Ulcerative colitis is a chronic inflammatory bowel disease that involves the colonic mucosa. It typically affects the rectum first and may extend proximally in a continuous manner. The disease runs a relapsing and remitting course. Treatment involves 5-aminosalicylates and corticosteroids to induce and maintain remission. For moderate to severe disease, immunosuppressants like azathioprine, anti-TNF agents, and vedolizumab may be used. Surgery with proctocolectomy and ileal pouch-anal anastomosis is the treatment of choice for those who require colectomy.
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
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
Irritable Bowel Syndrome: An Update in Pathophysiology and Management Monkez M Yousif
Irritable bowel syndrome is the commonest health problem in hospital outpatient clinics and in private health care facilities and represents a big challenge for patients and physicians. This presentation discusses a different aspect of the disease from pathophysiology, clinical presentation and management
NAFLD is a vast topic and recently gaining a lot of importance. Fatty liver, NASH, are other topics discussed here. sleissenger, sheila sherlock and Harrisons are used for reference
Irritable Bowel Syndrome: An Update in Pathophysiology and Management Monkez M Yousif
Irritable bowel syndrome is the commonest health problem in hospital outpatient clinics and in private health care facilities and represents a big challenge for patients and physicians. This presentation discusses a different aspect of the disease from pathophysiology, clinical presentation and management
NAFLD is a vast topic and recently gaining a lot of importance. Fatty liver, NASH, are other topics discussed here. sleissenger, sheila sherlock and Harrisons are used for reference
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.
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.
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!
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
- 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
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
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.
2. DEFINITION
Chronic inflammatory condition
Mucosal inflammation without granuloma
Involvement of the rectum with variable proximal extension
Continuous fashion
Relapsing and remitting course
3. EPIDEMIOLOGY
More common in western countries
Onset: Peak age of onset 2nd and 3rd decade, second smaller peak at
60 and 70s
Male >Female
More common in nonsmokers and ex-smokers
5. PATHOLOGY
Always involves the rectum with variable proximal extension
Sharp transition between diseased and healthy segment of the colon
Small intestine is normal, although mild mucosal inflammation of
distal ileum(backwash ileitis) may be present
6. MACROSCOPIC FEATURES
Mucosa appears hyperemic, edematous and granular in mild disease
Hemorrhage, with visible punctate ulcers
Pseudopolyps
Mucosal bridges
In long standing disease, mucosal atrophy with a flat and smooth
mucosal surface that lacks normal folds(featureless colonic mucosa)
7. GROSS PATHOLOGY OF ULCERATIVE COLITIS
B. Sharp demarcation between active UC and normal mucosa
A Total colectomy with pancolitis showing active disease,
with red, granular mucosa in the cecum (left) and
smooth, atrophic mucosa distally (right).
C, Inflammatory polyps. D, Mucosal bridge
8. MICROSCOPIC FEATURES
Clusters of neutrophils within a crypt (cryptitis, crypt abscesses)
Architectural crypt distortion
Inflammation generally confined to mucosa and superficial
submucosa
Epithelial metaplasia
9. C. Disease is limited to the mucosa
MICROSCOPIC PATHOLOGY OF ULCERATIVE COLITIS
A. Crypt abscess.
B. Pseudopyloric metaplasia (bottom).
A
C
B
10. CLASSIFICATION
EXTENT ANATOMY
E1 Proctitis limited to rectum(Distal to rectosigmoid junction)
E2 Proctosigmoiditis or left
sided colitis
Affects the rectum and left colon( distal to splenic flexure)
E3 Pancolitis or extensive
colitis
Affects the rectum and colon proximal to splenic flexure
According to disease extent (Montreal classification)
11. CLASSIFICATION (according to disease severity)
SEVERITY
S0 Clinical remission
S1 Mild UC
S2 Moderate UC
S3 Severe UC
13. ULCERATIVE PROCTITIS
Rectal bleeding
Rectal urgency
Constipation
Systemic features are uncommon but skin or joint symptoms can
occur
14. LEFT SIDED COLITIS
Diarrhea or constipation
Tenesmus, urgency, rectal bleeding
Colicky left lower quadrant pain and extraintestinal manifestations
are more common than with proctitis
15. EXTENSIVE COLITIS
Diarrhea
Urgency, tenesmus, cramping abdominal pain
Systemic features
o weight loss
oFever
oNight sweats
oNausea, vomiting
18. LABORATORY INVESTIGATIONS
BLOOD TEST :
CBC- anemia, leukocytosis, thrombocytosis ,high ESR
Electrolytes
Liver enzymes- minor elevation of AST and ALP
S. albumin –To assess severity and prognosis
Baseline kidney function
CRP- Elevated in active UC
19. STOOL TEST
Stool RE and CS: To exclude infectious colitis
Assay for toxins A and B of C. difficile
Fecal calprotectin is a marker of intestinal inflammation
o >250 mcg/g is predictive of relapse of UC
o < 50 mcg/g is predictive of remission
21. COLONOSCOPY / SIGMOIDOSCOPY
Colonoscopy contraindicated in severe UC
Risk of perforation
Risk of megacolon
Risk of sedation
Flexible sigmoidoscopy instead
Minimal insufflation
No/minimal sedation
Limit exam to rectum
No retroflexion
22. Findings
Mucosal erythema and edema
Loss of normal vascular pattern
Mucosal granularity(fine or coarse)
Coarse granularity represent microscopic or pinpoint ulceration, and
associated with friability(spontaneous or scope induced contact
bleeding)
Ulcearation(usually shallow)
Exudates of mucopus
Pseudopolyps with long standing disease
25. HISTOLOGY
ACTIVE UC: Distorted colonic
crypts , inflammatory
infiltrate , crypt abcess
QUISCENT UC: Branched
colonic crypts but no active
inflammatory infiltrates
26. IMAGING STUDIES
Plain X-Ray abdomen: useful in severe attack of UC
Thumbprinting or thickening of colon wall severe colitis with
bowel edema
Distended bowel with loss of haustration toxic megacolon
Barium enema less commonly used
Colon typically appears granular and shortened
29. ASSESSMENT OF DISEASE ACTIVITY
There are numerous indices to measure disease activity in UC
The truelove and Witts classification is reliable and simple to use in
clinical practice
It is most applicable for patients with extensive colitis
33. MEDICAL THERAPY
The Rx Strategy for UC is mainly based on -
• Distribution (proctitis, left sided or extensive colitis)
• Severity(mild, moderate, severe)
• Prior therapy (response, side effect, compliance)
34. Indduction of remission in mildly active UC
Proctitis Left sided colitis Extensive colitis
Rectal 5-ASA(1g/d) • Rectal 5-ASA
enema(1g/d)
preferred over rectal
steroids
• Suggest rectal 5-ASA
enemas(1g/d)
combined with oral
5- ASA
(2g/d)compared with
oral 5-ASA alone
• Oral 5-ASA (2g/d)
If intolerant or nonresponsive to 5-ASA therapy, recommend oral budesonide MMX
9mg/d or oral systemic corticosteroid for induction of remission
35. Maintenance of remission in mildly active UC
Proctitis Left-sided or extensive UC
Rectal 5-ASA at a dose of at
least 1g/d
Recommend oral 5-ASA therapy at a dose at least
2g/d for maintenace of remission
Recommend against systemic corticosteroids for maintenance of remission in patient
with UC
36. Induction of remission for moderate to severe UC
Moderately active UC Moderately to severely active UC of any
extend recommended
Recommend oral budesonide MMX • Oral systemic corticosteroids
• Anti-TNF therapy in combination with
azathioprine
• Vedolizumab
• Tofacitinib 10 mg orally b.i.d. for 8 wks
Moderately to severe UC who have
previously failed anti-TNF therapy
recommend
• Vedolizumab
• Tofacitinib 10 mg orally b.i.d. for 8 wks
37. Maintenance of remission moderate to severe UC
• Recommend against systemic corticosteroids or MTX for maintenance
of remission
• Now in remission due to corticosteroids induction, suggest thiopurines
for maintenance of remission compared with no treatment or
corticosteroids. Recommend
• Continuing anti-TNF therapy to maintain remission after anti-TNF
induction
• Continuing vedolizumab to maintain remission after Vedolizumab
induction
• Continuing tofacitinib to maintain remission after Tofacitinib induction
38. MANAGEMENT OF HOSPITALIZED PATIENT WITH ACUTE SEVERE UC (ASUC)
• ASUC is defined as presence of 6 or more bowel movement plus 1
systemic sign of toxicity including tachycardia, fever, anemia
(Hb<10.5 gm/dl)or elevated inflammatory markers(ESR and CRP)
• All patients with ASUC should have stool testing to rule out CDI and
should undergo flexible sigmoidoscopy to asses endoscopic severity
of inflammation and to obtain biopsies to evaluate for
cytomegalovirus(CMV) colitis
• Recommend against routine use of broad spectrum antibiotic and
total parenteral nutrition (TPN)
39. MANAGEMENT OF HOSPITALIZED PATIENT WITH ACUTE SEVERE UC (ASUC)
Induction of remission:
A total of 60mg/d of methylprednisolone, hydrocortisone 100 mg 3/4 times daily for
3-5 days
If fail to adequately respond to IV steroids, recommend rescue therapy with
infliximab or cyclosporine
Maintenance of remission:
if achieve emission with Infliximab, recommend maintenance of remission with
same agent, who achieve remission with infliximab treatment
If achieve remission with cyclosporine treatment, suggest maintenance of
remission with thiopurine or Vedolizumab
40. SURGICAL TREATMENT ( 25% cases )
Colonic dysplasia or carcinoma
Chronic refractory UC not responding to traditional medical therapy
Toxic megacolon, colonic perforation
Intolerable or unacceptable side effects of medical therapy
Systemic complications that are recurrent or unmanageable
Uncontrollable colonic hemorrhage
41. PROCEDURES
Proctocolectomy with ileal Pouch-Anal Anastomosis(IPAA)
Currently operation of choice who require elective colectomy
Total proctocolectomy and end ileostomy
Total proctocolectomy and continent ileostomy
42. E. Proctocolectomy with ileal Pouch-Anal
Anastomosis(IPAA)
C. Total proctocolectomy and end ileostomy
D. Total proctocolectomy and continent ileostomy