Isoniazid Liver Injury Case Study

How To Write A Case Study Isoniazid
TITLE: ISONIAZID INDUCED ACUTE LIVER INJURY
INTRODUCTION: Treatment with Isoniazid (INH) has been proven effective in preventing
activation of latent tuberculosis (TB) into clinical disease. The recommendation of INH treatment
ranges between 6 to 12 months of continuous therapy (1, 2). The most common side effects of INH
are gastrointestinal adverse events. Prospective clinical trials have shown the risk of INH–induced
hepatitis, mostly with gradual increased levels of AST and ALT.
CASE: 51–years–old male visiting from Guyana with past medical history of hypertension and
hyperlipidemia presented with non–obstructive jaundice for 3 weeks. Patient is a former heavy
alcohol drinker (15 years), and a former cigarette smoker (15 years). Patient was prescribed INH for
latent TB 2 months ago. Also, 7 days prior to admission he was prescribed Gemfibrozil 600mg.
Other home medications were Metformin 500mg, Ramipril 5mg, Metoprolol 50mg, and
multivitamins. Patient denies Hepatitis A and B vaccination, blood transfusion, family history of
liver cancer/chronic disease, drug use, recent sexual activity/STDs. Physical exam remarkable only
for scleral icterus, jaundice and bright yellow urine and clay colored stools. Labs revealed AST 1626
ans ALT 1250, trending up form 2 months ago ... Show more content on Helpwriting.net ...
The metabolism of INH is primarily hepatic via acetylation and hydrolysis. Their reactive
metabolites induce oxidative stress or alter lipid metabolism, resulting in hepatic apoptosis or
steatosis. Genetic polymorphisms of NAT–2 are commonly found among people of Asian descent
and Native Americans. Approximately 12% – 15% of patients on INH will develop temporary
elevations of serum transaminases within the first 3 months. Patients with severe hepatotoxicity may
present gastrointestinal symptoms with AST level exceeding three to five times the upper limit of
the normal value. In such cases, immediate discontinuation of INH is
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Reverse Transcriptase Polmerase Chain, Reaction is an...
Reverse transcriptase polymerase chain reaction, also known as RT–PCR, has been recognized as a
reliable, accurate, and sensitive method for quantifying gene transcription. Polymerase chain
reaction, also known as PCR, is considered an essential tool in molecular biology that allows for the
amplification of nucleic acid sequences. Specifically, the three main consecutively repeating steps in
PCR are denaturation, annealing, and elongation. If the reaction runs with 100% efficiency, there
will be a two–fold increase in target amplicons after each cycle of PCR. Therefore, with n cycles of
the reaction, the copy number of the target sequences will be 2n. However, one of the main
disadvantages of conventional PCR, also called end–point PCR, is that the results of amplification
can only be visualized after all the cycles of amplification are complete (Nestorov 326). Therefore,
in recent years, modifications of conventional PCR methods have been developed to improve the
performance and specificity of the technique. One such example is RT–PCR, which has many
advantages over conventional PCR methods. For instance, RT–PCR is a quantitative method for
determining gene expression levels, while endpoint PCR is only semi–quantitative. Additionally,
through RT– PCR, data can be collected during the exponential phase of the PCR amplification
process, in which the PCR reaction is not limited by enzymatic activity or substrate concentration.
Alternatively, in end–point PCR, data is

Acetaminophenol Research Paper
Acetaminophen (N–acetyl–p–aminophenol, abbreviated as APAP) is one of the most widely used
analgesic, antipyretic, and anti–inflammatory drugs worldwide [1]. While generally considered to be
safe for humans at a maximum recommended daily dose of 4,000 milligrams (mg) per healthy adult
[2], at higher concentrations this drug can cause serious adverse effects, especially toxicity to the
gastrointestinal, renal, and hepatic systems [1]. Moreover, APAP poisoning, either by accidental or
intentional overdose, is a frequent problem in current medical practice. For example, it is the
paramount cause of acute liver failure in the Western Europe, the United States, Canada, and
Australia [3]. Therefore, an extensive body of literature dealing with acetaminophen ... Show more
content on Helpwriting.net ...
Linoleic acid is as an additional source of arachidonic acid, and therefore, this compound also serves
as a key player in eicosanoid biosynthesis [11,12]. The cyclooxygenase enzymes convert
arachidonic acid via the cyclic pathway of eicosanoid biosynthesis to prostaglandin H2, which is
further metabolized to prostaglandins (e.g., PGE2, PGF2α, PGD2, PGI2) and thromboxane, many of
them with pro–inflammatory properties [13,14]. There are three types of cyclooxygenases, sharing
60% of their primary structure: COX–1, which is generally localized in the endoplasmic reticulum;
COX–2, which is found on the nuclear envelope [14,15]; and COX–3, which occurs only in the
cerebral cortex [16]. In the healthy liver, COX–1 and COX–2 work together to induce the
inflammation state, and when needed, to reinstate the normal hepatic function [17,18]. At hepatic
level, these cyclooxygenases are abundantly expressed during liver injury, cirrhosis, and induced
tumorigenesis [19], suggesting the involvement of eicosanoids in the pathogenic mechanisms of
liver injury. They are expressed by the liver macrophage–like Kupfer cells, identified by the
macrophage marker ED2 (CD168) and these cells are sites of intense eicosanoid production and
signaling [20]. Still, in spite of all these data, little knowledge exists about the interplay between
APAP treatment and cyclooxygenase–mediated signaling pathway in the liver. It is known, though,
that COX–2 overexpression in the mouse liver induces chronic hepatitis by inducing a persistent
inflammatory reaction involving macrophages that causes a persistent increase in the hepatocyte
death, which reinforces the inflammatory reaction and thus further death of hepatocytes

Cyp3a4 Research Paper
Endogenous factors
The endogenous factors that determine the extent of a xenobiotic metabolism are age, sex, species,
pathology, genetics and cofactor availability. The age of human or an organism play a vital role in
the metabolic capacities towards xenobiotics, neonates and fetuses have lower metabolic activities
than children and adults. For example, CYP3A4 is a key xenobiotic–metabolizing enzyme, and
developmental process affects its expression. The xenobiotic enzyme, CYP3A7 is mostly a fetal
enzyme, while CYP3A4 has limited expression in fetuses and does not meet adult expression after
birth(Croom, 2012). Sex is less vital as a factor that determines the metabolism in humans than in
other organism like rodents, that greatly exhibit sexual ... Show more content on Helpwriting.net ...
As doses shift from low to high, the relative importance of individual enzymes involved in the
metabolism may also shift. For example, at the high dose, oxon formation correlated best the
CYP3A4 activity, while at the low dose, oxon formation correlated best with the higher affinity
enzyme CYP2B6. Nutrition plays a role in metabolism(Croom, 2012). Poor nutrition limits the
available energy for metabolism. Metabolizing enzymes require cofactors and micronutrients that
may be lost with inadequate nutrition. Food itself can change the amount of xenobiotic available for
metabolism by affecting its solubility, as well as by altering gastric emptying and
bioavailability(Croom, 2012). Oral exposures involve first–pass metabolism, where the bulk of the
blood collected from gastrointestinal tract first passes through the liver before being transported to
the rest of the body(Croom, 2012). For xenobiotics with significant dermal absorption or significant
exposure through inhalation, this can dramatically increase the amount available in the circulation
and if the target organ is capable of bioactivation result in significant toxicity in that

Bayesian Evidence Synthesis And Decision Modeling For...
Bayesian Evidence Synthesis and Decision Modeling for Non–Alcoholic Fatty Liver Disease
Summary
The World Gastroenterology Organization (WGO) has recently declared NALFD as most common
cause of liver disease. Obesity is an increasing problem not only in the UK but worldwide. An
estimated 26% of the adults in the UK are considered to be obese 1, 2. Obesity induced metabolic
syndrome may lead to NAFLD, which can progress to Nonalcoholic Steatohepatitis (NASH), and in
turn to advanced fibrosis and an increased risk of Hepatocellular Carcinoma (HCC) 2, 3.
Background
Recent increases in the prevalence of obesity induced metabolic syndrome (MetS) resulted in an
upsurge in the global incidences of both Nonalcoholic fatty liver disease (NAFLD) ... Show more
Apart from their clinical implications, the current economic burden of NAFLD/NASH on the health
care system is substantial. A recent study analyzed outpatient resource utilization in the United
States (US) observed an increase in annual inflation adjusted total NAFLD/NASH outpatient
charges from $2,624 in 2005 to $5,132 in 2010 7. A simulation study estimated $103 billion ($1,613
per patient) annual direct medical cost attributed to NAFLD, which further increased to $189 billion
upon including societal cost 8. In the UK, the total annual cost of NAFLD is estimated to be £31.26
billion, of which, £5.24 billion is in direct cost 8. With the manifold health consequences of
metabolic syndrome are projected to considerably increase in the next decade, the clinical and
economic burdens of NAFLD/NASH are bound to surge in upcoming years.
Research Problem
NAFLD is the hepatic manifestation of the metabolic syndrome (MetS). However, little is known
about the natural history of NAFLD. Furthermore, the pathophysiological relationships between
MetS and hepatic steatosis is not fully understood. The diagnosis of the MetS involves the presence
of three of the following five risk factors: 1) hyperglycemia (fasting glucose ≥ 100 mg/dL), 2) low
concentrations of high–density lipoprotein (HDL) cholesterol ( (–– removed HTML ––) than 150
mg/dL), 4) increased waist circumference (102 cm for men and 89

Lithium Carbonate Interview
With technology advancing and new medications being made to help cure or prevent a disease,
countless amount of people are on a medication or multiple medication. The person I choose to
interview was initials are D.B., who is a male and is in his early 50's. He is on multiple different
medications. The medication that we will be talking about is Lithium Carbonate. Lithium Carbonate
is a mood stabilizer. D.B. has been taking Lithium Carbonate for about 5 years. Lithium Carbonate
is also known as Lithobid or also Eskalith. When taking Lithium, it alters the sodium transport nerve
and muscle cells. The alterations of the sodium transport in the two areas can cause the intraneuronal
metabolism of catecholamines. When taking any medication, ... Show more content on
Helpwriting.net ...
Interviewing D.B. will have some effect developing my RN role When becoming an RN, you
include different learning approaches when communicating with others. Some ways you might earn
a little information from a person as well as obtaining abundant amount. Learning about Lithium
Carbonate I needed do my own research on learning about this drug. Researching data will help you
not only build a better understanding of the medication but it will help you teach your patients about
it along with make sure they absolutely understand the information. I learned that not everyone
retains information the same. Some patients like to have handouts but some need hands on teaching.
Knowing more facts about your patient is always key to a successful training along with a successful
patient–provider relationship. Lithium Carbonate is not typically prescribed to many people.
Lithium, being a dangerous drug can result in a risk of potential toxicity. This drug has to be closely
monitored by having labs done every 3 months to prevent toxicity. In order to be prescribed Lithium
Carbonate you have to be seen someone in behavioral health vs. by your family doctor. After
someone has been on a medication for a few years they tend to let slip from memory the serious
adverse effects along with patient teaching. It is always valuable to just review the basic teaching.
When prescribing a drug, you will know the side effects for that drug, but you also need to know the
drug interactions it will have on other drugs if someone is taking multiple

Chronic Liver Disease Research Paper
The multidimensional function of the liver makes it prone to various diseases. These diseases
interfere with liver function and leads to its derangement. However, the liver has a great reserve
capacity to regenerate and it only produces symptoms after extensive damage. The liver diseases are
categorized into chronic and acute disease. Acute disease occur rapidly and exist for a short period
while chronic liver disease involves a process of progressive destruction and regeneration of liver
parenchyma leading to fibrosis and cirrhosis (Crawford 2007). The burden of chronic liver disease is
on the increase in both developed as well as developed countries. There are various forms of liver
disease. The non–alcoholic fatty liver disease (NAFLD) is one of the most common forms of
chronic liver ... Show more content on Helpwriting.net ...
Patients with fatty liver are asymptomatic so that they rarely present with liver related problems.
Fatty liver is reversible with abstention but it is a risk factor for progression to alcoholic hepatitis
and cirrhosis in patients who continue drinking (Beckingham , 2001).
Hepatitis is another common condition of inflammation of the liver. The most usual cause of this is
viral, and the most common of these infections are hepatitis A B C D and E. Some of these
infections are sexually transmitted. Infection with hepatitis B virus or hepatitis C virus is the main
cause of liver cancer (Wong et al., 2006; Luis et al. 2009).
Liver cancer is another common form of liver disease. It manifests as hepatocellular carcinoma or
cholangiocarcinoma. Most of the liver malignancies are secondary lesions that have metastasized
from primary cancers in the gastrointestinal tract and other organs, such as the kidney, lungs, breast
or prostate. Other diseases of the liver include fascioliasis, cirrhosis, Budd– Chiari syndrome,
hereditary associated liver diseases and sclerosing

Focal Nodular Hyperplasia (FNH)
Focal nodular hyperplasia (FNH), defined as a nodule composed of normal–appearing hepatocytes
in an otherwise normal liver (30), is the second most common benign hepatic tumor after
hemangioma. Histopathologically, FNH is categorized into two major groups: (i) classic (80%) and
(ii) nonclassic (20%). The nonclassic–type is further subcategorized as the telangiectatic FNH
(15%), FNH with cytologic atypia (3%) and mixed hyperplastic and adenomatous FNH (2%). Three
key elements are present in classic FNH lesions including an abnormal nodular architecture,
cholangiolar proliferation, and malformed vessels. In nonclassic–type, the cholangiolar proliferation
is always present but one of the other two elements may be missing (31). In approximately ... Show
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In large hemangiomas, the central scar is typically brighter and larger on T2–weighted images.
Because of the presence of calcifications, necrosis, and scar tissue the central scar in hepatocellular
carcinoma shows low signal intensity on both T1– and T2–weighted images and the enhancement is
slight (37).
The pseudocapsules around some FNH lesions result from compressed liver parenchyma and vessels
surrounding the lesion and an inflammatory reaction. The pseudocapsule of FNH is often seen with
high signal intensity on T2–weighted images and enhances on delayed contrast–enhanced
sequences. In contrast to this pseudocapsule, the true capsule of hepatocellular carcinoma shows low
signal intensity on both T1– and T2–weighted images, with persistent enhancement on delayed
contrast–enhanced sequences (37).
Nuclear medicine: because of the presence of Kupffer cells in FNH, technetium 99m sulfur colloid
can be taken up by this tumor. This ability differentiates FNH lesions from hepatocellular adenomas,
hepatocellular carcinoma and hepatic metastasis that usually don't have functionally active Kupffer
cells

Indications For Liver Biopsy And Histological Assessment...
INDICATIONS FOR LIVER BIOPSY
Liver biopsy and histological assessment of the liver has now taken on an important role in clinical
management. Therefore liver biopsy currently has two major roles:
(A) Diagnostic purposes: Liver biopsy is helpful in diagnosis of many forms of liver disease such as
acute and chronic hepatitis (Wilson disease, alpha–1–antitrypsin disease, glycogen storage diseases,
AIH, NiemannPick disease and others), cholestatic disorders, fatty liver disease, vascular diseases,
inﬁltrative or storage diseases, some infectious diseases, and other disorders that may be associated
with characteristic histological abnormalities. It also plays a role in the diagnosis of patients with
abnormal liver tests of unknown etiology (Czaja et al., 2007). (B) Liver biopsy in the assessment of
known liver disease: Liver histology is also commonly used in disease monitoring of patients with
AIH. First, the portal–based plasma cell inﬁltrate may predict relapse and second, liver biopsy is
often obtained prior to steroid dose reduction and/or discontinuation of immunosuppressive therapy
(Rockey et al., 2009). 1– Neonatal Cholestasis Some forms of neonatal cholestasis can be identified
biochemically and genetically, but others require LB.
Biliary atresia (BA): Typically neonates with BA have acholic stools, firm livers, and abnormal
values for biochemical markers of hepatobiliary injury. Histopathologic evaluation permits
diagnosis of BA in 96% of adequate LB

Obesity : The Wild And Wonderful State Of West Virginia Essay
Obesity, and more importantly childhood obesity, is drastically effecting the United States of
America and other parts of the world, more and more each day. In the last 30 years, the amount of
children who are six to eleven years old have doubled, and children who are twelve to nineteen
years old have more than quadrupled. ("Facts") The wild and wonderful state of West Virginia
unfortunately has the title of the 2nd highest obesity rate in the United States at 35.7% as of 2014.
The childhood obesity rate in West Virginia is 14.0% for two to four year olds, 18.5% for ten to
seventeen year olds, and 15.6% for high school students in general. ("WV") There was a census
conducted in 2012 that showed that greater than one–third of children were overweight or obese too.
("Facts") There is clearly a problem with West Virginia, the United States, and the world. Even
though childhood obesity increases every year and is caused by many factors, it can be prevented.
Before the causes, effects, and prevention of Childhood Obesity can be debated, there must be a
clear difference made between overweight and obesity. Being overweight is the state of "having
excess body weight for a particular height from fat, muscle, bone, and or water." Being obese
includes the definition of overweight, but it also includes "having excess body fat." ("Facts") In
short, the state of being obese is worse than being in the state of overweight, and has more
considerable causes and effects. Obviously,

Truman Medical Case
This 49–year–old African–American female was presented to Truman Medical Center – Emergency
Department, on November 24, 2014 due to nausea, vomiting, and headaches for two days. She
stated that she has no appetite and left lower quadrant pain. She was previously treated at Saint Luke
Hospital – Emergency Department for her diarrhea, nausea and vomiting before transferred to TMC
Hospital. At SLH – ED, she was given some Benadryl, Tylenol and IVF which showed no
improvement and continue to have three to four times watery diarrhea with no blood or mucus
associated with nausea and vomiting. Her medical history is significant of diabetes mellitus type 2,
hypertension, intracardiac loop recorder and cerebro–vascular disease. Vital signs included a high
oral temperature ... Show more content on Helpwriting.net ...
Physical examination showed soft, right upper quadrant tenderness with mild hepatomegaly.
Ultrasound of abdomen revealed contracted gallbladder and hepatic steatosis. CT of abdomen and
chest without contrast revealed bibasilar heterogeneous opacities, bilateral pleural effusions,
prominent lower right paratracheal lymph node, and two hyper enhancing foci within the liver.
Abdominal MRI showed liver masses. With this, medical concerned was for neutropenia fever due
to viral infection vs HIV vs malignancy vs drug induced. Plan of care included, CT of the abdomen
and chest, ultrasound of abdomen, MRI, blood culture, urine culture, stool analysis, peripheral
smear, Infectiologist and Oncologist consultation, C differential toxins, mono spot test, A1C and
TSH test, intravenous fluid of 150 cc/hr of NS, Lyrica: 25 mg, 1 cap, oral, twice a day , Zofran: 4
mg, 2 mL, IV Push, every 6 hours, Zosyn IVPB: 3.375 gram, 100 mL, 25 ml/hr, IVPB, every 8

Nonalcoholic Fatty Liver Disease (Nafld), Is A Form Of
Nonalcoholic fatty liver disease (NAFLD), is a form of chronic liver disease ranging in severity
from simple fat infiltration (steatosis) to an advanced form, nonalcoholic steatohepatitis (NASH,
steatosis with liver inflammation) with subsequent progression to fibrosis.1 The relationship
between gut flora and the development of NAFLD have been under study for almost the last decade.
Uncontrolled growth of gut bacteria and translocation of gut microorganisms from the intestinal
lumen predispose patients to multiple bacterial infections. 2
The portal vein carries blood containing digested products and gut microbiota products to the liver.3
Factors like increased gut permeability, and increased bacterial endotoxins, especially ... Show more
liver damage and mitochondrial dysfunction will follow which contribute to fat accumulation and
development of NAFLD.9
Therefore, the liver–gut interaction is central to understand the pathophysiology of liver diseases,
including non–alcoholic fatty liver disease (NAFLD) and hepatic encephalopathy. Current
knowledge on the association between gut microbial composition and NASH is incomplete. Liver
malfunction leads to altered genetic composition of gut microbial, and in the meantime specific
bacterial species are present during liver pathogenesis, and the abundance of some bacteria is
correlates with grade of liver disease, implying the term "gut–liver axis".
Toll–like receptors (TLRs) constitute very important players in this microbiome balance. TLRs are
trans membrane non–catalytic receptor proteins that prompt activation of innate and adaptive
immune responses to microorganisms through recognition of conserved molecular patterns of
organisms. In order to maintain immune tolerance to the luminal microorganisms the expression of
TLRs by intestinal epithelial cells is normallyat its minimal.

Paralytic Shellfish Poisoning Research Paper
Paralytic shellfish poisoning (PSP) is caused by the consumption of the water soluble alkaloid
neurotoxin known as saxitoxin from shellfish (mussels, clams, cockles, oysters and scallops) from
waters contaminated by Algal blooms. The algal bloom that forms in the water has a fluorescent
greenish hue and contains dinoflagellates that produces these neurotoxins and is found in both the
temperate and tropical areas. Along with medications, the symptoms of may PSP resolve with the
excretion of the toxin. Patients are treated by providing them with respiratory support and fluid
therapy. PSP is confirmed by the urine test of the affected individual to check for saxitoxin by high
performance liquid chromatography– mass spectroscopy. Although the HPLC–MS

Drunk Driving Research Paper
Driving a vehicle with an excessive amount of alcohol in the blood is dangerous for the driver,
passengers, and other innocent civilians around. Driving under the influence (DUI) commonly
known as "drunk driving" refers to a person who is operating a motor vehicle while one's blood
alcohol concentration (BAC) is above the legal limit of .08 percent. Drunk Driving is a major issue
in America, especially for young adults, which is why the government enforces many laws to
prevent car accidents. One of the most commonly cause of drunk driving is due to peer pressure.
Teenagers want to act tough and pretend not to be drunk just to impress their peers or because they
do not want anyone to drive their cars. It is more difficult for young adults to ... Show more content
on Helpwriting.net ...
Alcohol can affect many parts of the body, which includes the following: brain, heart, liver, and
pancreas. Drinking too much alcohol can affect how the brain functions and looks. Consuming too
much alcohol can change a person's mood or behavior as well as making it harder for that individual
to think clearly and move with coordination. Alcohol can damage the heart, causing problems
including: cardiomyopathy, arrhythmias, stroke, and high blood pressure. Cardiomyopathy is the
disease of a heart muscle usually leading to heart failure. Those who have cardiomyopathy are often
as risk with irregular heart rate. Arrhythmias is a condition where the heart is beating either faster or
slower than average. A heartbeat that is too fast is called tachycardia and a heartbeat that is too slow
is called bradycardia. Usually a heart rate of over 100 beats per minute is considered tachycardia
and a heart rate of under 60 beats per minute is considered bradycardia. Stroke occurs when the
supply of blood to the brain is either disrupted or diminished. When this happens, the brain does not
get enough oxygen or nutrients which causes brain cells to die. Heavy drinking takes a toll on the
liver and can lead to various problems like steatosis, alcoholic hepatitis, fibrosis, and cirrhosis.
Steatosis is also known as fatty liver, which infiltrates the liver cells with fat due to alcoholism.
Alcoholic hepatitis is caused by

The Effects Of Alcohol On The Human Body
The Impact of Alcohol on the Human Body
Alcohol is a dangerous substance that deteriorates the human body if consumed on a regular basis.
Even if a person is not a heavy drinker, their body still go through changes when they drink alcohol
(NIH, 2010). Alcoholic beverages are an extremely toxic substance that affects one physical
wellness. The National Institute on Alcohol Abuse and Alcoholism known as NIH, discusses how
alcoholic beverages affects a person's brain, heart, and liver. Also, the NIH explains how alcohol
abuse can lead to cancer in the mouth, esophagus, breast, liver, pharynx, and larynx. It has been
noted that alcohol abuse can cause the immune system of a person to weaken (NIH, 2010). Various
research has been conducted in order to determine which parts of the brain is impacted because of
alcohol consumption (NIH, 2010).
According to NIH, the cerebellum, limbic system, and the cerebral cortex are the three areas of the
brain that are most affected by alcohol. The cerebellum is the area of the human brain that controls a
person's coordination. When a person is intoxicated, damage to the cerebellum causes loss in
balance and emotional response is altered (NIH, 2010). In addition, the limbic system of the brain is
responsible to store a person's memory, yet it is also greatly affected when alcohol is consumed.
Furthermore, the cerebral cortex is the area of the brain that gives a human the ability to think,
behave intelligently, and interact socially. When a

Carbohydrates Shakes Isn 't As Bad
8 Facts why Fat in Protein Shakes isn't as Bad as You Think
When building muscle is the goal, most athletes try to eliminate their fat intake. Fat is not "bad" but
an important part of everyone's nutritional needs. Despite the fact that fat is high in calories, there
are many health benefits that come from them. In proper balance and moderation, they will aid you
in your training regimen and get you stronger, more defined and keep you healthy.
1. Energy during Exercise
Twenty minutes into a workout and it feels like you hit a wall. Energy levels drop and so does your
performance. By adding a small amount of fat to your pre–workout protein shake, when the
carbohydrates run out at the twenty minute mark, the body can then start to burn the fat.
The carb crash causes an increase of insulin in the blood stream followed by a rapid decrease in
blood sugar when the carbs are all used up. When fat burns, the body does not release extra insulin
and give you a sustained level of energy.
2. Hormones
Both men and women each have certain amounts of both testosterone and estrogen in their bodies.
The cholesterol found in saturated fats produces hormones. Not only does the saturated fat help
produce hormones, it helps to balance them or to raise the testosterone levels. An increase in
testosterone helps to build muscles. With more muscle mass the body burns more fat.
3. Improve Vitamin and Supplement Absorption
There are two kinds of vitamins: water soluble and fat soluble.

Chemical-Induced Toxicity
Chemical–induced organ and tissue toxicity is a worldwide health concern. Liver toxicity, because
of the primary role of the liver in the metabolism, detoxification, and elimination of xenobiotics,
caused by the exposure to the growing number of chemical toxicants in the form of agricultural,
industrial, and pharmaceutical products and food components, additives, and contaminants is the
most common organ injury [1–3]. Toxicant–associated liver injury has been associated with a broad
spectrum of liver pathologies ranging from acute necrosis to several types of chronic pathological
states, including simple hepatic steatosis, nonalcoholic steatohepatitis (NASH), toxic liver fibrosis,
and cirrhosis [1,3]. Furthermore, some toxicants may act as carcinogens causing the development of
cancer not only in the liver, but in other human organs and tissues as well [4,5]. This indicates that
detecting, evaluating, and predicting the potential human risk posed by chemicals continues to
remain of great importance. ... Show more content on Helpwriting.net ...
The first approach is based on the use of the genomic technologies to discover sets of genes that
may be chemical–specific and distinctive to organ–injury [3,4,6]. The second approach is based on
identifying selective and sensitive biomarkers of toxicity. Each of these approaches has some
advantages and limitations; however, none of the recent biomarkers identified by either of these two
methodologies have been able to demonstrate enough specificity and sensitivity in detection of liver

Macrohih2a1 Case Study
MacroH2A1.1–overexpressing cells display ameliorated glucose metabolism, 214 reduced
expression of lipogenic genes and fatty acid content (40). These associative 215 studies indicate a
possible conserved involvement of macroH2A1 isoforms, in lipid 216 metabolism. A number of
mechanistic studies using animal have explored this 217 possibility, yielding conflicting outcomes
(Table II). Two mouse models with a 218 macroH2A1 knockout have been reported under a
standard diet feeding. In the first 219 model, generated in the pure C57Bl/6J background,
developmental changes in 220 macroH2A1–mediated gene regulation were observed (42): up–
regulation of 221 lipogenic genes was detected in the liver of the knockout mice (42), which
displayed 222 ... Show more content on Helpwriting.net ...
The changes in lipogenic gene expression 226 have subsequently been associated with differential
physical occupancy of the gene 227 body by macroH2A1 (42, 43). In the second model, knockout of
macroH2A1 in a 228 mixed background led to a variable hepatic lipid accumulation in 50% of the
229 females (44). In this model, the X–linked thyroxine–binding globulin (Tbg) gene was 230 found
to be upregulated in steatotic livers. Tbg is the main carrier of the thyroid 231 hormone T4
(thyroxine), a major regulator of energy metabolism, which could be 232 responsible for the
enhanced fat accumulation. Enrichment of macroH2A1 at the 233 Tbg promoter in female animals
indicated that increased Tbg expression in 234 macroH2A1–knockout mice could be a direct
consequence of the absence of this 235 histone (44). In contrast, our analysis of the in vivo role of
macroH2A1 in response to 236 nutritional excess led us to discover that genetic eviction of
macroH2A1 confers 237 protection against high fat diet–induced obesity and metabolic
derangements in 238 mice (45). Together, these mice studies did not address the role of the single
239 macroH2A1 isoforms; moreover if these histone variants can impact energy 240 turnover in
extra–hepatic depots, was unknown until recently. In the skeletal 241

Hepatic Hemangioma Research Paper
Hemangioma is the most common non–cystic benign hepatic lesion. Depending on imaging
findings, hepatic hemangiomas can be categorized as typical and atypical. Typical hemangiomas
comprised of three distinct histological subtypes, including (i) the cavernous hemangioma, (ii) the
capillary hemangioma and (iii) the sclerosed hemangioma (1). The atypical group includes various
categories such as giant and heterogeneous large hemangiomas (2, 3). A.1.Typical hepatic
hemangiomas Ultrasonography (US): Generally, typical hepatic hemangiomas are homogeneous
hyperechoic masses with well–defined margins and posterior acoustic enhancement at US
examination. In 10% of cases, the lesion may be seen as a hypoechoic lesion due to the presence of
an underlying ... Show more content on Helpwriting.net ...
On T2–weighted images, the lesion is hyperintense with well–defined margins, but the intensity is
less than that of the cerebrospinal fluid (CSF) or a hepatic cyst. After administration of gadolinium,
the lesion shows peripheral nodular discontinuous enhancement that progresses centripetally in the
delayed phases. At diffusion–weighted imaging (DWI), hepatic hemangiomas are typically
hyperintense even with high b–values because of slow blood flow and are hypointense on ADC map
because of restricted diffusion (1, 10, 11). The contrast kinetics in capillary hemangiomas is similar
to that of the CT, i.e. a uniform and rapid enhancement occurs (12). When an arterioportal shunt is
also present a transient perilesional enhancement is observed (13). In sclerosed hemangiomas, the
zones of central sclerosis appear hypointense and the overall signal of the lesion is heterogeneous on
T2–weighted images. After administration of contrast material, a peripheral nodular enhancement
develops and progresses very slowly. An early transient perilesional enhancement is a classical
finding. Sometimes, sclerosed hemangiomas do not enhance at

Liver Disease Research Paper
Pediatric non–alcoholic fatty liver disease:
Increasing awareness in the primary care setting
By Hanna Sauer, RN, BSN
495 Cicada Court, Reno, NV 89521
(775) 303–4779 sauerhanna@gmail.com Abstract: Non–alcoholic fatty liver disease (NAFLD) can
lead to cirrhosis and hepatocellular carcinoma in children and adolescents. Primary care providers
have a unique position to identify and screen for the disease in its early stages. This article provides
an overview of prevalence, expert guidelines, screening, treatment, and implications for the
advanced practice registered nurse (APRN).
Introduction
Non–alcoholic fatty liver disease (NAFLD) is a major complication of childhood ... Show more
According to a landmark article by Browning et al, prevalence of NAFLD was described as being
highest in the Hispanic population and lowest among Black Americans, and Caucasians with an
intermediate prevalence. The differences were thought to be related to insulin resistance, visceral
adiposity, genetics and socioeconomic status9.
Overnutrition, specifically excessive consumption of fructose, is fundamental to NAFLD
development10. Fructose metabolism, unlike glucose, occurs nearly exclusively in the liver and is
preferentially selected for lipogenesis. The triglyceride production and storage that results from
fructose ingestion is highly associated with central obesity, dyslipidemia, and insulin resistance11.
This relevant finding is especially important to clinicians, as this modifiable risk factor may be
easily addressed.
Screening Guidelines and Recommendations
The majority of children with NAFLD are asymptomatic. Occasionally patients may complain of
vague abdominal pain, fatigue, or malaise, however, liver disease is usually found incidentally on
physical exam or routine lab work1. Children may have mild to moderate hepatomegaly; however,
the majority of these children are overweight or obese, making liver palpation a challenge. In
addition to obesity and visceral adiposity, children with NAFLD often present with acanthosis
nigricans on the back of their neck or intertrigenous areas, which is suggestive of insulin

Fatty Liver Disease Case Study
Methods: Four different clinical trials were selected for this paper. First trial focuses on the
management of fatty liver disease with vitamin E and C combined compared to usrodeoxycholic
acid treatment. Second trial focuses on only vitamin E, pioglitazone, or placebo on NAFLD patients.
Third trials focuses on the treatment of nonalcoholic steatohepatitis with vitamin E and vitamin C
combined. Final trial focuses on pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis,
similar to the second trial. First trial had patients who were randomly prescribed either vitamin E
plus vitamin C (500 mg/day) or ursodeoxycholic acid (10 mg/kg/day). After a period of six months,
there was no significant change in BMI before and after the ... Show more content on
Helpwriting.net ...
Vitamin E (300 mg/day) and vitamin C (300 mg/day) were given to each patient orally for 12
months. Half of the patients had a liver biopsy done on them before and after the trial treatment. The
findings of this trial concluded that using both vitamin E and vitamin C combined can help patients
with NASH by minimizing the damage from oxidative stress, significantly improving fibrosis, and
actually slowing down the process that eventually leads to cirrhosis. When vitamin E is administered
along with vitamin C, the combination of both can actively fight against the oxidative stress in the
liver. In this study, serum alanine aminotransferase levels improved, along with a decrease in serum
thioredoxin, high–sensitivity C–reactive protein, and 8–hydroxydeoxyguanosine levels. This trial
suggests that the combination of vitamin C and E should be investigated further to be able to take
advantage of the full benefits of vitamin E against nonalcoholic steatohepatitis (11). Last trial on this
research was similar to the second trial discussed. This trial focused only on adults without diabetes
and without a developed case of cirrhosis. The reason these patients were excluded was due to the
fact that it is unclear whether these patients would have the same response to the therapy being
offered as patients without these conditions. The results on this trial were slightly different than the
second trial discussed. In this trial, significant

Persuasive Research Paper
Richard Branson once said, "Every risk is worth taking as long as it's for a good cause, and
contributes to a good life." Drinking alcohol is a risk itself, let alone drinking alcohol as a teenager.
Drinking can cause interferences with the brain's communication pathways, cardiomyopathy, high
blood pressure, pancreatitis, steatosis, puts you at risk for certain cancers, and weakens your
immune system. These are just a portion of what drinking can do to you. As a teenager your brain
and body are still developing, drinking at an early age can stunt your development. Weed has effects
of major effects on your emotional well being, and you don't know whether they will be negative or
positive effects, smoking weed puts you at risk for lung and respiratory problems. Smoking weed
and drinking alcohol are risks teenagers our age our taking in order to release stress or they believe
it will help them have a good time. Neither drinking nor smoking are risks that contribute to a ...
Show more content on Helpwriting.net ...
Personally, I do not support adult drinking and smoking. For adults though, I believe having a drink
once and a while is okay, it's the heavy drinking I do not support. For teens though, I think that the
use of these drugs is preposterous. In no way, is the use of these substances contributing to a better
life for yourself, and the people you love. Now as I myself do not drink or smoke, I don't understand
why teenagers take in these substances. But from what I can conclude of seeing endless snapchat
stories of people drinking and smoking is the belief that to have a good time or party with people is
to have alcohol, smoke weed, and vape. Some people may feel the need to 'escape' reality, and want
to feel nothing besides the freedom of your body while under the influence. For example, if some
people have a rough home life, they may resort to these forms of what some call stress relief, to feel
better about the reality of their

The Factors That Cause Liver Failure
Many common liver diseases causes liver to become inflamed. The progress of this inflammation
can progress to liver cancer or liver failure. Factors which causes live disease includes viral
infection, alcohol abuse, use of certain drugs, poison or cancer.
More than 100 forms of liver disease are there. Liver diseases are caused by a variety of factors
which can affect everyone from infants to adults7. This can affect the morphology and fuction of the
liver8. It is estimated that 1 in 2500 live birth suffers from liver disease9.
The viral hepatitis B and Hepatitis C, alcoholic liver disease (ALD), non alcoholic fatty liver disease
(FLD), cirrhosis and hepatocellular cancer [1,2] are known to cause most morbidity and mortality
among ... Show more content on Helpwriting.net ...
Hepatic metabolism of insulin and peripheral glucose metabolism contribute to diabetes however
diabetes itself mey be a cause of liver disease. Hepatitis C virus may have direct hepatogenic effect.
Diabetes generates the liver disease of metabolic origin in association with obesity, dyslipidemia and
hypertension.
Symptoms: Usually asymptomatic however mild right upper quadrant discomfort, elevated ALT and
AST19.
d) Obesity: Non alcoholic Fatty Liver is strongly associated with the obesity especially with visceral
fat. Elevated levels of free fatty acids in the liver alters the hepatic metabolism which results in the
hepatic steatosis. This process is subsequent responsible for the inflammation. Also, Insulin
resistance and hyperinsulinaemia are common in obesity as insulin plays key role in the regulation
of regional fatty acid metabolism. In obesity visceral lipolysis is resistant to insulin results in the
accumulation of the free fatty acids in the liver which results in fatty liver and liver steatosis. liver,
fatigue, pain in upper right abdomen, ascites, enlarged spleen, red palms, yellowing of the skin and

Differences On Body And Tissue Weights
Results and Discussion
Body and Tissue Weights
The initial body weight of rats was similar (p–value=0.19). At the end of the experimental period,
the HFFr+S rats had a near doubling of visceral fat weight, compared to the control group (6.9±1.1 g
vs. 3.4±0.4 g, p–value=0.009), while it was slightly and non–significantly lower in the other groups,
especially in the rats gavaged with the high dose of metformin (200 mg/kg/day). After 60 days, no
significant differences were found between the groups regarding the final body weight and
liver/body weight percentage (Table 2). This suggests that the excess energy intake of HFFr rats
have led to a greater adiposity, but not to a higher body weight.
Serum Biochemistry
Compared to the control rats, ... Show more content on Helpwriting.net ...
In this line, Linden et al.35,36 reported that metformin (300 mg/kg/day) lowered adiposity,
hemoglobin A1c levels, hepatic triglycerides and markers of hepatic de novo lipogenesis in diabetic
Otsuka Long–Evans Tokushima Fatty (OLETF) rats. These were not accompanied by any
improvement in fasting and post–challenge glycemic control, and either in the increased serum
levels of triglyceride and free fatty acids. Indeed, there are some other studies, showing no effect
exerted by either dietary calcium and/or vitamin D3 on glucose intolerance37–41.
In this study, HFFr diet, calcium–vitamin D3 supplementation and oral gavage administration of
metformin did not alter the serum concentrations of triglycerides, total cholesterol and Non–HDL–C
(p–value>0.05). The rats in the CaD+S group exhibited clearly higher levels of serum HDL–C,
compared to the groups receiving recommended levels of calcium and vitamin D3. Moreover, the
levels of serum CTRP3 (also known as cartonectin, cartducin, CORS–26) was significantly higher
in the +Met200 group, compared to the other groups (except the +CaD+Met200 group). There was
no effect of HFFr diet and no additive effect of metformin and CaD on serum HDL–C and CTRP3
(Table 3).
CTRP3 is a novel adipokine and a member of CTRP superfamily, which has been shown to reduce
glucose levels, hepatic steatosis and gluconeogenesis, by its regulatory

Coronary Disease: The Role Of Heart Disease In Children
Heart disease is one of physiological result that correlates with the premature aging process
associated with obese children's bodies. Most cases of high blood pressure in children are the result
of heart or kidney disease. The blood flow through blood vessels might not be normal. This situation
may affect the function of the heart. Because of their over–weight kids have a chance to get heart
disease. The fat that stored in their bodies might leads to heart problem and create tension on their
heart. This affects the function of the heart in the body.. Obese children bodies can leads to one of
heart disease called Coronary artery disease. It is the common term for buildup plaque in the hearts
arteries that could lead to heart attack. It may be chronic, caused narrowing of coronary artery and
limitation of the blood supply to part of the muscle. Or it can be acute, resulting from a sudden
plaque that ruptures. The cultural Practice of encouraging children to eat has turned from protective
to destructive. Heart disease and diabetes are become epidemic because over fed children often
grown up to become overweight adults. An article in the Lancet predicts that by 2020,228 million
adults worldwide will have diabetes because ... Show more content on Helpwriting.net ...
Deposition of lipid within the liver represents part of an abnormal lipid partitioning pattern, most
commonly associated with increased intra–abdominal fat. The typical obese child with NAFLD will
usually manifest other components of the insulin resistance syndrome such as dyslipidemia,
hypertension and altered glucose metabolism. As liver steatosis itself is usually asymptomatic, a
high index of suspicion for its presence should be present in obese insulin resistant kid who present
with dislipidemia or altered glucose metabolism or manifest anamnesttic or physical signs that
suggest the presence of insulin

Non-Alcoholic Tumor Disease
Non–alcoholic fatty liver disease (NAFLD) is defined as liver abnormalities ranging from simple
steatosis to non–alcoholic steatohepatitis with or without developing cirrhosis, which occurs in the
absence of significant alcohol intake or use of teratogenic drugs or hereditary disorders. There is a
significant association between NAFLD and metabolic syndrome. Obesity, dyslipidemia and Type 2
diabetes mellitus (T2DM) are the most common metabolic risk factors associated with NAFLD. Due
to increase in prevalence of metabolic syndrome, NAFLD is the most common cause of chronic
liver disease in adult population. . It is estimated that 10%–29% of patients with NASH will
eventually develop cirrhosis within a 10 year duration. The mortality of cirrhosis ... Show more
But many of genetic mutations are rare single protein or enzyme mutations that do not explain the
vast majority of the cases of NAFLD
Metabolic changes
The peroxisome proliferators activated receptors (PPAR) are a group of nuclear receptors involved
in regulation of fatty acid metabolism and storage. PPARα is a regulator of β–oxidation and PPARγ
is involved in insulin sensitivity and triglyceride storage. PPARα increases the β–oxidation, uptake
and clearance of fatty acids. PPARα have shown a marked development of steatosis, implicating a
possible role in the disease. Hormone changes
Insulin resistance is found in those with metabolic syndrome, obesity and/or diabetes, is frequently
considered the key factor in developing hepatic steatosis. The prevalence of diabetes is increasing
because of obesity and insulin résistance as common risk factor for both diabetes and NHFLD.
Hence the prevalence of NHFDL is also increasing.
Inflammation
Tumor necrosis factor alpha (TNFα) and Interleukin–6 (IL–6) are identified to cause NAFLD. But,
(TNFα) is linked to cause insulin resistance and progression to NASH. Treatment with anti–TNFα
therapy shows improvement in NAFLD.
Diet and physical

Liver Biopsy Essay
Chronic liver diseases and liver biopsy. Chronic liver diseases encompass many different causes,
including viral infections, nonalcoholic fatty liver disease (NAFLD), alcohol abuse, primary
sclerosing cholangitis, primary hemochromatosis, and autoimmune disease. All of these precipitate
chronic damage to the liver via necroinflammation and subsequent cellular injury and accumulation
of extracellular matrix (ECM) proteins distorting the hepatic architecture by forming hepatic fibrosis
with abnormal collagen deposition. Without treatment, the eventual development of cirrhosis (the
end stage of fibrosis) can accelerate to hepatocellular dysfunction, hepatic insufficiency, portal
hypertension, and hepatocellular carcinoma (HCC), thus ... Show more content on Helpwriting.net
...
For example, a NAS only has Kappa values of 0.6 for interobserver and intraobserver agreement.7,
8 Due to the growing concern about NAFLD, there is an urgent need for safer, less expensive, and
more accurate imaging biomarkers of a NASH diagnosis and longitudinal follow–up.
Noninvasive Magnetic Resonance Elastography imaging biomarkers for NASH. The translation of
basic research into improved therapeutics and management of NAFLD patients is still poor. This is
partly because the foundations of hepatology were built upon histologic assessments of liver tissue,
and thus percutaneous biopsies have been bedrock for the diagnosis and staging/grading of liver
diseases. There are also critical barriers to a translational study design due to the prolonged natural
history of NAFLD and the lack of accurate noninvasive assessments of liver injuries, such as
hepatocellular ballooning in NASH. Therefore, noninvasive imaging biomarkers are critically
important for clinical management to better understand the progression from simple steatosis
(NAFL) to NASH with advanced stages of fibrosis. Timely identification of NASH before the onset
of fibrosis would also allow for early intervention to avoid progression to end–stage liver disease.
Magnetic Resonance Imaging (MRI) offers chemical–shift imaging and spectroscopic methods for

Hepatic Steatosis Research Paper
Fatty liver disease is a growing epidemic with a prevalence of 20–30% in the adult global
population [1] and in 70% patients with diabetes due to increased hepatic triglyceride content [2]. In
patients with non–alcoholic steatohepatitis (NASH), 50% will evolve to fibrosis, 10–15% to
cirrhosis and 5.4% to hepatic impairment [1] Hepatic steatosis may affect the whole liver diffusely
or in focal circumscribed areas near anatomical landmarks [3]. It can be identified in specific
locations such as the gallbladder fossa, the subcapsular region, and the porta hepatis. Focal hepatic
steatosis may attain a wedge–shaped or geographic appearance with absence of a mass effect and
visualization of normal vasculature passing through these fatty regions [4]. The natural prevalence
of hepatic steatosis was analyzed in the abdominal CT scans of 1,425 healthy adults and revealed
that fatty infiltration occurred in 9.7%, of which 68% were diffuse, 9% being focal and solitary, and
22% being focal and multiple in distribution and the prevalence increases with age suggesting that
focal patterns of hepatic steatosis are not rare mainly in older males with central

Hepatic Lipids Lab Report
The results shown are the average of 10 different experiments ± SEM. (*) Indicates significant
difference regarding to control group p ≤ 0.05 by Student "t" test.
Figure 1. Effect of CdCl2 exposition on hepatic lipids. A) Cd concentration, (in the control groups,
were not detected). B) Triglycerides level (TG). C) Phospholipids level (PL). D) Esterified
cholesterol level (Chol). The results shown are the average of 10 different experiments ± SEM. (*)
Indicates significant difference regarding to control group p ≤ 0.05 by Student "t" test.
Figure 2. Liver histology. Photomicrographs of lipid droplets stained with Oil Red O. Liver
morphology of control groups at 3, 4 and 5 months (A, C and E, respectively) with few lipid
droplets present, indicated by the arrows. Liver morphology of groups exposure to CdCl2 at 3, 4 and
5 months (B, D and F respectively), lipid droplets indicated by the arrows. Cadmium groups showed
both macrovesicular (ballooning of hepatocytes, white dotted circles) and microvesicular injurie
(foaming in hepatocytes, blue dotted circles); lesions are characteristic of hepatic steatosis. Scale
bars, 50µm. ... Show more content on Helpwriting.net ...
Electropherograms of lipoproteins and area under curve of lipidic mobility zones. A)
Electropherogram of 3–months of groups exposed and non–exposed to CdCl2. B) Area under curve
of lipidic mobility in 3–months groups. C) Electropherogram of 4–months of groups exposed and
non–exposed to CdCl2. D) Area under curve of lipidic mobility in 4–months groups. E)
Electropherogram of 5–months of groups exposed and non–exposed to CdCl2. F) Area under curve
of lipidic mobility in 5–months groups. The results shown are the average of 10 different
experiments ± SEM. (*) Indicates significant difference in comparison the control group P ≤ 0.05
group by Student "t"

Acute Liver Failure ( Alf )
1. Introduction
The liver is the one of the most important organs in the body, it helps maintain the body's normal
activities with many essential functions such as drug detoxification, also the liver is considered the
main site for metabolism inside the body, It organize many metabolic reactions in the body, as well
as providing the body with major secretory functions.(1)
Liver dysfunction is related to the abnormality in the liver's ability to perform its normal functions,
mainly due to exposure to various stimuli such as toxic substances, viral infections, and trauma,
which eventually lead to massive damage to the hepatocytes as well as abnormal functions of the
liver.(1)
1. Types of Liver diseases:–
1.1. Acute liver failure (2)
Description of acute liver failure (ALF) is the sudden loss of function of liver cells in a patient with
formerly normal liver function, which includes blood clots and hepatic encephalopathy disease.
However, the causes of pathological and the clinical causes of acute liver failure are variables, these
causes are recognized as the severe acute Wilson, activated (illuminated) of hepatitis B and hepatitis
autoimmune usually be chronic liver disease instead of the acute liver failure Foundation. (2)
Even with the histological studies, however, the architectural collapse of the liver, which is a feature
of the acute liver failure, may be difficult to distinguish from fibrosis associated with chronic liver
disease. It can define the process of acute

Nonalcoholic Fatty Liver Disease Essay
Nonalcoholic Fatty Liver Disease, one of the most common liver disorders, can have several causes,
such as congenital, pharmaceutical, or other miscellaneous sources, but the most clinically important
etiology is metabolic disorder. Metabolic Disorder, also known as syndrome X, is a collection of
symptoms that occur in clusters, and cause a patient to have a higher risk of heart disease, stroke,
and diabetes. Metabolic syndrome has several hallmark signs. Many of these conditions can occur
alone, or secondary to another condition and do not individually point to metabolic syndrome. These
characteristic signs are a large waist circumference, high triglyceride levels, reduced HDL
cholesterol, increased blood pressure, and elevated fasting ... Show more content on Helpwriting.net
...
The basic mechanism of steatosis is that insulin resistance causes increased lipid deposition in the
hepatocytes of the liver. This abnormal amount of fat causes cell death. When a hepatocyte
undergoes lysis, liver enzymes such as aminotransferases are released. This elevation of liver
enzymes in the bloodstream is a major sign of steatosis since most patients are asymptomatic at this
stage. It is important, however, to rule out the many causes of cell death that would have the same
presentation. As discussed in the research by Birkenfeld, the accumulation of fatty deposits
decreases the metabolic capacity of the liver, and causes inflammation of the hepatic tissue, causing
hepatomegaly. This deposit of triglycerides in the liver instead of the adipose tissue is thought to be
caused by altered levels of cellular products involved in the uptake of fatty acids. While the
concentrations of enzyme lipoprotein lipase, fatty acid transport proteins, and FAT/CD36 are
typically high enough in the muscle to cause lipid uptake into adipose tissue, it is inhibited in
insulin–resistant NAFLD patients. Insulin plays a key role in the action of lipoprotein lipase.
Without insulin the normal uptake of lipids to adipose decreases, and their uptake in the liver
increases. This is shown by the disproportionally high level of lipoprotein lipase, fatty acid transport
proteins, and FAT/CD36 in the liver to the bodily adipose tissue. (3) Steatosis is the first stage of
NAFLD

Hemangioma Essay
A.2. Atypical features A.2.1. Heterogeneous large and giant hepatic hemangiomas At US, large
hemangiomas seem heterogeneous. With using non–contrast CT, the lesion may be seen
hypoattenuating and heterogeneous with low attenuated central areas. After administration of
contrast material, the filling is incomplete during the portal venous and delayed phases. On T1–
weighted images, the lesion is observed as a marginated hypointense mass containing hypointense
septa and a hypointense cleft. On T2–weighted images, the internal septa remain hypointense, but
the cleft is hyperintense. The enhancement is similar to that of CT imaging and the internal septa
and cleft remain hypointense (14, 15). A giant hemangioma is a large (over 4 cm in diameter)
cavernous ... Show more content on Helpwriting.net ...
The FNH lesions are often multiple in these patients (17, 18). In fact, multiple hemangiomas provide
adequate arterial flows for the development of multiple FNH lesions (a hyperplastic response) (2).
A.2.7. Hemangioma with capsular retraction This finding usually reflects the presence of a marked
focal fibrous stromal reaction in the sclerosed hemangiomas and should not be considered a definite
marker of malignancy (5, 19). A.2.8. Hemangiomas and the dilation of the bile duct This condition
is seen when a hemangioma is located in segment IV or close to the hepatic hilium (20). A.2.9.
Hemangioma and hepatic steatosis In the severe fatty liver, the typical appearance of hemangiomas
is altered. The lesion may appear hyperechogenic, isoechogenic or hypoechogenic compared to the
steatotic liver with or without a posterior acoustic enhancement at US examination. In non–contrast
CT the lesion may be found hyperdense or isodense (2, 21). When a contrast material is used or
when T2–weighted images are acquired the presence of hepatic steatosis does not affect the
appearance of hemangiomas. A perilesional zone may be seen without fat infiltration (22,

Pathophysiology: HCV Analysis
Pathophysiology
HCV is an enveloped single stranded RNA virus and belongs to the genus Hepacivirus of the family
Flaviviridae (Irshad el al., 2013). Analysis has identified 6 different types of HCV genotypes
numbered 1 to 6 (Pawlotsky, 2003). Genotype 1 is the common type of HCV currently in the United
States (Irshad el al., 2013). Differentiating between the genotypes when determining the which
antiviral regimen to treat the patient with. Humans are the only known natural host for HCV
(Pawlotsky, 2003). HCV is a non–cytopathic virus that enters the liver cell and replicates causing
hepatocytes necrosis by several mechanisms by immune mediated cytolysis and metabolic changes
including hepatic steatosis, oxidative stress and insulin resistance ... Show more content on
Helpwriting.net ...
During the acute viral infection, the HCV alters the host's defense and innate immunity triggering a
non–specific immune response. The adaptive immune response plays a major role in establishing a
persistent infection, which results in chronic HCV infection (Irshad el al., 2013). Fibrosis is the
main complication of chronic HCV infection and is ultimately the culprit of HCV morbidity and
morality (Irshad el al., 2013). Fibrosis progressin occurs as a direct result of chronic inflammation of
the liver which is caused by chronic injury and destruction of the liver cells (Irshad el al., 2013).
HCV eradication reserves the fibrotic state and according to recent studies suggest that cirrhosis
may be reversed over time (Irshad el al., 2013). HCC is the ultimate complication of HCV infection
aNd it occurs in 1–4% of HCV cirrhotic patients (Irshad el al., 2013). Cirrhosis is the main risk
factor for HCC in addition to other exogenous factors such as alcohol consumption, viral co–
infections, diabetes and obesity

Alcohol Consumption And Metabolic Syndrome
Both alcohol consumption and metabolic syndrome are risk factors for development of fatty liver
diseases with similar pathology which ultimately can result in development of liver cancer.3, 4, 24–
273, 4, 23–26 Using a two–stage mouse model in which tumor initiation by DEN was followed by a
35% high fat diet, we have previously reported increased tumor incidence, suggestive of a diet–
related promotional effect.11 Consistent with these findings, in the current study, we observed
increased adenoma incidence and tumor multiplicity in the HF/CAS group relative to chow controls.
More importantly, substituting SPI for casein in the diet produced a marked reduction in hepatic
lipid accumulation, inflammation and cell proliferation, resulting in lower tumor incidence and
multiplicity. SPI feeding prevented liver weight increase and hepatic steatosis in HF–fed mice
relative to mice fed casein (Figure 1). In rats, replacing casein with soy in various feeding regimes
has also led to significant reductions in hepatic weight and steatosis .17, 28, 29 This was found to be
associated with hepatic activation of PPAR–signaling pathways and inhibition of SREBP signaling
which might promote fatty acid utilization over fatty acid synthesis.17 Similar mechanisms may be
operating in our mouse model, as SPI induces genes involved in fatty acid uptake, fatty acid
degradation and oxidative phosphorylation. The employed model demonstrates protective effects of
SPI in early tumorigenesis.

Liver Disease Essay
For the past few decades there has been a chronic disease plaguing society's young children. This
chronic disease has spread worldwide with the numbers of diseased children is expected to increase
in the next decade. This chronic disease is obesity. Along with the rise of obesity among youth, there
is a new silent killer linked to childhood obesity. This new chronic disease, typically found in
alcoholics, is now becoming prevalent in obese children and is called non–alcoholic fatty liver
disease (NAFLD). NAFLD is defined as a liver disease in people who have not consumed alcohol in
significant amounts to cause liver damage, and in whom no other etiology for fatty liver is present
(Prashant, 2007, p. 401). Ulrich, an MD at the Birmingham ... Show more content on
Helpwriting.net ...
In a study by Giorgio, an MD at regional hospital of Bolzano, found that using MRI, "14 children
had steatosis, with 8 of 14 subjects with severe fatty infiltration and 6 of 14 with mild form"
(Giorgio, 2005, p. 834). Ultrasound has been helpful in detecting fat accumulation, but it does not
detect fibrosis as effectively. Prashant reported an ultrasound study by Joseph et al reported," A
sensitivity of 89% and specificity of 93% in detecting steatosis in the liver, and a sensitivity of 77%
and specificity of 89% in detecting increased fibrosis in the liver" ( Prashant, 2007, p. 402). That
same study showed that the MRI reported a sensitivity of 92% and specificity of 100% in detecting
NAFLD when combined with serum aminotransferases (ATL) levels (Prashant, 2007, p.402). With
these findings, it can be concluded that MRI is better at detecting NAFLD than ultrasound.
However, MRI is only accurate at 100% when combined with taking ALT and aspartate
aminotransferases (AST) serum blood levels. ALT and AST are liver enzymes in the blood, and
when found at high concentrations are associated with obese children, and linked to be a good
indicator of detecting NAFLD. Prashant (2007) stated, "In NAFLD the ALT and AST levels are
elevated to up to 5 times the upper normal limit (p.402). Therefore, studies have shown that 24–25%
of children referred to obesity centers have elevated ALT levels (Kerkar, 2004, p.614). With the
different

Liver Failure: A Case Study
Liver function:
The liver is a large, meaty organ that sits on the right side of the belly.
The liver is the main site of metabolism for drugs and other exogenous compounds.
It regulates the composition of blood, including the amounts of sugar, protein, fat , and nutrients.
Hepatotoxicity:
Damage or injury to the liver caused by a drug, chemical or other agent. Symptoms vary depending
on the degree of exposure and hence extent of the liver damage or injury. Mild liver damage may
cause few of any symptoms whereas severe damage can ultimately result in liver failure.
Symptoms of hepatotoxicity:
Signs and symptoms specific for hepatotoxicity:
Jaundice
Itching
Easily bruising
Symptoms of severely damaged cirrhosis ... Show more content on Helpwriting.net ...
This effect may well be due to the inhibition of protein synthesis caused by tetracycline which will
inhibit the production of the apolipoprotein complex involved in transport of the very low density
lipoprotein (VLDL) out of the hepatocyte
6. Chronic active hepatitis, cirrhosis and sub–acute necrosis:
Chronic active hepatitis, sometimes associated with cirrhosis is associated with the use of a number
of drugs such as oxyphenisatin a–methyldopa, nitrofurantoin and isoniazid. Long term
administration of the antitubercular drug isoniazid leads to hepatic dysfunction in a significant
proportion of recipients (10–20%).
8. Liver tumors:
Anabolic steroids have been implicated as responsible for primary hepatocellular carcinomas and
adenomas. Similarly use of contraceptive steroids has been connected with liver tumours,
particularly the oestrogenic components. The mechanism(s) is unknown .
9. Non–specific changes:
Certain hypotensives, vasodilators, anti–inflammatory agents and oral contraceptives cause a
transient increase in transaminase levels which revert to normal level after the drug is stopped.
These reactions cannot be predicted

Nonalcoholic Fatty Liver Disorder
Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is a metabolic disease commonly associated
with obesity, type 2 diabetes, and inflammation–all features of insulin resistant syndrome. However,
very limited data are available regarding the association of subclinical inflammation and insulin
resistance with NAFLD in a prediabetic state. We, therefore, conducted the study to assess this
relationship among this population.
Methods: We studied a cross–sectional analytical design of 140 [male/female, 77/63; age in years
(ranges), 45 (25–68)] prediabetic subjects after confirming with 75 g oral glucose tolerance test
(OGTT). The diagnosis of NAFLD was made by ultrasonic examination of the liver and divided into
groups of without NAFLD (n = 63) and NAFLD (n = 77). All individuals underwent anthropometric
and clinical examinations. Among laboratory investigations, serum glucose was estimated by
glucose oxidase method, serum lipid profile and liver enzymes were measured by the enzymatic
colorimetric method and glycated hemoglobin (HbA1c) was measured by high performance liquid
chromatography (HPLC) technique. Serum insulin and high sensitivity C reactive protein (hsCRP)
were measured by enzyme immunoassay technique. Insulin resistance (HOMA–IR) was calculated
by homeostasis model assessment (HOMA).
Results: There was significantly higher levels of hsCRP (2.82 ± 1.60 vs. 1.39 ± 0.66 mg/l, P <
0.001) and HOMA–IR (4.03 ± 1.39 vs. 1.98 ± 1.04, P < 0.001) in NAFLD subjects

Patient T. R: A Case Study
Patient T.R. presents for a routine physical exam and bloodwork. Patient reports a healthy diet,
exercises three–four times per week, takes a multivitamin daily, and omeprazole occasionally for
heartburn relief. His husband is HIV positive, but T.R. is not and has never received antiretroviral
therapy. T.R.'s labs are normal with the exception of CD4+ T–cell count: 210 cells/mm3; Viral load:
10,000 copies/ml; Genotype: No resistance mutations detected. He is diagnosed with asymptomatic
HIV infection. Treatment goals for T.R. include decreasing plasma HIV RNA, maintaining immune
system function, preventing opportunistic infections, and preventing transmission of HIV
("AIDSinfo | Information on HIV/AIDS Treatment, Prevention and Research," n.d.).
Pharmacologic treatment for HIV–infected patients consists of antiretroviral (ARV) medications
which cover six classes of drugs including nucleoside/nucleotide reverse transcriptase inhibitors
(NRTI), non–nucleoside reverse transcriptase inhibitors (NNRTI), protease inhibitors (PT), a fusion
inhibitor (FI), a CCR5 antagonist, and integrase ... Show more content on Helpwriting.net ...
should have labs drawn for hepatitis B & C, liver function studies, lipid panel, and a urinalysis
("AIDSinfo | Information on HIV/AIDS Treatment, Prevention and Research," n.d.). A CBC,
chemistry, liver function panel, HIV viral load, and CD4 count should be performed at 2–8 weeks
after treatment initiation, after changes to the regimen, and every 3–6 months ("AIDSinfo |
Information on HIV/AIDS Treatment, Prevention and Research," n.d.). T.R. should also be educated
on adverse reactions to the medications such as myelosuppression, headache, nausea, steatosis,
neutropenia, amylasemia, fatigue, insomnia, and rash (Edmunds & Mayhew, 2014). The goal of the
current medication regimen is to see an increase in CD4 count and decrease in viral load to
undetectable

Hepatic Steatosis
DIAGNOSIS
Initial evaluation
The diagnosis of NAFLD requires
(1) There is hepatic steatosis by imaging or histology;
(2) There is no significant alcohol consumption; (3) No competing etiologies are present for hepatic
steatosis; and (4) There are no co–existing causes for chronic liver disease
It is important to rule out common causes of liver injury, such as alcohol, drug use, and viral
hepatitis as well as other co–existing etiologies for chronic liver disease including alpha–1
antitrypsin deficiency, hemochromatosis, autoimmune liver disease (types 1 and 2), chronic viral
hepatitis, and Wilson's disease
Elevated alanine aminotransferase and aspartate aminotransferase levels may indicate the presence
of hepatic steatosis, inflammation, ... Show more content on Helpwriting.net ...
In particular, cytokeratin–18 fragments have shown the most promise in the diagnosis of NASH. It
is an indicator of hepatocyte apoptosis, may have clinical utility showing a sensitivity of 66% and
specificity of 82% in diagnosing NASH. Currently this assay is not commercially available and
there is no established cut–off value. Other serum biomarkers that have been evaluated for the
diagnosis of NASH include various cytokines, acute phase proteins, and oxidative stress markers.
Two acute phase reactants, C–reactive protein (CRP) and pentatrix–3, have been studied in the
diagnosis of NASH.
Radiological evaluation
Ultrasonography (US) is a cheap, fast, and widely available imaging technique with applications for
fatty liver. US has been reported to have a sensitivity ranging from 60% to 94% and a specificity of
66% to 95%.
Liver biopsy
Currently, liver biopsy remains the gold–standard for the diagnosis of NASH as it serves as the only
means of distinguishing hepatic steatosis from steatohepatitis through examination of liver
histology. According to current AGA guidelines, a liver biopsy should only be considered in patients
with NAFLD who are at increased risk to have steatohepatitis and advanced fibrosis, such as those
who have metabolic

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