Portal Vein Thrombosis On Patients With Liver

Portal Vein Thrombosis On Patients With Liver
ISSN 2320–5407 International Journal of Advanced Research (2015), Volume 3, Issue 12, 1539– 1548
1539
Journal homepage: http://www.journalijar.com INTERNATIONAL JOURNAL OF ADVANCED RESEARCH RESEARCH ARTICLE
Portal vein thrombosis in patients with liver cirrhosis Insights to risk factors, clinical presentation and outcome
Afifi F. Afifi 1
, Usama M. Basha 1
, Fady M. Wadea 1
, Abdelaziz E. Samack 2
, Raghda A. Elsherbini 3
1– GIT and hepatology unit, internal medicine department, faculty of medicine, zagazig university.
2– radiology department, faculty of medicine, zagazig university.
3– clinical pathology department, faculty of medicine, zagazig university. EGYPT
Manuscript Info Abstract
Manuscript History:
Received: xxxxxxx
Final Accepted: xxxxxxxxxxxxxx
Published Online: xxxxxxxxxxxx
Key words:
Portal vein, Thrombosis, risk factors, cirrhosis.
*Corresponding Author
Pawan Kumar Thakur
Background and objectives: Portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is associated with worsening
liver function, ascites and the occurrence of gastroesophageal variceal bleeding. The aim of this work was to clarify the risk factors, clinical
presentation and complications of portal vein thrombosis in patients with liver cirrhosis and to study the outcome with or without treatment after
6 months follow up.
Methods: Hospitalized cirrhotic patients (N = 80) were segregated into the
PVT and non–PVT groups. PVT was detected by

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Peritonitis Case Study
DISCUSSION In this study, we found that early technical complications, peritonitis, long–term PD, and patient survival were not higher in patients
with LC compared to those without LC. This study is the first to evaluate the clinical outcomes of PD patients, depending on the absence or presence
of LC, by using propensity score matching methods. However, we did find that ascites associated with early peritoneal leakage and suspected
primary bacterial peritonitis was not increased in LC patients compared to patients without LC. In addition, hepatic encephalopathy was not an
obstacle in maintaining PD in LC patients. However, this retrospective analysis showed that requiring transition to HD from PD occurred slightly
faster in LC patients compared to patients without LC. We suggest that physicians can recommend PD as a RRT without having an additional risk,
even in LC patients with ascites. Despite the widespread use of HD as the main RRT, PD as a RRT for cirrhotic patients with ESRD may have several
advantages over HD. The maintenance of relatively stable hemodynamics is one of the biggest... Show more content on Helpwriting.net ...
Three patients had HEP during PD, however, recovery of HEP by receiving PD was not identified. Lactulose were supplied to treat the HEP in these
patients. We found that the use of lactulose was associated with lower peritonitis rates, because of increased bacterial translocation and promoted
colonic motility (29). The Application on PD or HD treating HEP in ESRD patients with LC were case–reported. Previously reported cases have
shown HEP recovery by shifting from HD to PD (30). Conversely, other cases have reported an aggravated course of HEP in a patients receiving PD
(31, 32). Hypokalemia during PD may worse HEP and the abrupt changes in volume and plasma osmolality during HD may exacerbate HEP (10, 33).
Aggravation of HEP may be not related with dialysis modality; management of risk factors for HEP is more important in LC

Summary: The Concept Of Metabolism
The Concept of Metabolism:
Nursing Interventions and Diagnoses Related to Cirrhosis
Hannah E. Null
New Mexico State University
Introduction
The concept of metabolism which is regulated by the major body system known as the endocrine system and includes the biochemical processes,
including the body's need to produce energy, repair cells, and maintain life (Pearson, 2015). This includes a series of glands including the hypothalamus,
pituitary, thyroid, parathyroid, thymus, adrenal, and the three organs being the pancreas, female ovary, and the male testis. The major organ being
discussed for the purpose of this paper is the liver, a complex organ with multiple metabolic and regulatory functions (Pearson, 2015). ... Show more
content on Helpwriting.net ...
Over time the liver is unable to metabolize the alcohol and leads the liver to form fibrous tissue, develop nodules, and the liver shrinks and has a
nodular uneven appearance (Pearson, 2015). Biliary cirrhosis is another type of liver disease that is characterized by the inability of bile to be
excreted, causing build up within the liver which eventually destroys the cells within the liver. The third type of cirrhosis is known as posthepatic
cirrhosis and is the result of a patient having hepatitis B or C resulting from an unknown cause. This type of cirrhosis causes the liver to shrink and
become nodular and fibrous resulting in destruction of the liver cells. Risk factors for all three types of cirrhosis include high risk behaviors such as
consuming excessive amounts of alcohol, drug use (primarily IV), unsafe sexual behaviors leading to the development of hepatitis B or C. Clinical
manifestations of cirrhosis include portal hypertension, which is caused by the portal vein becoming inflamed and casing blood to be rerouted to
adjoining lower pressure vessels, splenomegaly, ascites which is the enlargement of the stomach due to a collection of fluid in the abdominal cavity,
esophageal varices, which are enlarged, thin walled veins that form in the esophagus, portal, systemic encephalopathy, which is due to neurotoxins
being rerouted into the blood, hepatorenal syndrome caused by imbalanced blood flow, and spontaneous bacterial peritonitis, which is a contamination
of the peritoneal cavity (Pearson,

Portal Vein Thrombosis, Risk Factors, Cirrhosis
Abstract
Manuscript History: Received: 14 October 2015 Final Accepted: 22 November 2015 Published Online: December 2015 Key words: Portal vein,
Thrombosis, risk factors, cirrhosis. *Corresponding Author
Pawan Kumar Thakur Background and objectives: Portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is
associated with worsening liver function, ascites and the occurrence of gastroesophageal variceal bleeding. The aim of this work was to clarify the risk
factors, clinical presentation and complications of portal vein thrombosis in Egyptian patients with liver cirrhosis and to study the outcome with and
without treatment after 6 months follow up period. Methods: Hospitalized cirrhotic patients (N = 80) were segregated into the PVT and non–PVT
groups. PVT was detected by Doppler ultrasonography; each group was divided in two sub groups (A and B) according to presence or absence of
HCC respectively. The 2 groups were compared as regards risk factors, clinical presentation and complications. The outcome of treatment with
anticoagulation in 6 patients was evaluated. Result: PVT developed as result of combination of both local and systemic risk factors. HCC, abdominal
infection especially spontaneous bacterial peritonitis and abdominal intervention were the most important local risk factors. Abnormalities of
coagulation system were among systemic risk factors. Most of cases were asymptomatic and accidentally discovered, others presented

Cirrhotic Essay
Abstract P.P.I therapy is often used in patients with cirrhosis, sometimes, in the absence of a specific indication (e.g.: acid related diseases), there are
conflicting reports for their use in cirrhotic patients. The dosage of most PPIs should be reduced in cirrhotic as they are metabolized by the liver and
associated with adverse effects of prolonged use. We aimed to review strict indications and adverse effects for their use in this group of patients.
Keywords Proton pump inhibitors, liver cirrhosis, peptic ulcer, H. pylori, esophageal band ligation. Abbreviations P.P.I: proton pump inhibitors. EVS:
esophageal variceal Sclerotherapy. EVL: esophageal variceal ligation. HE: hepatic encephalopathy. SBP: spontaneous bacterial... Show more content on
Helpwriting.net ...
A short course for 10 days post–EVL may be reasonable if we concern for ulcer healing. However, high–dose infusion (e.g., pantoprazole 8 mg/h) and
prolonged use in the absence of endoscopic procedures is not supported by the literature and should be discouraged until evidence of benefit
becomes available. (8) GERD Functional studies showed decreased LES function with a low amplitude of acid clearance and primary esophageal
peristalsis in cirrhotics with large varices [9]. These phenomena could also be due to a mechanical effect of the varices. Cirrhotic patients without
EV have also esophageal motor disorders and mixed acid and bile reflux as the main pattern whereas the cirrhosis itself was an important causative
factor. It is unclear whether this might contribute to bleeding from varices [8]. Data on management of GERD in cirrhosis are few, however, the
indications of use for PPIs may remain exactly the same also in patient with cirrhosis of the liver as general population for the treatment of erosive
esophagitis or in general the pathology secondary to gastroesophageal reflux acid (10) Peptic ulcer and H. pylori infection Prevalence of duodenal and
gastric ulcers in patients with liver cirrhosis increases as the disease progress[11] and this prevalence becomes higher in decompensated cirrhosis than
in compensated cirrhosis [12]. Currently, PPIs are the mainstay treatment option of peptic ulcers in the

Unknown Lab Report
Unknown Lab Report
Unknown Organism #6
Ann Le (Phuoc)
May 6, 2010
Dr. Carrington
Microbiology Lab– MW 12:50
Le 1
I. Introduction
My unknown organism #6 is Morganella morganii, which is a gram–negative bacillus rods commonly found in the environment and also in the
intestinal tracts of humans, mammals, and reptiles as a normal flora. (3, 5) This bacterium Morganella morganii, was first discovered in the 1906 by a
British bacteriologist named H. de R. Morgan. (2) Despite its wide distribution, it is an uncommon cause of community–acquired infection and is most
often encountered inpostoperative and other nosocomial settings. (2, 3) Morganella morganii infections respond well to appropriate antibiotic therapy;
however, its ... Show more content on Helpwriting.net ...
Next I performed a KOH test to further confirm that my organism was a Gram–negative species. For the KOH test, I added 3 drops of 10% potassium
hydroxide (KOH) to a small drop of distilled water onto a clean microscope slide, transferred a visible clump of organism to the KOH solution using
my inoculating loop. I than mixed the cells into the solution using small, circular motions for 60 seconds and then lifted up the loop to look for what
appears to be a "stringing" affect which means it's confirmed that it is gram– negative species. Next, I created a streak plate using nutrient agar so that I
could see pure culture of my organism. I aseptically obtained a loop full of my organism and gently inoculated one quarter of the nutrient agar plate by
running the loop back and forth across the surface. I then flame sterilized the inoculating loop, allowing it to cool for 10 seconds, and then streaked the
organism from quadrant I into quadrant II using a zigzag motion technique. I repeated those steps streaking from quadrant II to quadrant III and then
streaking from quadrant III to quadrant IV. Once completed, I put the streak plate in the incubator at 37В° for 24–48 hours. 48 hours later, I check my
streak plate and it had a lot of growth on it. I was able to determine that the organism was definitely an off white color, opaque. The IV quadrant was
the quadrant that best

Le 5 represented the colony. The whole colony was round, having

Risk Factors, Clinical Presentation And Outcome
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Portal vein thrombosis in patients with liver cirrhosis: insights to risk factors, clinical presentation and outcome
Article in International Journal of Advanced Research 3(12):1539–1548 В· December 2015
1st Afifi F Afifi
2nd Osama Basha
6.99 В· Zagazig University
+ 1
3rd Fady Maher
Zagazig University
Last Raghda Abd Ellatif Hafez
16.2 В· Faculty of medicine/Zagazig University.www.zu.edu.eg
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ISSN 2320–5407 International Journal of Advanced Research (2015), Volume 3, Issue 12, 1539–15481539Journal homepage:http:/
/www.journalijar.comINTERNATIONAL JOURNALOF ADVANCED RESEARCHRESEARCH ARTICLEPortal vein thrombosis in patients with
liver
cirrhosis:insights to risk factors, clinical presentation and outcomeAfifi F. Afifi 1, Osama M. Basha 1, Fady M. Wadea 1, Abdelaziz E. Samack 2,
Raghda Abd–elatif Hafez31–GIT and hepatology unit, Internal Medicine department, Faculty of Medicine, Zagazig University.2–Radiology
department, Faculty of Medicine, Zagazig University.3–Microbiology&Immunologydepartment, Faculty of Medicine, Zagazig University.
EGYPTManuscriptInfoAbstract Manuscript History:Received:14 October 2015Final Accepted: 22 November 2015Published Online: December
2015Key words: Portal vein,

Perforated Peptic Ulcer Paper
In our study we tried the safety of conservative treatment also known as the Taylor method of perforated peptic ulcer. Our results show that in the era
of PPI this approach can be applied in patients with acceptable morbidity and no mortality. Study of the natural history of peptic ulcer perforation has
shown that, after perforation occurs, it is promptly sealed by adjacent organs. A fibrin clot appears quickly on and around the perforation. This is the
initiation of definitive closure of perforation with the help of adhesions between perforated and adjacent organs [12–15]. According to Donovan, this
process of self–healing is sufficient in 50% of patients [16]. It is a not uncommon experience for surgeons operating on perforated peptic ulcer to find
that they first have to mobilize the perforation from adjacent organs or reperforate the already sealed perforation before being able to repair it.... Show
more content on Helpwriting.net ...
However, some patients develop peritonitis due to continuous fluid extravasation, higher bacterial load of the upper gastrointestinal tract and impaired
spontaneous sealing of the perforation. These observations were the basis for the development of conservative treatment. The morbidity and mortality
associated with surgical repair of perforated peptic ulcer are currently in the range of 3–9% whereas the result of very few series available for
conservative treatment shows mortality rates as 5.2%. In Taylor's initial series in 1957 for conservative treatment for perforated peptic ulcer, mortality
rates of 0% and more recent publications have reported morbidity rate upto 8% [17–21]. In our study, we had no mortality during hospital stay and
follow up

Portal Hypertension Paper
During chronic liver disease, hepatocyte cell death results in inflammation that leads to fibrosis. In addition, the loss of functional hepatocytes results
in loss of liver functions, such as the ability to metabolize bilirubin and synthesize proteins (e.g., albumin and clotting factors). Under normal
conditions, blood flows from splanchnic circulation to hepatic circulation (for removal of bacteria and toxins) via the portal vein, and blood is returned
to systemic circulation via the hepatic vein. Because of liver fibrosis, the distortion of hepatic architecture increases resistance to blood flow, resulting
in portal hypertension. The portal collaterals relieve some of the pressure in the portal system but may contribute to cirrhosis–related complications such
as varices (Liou, 2014).
Portal hypertension is usually estimated by the hepatic venous pressure gradient (HVPG). Normally, HVPG ranges from 3 to 5 mmHg. In the
compensated stage of cirrhosis, patients initially have moderate portal hypertension (>6 to <10 mmHg) with a low risk of decompensation. However,
as portal hypertension progresses to clinically significant levels (HVPG of в‰Ґ10 mmHg), the risk for developing decompensated cirrhosis increases.
Portal hypertension is a key driver of many of the clinical consequences of cirrhosis (Berzigotti et al., 2013). ... Show more content on Helpwriting.net
...
In addition, intestinal microbial translocation, which stems from increased intestinal permeability, small intestinal bacterial overgrowth (SIBO),
impaired immunity and the migration of bacteria and bacterial endotoxin from the gut to the lymph nodes and other organs have been implicated in
cirrhosis–related complications, such as spontaneous bacterial peritonitis (SBP), variceal bleeding and HE (Pinzone et al.,

Invasive Mycoses Research Paper
Invasive Mycoses
Fungi have emerged over the past several decades as major contributors to human disease.(1, 2) As populations of immunocompromised and/or
hospitalized patients continue to increase, so will the incidence of invasive fungal infections. A recent study reported that fungemia in theUnited States
increased by 207% between 1979 and 2000.(3) Moreover, as the populations at risk for fungal infection continue to expand, so will the spectrum of
pathogens capable of infecting those individuals.
Invasive mycoses may be categorized as i) opportunistic or ii) endemic. Endemic infections, which are generally confined to specific geographic
regions, are most often acquired via inhalation of spores. Infective agents include, but are not limited to, Histoplasma capulsatum, Coccidioides
immitis, and Blastomyces dermatitidis. These infections frequently mimic common pulmonary infections in initial stages and are therefore often
misdiagnosed. Dissemination and advanced disease follow. Dormancy may also occur, with reactivation of infection years later. This leads to
diagnosis in a geographic regions outside of the high risk area.(4, 5)
Opportunistic ... Show more content on Helpwriting.net ...
As the transition to the pseudohyphal growth phase occurs, production of an extracellular matrix begins and continues as the biofilm matures. This
matrix is composed primarily of carbohydrates, which differs from the protein–rich matrix of the C. albicans biofilm. As the biofilm grows,
non–adherent yeast cells are released from the biofilm and into the surrounding medium to facilitate the spread of infection.(89) Transcription factor
Bcr1 is the major regulator of biofilm formation in C. parapsilosis, as in C. albicans, and is required for proper biofilm formation. Bcr1 functions as
regulator of several cell wall and adhesion target genes, and at least some targets are conserved in C. parapsilosis.(90,

Essay on Streptococcus Pneumoniae
In accordance with the World Health Organization, pneumonia still remains one of the main killers of children under the age of five, taking more than
1.1 million lives of boys and girls annually (WHO Pneumonia factsheet, 2013). Pneumonia is more prevalent in South Asia and sub–Saharan Africa. It
is well known that pneumonia is a disease of respiratory system that affects the alveoli, which are the constituent part of the lungs. Normally alveoli fill
with air during the breath of a healthy person, while the one with pneumonia has alveoli, which are filled with fluid and pus; hence the breathing
process is painful and limits the oxygen consumption by organism. Pneumonia can be caused by several infectious agents, such as bacteria, fungi and ...
Show more content on Helpwriting.net ...
S. pneumoniae is capnophilic, preferring atmospheres of 5–10% carbon dioxide. Streptococcus pneumoniae can be distinguished from other
streptococci, owing to the fact that it is catalase negative; can be inhibited by ethyl hydrocupreine; it is soluble in bile (due to activation of autolytic
property, which consequently lead to cell lysis); it is О±–haemolytic (it can be easily identified on agar plates, due to greenish discoloration of blood
agar due to the production of pneumolysin) (Balakrishnan, 2006).
S. pneumoniae has some distinct virulence factors, which are proteins/enzymes that are expressed on the surface of gram–positive organisms. They are
also the main contributors to the pathogenic character of the bacterium and its survival against the host defense mechanisms. According to Poll et al.
(2009) virulence factors should be used in array, in order to be successful in coordinating ways for the tissue invasion. Some of the most important
virulence properties are the adherence factors, genes responsible for invasion, some heavy–metal transporters, evasion the immune system of the host,
production of pneumolysin and bacteriocin, quorum sensing and formation of bioп¬Ѓlms. Some centuries ago, S. pneumoniae's polysaccharide capsule
was considered to be the primary virulence factor, due to the fact that the capsule is crucial for colonization, invasion and dissemination from the
respiratory tract. This capsule is negatively charged and hence inhibits the

The Human Body Is The Liver
Introduction
The largest internal organ in the human body is the liver. The liver functions in many ways for the survival of the human body. Such as producing
blood proteins which help clotting, haemoglobin (oxygen transport), storing glucose, eliminating harmful toxins in the bloodstream, breakdown of
saturated fats and producing cholesterol (Robinson, 2016). Mr McGrath has 5 years past history of Alcoholic Cirrhosis in which there is irreversible
scarring of the liver and ultimately preventing the liver from functioning properly. Complications of Cirrhosis such as Ascites, variceal bleeding,
hepatic encephalopathy, jaundice, hypoxia, ecchymosis and high risk of infection are not uncommon with patients like Mr McGrath (Chalasani, 2013),
(Robinson, 2016) and (Moore & Aithal, 2006).
A liver transplant may be considered if initial treatment is ineffective (medication and dietary changes). Mr McGraths liver function test (LFT) displays
abnormal results which may indicate the evidence of his liver disease.
Ascites due to Cirrhosis
Ascites is the accumulation of fluid in the abdominal cavity which also indicate advanced liver disease. The development of ascites in cirrhosis can be
caused by portal hypertension which is the increase of blood pressure in the veins running through the liver called "portal veins" (Chalasani, 2013).
Mr McGrath was admitted to the hospital for abdominal swelling, displaying true signs of Jaundice (yellowing skin and eyes) fever (37.7В°C) and

Sepsis Associated Encephalopathy (SAE)
Sepsis associated encephalopathy (SAE) is a complex and potentially serious consequence of sepsis appearing in many clinical forms. SAE is no more
than the manifestation of a sinister cascade of damaging molecular interactions that can potentially lead to irreversible neurocognitive dysfunction. The
pathophysiology of SAE is unknown but recent animal studies have shed some important information about some of the responsible molecular
mechanisms and potential sites for future interventions. These pre–clinical studies have demonstrated the role of classic inflammatory factors that lead
to blood–brain barrier dysfunction, astrocyte dysfunction, apoptosis, and neuronal death. Further studies are warranted to enhance our understanding
of the process ... Show more content on Helpwriting.net ...
The sepsis induced by fecal peritonitis leads to the development of edema around the microvessels of frontal cortex in a rat model of sepsis. The
results suggest that the edema observed around the microvessels can have a role in the pathogenesis of the SAE probably by affecting the exchange of
oxygen and nutrients with carbon dioxide and waste products between the blood and brain parenchyma (73). Perimicrovascular edema together with
intact tight junctions has previously been reported in a pig model of sepsis (74). Further studies are warranted not only for understanding the
development of perimicrovascular edema associated with peritoneal sepsis in this model, but also for setting targets for the design of novel drugs to
treat perivascular edema and

Primary Peritoniitis
The abdominal cavity is the largest hollow space in the human body and contains the liver, pancreas, spleen, kidneys and adrenal glands, and the
digestive tract. The cavity is lined by a thin, silk–like membrane called the peritoneum which covers the inside wall of the abdominal cavity and every
organ or structure contained in it. A common affliction of the abdominal cavity is peritonitis, which is an inflammation of the peritoneum membrane
caused by the introduction of a fungal or bacterial infection in an otherwise sterile environment. The infection is often caused by an abdominal injury
that creates a rupture (perforation) within the abdominal cavity, or may arise from a complication of an underlying medical condition. The infection can
... Show more content on Helpwriting.net ...
Primary peritonitis is an infection that develops in the abdominal (ascitic) fluid of the peritoneal cavity. It is mostly seen in patients suffering from
advanced liver disease with cirrhosis, where abdominal fluid builds up (ascites) in the peritoneal cavity and may become infected. Although rare in the
absence of a perforation, there are many underlying conditions that can contribute to the growth of bacteria in the ascitic fluid. This type is called
spontaneous bacterial peritonitis and is the most common reason of primary peritonitis. Factors that increase risk of primary peritonitis include medical
procedures like peritoneal dialysis, medical conditions such as cirrhosis, kidney failure, and heart disease, and patient history of peritonitis. However, in
most cases the type of infection that develops is secondary peritonitis, which is usually caused by an infection that has spread from the digestive tract
after trauma or perforation of the abdominal viscera that allows infectious organisms to contaminate the sterile environment of the peritoneal cavity.
Most common causes of secondary peritonitis include injury or trauma to the peritoneum, a ruptured appendix, or stomach ulcer, digestive diseases
such as Crohn's Disease, and diverticulitis, perforations of the stomach, or intestines, and abdominal trauma such as injury from a knife or gunshot
wound. Both types of peritonitis are life threatening, and when left untreated can enter into the bloodstream spreading the infection throughout the
entire body leading to shock and organ

Alcohol And Hepatocellular Tumor
The liver is the organ responsible for filtering chemicals and metabolizing drugs. It also makes proteins responsible for blood clotting and other
functions. When alcohol reaches the liver, it produces a dangerous enzyme known as acetaldehyde. The liver needs water to do its basic functions.
Alcohol acts as a diuretic and dehydrates the body, depriving the liver of the water it needs to function. When acetaldehyde and other alcoholic toxins
build up in the liver, they can cause a variety of health problems.
One of the most commonly known problems of the liver caused by alcohol is hepatocellular carcinoma (HCC), a type of liver cancer. There are other
types of liver cancers, such as cholangiocarcinoma, a cancer of the bile duct, and hepatic angiosarcoma, a rare malignant mesenchymal tumor. Both of
these cancers are not caused by alcohol abuse. HCC is caused by cirrhosis or other long–term damage to the liver. Cirrhosis is most often caused by
alcohol abuse, hemochromatosis, or a hepatitis B or C infection. Symptoms of HCC include abdominal pain, easy bruising, enlarged abdomen,
jaundiced skin or eyes, and unexplained weight loss. Many tests are ordered to diagnosis liver ... Show more content on Helpwriting.net ...
Alcohol abuse and hepatitis B and C are the most common causes of cirrhosis. Cirrhosis can cause weakness, loss of appetite, jaundice, itching, and
fatigue, and can be diagnosed by blood tests, physical examinations, and a liver biopsy. There are many complications of cirrhosis, such as edema and
ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal vein hypertension, hepatorenal and hepatopulmonary syndrome,
hypersplenism, and liver cancer. One of the most common treatments of cirrhosis is a liver transplant. However, alcoholics have to be sober for six
months to prove that they are serious about taking care of their new liver and staying sober after the

Patho Case Study 1
Berlin Herrera Unit 1 Case Study
F.C. is a 54–year–old man with a history of chronic heavy alcohol use. He has frequent bouts of gastrointestinal bleeding for which he has been
hospitalized on six separate occasions over the years. He continues to drink and exhibits most of the common manifestations of alcoholic cirrhosis. He
was recently hit by a car and was hospitalized for a broken leg. He appeared to be under the influence of alcohol at the time of the accident and had a
blood alcohol level of 0.18. F.C.'s family reports that his mental functioning has deteriorated significantly over the past few months.
Discussion Questions 1. What are the common manifestations of alcoholic cirrhosis? Which of these are secondary to ... Show more content on
Helpwriting.net ...
* Hepatorenal Syndrome: defined as a rapid deterioration in kidney function that manifests from an acute insult to the liver. Changes in blood flow due
to decreased kidney function causes toxins to begin impairment of the kidneys since the liver cannot kill off the toxins before–hand. This condition is
considered secondary to portal hypertension for this reason.
* Edema: abnormal accumulation of fluid (aka swelling). This is important for cirrhosis because when the tissue starts turning into scar tissue, the
kidneys retain more salt. This increase in salt and water causes the visualized swelling. As time progresses, this swelling can affect abdomen area of the
body, making edema secondary to hepatocellular failure since it is the tissue cell morphing that causes edema to manifest.
* Esophageal Varices Bleeding: scarring of liver causes blood flow through the liver to decrease. With the decrease in liver blood flow, more blood
pumps through veins causing them to balloon outward. The increased amount of blood in the veins results in a vein bursting and leads to bleeding.
This condition is secondary to portal hypertension because of the alternate routes the blood takes due to the scarred liver, causing the veins to work
harder and accumulate more blood within a certain span of time, not being able to drain in a timely matter. 2. Why is

Aortic Aneurysm Case Study
Clostridial Aortitis Causing Ruptured Dissecting Aneurysm In A Young Adult Female Introduction Ruptured dissecting aortic aneurysm more
commonly occur in men age between 40 to 70 and most commonly associated with atherosclerosis. Other uncommon causes are previous hearts
surgery, connective tissue disorder and aortitis.1Infection of the aorta has an overall incidence between 0.7% and 2.6 % with salmonella spp.
representing the most commonly identified pathogens. A rare cause of aortic aneurysm is clostridium spp, which typically occurs in patients with
multiple co–morbidities.2Clostridium spp infection progresses very rapidly with mortality rate of approximately 79% in adults, typically occurring
within 48 hours of infection.3In younger individuals, aortic dissection is most commonly associated with... Show more content on Helpwriting.net ...
Diseases of the aorta. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 78.
2.Smith–Slatas CL, Bourque M, Salazar JC. Clostridium septicum infections in children: a case report and review of the literature. Pediatrics.
2006;117(4):e796–805. 3.Koransky JR, Stargel MD, Dowell VR Jr. Clostridium septicum bacteremia. Its clinical significance. Am JMed.
1979;66(1):63–6. 4.Saukko P, Knight B. Knight's forensic pathology. 3rd ed. London: CRC Press; 2004. 5.Todar K. Todar's online textbook of
bacteriology [Internet].Available from: www.textbookofbacteriology.net. 6.Hoeprich PD. Infectious Diseases. Philadelphia: Lippincott; 1994. p.
1255–8 7.Bahnson HT, Nelson AR. Cystic medial necrosis as a cause of localized aortic aneurysms amenable to surgical treatment. Ann Surg.
1956;144(4):519–29. 8.Wiesenfarth JM. Acute Aortic Dissection [Internet]. [cited 2010 Oct 10]. Available from: http://www.emedicine.com/emerg
/topic28.htm. 9.Carlson RG, Lillehei CW, Edwards JE.Cystic medial necrosis of the ascending aorta in relation to age and hypertension.Am J Cardiol.

Cirrhosis Research Paper
Dr. Robert Angel
2301
Cirrhosis
Cirrhosis refers to a combination of liver diseases that interfere with the normal function of the liver after destroying liver structures. The disease
causes the formation of scar tissue in the liver that kills liver cells thereby causing inflammation (Fabris 716). The cells that have survived would tend
to multiply rapidly to replace the dead cells. It results to regenerative nodules in the scar due to clustering of the newly formed liver cells. Cirrhosis is
caused in varied ways that range from the chemical cause like alcohol to viruses. Besides, heavy and toxic metals like mercury, lead, copper and iron
cause cirrhosis if they accumulate in the liver. The liver is a detoxicating organ of the body that purify ... Show more content on Helpwriting.net ...
If it is not possible to stop, then one should limit the rate of alcohol consumption and how often the consumption is done. Sexual behavior can also
lead to cirrhosis (Schuppan 849). One should, therefore, avoid unprotected sexual contact that appears risky. One should be careful while handling
chemicals. Besides, limiting exposure to a toxic environment where heavy metals and other poisonous substances are available is also important. In
case it is unavoidable, protective clothing should be worn (Wong, 1543). Hepatitis B is a risk to getting liver cirrhosis and therefore it is advisable to
vaccinate against it. Eating well–balanced diet incorporated with vegetables and fruits it helpful in minimizing the rate of infection of the disease. The
vegetables and fruits provides vitamin E that helps in boosting the immune system of the

Higher Risk Of Surgery As A Patient For Elective Total Hip...
The higher risk of surgery in a cirrhotic patient is due to the fact that the liver normally performs myriad metabolic and synthetic functions in the body.
The liver is vital for protein synthesis, coagulation homeostasis, glucose homeostasis, bilirubin excretion, drug metabolism, and toxin removal, among
other critical functions. The optimal management of a cirrhotic patient for elective total hip replacement surgery would involve:
1.Pre– operative assessment, including a detailed history, examination and investigations.
2.Risk assessment and stratification using various scoring systems available.
3.Optimisation and planning for reduction of peri– operative complications:
a.Correction of underlying conditions.
b.Meticulous planning of the intra and post– operative period, including:
i.Available infrastructure – the hospital should be sufficiently equipped to handle the complicated intra and post– operative course. ii. Personnel
available– there should be qualified gastro–enterologists or hepatologists to provide expert advice whenever required. iii. Post– operative care.
c.Pre– planned strategies to manage complications, in case they occur.
PRE– OPERATIVE ASSESSMENT (1, 2)
History
1.Presenting complaint: Pain in hip– duration, severity, character, effect on function (this is the determinant of the necessity and urgency of surgery)
2.History related to liver cirrhosis:
a.Duration of cirrhosis and how it was diagnosed initially.
b.Cause of cirrhosis– Was it

Essay On Cirrhosis
P.P.I therapy is often used in patients with cirrhosis, sometimes, in the absence of a specific indication (e.g.: acid related diseases), there are
conflicting reports for their use in cirrhotic patients. The dosage of most PPIs should be reduced in cirrhotic as they are metabolized by the liver and
associated with adverse effects of prolonged use.
Keywords
Proton pump inhibitors, liver cirrhosis, peptic ulcer, H. pylori, esophageal band ligation.
Abbreviations
P.P.I: proton pump inhibitors.
EVS: esophageal variceal Sclerotherapy.
EVL: esophageal variceal ligation.
HE: hepatic encephalopathy.
SBP: spontaneous bacterial peritonitis.
CDI: Clostridium difficile infection.
PHG: portal hypertensive gastropathy.
GERD: gastroesophageal ... Show more content on Helpwriting.net ...
However, high–dose infusion (e.g., pantoprazole 8 mg/h) and prolonged use in the absence of endoscopic procedures is not supported by the literature
and should be discouraged until evidence of benefit becomes available. (8)
GERD
Functional studies showed decreased LES function with low amplitude of acid clearance and primary esophageal peristalsis in cirrhotic patients
with large varices [9]. These phenomena could be due to a mechanical effect of the varices. Cirrhotic patients without EV have also esophageal
motor disorders and mixed acid and bile reflux as the main pattern, whereas the cirrhosis itself is an important causative factor. It is unclear whether
this might contribute to bleeding from varices [8]. Data on management of GERD in cirrhosis are few, however, the indications of use for PPIs may
remain exactly the same in patient with cirrhosis of the liver as general population for the treatment of erosive esophagitis, or in general the pathology
secondary to gastroesophageal reflux of acid (10)
Peptic ulcer and H. pylori infection
Prevalence of duodenal and gastric ulcers in patients with liver cirrhosis increases as the disease progress[11] and this prevalence becomes higher in
decompensated cirrhosis than in compensated cirrhosis [12]. Currently, PPIs are the mainstay treatment option of peptic ulcers in the general
population [13]. Helicobacter pylori infection contributes to the development of hyperammonemia [14] and subsequent episodes of

Cirrhosis Essay
Cirrhosis is the eighth leading cause of death in the United States and the thirteenth leading cause of death worldwide.1 Cirrhosis is the irreversible
fibrosis of the liver characterized by hepatic architectural distortion secondary to fibrous tissue and the formation of regenerative nodules.2 These
anatomical changes cause hepatic vascular resistance and an increase in blood flow leading to portal hypertension. Porto–systemic collaterals develop
in order to overcome the increased portal pressure gradient.3 Nitric oxide, an endogenous vasodilator is also released in effort to overcome portal
pressure with the expense of causing systemic vasodilation and a decrease in blood pressure. As a result, a marked activation of neurohumoral
vasoactive factors occurs in an effort to maintain an effective arterial blood pressure. Hypervolemia, increased cardiac index, decreased systemic
vascular resistance, and systemic hypotension are manifestations of portal hypertension.3 Chronic hepatitis B virus (HBV), hepatitis C virus (HCV),
alcoholism, nonalcoholic steatohepatitis (NASH), and non–alcoholic fatty liver disease (NAFLD) are all major causes of cirrhosis. ... Show more
content on Helpwriting.net ...
Decompensated cirrhosis is characterized by the development of a cirrhosis–related complication, including variceal hemorrhage, ascites, spontaneous
bacterial peritonitis, hepatorenal syndrome, and/or coagulopathies. For patients with compensated and decompensated cirrhosis, the risk of death is 4.7
and 9.7 times higher than the general population, respectively.4 Survival in patients with decompensated cirrhosis is considerably lower than that of
patients with compensated cirrhosis. The median survival times are as low as 2 years in decompensated patients and greater than 12 years in
compensated

Portal Vein Thrombosis On Patients With Liver Cirrhosis
Portal vein thrombosis in patients with liver cirrhosis: insights to risk factors, clinical presentation and outcome
Afifi F. Afifi 1, Osama M. Basha 1 , Fady M. Wadea 1, Abdelaziz E. Samack 2, Raghda Abd
–elatif Hafez 3
1– GIT and hepatology unit, Internal Medicine department, Faculty of Medicine, Zagazig University.
2– Radiology department, Faculty of Medicine, Zagazig University.
3– Microbiology&Immunology department, Faculty of Medicine, Zagazig University. EGYPT
Manuscript Info Abstract
Manuscript History: Received: 14 October 2015 Final Accepted: 22 November 2015 Published Online: December 2015 Key words: Portal vein,
Thrombosis, risk factors, cirrhosis. *Corresponding Author
Pawan Kumar Thakur
Background and objectives: Portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is associated with worsening
liver function, ascites and the occurrence of gastroesophageal variceal bleeding. The aim of this work was to clarify the risk factors, clinical
presentation and complications of portal vein thrombosis in Egyptian patients with liver cirrhosis and to study the outcome with and without treatment
after 6 months follow up period. Methods: Hospitalized cirrhotic patients (N = 80) were segregated into the PVT and non–PVT groups. PVT was
detected by Doppler ultrasonography; each group was divided in two sub groups (A and B) according to presence or absence of HCC respectively. The
2 groups were compared as regards risk factors,

The Progression of Streptococcus suis Meningitis Essay
There are three types of pathogens that cause meningitis. The first type of pathogen is Haemophilus influenzae type b. It is an aerobic gram–negative
bacteria, meaning they have relatively thin cell walls and can be resistant to antibiotic treatment. In 95% of invasive diseases are caused by type b.
Before the introduction of a vaccine, it was the leading cause of bacterial meningitis most common in infants. The organism colonizes in the
nasopharynx (the upper part of the throat behind the nose) and can sometimes invade the bloodstream and cause infection at a distant site.
Neisseria meningitides is a bacteria that causes meningoccal disease. It is aerobic, Gram–negative bacteria that causes serious, sometimes fatal, infection
... Show more content on Helpwriting.net ...
An MRI indicated inflammation of sulci, a groove in the brain, vascular congestion and cortical edema or fluid on the brain. A spinal tap was obtained
from the patient and because of possible pneumococcal meningitis, an intravenous therapy with a combination of a steroid and antibiotics.
Streptococcus suis was identified and the patient was asked about any recent contact with swine. For several weeks, he had been slaughtering, by hand,
several non– commercially raised pigs for a luau. And although he did not recall any mucosal exposure to the pig blood or secretions, there is no
known route for infection to humans. He did not wear any type of protective gear, i.e., gloves, apron or facemask. His exposure to pigs blood, skin and
organs was extensive. During the slaughter process, his hands sustained multiple cuts. It is possible that the bacteria entered through those cuts as no
other church members who participated in the preparation became ill. Treatment of ceftrixone and a 4–day course of dexmathasone was prescribed and
his headache improved. He was discharged after 6 days and given a 2– week course of IV ceftrixone. After 1 day of discharge, he was affected again
by headaches accompanied by a mild hearing loss. After a repeat spinal tap was administered, it was concluded that the headache was a result of
residual meningeal/cerebral edema (swelling) that resolved

Portal Vein Thrombosis On Patients With Liver

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Portal Vein Thrombosis On Patients With Liver