Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Slideshow is from the University of Michigan Medical
School's M1 Immunology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Immunology
easy description of common lut disorders. improvements on the slides accepted. text includes congenital and acquired disorders. more so the causes of bladder outlet obstructions. also management of the disorders are breifly described.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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
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.
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.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
3. ANATOMY OF SPLEEN
• Weight: Normal adult spleen weighs 100-150
grams.
• Size: Adult spleen measures 3 X 8 X 14 cm,
• The largest single mass of lymphoid tissue in
body & is completely covered by peritoneum
• Relations:
– Site: Beneath left diaphragm separating it from 9,
10, &11 ribs.
– Posterolaterally; Attached to left kidney by the
lienorenal ligament.
– Antero-medially; attached to the stomach by
4. ANATOMY OF SPLEEN
• Blood supply:
– Arterial: Splenic artery from the celiac trunk & run
a tortuous course over the upper border of
pancreas till it reaches the spleen.
– Venous: See portal circulation.
• Open & closed circulation of spleen:
– Closed circulation i.e. The arterioles branch into
capillaries that are contiguous with the venous
sinuses within the red pulp.
– Open circulation i.e.The capillaries drain freely
into splenic parenchyma & the blood cells flow
through the fenestrations in venous sinuses into
5. Functions of spleen
• Cellular Functions:
– Culling Action i.e. removal of aged RBCs & abnormal cells e.g. spherocytes. Because the spleen is not
the only site of RBCs destruction, the life span of RBCs is not affected after splenectomy.
– Pitting Action i.e. Removal of non-deformable structures from deformable cells e.g.→
• Nuclei (Howell jolly bodies).
• Iron granules (Papen heimer bodies).
• Denaturated hemoglobin (Heinz bodies).
• Nuclear remnant & excess membrane (Reticulocytes)
• Parasites & fungi.
– Hemopoiesis:
• Spleen is the site of hemopoiesis during intra uterine fetal life.
• Spleen is one of extra medullary hemopoietic site.
– Storage of Platelets:
• About ¼ of platelets are present inside the spleen.
• In hypersplenism, 80% of platelets are trapped in spleen → thrombocytopenia.
• Immunological Functions***
– Removal of blood borne bacteria in absence of pre-existing antibody against it.
– Phagocytosis of anti-body coated bacteria & phagocytosis of encapsulated organisms e.g.
Pneumococci. & hemophilus influenza.
6. CONGENITAL ANOMALIES OF
SPLEEN
1. CONGENITAL ABSENCE of spleen: Very rare &
occurs in association with cardiac anomalies.
2. WANDERING SPLEEN: the spleen has a long
splenic mesentery → great mobility (may
reach to any part of abdomen). It may
undergo torsion → severe pain & shock. The
condition is more commonly seen in children
& females between 20-40 years.
3. SPLENCULI
Incidence: 10% - 25%.
Sites:
7. ASPLENIC STATE OR
HYPOSPLENISM
• Causes:
– Splenectomy.
– Splenic atrophy.
• Auto splenectomy e.g. sickle cell anemia.
• Chronic illness e.g. celiac disease, hyperthyroidism, ulcerative colitis.
• Splenic arterial or venous thrombosis e.g. Pancreatitis.
• Complications → over whelming post-splenectomy sepsis
– Explanation: Spleen is capable of phagocytosis of micro organisms (especially
capsulated organism) in absence of pre-existing antibodies to these organisms.
– Post-splenectomy sepsis has a high mortality rate up to 40%.
– Prophylaxis :
• Vaccination: Polyvalent pneumococcal vaccine. (Vaccination against H influenza & meningococci.)
• Penicillin. , Pediatric follow up: For all splenectomized children below 10 years.
• Partial splenectomy instead of total splenectomy or splenic auto transplantation should be
practiced whenever possible.
8. HYPERSPLENISM
• Definition: hypersplenism is a syndrome
characterized by the followings:
– Splenic enlargement.
– Deficiency of one or more blood cell lines.
– Normal or hyperplasic cellularity of deficient cell
in bone marrow.
– If diagnosis is correct, splenectomy is expected to
correct defect.
• Pathogenesis:
– Deficiency of blood cell elements may be due to:
→
9. HYPERSPLENISM
• Types:
– Primary Hypersplenism : very rare
– Secondary Hypersplenism : due to →
• Congestive splenomegally e.g. Portal hypertension.
• Neoplastic diseases e.g. Lymphomas, leukemia’s,
myeloid metaplasia.
• Inflammatory diseases, sarcoidosis, SLE, Felty’s
syndrome.
• Infections e.g. acute septicemia, chronic TB infection,
brucellosis, malaria.
• Storage diseases e.g. Gaucher’s disease, amyloidosis.
• Myelo-proliferative disorders e.g. Myelo-fibrosis.
• Chronic hemolytic anemia.
10. RUPTURE SPLEEN
• Predisposing factors:
– Infectious mononucleosis, malaria, typhoid fever.
– Generalized infection e.g. septicemia, pyaemia.
• Causes:
– Direct trauma: Penetrating or closed trauma
(more common).
– Indirect trauma e.g. falls from height or
compression.
– Spontaneous: Rupture may be due to trivial
trauma overlooked by patient.
– Operative trauma: Common with operations of
esophagus, stomach.
11. RUPTURE SPLEEN
• CLASSICAL RUPTURE
– Initially; the victim develops a shock & then
recovered with signs & symptoms of internal
hemorrhage & peritoneal irritation.
– Internal Hemorrhage:
• General: Pallor, tachycardia, restlessness, sighing
respiration.
• Local (blood in peritoneal cavity)
• Shifting dullness ……Elicited on right side of abdomen.
• Balance’s sign i.e. fixed dullness on left side due to
hematoma in splenic bed.
• Cullen’s & Gray turner’s signs: Discoloration around
umbilicus & flanks few days after trauma (gravitation of
12. RUPTURE SPLEEN
– Peritoneal Irritation {reflex rigidity & tenderness
& irritation due to presence of blood} →
• Severe abdominal pain marked in flanks & left
hypochondrium.
• Kehr’s sign i.e. hyperthesia in left shoulder on palpation
of left upper abdominal quadrant & on Trendlenberg
position (Elevation of foot bed for ¼ hour, → blood
touches the under surface of diaphragm → irritation →
referred pain to left shoulder).
• P-R: Marked tenderness in rectovesical pouch + soft
boggy swelling (due to accumulation of blood in pelvis).
• Rigidity & tenderness: Early on left side. Later on,
generalized.
• Tenderness over 9th 10th & 11TH ribs.
13.
14. RUPTURE SPLEEN
• DELAYED RUPTURE
– Incidence: 10% of blunt trauma cases.
– Causes:
• Presence of sub capsular hematoma (absorbs more
water, → ↑pressure inside it → burst).
• Dislodgment of blood clot over a tear.
• Associated pancreatic tail injury “enzymes digest any
clot present”.
– Presentation:
• Effects of injury are delayed for hours, days & even
months {Latent period of Boudet}.
• 50% of cases; present in first week after trauma, (25%
in 2nd W).
16. RUPTURE SPLEEN
• Investigations for rupture spleen:
– Plain x-ray:
• Normal out line of spleen is strong evidence against
rupture.
• Signs suggestive of rupture spleen →
– Obliteration of splenic outline.
– Enlarged splenic shadow.
– Obliteration of psoas shadow.
– Indentation of left side of stomach air bubble.
– Fracture one or more of lower ribs on the left side (27%).
– Elevation of left copula of diaphragm.
– Sonogram & CT: advantages →
• DD splenic hematomas from lacerations.
• Diagnosis of associated renal or liver injuries.
17. RUPTURE SPLEEN
• Management of rupture spleen:
– Conservative Treatment : Allowed in 25% of
cases provided that →
• Trauma is blunt.
• No other associated injuries requiring surgical
interference.
• Patient is hemodynamically stable.
• Total transfusion requirement is not > 2 units.
• Regular follow up by radiology, scintiscan & CT.
– Concept: Anatomy of spleen favors spontaneous cessation of
bleeding after trauma as sinuses facilitate platelets
aggregation & clot formation.
– Surgery:
• Small Capsular Tear → Splenorrhaphy.
18. SPLENOMEGALLY
• Introduction:
– 10% of healthy children have a palpable spleen
normally.
– Approximately 3% of healthy young persons have
palpable spleens.
– Normal palpable spleen is soft, smooth, & non
tender.
– A pathologically enlarged spleen is often is firmer,
may abnormal surface or texture.
• Characters of splenic swelling:
– Site :Left hypochondrium
19. SPLENOMEGALLY
• Causes of splenomegaly:
– Infective:
• Bacterial e.g. typhoid, paratyphoid, typhus, anthrax, TB,
septicaemia, splenic abscess.
• Spirochetal e.g. syphilis, Weil’s disease
• Viral e.g. infectious mononucleosis, Psittacosis.
• Protozoal e.g. Bilharsiasis, malaria, Kala azar.
• Parasitic e.g. hydatid disease.
– Blood Diseases e.g.
• Leukaemia (myeloid, lymphatic).
• Pernicious anaemia, polycythaemia, erythroblastosis
foetalis.
• Spherocytosis acquired haemolytic anaemia.
20. SPLENOMEGALLY
• Investigations:
– Complete Blood Cell Count.
– Antinuclear Antibody Titre: To screen for systemic
lupus erythematosus.
– Immunoglobulin Levels, neutrophil function, & T-
cell subclasses (e.g. immuno deficiency).
– Viral Antibody Titres: To detect EBV, CMV,
toxoplasmosis, & HIV.
– Bone Marrow Biopsy: For leukaemia, lymphoma,
storage diseases, & disseminated fungal or
mycobacteria infections).
– Ultrasound: Confirm the presence of the enlarged
21. PORTAL HYPERTENSION
• Physiology
– Hepatic blood flow is 1.5 litre/minute = ¼ cardiac
output;
– 2/3 of hepatic blood flow comes through the
portal vein (50% of O2 supply)
– 1/3 of hepatic blood flow comes through the
hepatic artery (50% O2 supply).
– Normal portal vein pressure is 10-15cmH2O or 7-
10 mmHg.
– Variceal bleeding occurs when pressure rises
above 12 mmHg.
22. PORTAL HYPERTENSION
• Anatomy:
– Portal vein is formed by the confluence of the
superior mesenteric & splenic veins behind the
neck of the pancreas & runs for approximately 6
to 8 cm posterior to CBD & hepatic artery up to
the porta hepatis where it bifurcates.
– IMV drains into splenic vein.
– Right gastroepiploic vein drains into SMV.
– Left gastroepiploic vein & short gastric veins drain
into splenic vein.
– Main tributaries of portal vein include → Right
gastric vein, Left gastric vein & Umbilical vein
23. PORTAL HYPERTENSION
• Pathophysiology:
– Pressure in portal vein (PV) = Flow x Resistance
– Portal hypertension can result from flow or
resistance
– Resistance e.g. Bilharzias fibrosis, cirrhosis,
portal vein obstruction.
– Flow e.g. arteriovenous fistula which may be
due to
• Trauma
• Giant splenomegally, tropical splenomegally,
splenomegally due to myeloid dysplasia.
– Portal vein pressure Pressure in portal vein
24. PORTAL HYPERTENSION
• Pathophysiology:
– The type of collateral development depends on
the cause of portal hypertension e.g.
• In extra hepatic portal vein thrombosis without liver
disease , the collaterals are hepatopetal i.e. transport
the blood to liver around occluded vein e.g.
– Hepatopetal collaterals in diaphragm, hepatocolic & hepato-
gastric ligaments.
– Deep cystic vein, accessory vein of Sappy.
– Vein of suspensory ligament, epiploic vein.
• In presence of liver disease , the collaterals are
hepatofugal i.e. carry blood around the liver into
systemic circulation e.g.
– Collaterals at lower oesophagus (with azygos vein →
25. PORTAL HYPERTENSION
• Etiology of portal hypertension: it may be
presinusoidal, sinusoidal, or post sinusoidal.
– In Presinusoidal Portal Hypertension, liver
functions are normal.
– Cirrhosis is the major cause of sinusoidal portal
hypertension:
• The most common causes are viral hepatitis & alcohol.
• Both portal hypertension & hepato-cellular damage
exist.
• Liver functions are markedly affected.
– Post sinusoidal Portal Hypertension is rare &
caused by a hepatic venous outflow obstruction.
26. BLEEDING OESOPHAGEAL VARICES
• Causes: Either due to explosion from within or
erosion from without (e.g. Hcl & trauma by
food).
– Explosion from within: Occurs when expanding
force exceeds that of venous wall tension
(Pressure more than 250-300 cm H2O).
– In 30% of cases, the bleeding is due to associated
other causes e.g. peptic ulcer.
27. BLEEDING OESOPHAGEAL VARICES
• Investigations:
– Barium Swallow: Grape like filling defects in lower
oesophagus.
– Endoscopy: Diagnosis & management of bleeding
varices. Risk of rebleeding is high in big varices &
in presence of red whale markings (Long. dilated
venules).
– Duplex ultrasound : →
• Diagnosis of portal hypertension & varices (PV> 13mm).
• Diagnosis of ascites (sensitive up to300ml).
• Diagnosis of the cause of portal hypertension.
• Direction of blood in portal vein (hepatopetal or
28. BLEEDING OESOPHAGEAL VARICES
• Investigations:
– Measurement of Portal Venous Pressure:
• Measurement of Sinusoid or Post sinusoid Pressure:
The pressure can be obtained by getting the wedge
hepatic venous pressure through trans-jugular trans-
hepatic catheterization of hepatic vein.
• Measurement of Pre sinusoid Pressure : The pressure
can be obtained by one of following methods →
– Percutaneous catheterisation of splenic sinusoids.
– Percutaneous transhepatic catheterisetion of intra hepatic
branches of portal veins.
– Measurement of intra variceal pressure (through endoscopy)
using either micro needle introduced into varices or
pneumatic cuffs compressing varices at certain pressure.
29. BLEEDING OESOPHAGEAL VARICES
• CHILD'S-PUGH CLASSIFICATION:
• Grades: A, 5 to 6 points; B, 7 to 9 points; C,
10 to 15 points.
• The operative mortalities after shunt
determined by child- Pugh classification are
• For type A: 5 %......For type B: 10%.............For type C:
40%.
• Liver Biopsy: The severity of histological
changes in liver is correlating with immediate
death rate after shunt. The most ominous
findings are; the presence of hepatocellular
30. CHILD'S-PUGH CLASSIFICATION
Three points Two points One point Parameter
> 3.0 2.0-3.0 < 2.0 Bilirubin (mg/dl)
< 2.8 2.8-3.5 > 3.5 Albumin (g/dl)
> 6 4-6 1-3 Prothrombin time
(seconds above
control value)
Moderate slight None Ascites
3-4 (severe) 1-2 (mild) None Encephalopathy
31. BLEEDING OESOPHAGEAL VARICES
• MANAGEMENT OF BLEEDING VARICES:
– General resuscitative measures {fresh blood transfusion, antacids, VK
injection & repeated enemata to decrease absorption of ammonia, fluids}.
– Pharmacotherapy: To reduce portal pressure by 20% either in acute or chronic
setting → Vasopressin & somatostatin: Vasopressin is infused at 0.2 to 0.4 units/min..
– Inderal or propranolol.
– Endoscopic Sclerotherapy, endoscopic Banding Ligation or both:
• Intra variceal injection of one of the following sclerosants e.g. Sod. Marrhuate,
ethmoline, ethanolamine oleate, tetradecylsulphate…etc
• Complications of Sclerotherapy:
– Fever, retrosternal chest pain, septicaemia
– Pulmonary complications e.g. pneumonia, ARDS, pleural effusion, infiltration on chest
X ray.
– Oesophageal complications:
• Mucosal ulceration & bleeding.
• Oesophageal perforation, acute injection dysphagia.
• Oesophageal stricture.
– Technical difficulties:
• Poor results in fundic varices.
• Difficulties in visualization in 25% of cases.
32. BLEEDING OESOPHAGEAL VARICES
• Trans-jugular Intra-hepatic Portal Systemic
Shunt (TIPS)
– Technique: TIPS are introduced through the right
internal jugular vein → catheterisation of a main
hepatic vein → trans-parenchymal catheterisation
of portal vein, & serial dilation of track until large
enough to insert a stent. Technical success rate is
92 %.
– Complications:
• The rebleeding rate is 20 % at 1-year follow-up.
• Shunt dysfunction in 50-60% of cases at 6 months e.g.
thrombosis, migration, stenosis & obstruction.
33. BLEEDING OESOPHAGEAL VARICES
– Percutaneous Transhepatic Obliteration of
Varices: It is indicated in case of failure of
endoscopic sclerotherapy & the patient is unfit for
shunt surgery}.
– Angiographic Embolization of mid splenic, left
gastric & left gastro epiploic arteries.
– Emergency Operations:
• Tanner’s trans-gastric resection & anastomosis.
• Trans-thoracic trans-esophageal ligation of varices.
• Devascularisation procedure (Hassab’s operation):
This procedure consists of splenectomy, gastric &
oesophageal devascularisation by ligation of left
gastric, left gastroepiploic & phrenic veins.
• Emergency Shunt Operations e.g. portocaval shunts
34. BLEEDING OESOPHAGEAL VARICES
• Balloon Tamponade: types include →
– Sengestaken Black more Tube: Three luminal tube;
gastric (200 cc air), oesophageal (40 mmHg) &
central luminal tubes). The most important is
gastric tube; traction against cardia → obstruction
of collaterals at cardia.
– Minnesota Tube: This tube has an additional
lumen to aspirate saliva.
– Complications of Balloon Tamponade;
• Renewing of haemorrhage after removal
• Aspiration of saliva (use four lumen tubes )
• Necrosis of mucosa due to prolonged pressure (tube
36. BLEEDING OESOPHAGEAL VARICES
• SURGICAL SHUNTS
• Shunts can be total, partial or selective
• Role of shunts is to:
– Emergency control of variceal bleeding if TIPS is
not available or contraindicated.
– Reduce portal hypertension in patients awaiting
transplantation
– Relieve intractable ascites
– Reduce bleeding from rectal, colonic or stomal
varices
– All types of shunt will correct hypersplenism if
37. BLEEDING OESOPHAGEAL VARICES
• TOTAL SHUNTS
– End-to-Side Porto-caval Shunt: End of PV to side
of IVC.
– Side-to-side porto-caval shunt: Side-of PV to side
of IVC.
– Meso-caval Shunt: Prosthetic or internal jugular
vein graft is interposed between IVC & SMV.
– Central Spleno-renal Shunt : Splenic vein is
anastomosed to centre of renal vein after removal
of spleen )
38.
39.
40. BLEEDING OESOPHAGEAL VARICES
• PARTIAL OR SELECTIVE SHUNTS
• Introduction: The portal vein carries 50% of
oxygen supply to liver; hepatic oxygenation is
impaired by 50% in case of total shunt →
progressive hepatocellular damage & hepatic
encephalopathy. In partial shunt, still some
blood reaches the liver → ↓incidence of
hepatic encephalopathy.
• Definition: Selective drainage of variceal area
only while the rest of portal circulation
41. BLEEDING OESOPHAGEAL VARICES
• Types of Selective Shunts:
– Distal splenorenal shunt (Warren): The splenic
vein is inserted into the left renal vein.
Oesophageal varices is selectively decompressed
through the short gastric veins into the splenic &
then into renal veins.
– Left gastric vena caval shunt (Inokuchi): The left
gastric vein is anastomosed to IVC
• Advantages of selective shunt:
– Selective decompression of variceal area.
– Low incidence of hepatic encephalopathy
42.
43. BLEEDING OESOPHAGEAL VARICES
• Sugiura Operation: The operation is formed of
two stages;
– Thoracotomy (The first stage): All dilated venous
collaterals between oesophagus & adjacent
structures are divided & ligated. The oesophagus
at the level of diaphragm is transected &
reanastomosed.
– Laparotomy is done in the second stage (this stage
can be done with the first stage if there is active
bleeding): Upper 2/3 of stomach is devascularized.
Splenectomy, selective vagotomy & pyloroplasty
are carried out.
44. ASCITES
• Causes:
– Lymphatic ooze from liver surface
– Hypoalbuminemia
– Salt & water retention
– Portal hypertension ( ↑filtration force )
– 2% of cases, TB
• Investigations:
– Paracentesis:
• WBCs ( > 250 /µL i.e. silent bacterial peritonitis)
• Cytological examination to exclude malignancy
• Amylase level: the level is high in pancreatic sources.
– Ultrasound: Sensitive to detect up to 300 ml of
45. ASCITES
• Treatment:
• Medical Treatment:
– Sodium intake is restriction; Diuretics (see medical
side).
– Albumin transfusion
– Paracentesis: If above measures failed,
paracentesis can be used or more recently TIPS
has been shown to alleviate refractory ascites.
47. ASCITES
• Surgical Treatment:
• Portocaval Shunt.
• Peritoneal Jugular Shunt (Le Veen shunt):
– Procedure: Silastic catheter with unidirectional
valve is kept subcutaneous under between
internal jugular vein & peritoneal cavity.
– Indications:
• Refractory ascites failing to respond to high doses of
diuretics.
• Ascites due to Budd Chiarri syndrome
• Malignant ascites esp. if malignant cells are not present
in ascitic fluid.
49. 1. Acute abscess: This is a rare condition
occurring as a sequel of specific fever, e.g.
typhoid fever, it can also be blood borne from
a distant septic lesion or during systemic
pyaemia. The treatment is splenectomy if
possible, but if there are dense adhesions,
drainage of the abscess is only performed.
2. Chronic abscess: This is also rare and can
result form a neglected acute abscess or an
infected cyst. Treatment is splenectomy.
3. Tuberculosis: The disease is usually a
INFECTIONS OF THE SPLEEN
50. This category includes a wide spectrum of
disorders in which there is accelerated
destruction of mature red blood cells.
Haemolytic anaemias are generally classified to
congenital or acquired:
Congenital anaemias: are due to an intrinsic
abnormality of the red blood cells like hereditary
spherocytosis , thalassaemia and sickle-cell
anaemia.
Acquired anaemias: are related to extra-
corpuscular factors acting on normal red blood
CHRONIC HAEMOLYTIC ANAEMIAS
51. Hereditary spherocytosis
Aetiology:
There is a defect in the red-cell membrane due to
deficiency of certain proteins known as spectrins. As a
result, there is excessive permeability to sodium ions
and the red cell integrity can only be .maintained by
increasing the glycolytic activity to provide the energy
required to pump out the sodium ions.
1. The increased metabolic activity leads to the
development of microspherocytosis in the red – pulp
of spleen where the available glucose is diminished.
2. Microspherocytes are trapped in the red pulp
because they lack deformability and so they are
CHRONIC HAEMOLYTIC ANAEMIAS
52. Hereditary spherocytosis
Pathology:
1. Blood: Abnormal fragility; haemolysis occurs at
higher concentrations of saline than in the
normal .Normal haemolysis starts at 0.45%
saline solution. In spherocytosis ,haemolysis
starts at o.6%. In spherocytosis, the R.B.Cs are
biconvex instead of being biconcave.there is
anaemia with reticulocytosis.
2. Liver: Slightly enlarged, Pigment stones may form
in the biliary system, Biliary cirrhosis may occur
in late cases.
CHRONIC HAEMOLYTIC ANAEMIAS
53. Hereditary spherocytosis
Clinical features:
Usual course:
Jaundice is associated with anaemia.
Life span is not greatly affected.
Icterus index is usually not more than 50.
Severe cases: These are rare and are characterized by:
Haemolytic crisis; fever, severe anaemia and depth of
jaundice increases.
Striation of cranial bones may be detected in X-ray.
CHRONIC HAEMOLYTIC ANAEMIAS
54. Hereditary spherocytosis
Complications:
A. Pigment gall stones may occur in up to 60% of
patients.
B. Chronic leg ulcers may occur in long standing cases.
Treatment:
Splenectomy relieves jaundice and anaemia (as spleen is
the site of destruction of the RBCs), but it does not
affect the spherocytosis. The best timing for
splenectomy is at the age of 6-7 years. Before this age
there is a risk of increased liability to infection due to
loss of the immune functions of the spleen. If there are
any biliary stones, cholecystectomy should be done
CHRONIC HAEMOLYTIC ANAEMIAS
55. Idiopathic Thrombocytopenic purpura
Aetiology
This disease was formerly though to be idiopathic . But it
is now known to be an auto-immune disease. Platelets
are sensitized with an auto-antibody that results is their
early sequestration by the reticuloendothelial cells
(mainly in the spleen and liver).
Pathology
The term ITP should be reserved for the haemorrhagic
disorder characterized by:
1. Subnormal platelets count.
2. Bone marrow contains normal or increased
megakaryocytes.
CHRONIC HAEMOLYTIC ANAEMIAS
56. Idiopathic Thrombocytopenic
purpura
Clinical features
Symptoms
1. The disease occurs most commonly in children and
young adult females.
2. The course of the disease runs in remissions and
relapses.
3. It may present by an attack of bleeding under the skin
(ecchymosis) or mucous membrane or from an
orifice, as the nose, urinary or gastrointestinal tract.
Menorrhagia is a common complaint in affected
CHRONIC HAEMOLYTIC ANAEMIAS
57. Idiopathic Thrombocytopenic
purpura
Investigations
The red and white cells are diminished due to
repeated haemorrhages.
Platelets are diminished in number. Their count
may drop to 30.000/ul.
Bleeding time is prolonged up to 20 minutes
(normally 2-5 min). Coagulation time is
normal. The blood clot is soft, friable and fails to
retract.
CHRONIC HAEMOLYTIC ANAEMIAS