This document provides information on various liver, pancreas and biliary tract disorders. It begins with an introduction to cirrhosis of the liver, defining it as a chronic disorder characterized by replacement of normal liver tissue with diffuse fibrosis. It then discusses causes such as alcoholism and hepatitis B and C. Clinical manifestations, diagnostic studies, medical management and complications of cirrhosis are summarized. The document subsequently provides overviews of other conditions including jaundice, hepatitis, liver abscess, Wilson's disease, Gilbert's syndrome, hemochromatosis, portal hypertension and ascites.
collected from multiple general surgery references (2016) like bailey's and loves short practice of surgery , Schwartzs Principles of Surgery, 10th Edition , Schwartzs Principles of Surgery, 10th Edition and Matary's GIT surgery .
collected from multiple general surgery references (2016) like bailey's and loves short practice of surgery , Schwartzs Principles of Surgery, 10th Edition , Schwartzs Principles of Surgery, 10th Edition and Matary's GIT surgery .
Inflammatory bowel disease (IBD) is a group of disorders that cause chronic inflammation (pain and swelling) in the intestines. IBD includes Crohn's disease and ulcerative colitis. Both types affect the digestive system. Treatments can help manage this lifelong condition
Inflammatory bowel disease (IBD) is a group of disorders that cause chronic inflammation (pain and swelling) in the intestines. IBD includes Crohn's disease and ulcerative colitis. Both types affect the digestive system. Treatments can help manage this lifelong condition
Newstylesite luxurious Watch is One of the MostNew Style Site
Watches are one of the most beautiful gift, which one can plan for giving their loved ones. It is only the time which does not wait or stop for anyone.
A look at something we all have, but may not know how to manage. Your digital footprint is increasingly important and should be top of mind before sharing content online.
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Chronic Liver Disease in pediatric: a case presentation and discussionDr Abdalla M. Gamal
A presentation from a tutorial about an interesting case that came to the Pediatric Department of Sebha Medical Center and was imaged by the Radiology Department.
The tutorial was a joint effort between Dr Zeinab Salem Ali (from Pediatric Department) and me (from Radiology Department). In her slides, Dr Zeinab presented the case history, examination, investigations, differential diagnosis and discussed the clinical presentation, investigations and management for chronic liver diseases in pediatric patients.In my slides, I discussed the definition, etiology, natural history of this condition and explained the role of imaging in its diagnosis.
These are my slides after some modifications. I added an aknowlegement page to illustrate Dr Zeinab effort and to thank Dr Khaled Aljasem from Pediatric Department for his effort in revising the original presentations and the constructive feedback he provided which improved the quality of the presented material. Then I added a summary for the parts Dr Zeinab has presented to make this powerpoint presentation complete.
This presentation was presented by Dr Zeinab Salem (from Pediatric Department) and me in a joint tutorial between Pediatric Department and Radiology Department of Sebha Medical Center.
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism. ... As cirrhosis progresses, more and more scar tissue forms, making it difficult for the liver to function (decompensated cirrhosis)
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.
Similar to DISORDERS OF LIVER, PANCREAS AND BILIARY TRACT (20)
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
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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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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?
- 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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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4. INTRODUCTION
Liver is normally able to
regenerate damaged cells. Cirrhosis develops
when the factor damage the liver such as
alcohol and chronic infections are present
over a long period of time. When this
happens, the liver become injured and scarred.
A scarred liver cannot function properly and
cirrhosis results.
5. DEFINITION:
Cirrhosis is a chronic disorder
characterized by replacement of normal
liver tissue with diffuse fibrosis that
disrupts the structure and function of
the liver.
6. INCIDENCE:
Cirrhosis and chronic liver diseases were the
tenth leading cause of death for men and
twelth leading cause of death in women.
In India 2,08,185 total deaths due to
cirrhosis.
The age adjusted death rate is 23.59 per
1,00,000 of population ranks India 27 in
world.
17. INTRODUCTION:
Jaundice causes your skin and the whites of your
eyes to turn yellow. Too much bilirubin causes
jaundice. Bilirubin is a yellow chemical in
hemoglobin, the substance that carries oxygen in
your red blood cells. The term jaundice comes
from the French word jaune, meaning yellow.
18. DEFINITION:
Jaundice (also known as icterus ) is
a yellowish pigmentation of the skin, the
conjunctival membranes over the sclerae (whites of the
eyes), and other mucous membranes caused
by hyperbilirubinemia (increased levels of bilirubin in
the blood).
19. INCIDENCE:
Many healthy babies have some jaundice during
the first week of life. It usually goes away.
However, jaundice can happen at any age and may
be a sign of a problem.
20. ETIOLOGY:
Jaundice can happen for many
reasons, such as
Blood diseases
Genetic syndromes
Liver diseases, such as hepatitis or cirrhosis
Blockage of bile ducts
Infections
Medicines
23. CLINICAL MANIFESTATIONS:
The main symptom of jaundice is a yellow discoloration of
the white part of the eyes (sclera) and of the skin.
The conjunctiva of the eye are one of the first tissues to
change color as bilirubin levels rise in jaundice. This is
sometimes referred to as scleral icterus. However, the
sclera themselves are not "icteric" (stained with bile
pigment) but rather the conjunctival membranes that overlie
them.
The yellowing of the "white of the eye" is thus more
properly termed conjunctival icterus.
24.
25. ASSESSMENT AND DIAGNOSTIC STUDIES:
This hyperbilirubinemia subsequently causes increased levels of
bilirubin in theextracellular fluid. Concentration of bilirubin
in blood plasma is normally below 1.2 mg/dL (<25µmol/L). A
concentration higher than approx. 3 mg/dL (>50µmol/L) leads to
jaundice.
Laboratory findings include:
Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic
anemia causes increased heme metabolism; exception: infants
where gut flora has not developed).
Serum: increased unconjugated bilirubin.
26. MANAGEMENT:
Correction of coagulopathy
Fluid and electrollyte balance
Low fatty spicy foods
Blood transfusion if needed
Antibiotics
Encourage fluid and fiber diet
Biliary drianage with ERCP(Endoscopic retrograde
cholangiopancreatography)
27.
28. INTRODUCTION:
Hepatitis is an inflammation of
the liver.
Hepatitis is of various types that is:
Viral hepatitis
Non-viral hepatitis
29. VIRAL HEPATITIS:
DEFINITION:
It is a systemic viral infection in which
necrosis and inflammation of liver cells produce a
characteristic cluster of clinical, biochemical and
cellular changes.
31. INCIDENCE:
Approximately 61000 cases occur in U.S and 10
million cases world wide
The prevalance of HAV antibodies increases with
age and most people older than 50 yrs of age have
prior exposure.
32. ETIOLOGY:
Viral hepatitis is caused by one of the major viruses
that is A,B,C,D,E and G
Other viruses include
Cytomegalovirus
Herpes virus
Coxsackie virus
Rubella virus
33. MODE OF TRANSMISSION:
Over crowding
Poor sanitation
Faeceal-oral route
Infected food handler
Multiple sex partners
Blood transfusions
43. PREVENTION:
Vaccination
Hand washing
Safe drinking water
Proper control of sewage disposal
Caution about contaminated foods
Health education
45. DEFINITION:
Liver abscess is accumulation or
stagnantion of pus in the liver due to
infection
INCIDENCE:
It is most commonly occurs in developing
countries of the trophics and sub trophics
due to poor sanitation and hygiene
48. PATHOPHYSIOLOGY:
Due to infection
Infective organisms reach the liver through the
biliary, portal arterial loss lymphatic system
Bacterial toxins destroy the neighbouring liver cells
Necrotic tissue serves a protective wall for the
organisms
49. Leukocyte migrate serves a protective wall for the
organism
Abscess cavity full liquid containig living and dead
leukocytes, liquefied liver cells, and bacteria
LIVER ABSCESS
50. CLINICAL MANIFESTATIONS:
Fever with chills
Diaphoresis
Malaise
Anorexia
Dull abdominal pain
Tenderness in right upper quadrant
Anemia
51. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Blood culture
Aspiration of liver abscess guided by ultrasound
CT
MRI
Percutaneous drainage of pyogenic abscess
52. MEDICAL MANAGEMANT:
IV antibiotics thearpy depend on the organism
Continuous supportive care is provided
Open surgical drainage may be required if
antibiotic thearpy and percutaneous drainage is
ineffective
A catheter is left in place for continuous drainage.
53. NURSING MANAGEMENT:
Continuous monitoring of the drinage and skin
care is provided
Vital signs monitoring
Administer antibiotics as prescribed
Management of drainage
55. INTRODUCTION:
Wilsons disease is a
progressive, familial, terminal neurologic
disease accompained by chronic liver
disease leading to cirrhosis.It is
associated with increased storage of
copper.
57. INCIDENCE:
Wilsons disease occurs world wide with an average
prevalance of 30 individuals per million
population.
Wilsons disease is an inherited disorder that affects
about one to 4 in 30,000-1,00,000 individuals of
any race or ethnicity.
CAUSES:
The condition is due to “mutations” in the wilson
disease protein (ATP7B) gene.
66. INTRODUCTION:
Gilbert’s syndrome is often
shortened to GS also called Gilbert-Meulengracht
syndrome.
DEFINITION:
Gilberts syndrome is a genetic liver
disorder and the most common hereditary cause of
increased bilirubin and is found upto 5% of the
population.
67. INCIDENCE:
It is mostly seen in 5% of population
Gilbert syndrome is closer to 10% of caucasian
people.
CAUSES:
Idiopathic
Genetic disorder
Reduction activity of the enzyme.
68. PATHOPHYSIOLOGY:
Due to etiological factors
Reduced activity of enzyme gluuronyltransferase
It conjugates bilirubin and a few other lipophilic
molecules
Conjugation renders bilirubin water-soluble
Excreted in bile into the duodenum
69. CLINICAL MANIFESTATIONS:
Mild jaundice
Fatigue
Difficulty in maintaining concebtration
Loss of appetite
Abdominal pain
Weight loss
Itching
70. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Increased bilirubin levels
TREATMENT
Gilbert syndrome usually doesnot need any
treatment.
72. INTRODUCTION:
Haemochromatosis is a systemic disease that
affecs the liver, heart, pancreas and the endocrine
system. It is caused by increased and inappropriate
absorption of dietary iron.
73. DEFINITION:
Haemochromatosis is iron over
load indicates accumulation of iron in the body from any
cause.
INCIDENCE:
It is most common in white people and occurs in 0.6%
of the population.
It is uncommon in indian population due to low
prevalance of gene associated with haemochromatosis.
74. CAUSES:
Genetic disorder
Transfusional iron over load (repeated blood
transfusion)
Increased and inappropriate absorption of
dietary iron.
77. MANAGEMENT:
Phlebotomies
Deferoxamine drug
Dietary modifications such as avoidance of
vitamin c and iron supplements, uncooked
foods, and iron-rich foods.
Complications include cirrrhosis, liver
failure, hepatic carcinaoma, and cardiac
failure
79. DEFINITION:
The normal venous pressure is 5-10 mm of Hg. A
wedged hepatic venous pressure or direct portal
pressure that is more than 5 mm of Hg greater than
the inferior vena caval pressure, a splenic pressure
of more than 15 mm of Hg measured at suregry of
greater than 30 cm water is abnormal and indicates
the presence of portal hypertension.
87. CAUSES:
Cirrhosis of liver
Variceal bleeding
Hepatic encephalopathy
Jaundice
Portal hypertension
Increased flow of hepatic lymph
Impaired water excretion
88. PATHOPHYSIOLOGY:
Due to etiological factors(cirrhosis of liver)
Splenic arterial vasodilatation
Decreased in circulating arterial blood volume
Activation of renin angiotensin and symathetic nervous
system
90. CLINICAL MANIFESTATIONS:
Increased abdominal girth
Weight gain
Bulging flanks
Shortness of breathe
Fluid and electrollyte imbalances
Straie, distended veins
Umbilical hernia
91. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Ultrasound
Doppler examination
Serum levels
Ascites total protein and serum ascites albumin
gradient is 1.1g/dl
95. DEFINITION:
Fluminant hepatic failure or liver
failure is a clinical syndrome characterized b severe
impairement of liver function associated with hepatic
encephalopathy.
96. INCIDENCE:
It is uncommon with approximately 2,000 cases
per year in the united states.
It develops within 8 weeks after the first symptom
of jaundice
The survival rate is approximately 50%-80%
It is common in men than in women
98. PATHOPHYSIOLOGY:
Due to etiological factors
Disruption in the essential intracellular processes
Accumulation of toxic metabolic products
Liver cell failure
99. CLINICAL MANIFESTATIONS:
Anorexia, nausea
Epigastric and upper abdominal distress
Abdominal pain and GI bleeding
Tacchycardia
Oliguria, hyponatremia, hypokalemia
Altered mental status
Cerebral edema
Hepatic encephalopathy
100. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Doppler sonogram
ABG analysis
Elevation of serum alkaline, AST, ALT
Blood culture
Chest x-ray
Echocardiography
Coagulation studies
101. MANAGEMENT:
Administration of life saving antibodies
Fluid and electrollyte balance
N-acetylcysteine for acetaminophen toxixity
Plasmapharesis
Prostaglandins thearpy
Extra corporeal liver assist devices
Bio artificial liver
Liver transplantation
103. DEFINITION:
Hepatic tumours may be benign or malignant. It is
an abnormal proliferation of cells in the liver.
INCIDENCE:
It is most frequently in women in their
reproductive years
106. CLINICAL MANIFESTSTIONS:
Pain in epigastric right upper quadrant or back
Weight loss
Loss of sterngth
Anorexia
Anemia
Jaundice
Ascites
110. NURSING MANAGEMENT:
Constant infusion of 10% glucose may be required in
first 48hrs to prevent fall in blood glucose levels
Close monitoring
Hydration
Health education
Psychological reassurance
112. DEFINITION:
Cholecystitis is defined as acute
inflammation of gallbladder.
INCIDENCE:
It is more common after 40 yrs of age,
especially in women
It is uncommon in chidren and young
women
114. ETIOLOGY:
Gall stones
Emphysema of the gall bladder
Intestinal organisms like E.coli
Cytomegalovirus and cryptosporidium
Generalized peritonitis
115. PATHOPHYSIOLOGY:
Due to formation of gall stones
It obstructs the bile out flow
Bile in gall bladder intiates a chemical recation
Autolysis and edema occurs, and blood vessel are compressed
It results in gangrene of the gall bladder with perforation
CHOLECYSTITIS
116. CLINICAL MANIFESTATIONS:
Epigastric pain at right hypochondrial region
Nausea and vomiting
Flatulence
Sweating patient with swallow
Fever, Jaundice
Murphys sign:Right hypochondrial tenderness is present
and is exacerbated by inspiration
Muscle grading and rebound tenderness
118. MANAGEMENT:
Analgesics like buphine and atropine is administered
Antibiotics are given like amoxicillin
Oral feedings are stopped and intravenous fluid
administered
The patient should be frequently observed with
abdominal examination and sequential leukocyte cont
121. DEFINITION:
It is defined as formation of stones in
the common bile duct is called choledocholithiasis.
INCIDENCE:
About 50% of patients with cholelithiasis have
common bile duct stones
It increase with age
122. ETIOLOGY:
Common bile duct gall stones
Cholangitis
Carcinoma of bile duct and gall bladder
Sclerosing cholangitis
Metastatic carcinoma
Haemophilia
Biliary atrexia
Choledochol cyst
123. CLINICAL MANIFEASATIONS:
The classic traid of symptoms
Right upper abdominal pain
FEVER
Jaundice
Pain is colicky severe and persists for hours
Vomiting
Dark colour urine
Faces are pale
Itching
124. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Liver function test
Prolonged prothrombin time
Radiography
Ultrasonography
Cholangiography
125. MANAGEMENT:
Administer antibiotics
Maintain fluid and electrollyte balance
Maintain nutritional status
Administer parenteral vit k of prothrombin time is
prolonged
Sphinterotomy
Cholecystectomy
127. DEFINITION:
Pancreatitis is defined as inflammation of
the pancreas
INCIDENCE:
Men of 40-45 yrs of age
Women f 50-55 yrs of age
Hereditary
Autodigestion of pancreas
128. ETIOLOGY:
Use of alchol
Spasm and edema
Blunt abdominal trauma
Peptic ulcer disease
Ischemic vascular disease
Hyperlipidemia, hypercalcemia
Oral contraceptives
129. PATHOPHYSIOLOGY:
Due to etiological factors
Enter the common bile duct
Lodge at the ampulla of vater
Obstructing the flow of pancreatic juice
Reflux of bile from common bile duct into the
pancreatic duct
130. Activation of pancreatic enzymes
Vasodilatation and increased vascular permeability
Necrosis and erosion and haemorrhage
131. CLINICAL MANIFESTATIONS:
Severe abdominal pain and back pain
Low grade fever
Leukocytosis
Hypotension, tacchycardia, jaundice
Bowel sounds decreased
Cyanosis of abdominal wall
Ecchymosis
Mental confusion
Agitation
132.
133. ASSESSMENT AND DIAGNOSTIC
STUDIES:
History collection
Physical examination
Serum and lipase levels
Urinary amylase levels
White blood cell count increses
Elevated serum bilirubin levels
Ultrasound
CT-scan
ERCP
134. MANAGEMENT:
Parenteral nutrition
Nasogastric suction
Histamine 2 antagonist such as cimentidine and
rantidine
Proton pump inhibitors such as pantoprozole
Laporotomy
136. DEFINITION:
Pancreatic cancer occurs when cancer
cells develop from the pancreas a
glandular organ located behind the
stomach.
INCIDENCE:
In 2012 pancreatic cancer of all types
cause 330000 deaths globally the
seventh most common cause of deth
due to cancer.