LIVER DISEASE - Cleveland Clinic...Implications GGTP, GGT R=8-38 u/L Found on the surface of hepatocytes Sensitive indicator for biliary disease Chronic alcohol ingestion Albumin R=3.3-4.5

DOS CME Course 2011 1 Oxtober 2010 1 Confidential

Shannon A. Rives, MSN, RN, ACNS-BC, CCRN

Clinical Nurse Specialist Gastroenterology, Hepatology, and Transplant Nursing Education and Professional Practice Cleveland Clinic

© Cleveland Clinic 2015

LIVER DISEASE

DOS Course 2015 1

1. Recognize and describe the implications of abnormal laboratory tests as they apply to the liver.

2. Define non alcoholic fatty liver disease, hemochromatosis, and hepatitis C.

3. Explain the pathophysiology of non alcoholic fatty liver disease, hemochromatosis, and hepatitis C

4. Classify diagnostic measures to establish a diagnosis

5. Identify non-pharmacologic and pharmacological treatment options for nonalcoholic fatty liver disease, hemochromatosis, and hepatitis C

6. Apply interventions to aid in the management of specific liver diseases.

Objectives

DOS Course 2015 2

Overview

Synthesize Plasma proteins

Albumin Amino Acids

Complement proteins Clotting factors

Hormones

Metabolize Carbohydrate

Lipids Drugs

Bile production Conjugate bilirubin

Bile acids

Immune/Defense Remove bacteria from the blood Elimination of toxic by-products

LIVER

DOS Course 2015 3

http://jb.oxfordjournals.org/content/149/3/231/F1.large.jpg 4

Overview

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Presenter

Presentation Notes

The symptoms of hepatic encephalopathy may range from mild to severe and may be observed in as many as 70% of patients with cirrhosis. Symptoms are graded on the following scale: Grade 0 - Subclinical; normal mental status but minimal changes in memory, concentration, intellectual function, coordination Grade 1 - Mild confusion, euphoria or depression, decreased attention, slowing of ability to perform mental tasks, irritability, disorder of sleep pattern (ie, inverted sleep cycle) Grade 2 - Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, intermittent disorientation (usually with regard to time) Grade 3 - Somnolent, but arousable state; inability to perform mental tasks; disorientation with regard to time and place; marked confusion; amnesia; occasional fits of rage; speech is present but incomprehensible Grade 4 - Coma, with or without response to painful stimuli

Illustration Courtesy of Lisa Marie Galbraith, RN

Edema

Palmar erythema

Ascites

Bleeding

Bruising Jaundice

Hepatic encephalopathy

Spider angioma

Caput medusae

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Presenter

Presentation Notes

TIPS Blood and plasma Lactulose or rifaxim Paracentsis and albumin ATB The symptoms of hepatic encephalopathy may range from mild to severe and may be observed in as many as 70% of patients with cirrhosis. Symptoms are graded on the following scale: Grade 0 - Subclinical; normal mental status but minimal changes in memory, concentration, intellectual function, coordination Grade 1 - Mild confusion, euphoria or depression, decreased attention, slowing of ability to perform mental tasks, irritability, disorder of sleep pattern (ie, inverted sleep cycle) Grade 2 - Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, intermittent disorientation (usually with regard to time) Grade 3 - Somnolent, but arousable state; inability to perform mental tasks; disorientation with regard to time and place; marked confusion; amnesia; occasional fits of rage; speech is present but incomprehensible Grade 4 - Coma, with or without response to painful stimuli

Lab Interpretation

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• Aspartate aminotransferase (AST) – Serum glutamic oxaloacetic transaminase(SGOT)

• Alanine aminotransferase (ALT) – Serum glutamic pyruvic transaminase(SGPT)

• Alkaline phosphatase (ALP)

• Albumin

• Total Bilirubin

Labs

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–Gamma-glutamyl transferase (GGT)

–Unconjugated bilirubin (indirect)

–Prothrombin time –Lactate dehydrogenase (LDH)

Labs

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Labs

Lab Study Description Implications

AST (SGOT) R = 7-40 U/L

Higher than ALT when damage to the hepatocytes is caused by ETOH

Signifies cellular injury

ALT (SGPT) R = 5-36 U/L

More specific to the liver than AST Signifies cellular injury

ALP R=30-120 U/L

Highest concentrations are found in the liver, biliary tract epithelium.

Marker for cholestasis (lack of bile flow)

DOS Course 2015 10

Labs


GGTP, GGT R=8-38 u/L

Found on the surface of hepatocytes

Sensitive indicator for biliary disease Chronic alcohol ingestion

Albumin R=3.3-4.5 g/dl

Albumin is produced and secreted by the liver daily

Assess hepatic function Not to be used to assess acute liver disease

Prothrombin time R =12-15 sec

Indicator of liver’s ability to manufacture extrinsic coagulation factors

May be normal in chronic disease but elevated in acute dysfunction

DOS Course 2015 11

Presenter

Presentation Notes

GGT- men have higher level the women because of the levels in the prostate gland. Used to validate liver as The source for an increased AP. Where you may have have an elevated AP and a normal GGT I would think bone disease. GGT is not elevated in pregnancy

Labs


Total Bilirubin 0.3-1.3 mg/dl

Production of red blood cell breakdown

Direct Bilirubin (Conjugated) 0.1-1.3 mg/dl

Water soluble form of bilirubin. May indicate biliary tract obstruction

Indirect Bilirubin (Unconjugated) 0.1-1.0 gm/dl

Non-water soluble form of bilirubin Overproduction of bilirubin Inability to conjugate bilirubin

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LDH R = 92-200 U/L

Poor diagnostic sensitivity, iso-enzyme 5 is particular to the liver

Suggests ischemic hepatitis

Labs

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Non Alcoholic Fatty Liver Disease

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Non Alcoholic Fatty Liver Disease Steatosis (fatty liver)

• Fat accumulation in the liver cells

• Can be considered when more

that 5% of the hepatocytes contain liver droplets

Non alcoholic steatohepatitis (NASH)

• Presence of lobular inflammation and/ or fibrosis

• Can progress to cirrhosis, end

stage liver disease, and or hepatocellular carcinoma (HCC)

Source: http://liverbasics.com/hepatic-steatosis.jpg Source: http://geekymedics.com/2010/10/16/non-alcoholic-fatty-liver-disease

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Epidemiology • The most common cause of liver disease in the Western world and a

frequent reason for elevated liver enzymes (Bedgoni, Nobili, & Tiribelli, 2014)

• World wide prevalence is estimated at 6.3% to 33% with a median of 20% (Baran & Akyuz, 2014)

• NASH cirrhosis is the third leading indication for liver transplant in the United States (Machado & Cortez-Pinto,2014)


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Presenter

Presentation Notes

Hispanics may exhibit a more progressive disease process Highest prevalence in males between 45-60 years old

LIVER

INSULIN

ER stress Cytokine

s

TNF-a

SFA

Lipotoxicity

Kupffer

ATP

Pathophysiology

“Two hit theory”


Dysfunctional adiopocytes Decreased adiponectin

Insulin resistance Increased lipolysis

Increased free fatty acids

Decreased export of fatty acids from the

liver

Increased oxidative

stress Cytokines

Mitochondrial dysfunction Damage to hepatocytes

Excessive accumulation of triglycerides in the liver

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Clinical presentation

Physical

• The patient may be asymptomatic or exhibit very general symptoms of fatigue and abdominal discomfort (RUQ)

• Hepatomegaly

Laboratory

• Mild to moderate elevation in liver enzymes AST and ALT reflecting cellular damage


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Presenter

Presentation Notes

Assess for elements of the metabolic syndrome Assess alcohol intake

Liver biopsy- gold standard for diagnosis

Non alcoholic fatty liver disease

Source: http://www.skills.uct.ac.za/photos/liver%20biopsy.jpg

• Invasive

• Used to evaluate treatment

• Used for prognosis • Not a perfect

diagnostic tool

Source: http://www.cpmc.org/advanced/liver/patients/topics/HepatitisC-profile.html

Nursing Considerations Check coagulation status Assess site for bleeding Assess hemodynamics Pressure dressing.

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Presenter

Presentation Notes

High cost, not readily available, Sampling error, pathologist vary in their interpretation. We save it for those who have high ferritin levels, complication metabolic syndrome, and those suspected of having advanced fibrosis

Imaging

• Ultrasound (LUS) – Most commonly used – Inexpensive, goods specificity and sensitivity, non-invasive – Specificity and sensitivity are altered by mild disease, and

alterations in tissue appearance

Source http://www.e-moh.com/vb/t141782/ http://www.radrounds.com/photo/normal-liver-echotexture-on?context=album&albumId=1791588%3AAlbum%3A59578


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Presenter

Presentation Notes

Gold Standard for diagnosis is a liver biopsy Not used routinely because it is expensive, invasive and therefore has complications attached to it. Diagnosed from imaging results- trans-abdominal ultrasound can also be a huge benefit, non-invasive, inexpensive, has reasonable accuracy. 66-97% specificity and 60-94% sensitivity 1) Liver echo greater than renal cortex and spleen with attenuation of sound wave, 2) loss of definition of diaphragm, 3) poor delineation of intrahepatic architecture (to avoid false-positive diagnosis, all three findings should be fulfilled). Sensitivity 60-100%. Specificity 77-95%.

Intervention Instruction Implication

Diet Aim to lose 5-10% of initially Decrease hepatic inflammation

Exercise 150-180 min a week or 30 min a day

Improves insulin sensitivity Reduces steatosis

Bariatric surgery May be consider as a primary intervention for a person with

high BMI

Decreased inflammation and fibrosis


Non-Pharmacological Management

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Presenter

Presentation Notes

No well established treatment regime for NAFLD. Primary recommendation is control any symptoms of metabolic syndrome and life style modification to focused on weight loss and exercise. Cardioprotective measure in exercise Goal: Decrease insulin resistance Reduce visceral fat Decrease hyperlipidemia Decrease hypertension

Pharmacological Management


Drug Pros Cons/Limitations

Pioglitazone Improves inflammation and fat accumulation

Linked to weight gain, bone factures, CHF, bladder cancer

Statins Decreased steatosis Mild elevation in ALT may occur.

ACEs and ARBs Decreased liver fibrosis and stellate cell activation

Not specifically for treatment of NAFLD

Vitamin E Decrease liver enzymes, improve steatosis, inflammation and ballooning

Lacking evidence for patient with diabetes, liver cirrhosis

Orlistat Improve steatosis Fat soluble vitamin deficiency

DOS Course 2015 23

Presenter

Presentation Notes

No clear curative treatment for NAFLD Pharmacological choices are dependent on the co-morbidities associated with disease progression Decrease the accumulation of fat in the liver and injury Anit-fibrotic, anti apoptotic, and immune drug to target liver specifically in the pipeline and hopefully with materialize as viable option in the next ten years 70% pt. patient with fatty liver have hypertension

Nursing Implications

• Explain risk factors for progression of the disease

Older age, Diabetes, hypertension, and obesity

• Life style modifications

Change in eating habits and exercise

Weight loss with an initial goal target dependent upon the extent of the disease process

Avoid alcohol consumption


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Presenter

Presentation Notes

Behavioral modification are essential to lasting success Vaccination - Encourage Hepatitis A and B vaccines

Hemochromatosis

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• Transferrin – Transported form of iron

• Ferritin – Stored form of iron

• Ferroportin – Iron export protein

• Heterozygote – A pair of genes that are not alike

• Homozygote – A pair if genes that are alike

• Hepcidin – Peptide hormone that regulates absorption of dietary iron

Definitions

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• Autosomal recessive disorder that effects the absorption and storage of iron.

Hemochromatosis

http://peir.path.uab.edu/wiki/IPLab:Lab_5:Hemochromatosis http://library.med.utah.edu/WebPath/LIVEHTML/LIVER002.html

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Presenter

Presentation Notes

Hemochromatosis is a condition that causes excess absorption of iron from the digestive tract. Over time, the excess iron accumulates in tissues throughout the body, leading to iron overload. Signs of iron overload may include sexual dysfunction, joint pains, weakness, changes in skin coloration, liver damage (cirrhosis), heart failure, diabetes mellitus, and rarely, thyroid disease or liver cance

Epidemiology

•Common genetic disorder found in people with a European ancestry (Crownover & Covey, 2013; Salgia & Brown, 2015)

•Most common mutation found in the HFE gene (Ulvik, 2014)

•Clinical expression of the disease in more prevalent in men (24%-43%) than women (1%-14%) (Salgia & Brown, 2015)

Hemochromatosis

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Presenter

Presentation Notes

In the past, hemochromatosis was often advanced by the time a person noticed symptoms and sought medical care. Today, most people with hemochromatosis are identified at a young age because of abnormalities on routine blood tests or because they undergo testing after a family member is diagnosed. As a result, about 75 percent of people with hemochromatosis are diagnosed before they have symptoms, and most people do not have complications at the time of diagnosis. Symptoms typically do not occur until after the age of 40. The symptoms tend to occur later in women than in men because women lose iron throughout their lives through menstrual periods, pregnancy, and breastfeeding Hemochromatosis is caused by the excessive absorption of iron. The exact process is still being studied. As a general rule, a number of chemical events take place that regulate how much iron is absorbed. Central to this process is a gene called HFE. Mutations in this gene cause excessive amounts of iron to be absorbed. The most common mutation is referred to as C282Y. Hemochromatosis is most often seen in people who have two copies of this mutation (one inherited from their mother and the other from their father). However, other mutations causing hemochromatosis continue to be discovered. Furthermore, for unclear reasons, a majority of people with two copies of the C282Y mutation do not develop iron overload

Pathophysiology

Hemochromatosis

Genetic mutation

Altered hepcidin

Increased intestinal

absorption of iron

Out flow of iron from

macrophages

Iron accumulation

oxidative stress

Damage to hepatocytes

Excessive accumulation of iron; deposit in the liver

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Clinical presentation

Physical

• At first the patient is asymptomatic

• Patient can shows signs of congestive heart failure, diabetes, and arthritis

Laboratory

• Elevated serum ferritin greater >200ng/L in female and >300ng/L in males

• Elevated transferrin-iron saturation >45%

• Genetic analysis

Hemochromatosis

DOS Course 2015 30

Presenter

Presentation Notes

Most commonly seen clinical presentation is cirrohsis, fatigue, and hypergigmentation

Source https://www.hinsdale86.org/staff/kgabric/Disease12/Hemochromatosis/Hyperpigmentation.htm

Hemochromatosis

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Clinical suspicion for HH

Test SF and TS

HFE testing

Treatment and monitoring

Hemochromatosis

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Presenter

Presentation Notes

HFE should be don in patients with a family history of the HH. All first degree relatives

Imaging

Hemochromatosis

Liver biopsy

Elevated iron Elevated liver studies and Non-c282y genotype

Coexsiting liver

dieases

SF>1000 and homozygous

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Presenter

Presentation Notes

Liver biopsy is used to evaluate fibrosis, cirrhosis, and cancers These are the patient that you want to refer to a specialist for further evaluation if you can

Management

Phlebotomy (blood letting) • Goal of therapy is to decrease the serum ferritin 50-150 ng/L

• Fatigue and lethargy should improve if initially present – 400-500 ml of blood (1 unit) Is removed on a weekly basis (this

can change based on gender)

– Iron levels are monitored during therapy to assess for effectiveness and complications (every 1-2 months)

– Approximately 30-50 sessions needed to clear iron stores

– Maintenance blood removal every 2-4 months

Hemochromatosis

Source http://www.agalligani.com/photographyhrzu/How-Do-You-Get-Hemochromatosis.html

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Presenter

Presentation Notes

Phlebotomy procedure — Phlebotomy is generally safe and can be performed in a clinician's office, blood bank, hospital, or even a person's home. People undergoing phlebotomy should drink an adequate amount of fluids and avoid exercise within 24 hours of the procedure.��Typically, 1 unit of blood (about 473 mL or 1 pint) is removed per week; however, 1.5 to 2 units of blood can often be removed from men, whereas it may be necessary to remove only 0.5 units of blood from women or frail or elderly patients with other medical problems.��Iron levels are usually monitored every four to eight weeks during treatment. These values help to determine when the excess iron stores have been depleted; they also help determine if phlebotomy has caused anemia by depleting iron too rapidly. If anemia occurs, phlebotomy may be temporarily stopped.��In people with hemochromatosis who do not have symptoms at the time of diagnosis, the excess iron stores are depleted to normal after about 30 or fewer phlebotomy sessions. In people who have symptoms at the time of diagnosis, 50 or more phlebotomy sessions may be needed to deplete excess iron stores. Each unit of blood drops the ferritin by about 30 ng/mL.

Hemochromatosis

Source: http://www.cdc.gov/ncbddd/hemochromatosis/training/treatment/phlebotomy_treatment.html

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Management

• Phlebotomy may not be a option for those with poor venous access and those that have heart disease

Alternative treatment options

• Erythrocytapheresis

• Iron chelation – deferoxamine or deferasirox

• Follow up will depend on evaluation of cirrhosis

Hemochromatosis

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Presenter

Presentation Notes

No lesion- 6-12 months <1 cm Lesion 3-6 month > Of equal a 1 cm refer to specialist for HCC


• Phlebotomy is not a quick fix

• Adequate fluid intake (phlebotomy treatment)

• Avoid exercise (phlebotomy treatment)

• Avoid vitamin C and iron supplements

• Alcohol in moderation or avoid alcohol consumption

• Avoid eating uncooked shellfish

Hemochromatosis

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Presenter

Presentation Notes

Phlebotomy can prevent complications of iron overload in people who do not have complications. It can also help to ensure a normal life expectancy. For example, phlebotomy can help prevent the potentially life-threatening complications of cirrhosis and liver cancer. Phlebotomy can resolve or markedly improve weakness, fatigue, and lethargy; darkening of the skin; and high blood ferritin levels. It can also resolve or greatly improve poor liver function, liver enlargement, and liver pain. Phlebotomy is most likely to reverse liver disease when it is in an early stage, but phlebotomy can still improve liver function in people who have developed cirrhosis. Phlebotomy may resolve joint pain and heart disease. Studies suggest that phlebotomy improves joint symptoms in about 20 percent of people with hemochromatosis. Phlebotomy is most likely to reverse heart disease when it is in an early stage. Phlebotomy only rarely improves joint deformity, pituitary disease, elevated blood iron levels, susceptibility to certain infections, diabetes, and thyroid disease. Phlebotomy is most likely to restore normal levels of sex hormones in men who are less than 40 years. Phlebotomy may not reverse cirrhosis or lessen the risk of liver cancer that is associated with cirrhosis Dietary considerations — People who are receiving treatment for hemochromatosis do not have to follow a special diet. There is no evidence that the condition is worsened by consuming moderate amounts of iron-rich foods such as red meat and organ meats (eg, liver). However, people with hemochromatosis should avoid iron supplements, and they may also be advised to avoid vitamin C supplements, which promote iron absorption. Alcoholic beverages may be consumed in moderation. However, drinking more than two alcoholic beverages per day increases the risk of cirrhosis. People with hemochromatosis and liver disease should avoid alcohol completely. People with hemochromatosis should avoid eating uncooked seafood because it may contain bacteria that grow well in an iron-rich environment Colon cancer screening if iron defiencies ensures Avoid eating uncooked shellfish- bacteria that cause a potential fatal infection in patient that have high iron level

Hepatitis C

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VIRUS

TRANSMISSION

INCUBATION

HAV Fecal – Oral 15 - 45 days

HBV Parenterally Close Contact

30 – 180 days

HCV Parenterally Close Contact

20 – 90 days

HDV Parenterally Close Contact

30 – 50 days in superinfection

HEV Water-Borne 15 – 60 days

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Epidemiology

• More than 185 million people around the world have been infected with HCV, of whom 350 000 die each year. (WHO, 2014)

• Between 18-34 % of those infected spontaneously clear HCV. (Westbrook, R.H. & Dusheiko, G., 2014)

• Chronic infection occurs in 75-85% of those with acute Hep C

• One third of those chronically infected develop liver cirrhosis or hepatocellular carcinoma. (WHO, 2014)

Hepatitis C

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Presenter

Presentation Notes

Acute and chronic diease. Chronic diease is further promoted by HIV, immunosuppression, alcohol use, older age

Considerations

• Access and Cost of treatment

• Extrahepatic complications

• Co-infections

• Variability of the disease

• Prevention Measures

Hepatitis C

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http://apsolutionsltd.co.uk/ka-map-northern-africa/

Hepatitis C

http://commons.wikimedia.org/wiki/File:East_Asia.png

http://dupcasestudy.blogspot.com

Source : WHO, 2014

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Transmission

•Spreads through contact with infected blood.

• High risk – IV (highest risk) and intranasal drug users

– Persons with multiple sex partners

– Healthcare workers

– Transfused patients

Hepatitis C

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Presenter

Presentation Notes

PWID have the highest risk of infection: Globally, the prevalence of HCV is 67% among PWID. Strongly linked to persons with a preexisting HIV infection

Pathophysiology

Hepatitis C

Exposure to virus

Viral replication uninhibited

Destruction of infected

hepatocytes by immune

cells

Continuous cytokine secretion

fibrogenesis

Progression to chronic disease

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Clinical Presentation

Physical

• Patient may be asymptomatic, c/o fatigue, or have flu like symptoms

• Jaundice, abdominal pain, dark urine (not common)

Laboratory – Anti-HCV antibodies (repeat in 12 weeks) – HCV RNA – Elevated bilirubin, elevated ALT/AST

–Note there are 6 genotypes of Hepatitis C

Hepatitis C

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Presenter

Presentation Notes

Liver specific thing- jaundice, dark urine, anorexia, abdominal discomfort. The most common outcome of acute hepatitis is chronic hepatitis

Imaging

Liver biopsy to evaluate fibrosis

Hepatitis C

Stage Implication

Stage 0 No fibrosis

Stage 1 Slight scarring

Stage 2 Moderate scarring

Stage 3 Liver becoming fibrotic (bridging)

Stage 4 Cirrhosis

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Presenter

Presentation Notes

How often to perform liver biopsy? Other methods of monitoring- imaging studies to view rather or not there is fibrosis

Genotype distribution

Treatment

Region/Countries Genotype

North, Central, and South Americas 1a, 1b, 2a, 3a

Europe 1a, 1b, 2a, 2b, 2c, 3a

Middle East 1a, 1b, 3a, 4

South Africa 5a

Egypt 4

East Asia 1b, 2a, 6a

South Asia 1b, 3b, 5a, 6a

Source: WHO, 2014

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Treatment

Hepatitis C

Drug Class MOA Monitoring Cost

Sofosbuvir Polymerase inhibitor

Inhibits viral replication Anemia, skin rash $33, 600

(month supply)

Peg interferon Interferon

Antiviral immune regulating properties

Suicidal ideation Depression $3,961.25

Simeprevir Telapervir

Proteases inhibitor

Inhibit viral replication

Oral/skin rash, photosensitivity

$26,544.00 (month supply)

Ribavirin Nucleoside Inhibit viral protein synthesis

Anemia, platelet count $200-$1,100

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Hepatitis C

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Prevention is the KEY!

Avoid sharing any devices that would increase exposure to blood

Protected sex

Never donate blood

Abstain from ETOH, drugs

Medications/Treatment options

Vaccinations

Hepatitis C

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Presenter

Presentation Notes

Hep A and B vaccine

Acute Liver Failure

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Clinical manifestation

• Causes – ischemia, acetaminophen toxicity, viral hepatitis.

• Liver tissue quickly becomes necrotic resulting in sudden onset illness.

• Mental status changes leading to coma

• Marked elevation of liver enzymes, bilirubin, prothrombin time

Acute Liver Failure

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Secure Access (multiple lines)

Monitor mental status

(encephalopathy)

Monitor BP (SBP<80 mmg Hg)

Prophylatic ATB

PPI administration

Fluids resuscitation

Stop any visual bleeding

Get to a higher level of

care when available

Illustration Courtesy of Lisa Marie Galbraith, RN

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Presenter

Presentation Notes

Those with a increased degree of encepholopathy with warrant a high level of care. Protect airway Treat Amanita phalloides mushroom intoxication with IV penicillin G, even though its mode of action is unclear. Silibinin, a water-soluble derivative of silymarin, may be administered orally, and oral charcoal may be helpful by binding the mushroom toxin. Treat acetaminophen (paracetamol, APAP) overdose with N -acetylcysteine (NAC). Researchers theorize that this antidote works by a number of protective mechanisms. Early after overdose, NAC prevents the formation and accumulation of N -acetyl-p-benzoquinone imine (NAPQI), a free radical that binds to intracellular proteins, nonspecifically resulting in toxicity. NAC increases glutathione stores, combines directly with NAPQI as a glutathione substitute, and enhances sulfate conjugation. NAC also functions as an anti-inflammatory and antioxidant and has positive inotropic and vasodilating effects, which improve microcirculatory blood flow and oxygen delivery to tissues. These latter effects decrease morbidity and mortality once hepatotoxicity is well established. The protective effect of NAC is greatest when administered within 8 hours of ingestion; however, when indicated, administer regardless of the time since the overdose. Therapy with NAC has been shown to decrease mortality in late-presenting patients with fulminant hepatic failure (in the absence of acetaminophen in the serum). If patients present within 4 hours of overdosing on acetaminophen, give activated charcoal just prior to starting NAC.[3] Never administer aminoglycosides or nonsteroidal anti-inflammatory drugs (NSAIDs) to patients with acetaminophen hepatotoxicity, because the potential for nephrotoxicity is exaggerated greatly in this setting.

1. Baran, B. & Akyuz, F. (2014). Non-alcoholic fatty liver disease: What has changed in the treatment since the beginning? Worl J Gastroenterol, 20(39), 14219-14229. doi: 10.3748/wjg.v20.i39.14219 2. Basaranoglu, M. & Ormeci, N. (2014). Non-alcoholic fatty liver disease: Diagnosis, pathogensis, and management. Turk J Gastroenterol, 25, 127-32. 3. Bartnikas, T. (2014) Liver not making hepcidin? hemochromatosis! Blood, 123, 3535-3536. doi: 10.1182/blood-2014-04-565499 4. Bedgoni, G., Nobili, V. & Tiribelli, C. (2014). Epidemiology of fatty liver disease: An update. Worl J Gastroenterol, 20(27), 9050-9054. doi: 10.3748/wjg.v20.i27.9050 5. Cacoub, P., Gragnani, L., Comarmond, C., & Zignego, A. (2014) Extrahepatic manifestation of chronic hepatitis c virus infection. Digestive and Liver Disease,46, s165-s173. 6. Crownover. B. K. & Covey, C. J. (2013). Hereditary hemochromatosis. American Family Physician, 87(3),183-190 7. Dyson, J. K., Anstee, Q. M., & McPherson, S. (2014). Non-alcoholic fatty liver disease: a practical approach to treatment. Frontline Gastroenterolgy, 5, 277-285. 8. GUIDELINES FOR THE SCREENING,CARE AND TREATMENT OF PERSONSWITH HEPATITIS INFECTION. World Health Organization, 2014. 9. http://www.uptodate.com/contents/hemochromatosis-hereditary-iron-overload-beyond-the-basics 10. http://www.cdc.gov/ncbddd/hemochromatosis/training/treatment/phlebotomy_treatment.html 11. http://www.agalligani.com/photographyhrzu/How-Do-You-Get-Hemochromatosis.html 12. http://www.hepatitis.va.gov/provider/guidelines/2014hcv/summary-table-01.asp?backto=provider/guidelines/2014hcv/summary&backtext=Back%20to%20Summary%20Table%20and%20Figures 13. Krier, M. & Ahmed, A. (2009). The asymptomatic liver patient with abnormal liver function test. Clin Liver Dis, 13, 167-177. doi:10.1016/j.cld.2009.02.001 14. Machado, M. V. & Pinto, H. (2014). Non-alcoholic fatty liver disease: What every clinician needs to know. Worl J Gastroenterol, 20(39), 2956-12980. doi: 10.3748/wjg.v20.i36.12956 15. Salgia, R. & Brown, K. (2015). Diagnosis and management of hereditary hemochromatosis. Clin Liver Dis, 19, 187-198. 16. Ulvik, R. J. (2014). The liver in hemochromatosis. J Trace Elem Med Biol. Http:dx.doi.org/10.1016/j.jtemb.2014.08.005

References

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DOS CME Course 2011 56 DOS Course 2015 56

Documents

LIVER DISEASE - Cleveland Clinic...Implications GGTP, GGT R=8-38 u/L Found on the surface of hepatocytes Sensitive indicator for biliary disease Chronic alcohol ingestion Albumin R=3.3-4.5