Ischemic bowel disease results from inadequate blood flow to the intestines. It can range from mild to severe depending on the damage from lack of oxygen. The major causes are arterial thrombosis, embolism, venous thrombosis, and non-occlusive ischemia. Symptoms include abdominal pain, bloody stools, diarrhea, and nausea. Diagnosis involves imaging tests and endoscopy. Treatment depends on severity but may include bowel rest, antibiotics, or surgery to remove ischemic sections of bowel. Complications can include bowel necrosis, sepsis, and death if not treated promptly.
Information about Ischemic Colitis by Dr. Dhaval Mangukiya.
Details of Ischaemic colitis, Colonic circulation, CT diagnosis of colonic ischemic, Management of colonic ischaemia, Dignosis of colonic ischaemia, Colours of ischaemia, cleveland clinic guidelines, Indications for surgery in colonic ischaemia, Surgery for colonic ischaemia, Outcome of ischaemic colitis.
https://drdhavalmangukiya.com/
http://www.youtube.com/c/DrDhavalMangukiyaGastrosurgeonSurat
https://gastrosurgerysurat.blogspot.com/
Information about Ischemic Colitis by Dr. Dhaval Mangukiya.
Details of Ischaemic colitis, Colonic circulation, CT diagnosis of colonic ischemic, Management of colonic ischaemia, Dignosis of colonic ischaemia, Colours of ischaemia, cleveland clinic guidelines, Indications for surgery in colonic ischaemia, Surgery for colonic ischaemia, Outcome of ischaemic colitis.
https://drdhavalmangukiya.com/
http://www.youtube.com/c/DrDhavalMangukiyaGastrosurgeonSurat
https://gastrosurgerysurat.blogspot.com/
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
this ppt presents pancreatitis and tumors of the pancreas
The fourth leading cause of cancer-related death in the United States and has a mean age of 55 at diagnosis.
I GET SMASHED
G I bleeding with radiological interventions(ACR Appropriateness Criteria).Tc-99m RBC scintigraphy,Catheter-directed Angiography,Pharmacological control,Embolization,Arterial interventions,Endoscopy,CT Angiography
Portal hypertension is elevation of portal venous pressure
above 10-12 mm Hg (normal 5-10 mm Hg). Portal
hypertension results from (a) increased resistance to portal
blood flow and (b) high portal blood flow.
Ischemic colitis is the most common form of intestinal ischemia. It manifests as a spectrum of injury from transient self-limited ischemia involving the mucosa and submucosa to acute fulminant ischemia with transmural infarction that may progress to necrosis and death. Although there are a variety of causes, the most common mechanism is an acute, self-limited compromise in intestinal blood flow.
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
this ppt presents pancreatitis and tumors of the pancreas
The fourth leading cause of cancer-related death in the United States and has a mean age of 55 at diagnosis.
I GET SMASHED
G I bleeding with radiological interventions(ACR Appropriateness Criteria).Tc-99m RBC scintigraphy,Catheter-directed Angiography,Pharmacological control,Embolization,Arterial interventions,Endoscopy,CT Angiography
Portal hypertension is elevation of portal venous pressure
above 10-12 mm Hg (normal 5-10 mm Hg). Portal
hypertension results from (a) increased resistance to portal
blood flow and (b) high portal blood flow.
Ischemic colitis is the most common form of intestinal ischemia. It manifests as a spectrum of injury from transient self-limited ischemia involving the mucosa and submucosa to acute fulminant ischemia with transmural infarction that may progress to necrosis and death. Although there are a variety of causes, the most common mechanism is an acute, self-limited compromise in intestinal blood flow.
Disorders that perturb cardiovascular, renal, or hepatic function are often marked by the accumulation of fluid in tissues (edema) or body cavities (effusions).
Vascular disease is a condition that develops when the arteries that supply the intestines with blood become narrowed due to the build-up of plaque. This results in a lack of blood supply to the intestines.
The lecture overviews the different situations where cholecystitis can be fatal,if not accurately diagnosed.Different types of dangerous cholecystitis are illustrated with their imaging findings.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
3. Definition
Ischemic bowel disease results from
inadequate flow of oxygenated
blood to the intestines.
• The extent of ischemic bowel disease can range
from mild to severe based on the amount of
damage from lack of oxygenated blood.
4. • Ischemic lesions may be restricted to the
•Small intestine mesenteric ischemia
•Large intestine ischemic colitis or
•Both enterocolitis
5. Blood Supply
• The majority of the GI tract is supplied by the
celiac, superior mesenteric, and
inferior mesenteric arteries.
• As they approach the intestinal wall the superior
and inferior mesenteric arteries ramify
into the mesenteric
arcades.
6. • Interconnections between arcades, as well as
collateral supplies from the proximal celiac
and distal pudendal and iliac circulations,
make it possible for the small intestine and
colon to tolerate slowly progressive loss of
the blood supply from one artery.
• In contrast, acute compromise of any major
vessel can lead to infarction of several
meters of intestine.
7. Levels of infarction
• Transmural infarction involving all layers of the gut.
• Mural infarction– mucosa & submucosa
• Mucosal infarction- mucosa
Mural-Of Wall
8. • Transmural infarction is caused by acute
occlusion of a major mesenteric artery.
• Mural or mucosal infarction more often results
from either physiologic hypoperfusion or more
localized anatomic defects and may be
acuteor chronic.
10. Arterial thrombosis
• Severe atherosclerosis
• Systemic vasculitis
• Dissecting aneurism An aneurysm in which the wall of an artery rips (dissects) longitudinally
• Angiographic procedures
• Aortic reconstructive surgery
• Surgical accidents
• Hypercoagulable states
• Oral contraceptives
11. Arterial embolism
•Cardiac vegetation An abnormal growth of tissue around a valve, composed of blood platelets, bacteria, and a protein involved in clotting.
•Angiographic procedures
•Aortic atheroembolism
12. Venous thrombosis
• Hypercoagulable states induced, for example, by oral contraceptive or antithrombin III deficiency,
• intraperitoneal sepsis,
• the postoperative state,
• vascular invasive neoplasm (particularly hepatocellular carcinoma),
• cirrhosis,
• abdomina trauma.
15. Causes
• Ischemic bowel disease occurs when an artery that
supplies blood becomes blocked or narrowed.
There are several possible causes of ischemic bowel
disease, including:
• Blockage in the arteries due to a tumor or blood
clot
• Narrowing of the arteries supplying blood to the
bowel from atherosclerosis
• Obstruction in the colon (large intestine)
16. Risk Factors
• Advanced age
• Shock induced by conditions such as blood
stream infection and blood loss
• Recent heart attack
• Sustained abnormal heart beat
• Congestive heart failure
• Peripheral vascular disease
• Coronary artery bypass surgery or other vascular
surgeries
17. • Colon cancer
• Certain medications that cause arteries to narrow
• Diabetes
• Hemodialysis
• Sickle cell disease
• Dehydration
• Pregnancy
18. Pathophysiology
• Arterial sources v.s. venous sources:
proximately 9:1. Similarly, arterial occlusive
disease occurs more frequently than
nonocclusive disease approximately 9:1
• The SMA and IMA, and their branches, are
more frequently than the celiac artery.
19. Pathophysiology (a. source)
Acute:
1.atheromatous plaque with intimal calcifications
2.embolic from cardiac disease
3. abdominal aortic aneurysms with dissection into
SMA
4. hypoperfusion secondary to hypovolemic shock or
low-flow cardiac failure.
20. Pathophysiology (a. source)
Chronic :
1.atherosclerosis
2.fibromuscular dysplasia
3.vasculitis.
Both occlusive and nonocclusive subtypes can occur .
21. Pathophysiology (v. source)
• are less frequently.
• In these cases, bowel ischemia results from
decreased mesenteric outflow of
deoxygenated blood rather than from decreased
perfusion of oxygen-rich blood
• Mortality rates generally are low.
• SMV is involved more often than the IMV.
22. 3.Nonocclusive mesenteric ischemia
– more frequently in older patients than other
forms and often already in an ICU setting .
– Symptoms typically develop over several days,
and may have had a prodrome of malaise and
vague abdominal discomfort.
– When infarction occurs, increased pain associated
with vomiting,hypotensive and tachycardic, with
loose bloody stool.
23. 4.Mesenteric venous thrombosis
in a much younger patient population than other types .
– acute or subacute abdominal pain involvement of the
small intestine rather than the colon.
– The symptoms are frequently less dramatic. 27% have
symptoms for >30 d.
– Many patients have a history of the risk factors for
hypercoagulability. include oral contraceptive use, deep
vein thrombosis (DVT), liver disease, tumor, or portocaval
surgery.
24. Pathogenesis
Intestinal responses to ischemia occur in two
phases.
I. The initial hypoxic injury occurs at the onset
of vascular compromise. While some damage
occurs during this phase, the epithelial cells
lining the intestine are relatively resistant to
transient hypoxia.
25. II. The second phase, reperfusion injury, is initiated
by restoration of the blood supply and it is at this
time that the greatest damage occurs.
In severe cases this may trigger
multiorgan failure.
While the underlying mechanisms of reperfusion
injury are incompletely understood, they involve
free radical production, neutrophil infiltration, and
release of inflammatory mediators, such as
complement proteins and TNF.
26. • Activation of intracellular signaling
molecules and transcription factors,
including hypoxia-inducible factor 1 (HIF-1)
and NF-κB(nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that
controls the transcription of DNA) also contribute to intestinal
ischemia-reperfusion injury
27. • The severity of vascular compromise,
• the time frame during which it develops, and
• the vessels affected
are the major variables in
ischemic bowel disease.
28. • Two aspects of intestinal vascular anatomy also
contribute to the distribution of ischemic damage.
1. Intestinal segments at the end of
their respective arterial supplies
are particularly susceptible to
ischemia.
Tail enders
29. • These watershed zones include the
splenic flexure, where the superior
and inferior mesenteric arterial circulations
terminate, and, to a lesser extent,
• the sigmoid colon and rectum where
inferior mesenteric, pudendal, and iliac arterial
circulations end.
30. • Generalized hypotension or hypoxemia can
therefore cause localized injury, and ischemic
disease should be considered in the
differential diagnosis of focal colitis of the
splenic flexure or
• rectosigmoid colon.
32. •This allows oxygenated
blood to supply crypts but
leaves the surface epithelium
vulnerable to ischemic injury.
• This anatomy protects the crypts, which contain
the epithelial stem cells that are necessary to
repopulate the surface.
33. • Thus, surface epithelial atrophy,
or even necrosis and sloughing,
with normal or
hyperproliferative crypts
is a morphologic signature of ischemic
intestinal disease.
34. Morphology
Transmural Intestinal Infarction-
may involve a short or long segment, depending on
the particular vessel affected and the patency of
the anastomotic supply. Whether the occlusion is
arterial or venous, the infarction
always has a
dark red hemorrhagic appearance (Red
Infarction).
35. • The ischemic injury usually begins in the
mucosa and extends outwards;
within 18 to 24 hours.
• There is a thin, fibrinous exudate
over the serosa.
36. • With arterial occlusion the demarcation
from adjacent normal bowel is fairly sharply
defined, but
• with venous occlusion the margins are less
distinct.
37. • Affected foci may or may not be visible
from the serosal surface, because by
definition the ischemia does not affect the
entire thickness of the bowel.
• When the bowel is opened, hemorrhagic
edematous thickening of the mucosa,
sometimes with superficial ulcerations, is
seen.
38. EHNE
Histologic features are those of
acute injury:
Edema, hemorrhage, and outright necrosis of
the affected tissue layers.
Inflammation develops at the margins of the
lesions, and an inflammatory fibrin-containing
exudate (pseudomembrane), usually
secondary to bacterial superinfection, may
coat the affected mucosa.
39. • Alternatively, Chronic vascular insufficiency may
produce a
chronic inflammatory and ulcerative condition,
mimicking idiopathic inflammatory bowel disease.
41. Morphology –Transmural infarction
• Histologically, the changes are typical of ischemic
damage with
• marked edema,
• interstitial hemorrhage,
• necrosis and sloughing of the mucosa.
• Within 24 hours intestinal bacteria produce
outright gangrene and sometimes perforation of
the bowel.
42. Mural & mucosal infarctions-
are recognised by multifocal lesions
interspersed with spared areas.
Their location depends in part on
the extent of preexisting atherosclerotic narrowing of
the arterial supply;
lesions can be scattered over large regions of the
small or large intestines.
Patchy lesions
(Necrosis)
43. Symptoms
• Cramping and abdominal pain
• Bloody stools
• Frequent urge to defecate
• Diarrhea
• Nausea or vomiting
• Abdominal distension
45. Acute transmural infarction
typically presents with
sudden, severe abdominal pain
tenderness (more sudden with mesenteric embolism),
sometimes accompanied by
nausea,
vomiting,
bloody diarrhea, or
grossly melanotic stool.
46. Patients may progress to shock and vascular collapse within hours as a result of blood
loss. Peristaltic sounds diminish or disappear, and
muscular spasm creates
board-like
rigidity of the
abdominal wall.
47. Because these physical signs overlap with those of
other abdominal emergencies, including
acute appendicitis,
perforated ulcer, and
acute cholecystitis,
the diagnosis of intestinal necrosis may be
delayed or missed,
with disastrous consequences.
48. As the mucosal barrier breaks down, bacteria enter the circulation and
sepsiscan develop;
mortality may exceed 50%.
The overall progression of ischemic enteritis depends on the underlying
cause and severity of injury.
49. • The mortality rate with infarction of
the bowel approaches 90%, largely
because
the window of time between onset
of symptoms and perforation
caused by gangrene is so small.
50. Mucosal and mural infarctions
by themselves may not be fatal. However, these may progress to more extensive
infarction
if the vascular supply is not restored by correction of the
insult
or,
in chronic disease, by development of adequate
collateral supplies.
51. • The diagnosis of nonocclusive ischemic enteritis and
colitis can be particularly difficult because there may be a confusing array of
nonspecific abdominal symptoms, including
intermittent bloody diarrhea
and
•intestinal pseudo-obstruction.
52. ,
Chronic ischemia may masquerade as
inflammatory bowel disease, with episodes of
bloody diarrhea interspersed with periods of healing.
53. Diagnosis
• X-ray of abdomen
• CT Scan or MRI of the abdomen
• Colonoscopy—a procedure where a long
flexible tube is inserted through the rectum to
inspect the colon and rectum.
• Angiography—an x-ray test used to view the
arteries supplying the bowel
55. Treatment
Supportive Care
• Bowel rest and intravenous fluids are given in mild
cases without significant progressed damage to the
bowel.
• Antibiotics
• Antibiotics are administered to minimize infection,
which can quickly complicate an ischemic bowel.
• Surgery
• In more severe cases, surgery is required to remove
the ischemic colon.
56. Complications
• Bowel necrosis (requiring bowel resection)
• Septic shock
• Death
• Patients in whom the diagnosis is missed until infarction
occurs have a mortality rate of 90%. Even with good
treatment, up to 50-80% of patients die.
• Survivors of extensive bowel resection face lifelong disability.
57. Prevention
• Stay well hydrated.
• Reduce your risk of cardiovascular disease
through regular exercise and a balanced diet
low in fat and calories.
• Consume plenty of fresh fruits, vegetables,
and fiber, which may reduce your risk of colon
cancer.
59. Major Causes of Intestinal Obstruction
Mechanical Obstruction:
• Hernias
• Adhesions
• Intussuception
• Volvulus 80%
60. Intestinal obstruction. The four major causes of intestinal obstruction are (1)
herniation of a segment in the umbilical or inguinal regions, (2) adhesion between
loops of intestine, (3) volvulus, and (4) intussusception.
61. Other less frequent conditions
• Tumors & Infarction 10-15 %
• Inflammatory strictures
• Obstructive gall stones, fecaliths, foreign bodies
• Congenital Strictures, atresias
• Congenital bands
• Meconium in cystic fibrosis
• Imperforate anus