptoms.
12. Diagnosis
How can you diagnose CD?:-
History and Examination
Presenting complain:- insidious or acutely abdominal
pain. Non-bloody Diarrhea but sometimes it maybe
bloody and Steatorrhea
systemic review is very important because of extra GI
manifestations
13. Family history is important because of genetic
predisposition.
Drug and social history due to NSAIDs and smoking
which is said to exacerbate CD.
14. Examination:-
Loss of weight and sign of malnutrition. aphthous
ulcer in the mouth is often seen.
15. Abdominal examination:-
• Maybe normal or shows tenderness and or right iliac
fossa mass are occasionally found.
• The anus should be examined to look for edematous
anal tags, fissures or perianal abscesses.
• And the presence of extra GI features should not be
forgotten.
16.
17. Investigations
Complete blood count (CBC):- for the presence of
anemia either normocytic normochronic anemia of
chronic diseases. However iron deficiency and or folate
also occur.
Erythrocyte sedimentation rate (ESR) & C-reactive
protein (CRP) may raised, white cells & platelets count
is also high.
Hypoalbuminemia is present in severe disease or as
part of an acute phase response to inflammation
associated with raised CRP.
18. Liver function test (LFT)
Blood culture for suspected septicemia
Serologic test:- anti-saccharomyces cerevisiae
antibodies (ASCA) often positive.
Stool culture for C. difficile toxin assay should always
be performed if diarrhea is present.
19. Endoscopy & radiological imaging
Colonoscopy/sigmoidoscopy in patient with severe
disease.
Upper GI endoscopy to exclude esophageal &
gastroduedenal involvement.
Small bowel imaging is mandatory in patient with CD
Perianal MRI or endoanal ultrasound.
Capsule endoscopy in CD with normal radiological
findings.
Radionuclide scan.
20. MRI shows linear fluid-filled
perianal fistula in the right
ischioanal fossa
22. Complications of CD
Malaborption
Peritonitis
Intestinal obstruction in 40%
Massive hemorrhage
Skin tags
Ischiorectal abscess
Anorectal
Fistula
23. Medical Management
The aim of management is to induce and maintain
clinical remission & achieve mucosal healing to
prevent complications.
Stop smoking
Induction of remission:- oral or I.V
glucocortic0steriods (e.g. 6 mercaptorine,
methotrexate) and TNF antibodies (e.g. infliximab,
adalimumab)
25. Surgical management of CD
Approximately 80% of patient will required surgery at
some course of the disease.
INDICATION FOR SURGERY ARE:-
Failure of medical therapy with acute or chronic
symptoms producing ill-health
Complications (e.g. toxic dilation, obstructions,
perforation, abscesses and enterocutenous fistula)
Failure to grow in children despite medical therapy
Presence of perianal sepsis
26. Surgical intervention
Colectomy
Stricturoplasty
Ileorectal anastomosis
Panprocolectomy with an end ileostomy (if the whole
colon & rectum is involved)
27. Problems associated with
ileostomies
Mechanical problem
Dehydration particularly if there is a short length of
small bowel remaining.
Psychosexual problems
Erectile dysfunction in men and reduced fueundity in
women (due to prior surgery)
Recurrence of CD
29. Ulcerative colitis UC
Ulcerative colitis (UC) can affect the rectum alone
(proctitis) & can extend to proximally to involved the
sigmoid and descending colon (left sided colitis) or
may involve the whole colon (extensive colitis). In a
few of these patients there is also inflammation of the
distal terminal ileum (backwash ileitis).
30.
31. Macroscopic changes in colitis
The mucosa looks reddened, inflamed and bleed easily
(friability). In severe disease there is extensive
ulceration with the adjacent mucosa appearing as
inflammatory (pseudo) polyps.
32. Microscopic changes in UC
The mucosa shows a chronic inflammatory cells
infiltrate in the lamina propria. Crypt abscesses and
goblet cell depletion are also seen.
33. Sign & symptoms of UC
Bloody Diarrhea with mucus
Lower abdominal discomfort
Malaise
Lethargy
Anorexia
Weight loss more often in UC than CD
34. Diagnosis
History and examination:-
History:- patient usually complain about frequent
passage of blood and mucus in his stool with urgency
and tenesmus. And frequency of defecation. About 10-
20 liquid of stool per day. Diarrhea mainly occurs at
night with incontinence and urgency.
In system review extra GI symptoms, +/- family history
35. Examinations
In general there are no specific sign in UC but the
abdomen maybe slightly distended or tender to
palpation.
Pyrexia, tachycardia, are sign of severe colitis and
require urgent admission.
Rectal examination will show presence blood.
Rigid sigmoidoscopy is usually abnormal, showing an
inflamed, bleeding, friable mucosa.
37. Investigations
Complete blood count (CBC):- iron deficiency and
raised WBC & platelet.
ESR & CRP are often raised
Liver function test (LFT)
Serologic test:- perinuclear anti-neutrophil
cytoplasmic antibodies (pANCA) often positive
Stool culture for C.difficile toxin.
Colonoscopy with mucosal biopsy is the gold standard
X-ray
39. Complications of UC
Short term complication:-
Toxic megacolon
Hemorrhage
Perforation
Long term complication:-
Stricture leading to obstruction
Dysplasia leading to cancer.
40.
41.
42. Medical Management
Multidisplinary term
Aminosalicyclic acid (5-ASA)(e.g. sulfasalazine,
balsaladize & olsalazine)
Suppositories and enemas of 5-ASA can be use
Oral prednisolone
In severe cases admission give I.V hydrocortisone
100mg 6 hourly with subcutaneous low molecular
weight heparin to prevent thromboembolism
43. Salvage therapy
To avoid Colectomy is required for patient with
CRP>40mg/L or more than eight bowel motions after 3
days of hydrocortisone.
Oral cyclosporine 2mg/kg/day
Infliximab 5mg/kg as an Infusion
SMOKING?
44. Surgical Management
While the treatment of UC remains primarily
medical, surgery continues to have a central role
because it maybe life saving is curative and eliminated
the long term risk of cancer.
Acute disease:- subtotal Colectomy with end ileostomy
Severe disease:- proctectomy with permanent
ileostomy.
45. Indications for surgery
Fulminate acute attack:-
failure of medical therapy
Toxic dilation
Hemorrhage
Imminent perforation
Chronic disease:-
Incomplete response to medical treatment
Dysplasia on surveillance colonoscopy
51. Features that distinguished CD
from UC
Crohn's gives GIFTS:-
Granulomas
Ileum
Fistula and fissure
Transmural
Skip lesions
52. Cancer in inflammatory bowel
diseases
Patients with UC and extensive Crohn’s colitis have
an increased incidence of developing dysplasia and
subsequent colon cancer. The risk of dysplasia is
related to the extent and duration of disease as well as
the presence of untreated mucosal inflammation.
53. Pregnancy and inflammatory
bowel disease
Women with inactive IBD have normal fertility.
Fertility, however, may be reduced in those with active
disease, and patients with active disease are twice
more likely to suffer spontaneous abortion than
those with inactive disease.
54. Listen to your patient he is telling you the diagnosis.
Dr. Williams Osler