This document discusses various hemodynamic disturbances including congestion, hemorrhage, and edema. It defines these conditions and describes their morphological features. Congestion is a passive increase in blood volume due to impaired outflow, causing tissues to appear cyanotic or red-brown. Hemorrhage can be external or internal, and results from vessel rupture. Edema is the accumulation of fluid in interstitial spaces or cavities, and can be localized or generalized. It results from increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, sodium retention, or inflammation. The morphology of congestion, hemorrhage and edema in various organs is described.
Slide Note: Edema Congestion
Title: Edema Congestion: Understanding the Mechanisms and Clinical Implications
Introduction:
Edema congestion is a pathological condition characterized by the abnormal accumulation of fluid within tissues or body cavities, leading to swelling and impaired tissue function. It is a complex physiological process that can arise due to various underlying factors and may manifest in different regions of the body. Understanding the mechanisms and clinical implications of edema congestion is crucial for healthcare professionals to effectively diagnose, manage, and treat patients presenting with this condition.
I. Mechanisms of Edema Congestion:
A. Increased Capillary Hydrostatic Pressure:
- Elevated pressure within the capillaries due to factors such as venous obstruction, heart failure, or localized inflammation.
- Higher hydrostatic forces cause an excessive filtration of fluid from the capillaries into the interstitial spaces, contributing to tissue swelling.
B. Decreased Plasma Oncotic Pressure:
- Reduction in plasma protein levels, particularly albumin, results in decreased oncotic pressure.
- Lower oncotic pressure leads to reduced fluid reabsorption from the interstitial spaces back into the capillaries, exacerbating fluid accumulation.
C. Lymphatic Obstruction or Insufficiency:
- Impaired lymphatic drainage due to lymphatic vessel obstruction, surgical intervention, or congenital malformations.
- Inadequate lymphatic clearance results in the retention of interstitial fluid, leading to edema.
D. Sodium and Water Retention:
- Dysregulation of sodium and water balance in conditions like kidney dysfunction, cirrhosis, or hormonal imbalances.
- Sodium retention leads to increased osmotic pressure, causing water to accumulate in the interstitial spaces.
II. Clinical Implications:
A. Peripheral Edema:
- Swelling predominantly in the extremities, commonly observed in conditions such as heart failure, deep vein thrombosis, or venous insufficiency.
- Patients may experience discomfort, reduced mobility, and skin changes due to chronic edema.
B. Pulmonary Edema:
- Accumulation of fluid in the lungs, often resulting from heart failure, acute respiratory distress syndrome (ARDS), or pneumonia.
- Respiratory compromise, cough, and shortness of breath are common symptoms requiring urgent medical intervention.
C. Cerebral Edema:
- Swelling within the brain due to trauma, stroke, or tumors.
- Potentially life-threatening, as it can lead to increased intracranial pressure, neurological deficits, and herniation.
D. Ascites:
- Edema within the peritoneal cavity, commonly associated with liver cirrhosis, malignancies, or congestive heart failure.
- Abdominal distension, discomfort, and respiratory compromise are typical manifestations.
III. Diagnostic Approach:
A. Clinical Examination:
- Careful assessment of the patient's medical history, physical symptoms, and risk factors.
Slide Note: Edema Congestion
Title: Edema Congestion: Understanding the Mechanisms and Clinical Implications
Introduction:
Edema congestion is a pathological condition characterized by the abnormal accumulation of fluid within tissues or body cavities, leading to swelling and impaired tissue function. It is a complex physiological process that can arise due to various underlying factors and may manifest in different regions of the body. Understanding the mechanisms and clinical implications of edema congestion is crucial for healthcare professionals to effectively diagnose, manage, and treat patients presenting with this condition.
I. Mechanisms of Edema Congestion:
A. Increased Capillary Hydrostatic Pressure:
- Elevated pressure within the capillaries due to factors such as venous obstruction, heart failure, or localized inflammation.
- Higher hydrostatic forces cause an excessive filtration of fluid from the capillaries into the interstitial spaces, contributing to tissue swelling.
B. Decreased Plasma Oncotic Pressure:
- Reduction in plasma protein levels, particularly albumin, results in decreased oncotic pressure.
- Lower oncotic pressure leads to reduced fluid reabsorption from the interstitial spaces back into the capillaries, exacerbating fluid accumulation.
C. Lymphatic Obstruction or Insufficiency:
- Impaired lymphatic drainage due to lymphatic vessel obstruction, surgical intervention, or congenital malformations.
- Inadequate lymphatic clearance results in the retention of interstitial fluid, leading to edema.
D. Sodium and Water Retention:
- Dysregulation of sodium and water balance in conditions like kidney dysfunction, cirrhosis, or hormonal imbalances.
- Sodium retention leads to increased osmotic pressure, causing water to accumulate in the interstitial spaces.
II. Clinical Implications:
A. Peripheral Edema:
- Swelling predominantly in the extremities, commonly observed in conditions such as heart failure, deep vein thrombosis, or venous insufficiency.
- Patients may experience discomfort, reduced mobility, and skin changes due to chronic edema.
B. Pulmonary Edema:
- Accumulation of fluid in the lungs, often resulting from heart failure, acute respiratory distress syndrome (ARDS), or pneumonia.
- Respiratory compromise, cough, and shortness of breath are common symptoms requiring urgent medical intervention.
C. Cerebral Edema:
- Swelling within the brain due to trauma, stroke, or tumors.
- Potentially life-threatening, as it can lead to increased intracranial pressure, neurological deficits, and herniation.
D. Ascites:
- Edema within the peritoneal cavity, commonly associated with liver cirrhosis, malignancies, or congestive heart failure.
- Abdominal distension, discomfort, and respiratory compromise are typical manifestations.
III. Diagnostic Approach:
A. Clinical Examination:
- Careful assessment of the patient's medical history, physical symptoms, and risk factors.
Disorders that perturb cardiovascular, renal, or hepatic function are often marked by the accumulation of fluid in tissues (edema) or body cavities (effusions).
This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Disorders that perturb cardiovascular, renal, or hepatic function are often marked by the accumulation of fluid in tissues (edema) or body cavities (effusions).
This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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?
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- 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
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
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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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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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
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
2. Hemodynamic disturbances
• Problems related to the flow of blood and
consequences thereof. Include:
• Hyperemia /congestion
• Hemorrhage
• Edema
• Thrombosis
• Embolism
• Infarction
• Shock
3. Hyperemia
• An active process resulting from
augmented tissue inflow due to arteriolar
dilatation causing increased volume of
blood in a particular tissue.
• Area is red due to oxygenated blood
• E.g. exercise, inflammation
4.
5.
6. CONGESTION
• A passive process resulting from impaired
outflow of venous blood from a tissue causing
increased volume of blood in that tissue.
• Poor oxygenation – blue red in color cyanosis
hypoxia - cellular degeneration - secondary
fibrosis
• Elevated intravascular pressure- capillary
rupture - focal hemorrhage
• Cardiac failure, local venous obstruction.
7. MOPRHOLOGY
Gross: cut surfaces are wet and hemorrhagic
Microscopic:
Acute Pulmonary congestion
alveolar capillary dilatation with blood
alveolar septal edema
intra alveolar hemorrhage.
Chronic Pulmonary congestion
Septa thickened and fibrotic, alveolar
septal edema.
Hemosiderin laden macrophages in
alveolar spaces - heart failure cells.
9. Acute hepatic congestion:
Distention of central vein and sinusoids with blood,
Central hepatocyte degeneration, Fatty change in
peri-portal hepatocytes
Chronic hepatic congestion:
Gross: central region of hepatic lobule is red brown
and depressed – surrounding zones uncongested.
Nutmeg Liver
Microscopic: Centri-lobular necrosis, hepatocyte drop
out, hemorrhages, hemosiderin laden macrophages,
hepatic fibrosis -Cardiac Cirhosis
MORPHOLOGY…
11. Hemostasis: process of blood clotting preventing
excessive bleeding after blood vessel damage
Hemorrhage: Extravasations of blood because
of vessel rupture.
External
Internal
Capillary hemorrhage - Chronic congestion
Large artery and vein – injury of blood vessels,
atherosclerosis, inflammation, neoplastic
erosion
Petechiae: minute hemorrhage into the skin 1-2
mm, mucous membrane or serosal surfaces.
15. Hematoma : an extra-vascular hemorrhage
enclosed in the tissue.
Subdural Hematoma
16. Clinical Significance of Hemorrhage
Depends on :
Volume of blood loss:
• Greater loss hemorrhagic – hypovolemic shock.
• Small amount, Subcutaneous Trivial effect.
Rate of blood loss: Rapid loss of small blood,
gradual volume loss of larger blood little effect
on healthy person.
Site of hemorrhage.
• Brain Skull unyielding increase Intracranial
Pressure.
• external loss - Iron deficiency anemia
• Internal in body cavities /tissue - Iron reuse.
.
17. Edema
• Accumulation of fluid in the interstitial space or
body cavities
• Variously named according to the site:
• Hydrothorax
• Hydropericardium
• Hydroperitoneum /Ascites
• Total body water = 60% of body weight
• Intracellular = 40%
• Extracellular = 20% (Plasma 5% + Inters 10%)
18. Edema
• Two types
• 1. Localized edema involves an increase of fluid
in extracellular space locally
• 2. Generalized edema is due to increase in both
total body water and sodium
• Anasarca: Severe and generalized edema with
subcutaneous swelling
19. Fluid movement in body
• There is free exchange of water, electrolytes and
small molecules between intra and extracellular
compartments of body.
• Primary site - capillaries
• Fluid movement is governed by two forces
–Hydrostatic pressure
–Colloid osmotic pressure
• Overflow through lymphatics
23. 1.Increased Hydrostatic pressure.
a. Local increase – venous obstruction or
compression.
i. Thrombosis
ii. External Pressure (Tumor, mass, torniquet etc)
iii. Venous return due to lower extremity inactivity
iv. Arteriolar dilatiation, Heat Neurohumoral dys-
regulation.
b. General increase.
i. Congestive cardiac failure.
ii. Constrictive pericarditis.
iii. Ascites ( liver cirhosis).
24. Reduced osmotic pressure
• Protein loss /deficiency/ hypoproteinemia due to
• Protein losing glomerulopathies
Glomerulonephritis, nephrotic syndrome
• Liver cirrhosis – reduced synthesis
• Malnutrition
• Malabsorption, Protein losing gastroenteropathy,
28. Clinical Correlation:
• Mild to fatal
• Indication of underlying cardiac or renal
disease, Infection, neoplasm
• Impaired healing
• Pulmonary edema: Interference with
respiration
• Compression of blood supply. ischemia
29. MORPHOLOGY
• Most commonly encountered in
subcutaneous tissue, brain and lungs.
• Most easily recognized on naked eye
appearance.
• Microscopically: Edematous tissue
appears as subtle cell swelling with
clearing and separation of ECM elements
Subcutaneous edema: It may be
Diffuse : e.g. in nephritic syndrome
Of dependent parts, in legs, sacrum e.g. CCF
Periorbital: renal dysfunction
Pitting by Finger pressure displacing interstitial
fluid.
31. simple edema, or fluid collection within tissues.
Pitting on pressure
32. Pulmonary Edema
Lungs are 2-3 times heavier, frothy and
blood tinged fluid escapes on cross –
sectioning.
e.g. in ARDS, LVF, renal failure.
Microscopic: Alveoli filled with edema
fluid ( light pink) and few RBCs.
Congested blood vessels.
33. Cerebral edema
It may be
Localized ~ at site of lesion e.g.
abscess , neoplasms
Generalized~ e.g. in encephalitis,
hypertensive crisis, or venous outflow
obstruct.
Brain is grossly swollen with narrowed
sulci and distended gyri.
34. cerebral edema seen at the right
which obscures the structures. There
is a shift of the midline to the left.
