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.
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.
Learn Barium Meal & Follow Through for the beginners from a Radiology Resident.For some image description please go through the text book "David Sutton" because i have described these image during my presentation Verbally..There are many animations used inside this presentation so to see all the pictures which are placed layer by layer with the help of animations you simple need to download this presentation first.... Thanx.
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
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 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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of 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
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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
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.
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
INFLAMMATORY BOWEL DISEASE IMAGING(RADIOLOGY)
1. IMAGING IN INFLAMMATORY
BOWEL DISEASE
DR.KHYATI VADERA REFERENCES: RADIOGRAPHICS
RESIDENT DOCTOR RUMACK
M.D RADIODIAGNOSIS RADIOLOGY ASSISTANT
MEDICAL COLLEGE BARODA
SSG HOSPITAL
2. • INTRODUCTION
• DEFINATIONS
• IMAGING MODALITIES
• DIFFERENCE BETWEEN CHRON’S AND UC
• DIFFERENTIAL DIAGNOSIS
• CONCLUSION
PROTOCOLS
3. Group of chronic disorders that cause inflammation
and ulceration in small and large bowel.
Mainly two most common diseases are –chron’s
disease and ulcerative colitis
INTRODUCTION
4.
5. Idiopathic, chronic, transmural inflammatory process
of bowel - affect whole GI system starting from
mouth to anus.
Most commonly involved- terminal ileum, ileocaecal
valve and caecum with regional enteritis.
SKIP LESIONS ARE PATHOGNOMIC
Diagnosed typically between 15-25 years of age group.
No gender predilection, runs in families.
Smokers - more affected.
CHRON’S DISEASE
6. • Chron’s disease can be –Stricturing,Penetrating,Inflammatory
• Etiology – idiopathic, genetic(DR5 DQ1 alleles), immunologic, microbial,
psychosocial
• Clinical presentation- diarrhoea, abdominal pain, weight loss
• Intermittent attacks of active disease followed by periods of remission.
• Disease re-activation by triggers like stress, dietary factors, smoking.
• Risk of colonic adenocarcinoma is increased in long standing cases.
7. • on X-ray- plain radiograph of abdomen is usually helpful in cases of
obstruction secondary to chron’s or extraintestinal manifestations
8. MUCOSAL ULCERS
APHTHOUS ULCERS initially
deeper transmural ulcers typically either longitudinal or circumferential in
orientation
when severe leads to COBBLESTONE APPEARANCE
may lead to sinus tracts and fistulae
thickened folds due to oedema
pseudodiverticula formation: due to contraction at the site of ulcer with
ballooning of the opposite site
STRING SIGN: tubular narrowing due to spasm or stricture depending on
chronicity partial obstruction
Barium small bowel follow-through
14. ULTRASOUND
limited role, it has been evaluated as an initial screening tool
Typically examination is limited to the small bowel and wall
thickness assessed:
Bowel wall thickness should be <3 mm, normally
thickness < 3 mm helps exclude the disease in a low risk patient.
thickness > 4 mm helps establish the diagnosis in a high risk patient.
Ultrasound in the assessment of extraintestinal manifestations.
15.
16. US image - stricture in a patient with active
Crohn's disease
18. Fat halo sign in chron’s disease
Transverse CT scan shows the central fatty
submucosal layer of low attenuation (*)
surrounded by higher-attenuation inner (long
arrow) and outer(short arrow) layers grossly
corresponding to the mucosa and muscularis
propria and serosa of the descending colon,
respectively.
19. COMB SIGN:Hypervascular appearance of the mesentery in active Crohn's disease.
Fibrofatty proliferation and perivascular inflammatory infiltration outline the
distended intestinal arcades. This forms linear densities on the mesenteric side of
the affected segments of small bowel, which give the appearance of the teeth of a
comb.
20.
21. CECT image, coronal section,
venous phase - enterocecal
fistula with secondary
traction of the cecum and
right psoas muscle abscess
22. CT AND MR ENTEROGRAPHY
Useful for both mural and extramural spread of
disease.
Inflammed bowel loops show thickening and contrast
enhancement.
Extramural spread: fibrofatty proliferation-thickening
of extramural fat
:vascular engorgement(comb sign)
Stenosis and strictures
23.
24. MRI enteroclysis - placement of a nasojejunal catheter
through which 1.5-2 L of contrast solution (e.g. water
with polyethylene glycol and electrolytes) are
injected.
When disease is transmural, with cobblestone
appearance, the abnormalities are evident as high T2
signal linear regions.
CT AND MR ENTEROCLYSIS
25. Introduction of the 12 to 14-F enteroclysis tube (under
fluoroscopy or through duodenoscope).
Contrast is administered either on the fluoroscopy table or after
transferring the the patient to the CT unit for commencement
of the CT scan (usually 1.5-2L of oral contrast).
In the CT unit, the position of the enteroclysis tube is checked in
the topogram.
In case negative oral contrast will be used, intravenous contrast
injection will be given (approximately 100-150ml).
CT ENTEROCLYSIS
26.
27. placement of a nasoduodenal tube under fluoroscopic guidance
the small-bowel is distended with 1-3L of methylcellulose (0.5%)
and water solution or isosmotic water solution through an
electric infusion pump infusion rate: 80-200 mL/min.
multislice HASTE(half-Fourier acquisition single-shot turbo spin-
echo) images with fat saturation and unenhanced and
enhanced (0.1 mmol/kg gadolinium) T1 coronal and axial fast
low-angle shot (FLASH) 2D images with fat saturation are
obtained 60 seconds after contrast injection
MR ENTEROCLYSIS
28.
29.
30. Perirectal phlegmon on axial T2 Single Shot TSE (left) and T1 contrast
enhanced (right) sequences. Rectal wall thickening with avid contrast
uptake due to active disease. Perirectal phlegmon surrounded by a
hyperenhancing perirectal fascia, displaces the rectum anteriorly.
32. Causes superficial ulceration of colon and rectum.
It starts from rectum and retrogradely involves whole colon
continuously.
In total colitis- back wash ileitis.
More common in DR2 related genes.
More female predilection, age group 30-40 yrs.
Clinical symtoms- diarrhoea, tenesmus, bleeding per rectum, passage
of mucus, crampy abdominal pain.
ULCERATIVE COLITIS
33. MILD DISEASE: fine granularity
MODERATE: marked erythema, coarse granularity, contact bleeding
and no ulceration.
SEVERE: spontaneous bleeding,edematous and ulcerated
Long standing cases epithelial regeneration- pseudopolyps, pre
cancerous condition
Eventually shortening and narrowing of colon
FULMINANT DISEASE: toxic colitis/megacolon
PATHOGENESIS
34. Acute UC – descending colon
has irregular outline. No fecal
residue in colon S/O total colitis
35. Mucosal inflammation-granular appearance to the surface of
the bowel.
Mucosal ulcers are undermined -button-shaped ulcers
Islands of mucosa remain giving it a pseudo-polyp appearance
In chronic cases the bowel becomes featureless with loss of
normal haustral markings, luminal narrowing and bowel
shortening- lead pipe sign
BARIUM ENEMA
40. Back wash ileitis : patulous
IC valve and dilated granular
terminal ileum
41. CT FINDINGS
Inflammatory pseudopolyps
Inflamed and thickened bowel - target appearance, due concentric
rings of varying attenuation- mural stratification
In chronic cases, submucosal fat deposition is seen particularly in the
rectum fat halo sign
Extramural deposition of fat, leads to thickening of the perirectal
fat, widening of the presacral space
Marked muscularis mucosa hypertrophy-lead pipe sign.
45. Wall Thickening- median wall thickeness of colon
ranges from 4.7 to 9.8 mm, more severe the disease
more thicken the wall
Increased Enhancement- enhancement of the mucosa
with no or less enhancement of the submucosa
Loss of haustral markings
MRI
46. Mri image reveals thickening
of colon with loss of haustral
markings
47.
48. DIFFERENCE
CHRON’S DISEASE
70-80%Small bowel involvement
Skip lesions
Fat halo sign seen in 8%
Apthous ulcers are seen
Bowel wall more thicker
Irregular serosal surface
Perianal fistula/sinus/abscess
more common
Creeping fat and abscess are
very common in chronic cases
ULCERATIVE COLITIS
95% cases rectal involvement
Continuous spread from rectum
upwards
Fat halo sign is commonly seen
Collar button ulcers are seen.
Smooth serosal surface
Perianal disease rare
Mesenteric creeping fat and abscess
are uncommon.
Carcinoma is more common in long
standing cases.
59. • Lymph nodes with peripheral
rim enhancement giving
multilocular appearance
• Bowel wall thickening
60. TB CROHN’S
Involvement of
terminal ileum
shorter longer
Features Narrowed,
thickened, rigid
terminal ileum with
pulled up ceacum
Asymmetry and
cobblestoning
Longitudinal
Ulceration
absent present
TUBERCULOSIS VS CHRON’S
67. Acute diverticulitis
Pericolic stranding- disproportionate to the amount of bowel
wall thickening
segmental thickening of the bowel wall
enhancement of the colonic wall
diverticular perforation - air and fluid into the pelvis and
peritoneal cavity
abscess formation (seen in up to 30% of cases)
may contain fluid, gas or both
fistula formation-gas in the bladder/direct visualisation of
fistulous tract
70. Ischemic colitis
On CT:
segmental region of abnormality
submucosal oedema may produce low-density ring bordering
lumen (target sign)
intramural or portal venous gas
mesenteric oedema WITH NON ENHANCING BOWEL WALL
superior mesenteric artery or vein thrombus/occlusion may be
demonstrated
74. Pseudomembranous colitis
Pseudomembranous colitis-caused by the bacterium
Clostridium difficile due to bacterial overgrowth of
the colon in patients who are treated with broad-
spectrum antibiotics.
ascites and hyper enhancement of the bowel wall
with submucosal edema and edema in the
mesocolon.
76. Accordion sign
The sign is described as alternating edematous
haustral folds separated by mucosal ridges filled with
oral contrast material
77.
78. CONCLUSION
Inflammatory bowel diseases are chronic group of disorders which have a long
course of disease with intermittent periods of active disease and remission.
They can be easily diagnosed by multimodality approach combining clinical
symptoms , colonoscopy, and radiology.
Conventional radiological investigations like barium studies are still necessary for
diagnosis of characteristic intramural changes.
However the CT and MRI investigations are nowadays frequent and less
invasive, useful for detection of extraintestinal manifestations of IBD.
Colonoscopy at regular intervals is also must to look for progression of disease
and malignancy in long standing cases
Postcontraste axial image showing the presence of an acute fistula (arrows) between an inflamed ileum loop and the right psoas muscle.
Fibrotic stenosis. Axial T2 Single Shot (upper) and axial T1 post-contrast (lower) images of a patient with a history of recurrent Crohn's disease and episodes of partial bowel obstruction, show fibrotic stenosis. Thickening and stenosis of the distal ileum with homogeneous contrast enhancement are seen.
Note prominent right mesenteric fat wrapping displacing surrounding intraperitoneal structures