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LIVER
CIRRHOSIS
TABLE OF CONTENTS
01
EPIDEMIOLOGY
03
02
PATHOPHYSIOLOGY
04
MANAGEMENT
DIAGNOSIS
Liver Structure and Function
● Liver is the largest internal organ of the body
● Located at the right upper quadrant of the abdomen under the right right cage against the
diaphragm
● Held my ligamentous attachments to the diaphragm, peritoneum, great vessels and upper GI
organs.
● Receives a dual blood supply:
○ 20% from oxygen-rich blood of the hepatic artery
○ 80% nutrient-rich blood from the portal vein, arising from the stomach, intestines, pancreas
and spleen
● Majority of the cells in the liver are hepatocytes, which constitute 2/3rds of the organ’s mass
● Remaining cells are the Kupffer cells, stellate, endothelial/blood vessel cells, bile ductular cells and
cells of supporting structures.
● Histologically, the liver is organized in lobules, with portal areas at the periphery and central veins
in the center of each lobule
● Functionally, the liver is organized into acini which flow from the hepatic zone (zone 1) and flow
through the sinusoids to the terminal hepatic veins (zone 3)
Definition of Liver Cirrhosis
● Histopathologically
○ Development of liver fibrosis to the point of architectural distortion with
the formation of regenerative nodules.
■ Decrease in hepatocellular mass
■ Hepatocellular function
■ Alteration of blood flow
● Clinical Features
○ Mirror the severity of disease
○ Decompensated vs Compensated Cirrhosis
■ Ascites
■ Hepatic Encephalopathy
■ Variceal Bleeding
○ Portal Hypertension is responsible for the development of ascites and
bleeding varices
○ Jaundice, coagulation disorders and hypoalbuminemia are common
contributions to portosystemic encephalopathy
Causes of Cirrhosis
● Alcohol Consumption
● Chronic Viral Hepatitis
○ Hepatitis B
○ Hepatitis C
● Autoimmune Hepatitis
● Nonalcoholic Steatohepatitis
● Biliary Cirrhosis
○ Primary Biliary Cholangitis
○ Primary Sclerosing Cholangitis
○ Autoimmune Cholangiopathy
● Cardiac Cirrhosis
● Inherited Metabolic Liver Disease
○ Hemochromatosis
○ Wilson’s Disease
○ Alpha-1 antitrypsin deficiency
○ Cystic Fibrosis
● Cryptogenic Cirrhosis
EPIDEMIOLOGY
01
Chronic Liver Disease
● Cirrhosis is a leading cause of mortality and morbidity worldwide. 11th
leading cause of death and 15th leading cause of morbidity
● Most common causes of prevalent diseases:
○ Nonalcoholic Fatty Liver Disease (59%)
○ Hepatitis B Infection (29%)
○ Hepatitis C Infection (9%)
○ Alcoholic Liver Disease (2%)
○ Others (1%)
● Others refers to Primary Biliary Cholangitis, Primary Sclerosing
Cholangitis, Alpha-1-Antitrypsin Deficiency, Wilson’s Disease and
Autoimmune Hepatitis
PATHOPHYSIOLOGY
02
Alcohol-Associated Cirrhosis
● Due to excessive chronic alcohol use
● Associated with various types of chronic liver disease
○ Alcohol Associated Fatty Liver
○ Alcoholic Hepatitis
○ Alcohol Associated Cirrhosis
● Alcohol use with the presence of other liver diseases can
contribute to the development of liver cirrhosis
○ Hepatitis C
○ Hemochromatosis
○ Fatty Liver Disease related to obesity
Alcohol-Associated Cirrhosis
● Ethanol intake increases intracellular accumulation of
triglycerides
○ Increases fatty acid uptake
○ Reduces fatty acid oxidation
○ Reduces lipoprotein secretion
● Formation of reactive oxygen species causes oxidative
damage to the hepatocyte membranes and also result in
kupffer cell activation
○ Profibrogenic cytokines are produced and initiate stellate
cell activation, creating excess collagen and extracellular
matrix
Alcohol-Associated Cirrhosis
● Connective tissues connect with the portal triads with the
central veins forming regenerative nodules.
● Combination of hepatocyte loss and collagen deposition leads
to contraction and decrease in size of the liver over a number
of years.
Cirrhosis due to Chronic Viral
Hepatitis B or C
Hepatitis C
● Noncytopathic Virus, therefore more likely immune related
● Portal-based fibrosis with bridging fibrosis and development of nodules.
● Liver is characterized as small and shrunken with micro and
macronodular cirrhosis.
● Inflammatory infiltrates are seen in portal areas with interface hepatitis
Hepatitis B
● Similar findings as with Hepatitis C
Nonalcoholic Fatty Liver Disease
● Occurs when triglyceride synthesis leads to accumulation of fat within
hepatocytes.
● Stimulated by obesity which reduces intestinal barrier function,
stimulating liver cells and inflammatory mediators
● Adipose depots decreases insulin sensitivity, causing hyperinsulinemia,
promoting lipid uptake, fat synthesis and fat storage, ultimately leading to
hepatic triglyceride accumulation (steatosis)
DIAGNOSIS
You can enter a subtitle here.
03
General Diagnosis for Cirrhosis
● Clinical Features
○
○ May present with non-specific symptoms
■ Vague RUQ Abdominal Pain
■ Fever
■ Nausea/Vomiting
■ Diarrhea
■ Anorexia
■ Malaise
General Diagnosis for Cirrhosis
● May present with more specific complications
○ Ascites
○ Edema
○ Upper GI Hemorrhage
○ Jaundice
○ Encephalopathy
● Physical Examination
○ Liver and spleen enlargement
■ Firmness of liver edge with possible nodules
○ Scleral Icterus
○ Palmar Erythema
○ Spider Angioma
○ Parotid Gland Enlargement
○ Digital Clubbing
○ Muscle Wasting
○ Edema
General Diagnosis for Cirrhosis
● Laboratories
○ Anemia from GI blood loss
○ Hypersplenism
○ Platelet counts reduced early on in the disease
■ Reflective of hypertension with hypersplenism
○ Serum total bilirubin can be normal or elevated in
advanced disease
○ Prothrombin time is often increased and isn’t decreased
with administration of Vitamin K
○ Sodium levels can be decreased if patient presents
ascites.
Alcohol-Associated Cirrhosis
● Accurate history of amount and duration of alcohol
intake/consumption
● Men
○ Decreased Body Hair
○ Gynecomastia
○ Testicular Atrophy
● Women
○ Menstrual Irregularities
○ Amenorrhea
Alcohol-Associated Cirrhosis
● Laboratories
○ May be normal in early compensated alcohol-associated
cirrhosis
○ Zieve’s Syndrome
■ Jaundice
■ Hemolytic Anemia
■ Hyperlipidemia
○ ALT/AST levels are elevated in active drinkers, with an
AST:ALT ratio of 2:1
Alcohol-Associated Cirrhosis
● Diagnosis is done based on the previously mentioned findings
as well as the patient’s drinking history.
● Other causes of chronic liver disease should be ruled out or
included as their presence may hasten the speed of disease
development.
● Liver biopsy can help confirm diagnosis but is generally not
performed.
● Patients who have complications of cirrhosis who continue to
drink have <50% 5-year survival.
● Abstinent patients have significantly higher prognosis but may
sometimes not improve
Hepatitis C or B
● Present with the usual signs and symptoms of chronic liver
disease
○ Fatigue, malaise, RUQ Abdominal Pain
● Hepatitis C
○ HCV RNA Testing
○ Analysis for HCV Genotype
● Hepatitis B
○ Serologies
■ HBsAg, anti-HBs, HBeAg, anti-HBe
○ Quantitative HBV DNA Levels
Nonalcoholic Fatty Liver Disease
● Patients with nonalcoholic steatohepatitis can progress to
increased fibrosis and cirrhosis.
● Generally presents with similar signs, symptoms and labs as
the above-mentioned diseases
● NAFLD and FIB-4 Score can assess severity of liver fibrosis in
NAFLD and NASH patients.
● Transient Elastography
○ Inexpensive
○ Rules out cirrhosis when the elasticity is low
Diagnostic Imaging
● Ultrasound
○ Widely available
○ Operator dependent
○ Imprecise qualitative assessment of fat severity in mild
steatosis
○ Initial screening test for suspected liver fat
● Transient Elastography
○ Requires specialized equipment and software
○ Good alternate screening test for suspected liver fat
○ Helps provide an indirect assessment of fibrosis and
cirrhosis
Diagnostic Imaging
● CT Scan
○ Rapid Assessment
○ Imprecise quantitative assessment of fat
○ Generally not recommended for clinical assessment of
liver fat
● MRI
○ Direct assessment of liver fat
○ Highly sensitive and specific
○ Test of choice for quantitative assessment of liver fat
Non-Invasive Methods of Assessing Hepatic
Fibrosis and Cirrhosis
Method Parameters Advanced Fibrosis Cirrhosis
APRI AST, platelet count >1 > 1.5
ELF Age, hyaluronic acid, MMP-3, TIMP-1 >7.7 > 9,3
FIB-4 Age, AST, ALT, Platelet Count >1.45 > 3.25
Fibrotest Haptoglobin, Alpha 2-macroglobulin, apolipoprotein
A1, gamma-GT, Total Bilirubin
>0.45 >0.63
Transient Elastography Speed of a shear wave generated by vibration
through liver tissue
>7.3 kPa > 15 kPa
Acoustic Radiation Force
Impulse
Speed of shear wave generated by acoustic radiation
force through liver tissue
> 1.3m/s >1.87 m/s
MELD Score and PELD Score
MANAGEMENT
You can enter a subtitle here.
04
Alcohol-Associated Cirrhosis and Alcoholic
Hepatitis
● Abstinence is the cornerstone of therapy for patients
with alcohol associated liver disease
● Nutrition and constant medical follow-ups
● Complications such as ascites, edema, variceal
hemorrhage, portosystemic encephalopathy have
specific management
● Glucocorticoids may be used in the absence of infection
along with N-acetylcysteine.
● Acamprosate calcium and baclofen can be used to
reduce the craving for alcohol.
Cirrhosis due to Chronic Viral Hepatitis B or C
● Chronic Hepatitis B
○ Antiviral Therapy
■ Lamivudine
■ Adefovir
■ Telbivudine
■ Entecavir
■ Tenofovir
● Chronic Hepatitis C
○ Glecaprevir-Pibrentasvir
○ Sofosbuvir-velpatasvir
● Interferon-Alpha should not be used for cirrhotics
Nonalcoholic Fatty Liver Disease
● Diet and Exercise
○ 3-5% weight loss improves steatosis and greater weight loss (>7%) improves
steatohepatitis and hepatic fibrosis
○ Mediterranean-type diet with reduced fructose and increased coffee intake
has been shown to lower risk of liver fibrosis
● Improve the risk factors of NAFLD and NASH
○ Insulin Resistance/Diabetes
○ Metabolic Syndrome
○ Dyslipidemia
● Incretin Mimetics have been used to optimise insulin and glucagon release which
improved enzyme elevations
● Antioxidants such as Vitamin E have shown some improvements to the histologic
features of NASH
Major
Complications of
Cirrhosis
Portal Hypertension
● Elevation of the hepatic venous pressure (HVPG) to >5 mmHg
● Increased intrahepatic resistance of the passage of blood flow
due to cirrhosis, regenerative nodules and microthrombi
● Increased splanchnic blood secondary to vasodilation in the
splanchnic vascular bed
● Clinically Significant Portal Hypertension (HVPG >10 mmHg) has
substantial risk of decompensation with variceal bleeding, ascites
or hepatic encephalopathy
● CT and MRI can be used to detect nodular liver and other
changes
● Measuring the HVPG via interventional radiology is rarely done.
Esophageal Varices
● Common practice to screen known cirrhotics with
endoscopy to look for varices
● Majority of patients with cirrhosis will develop
esophageal varices over their lifetime.
● ⅓ of patients with varices are expected to develop
bleeding
● Risk of bleeding depends on the severity of
cirrhosis (Child-Pugh class, MELD score), height of
wedged-hepatic vein pressure, size of varix,
location of varix, red wale sign, hematocystic spots,
diffuse erythema, white nipple spots, etc.
● Patients with tense ascites are also at risk for
bleeding from varices
Variceal Hemorrhage
● Patients with cirrhosis are encouraged routine
surveillance by endoscopy
● Primary Prophylaxis
○ Nonselective Beta Blockade
■ Goal HR 55-60 beats/min
■ Systolic BP >90 mmHg
○ Variceal band ligation
■ Shown equal efficacy when compared to
NSBB
● Fluid and RBC replacement to stabilize
hemodynamics
● Vasoconstricting agents (somatostatin and
octreotide) show improved initial bleeding control
Variceal Hemorrhage
● Transjugular intrahepatic portosystemic
shunt (TIPS)
○ If with endoscopic failure
○ If recurrent variceal bleeding occurs
despite repeated band ligation and
NSBB treatment
Ascites
● Accumulation of fluid within the peritoneal cavity
● Mostly caused by portal hypertension related to cirrhosis
○ May also be caused by malignant, infectious and cardiac sources
● Increased production of splanchnic lymph
○ Increase in intrahepatic resistance, causing increased portal pressure
○ Increase in vasodilation of splanchnic arterial system causes increase in
portal venous inflow
● Activation of Renin-Angiotensin-Aldosterone due to underfilling of arterial
dilation of the vascular bed
○ Increased aldosterone and activation of sympathetic nervous system lead
to Na retention
■ Fluid accumulation and expansion of extracellular fluid volume,
causing peripheral edema and ascites
Ascites
● Hypoalbuminemia from decreased synthetic function in cirrhotic liver results in
reduced plasma oncotic pressure, contributing to loss of fluid from vascular
compartment into the peritoneal cavity
● Clinical Features
○ Increased Abdominal Girth
○ Often accompanied with peripheral edema
○ Patients with massive ascites are often malnourished and have muscle
wasting and excessive fatigue and weakness
● Diagnosis
○ PE Findings
■ Bulging Flanks, Fluid wave, Shifting Dullness
Ascites
● Diagnostics
○ Diagnostic paracentesis should be performed to characterize the fluid
○ SAAG and Protein concentration should be calculated, along with blood cell
counts and cultures.
Ascites
● Treatment
○ Small amounts of ascites can be managed with dietary sodium restriction
alone (Target only 2g of sodium per day), eating fresh or frozen foods,
avoiding canned/processed foods.
● Diuretic therapy is indicated for moderate amounts of ascites
○ Spironolactone
○ Furosemide
● Refractory Ascites
○ Large amount of ascites despite diet and drug compliance
○ Large volume paracentesis may be indicated
○ TIPS procedure may also be done
Ascites
Hepatic Encephalopathy
● Alteration of mental status and cognitive function
occurring in the presence of liver failure.
● Increased ammonia levels are present
● Brain edema can be seen with severe
encephalopathy associated with swelling of the
gray matter.
● In cirrhosis, often a result from hypokalemia,
infection, increased dietary protein load or
volume depletion.
● Patients may be uncooperative and violent, or
very sleepy and difficult to rouse.
● Asterixis is often present
Hepatic Encephalopathy
● Treatment
○ Management of the above-mentioned
precipitating factors
■ Hypokalemia, Infection, Protein Load,
Volume Depletion
○ Lactulose
■ Colonic acidification
■ Elimination of nitrogenous products in
the gut
■ Promotion of 2-3 soft stools per day
○ Rifaximin
■ Lowers Bacterial Endotoxin and
Ammonium Neurotoxins
○ Zinc Supplementation
CREDITS: This presentation template was
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THANKS!
Source: Harrisons, T.R., Fauci, A.S., Hauser, S.L., Jameson,
J.L., Kasper, D.L., Longo, D.L., & Loscalzo, J. (2018).
Harrison’s Principle of Internal Medicine 20th Edition. New
York, NY. McGraw-Hill Education
Cheemerla, S., &amp; Balakrishnan, M. (2021). Global
epidemiology of chronic liver disease. Clinical Liver Disease,
17(5), 365–370. https://doi.org/10.1002/cld.1061
INTRODUCTION
https://aasldpubs.onlinelibrary.wiley.com/d
oi/10.1002/cld.1061
AWESOME WORDS
Mercury is the closest planet to the Sun and the smallest one in the Solar
System—it’s only a bit larger than the Moon.
ABOUT THE DISEASE
Saturn is composed
mostly of hydrogen and
also helium.
JUPITER
Mars is full of iron oxide
dust, which gives the
planet its reddish cast.
MARS
It’s a gas giant and the
biggest planet in the
Solar System.
JUPITER
ABOUT THE DISEASE
01 02 03 04
Jupiter is a gas
giant and the
biggest.
It’s composed of
hydrogen and
helium.
Mars is a planet
is full of iron
oxide dust.
Earth is the
planet where we
live on.
YOU COULD USE TABLES
DISEASES PATIENTS TREATMENT
MERCURY 267 187 65%
MARS 669 224 10%
CONCEPTS AND TYPOLOGY
Saturn is composed
mostly of hydrogen and
also helium.
TYPE A
It’s a gas giant and the
biggest planet in the
Solar System.
TYPE B
Mars is full of iron oxide
dust, which gives the
planet its reddish cast.
GESTATIONAL
PATHOLOGY
The planet is full of
iron oxide dust.
Despite being red,
Mars is a cold place.
Saturn is the ringed
one. It’s a gas giant.
Jupiter is a gas giant
and the biggest planet.
SYMPTOMS OF THE DISEASE
Despite being red, Mars
is a cold place. It’s full of
iron oxide dust.
SYMPTOM 1
Jupiter is a gas giant and
the biggest planet in the
Solar System.
SYMPTOM 2
RISK FACTORS
Despite being red, Mars is a
cold place. The planet is full
of iron oxide dust.
JUPITER
To modify this graph, click on them, follow the link,
change the data and paste the new graph here.
SATURN
MERCURY
VENUS
20%
15%
25%
40%
Mercury is the closest planet.
50,000
Patients in the hospital.
20,000
A PICTURE IS
WORTH A
THOUSAND
WORDS
923,857
People have suffered from fatty liver disease.
SOMEONE FAMOUS
“This is a quote, words full of wisdom that
someone important said and can make the
reader get inspired.”
DIAGNOSIS
Mercury is the closest
planet to the Sun.
It is the smallest
one in the Solar System.
Despite being red, Mars
is a cold place.
The planet is full
of iron oxide dust.
Venus is the second
planet from the Sun.
It’s a gas giant and the
biggest planet.
PREVENTION
Jupiter is the biggest
of them all.
The planet is full
of iron oxide dust.
It is the smallest one in
the Solar System.
Venus is the second
planet from the Sun.
TREATMENT
Despite being red, Mars
is a cold place. It’s full of
iron oxide dust.
TREATMENT 1
Jupiter is a gas giant and
the biggest planet in the
Solar System.
TREATMENT 2
● Here you can
describe what the
patient shouldn’t do
● Here you can
describe what the
patient shouldn’t do
● Here you can
describe what the
patient shouldn’t do
RECOMMENDATIONS
● Here you can
describe what the
patient should do
● Here you can
describe what the
patient should do
● Here you can
describe what the
patient should do
PREVALENCE
25% - JUPITER
20% - SATURN
40% - MERCURY
15% - VENUS
CONCLUSIONS
Mercury is the closest planet to the Sun
and the smallest one in the Solar
System—it’s only a bit larger than the Moon.
The planet’s name has nothing to do with
the liquid metal, since it was named after
the Roman messenger god, Mercury.
OUR TEAM
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JOHN DOE
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● AUTHOR (YEAR). Title of the publication. Publisher
● AUTHOR (YEAR). Title of the publication. Publisher
● AUTHOR (YEAR). Title of the publication. Publisher
● AUTHOR (YEAR). Title of the publication. Publisher
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Liver Cirrhosis Presentation.pdf

  • 1. PGI Villanueva, Marius Paul L. LIVER CIRRHOSIS
  • 3. Liver Structure and Function ● Liver is the largest internal organ of the body ● Located at the right upper quadrant of the abdomen under the right right cage against the diaphragm ● Held my ligamentous attachments to the diaphragm, peritoneum, great vessels and upper GI organs. ● Receives a dual blood supply: ○ 20% from oxygen-rich blood of the hepatic artery ○ 80% nutrient-rich blood from the portal vein, arising from the stomach, intestines, pancreas and spleen ● Majority of the cells in the liver are hepatocytes, which constitute 2/3rds of the organ’s mass ● Remaining cells are the Kupffer cells, stellate, endothelial/blood vessel cells, bile ductular cells and cells of supporting structures. ● Histologically, the liver is organized in lobules, with portal areas at the periphery and central veins in the center of each lobule ● Functionally, the liver is organized into acini which flow from the hepatic zone (zone 1) and flow through the sinusoids to the terminal hepatic veins (zone 3)
  • 4. Definition of Liver Cirrhosis ● Histopathologically ○ Development of liver fibrosis to the point of architectural distortion with the formation of regenerative nodules. ■ Decrease in hepatocellular mass ■ Hepatocellular function ■ Alteration of blood flow ● Clinical Features ○ Mirror the severity of disease ○ Decompensated vs Compensated Cirrhosis ■ Ascites ■ Hepatic Encephalopathy ■ Variceal Bleeding ○ Portal Hypertension is responsible for the development of ascites and bleeding varices ○ Jaundice, coagulation disorders and hypoalbuminemia are common contributions to portosystemic encephalopathy
  • 5. Causes of Cirrhosis ● Alcohol Consumption ● Chronic Viral Hepatitis ○ Hepatitis B ○ Hepatitis C ● Autoimmune Hepatitis ● Nonalcoholic Steatohepatitis ● Biliary Cirrhosis ○ Primary Biliary Cholangitis ○ Primary Sclerosing Cholangitis ○ Autoimmune Cholangiopathy ● Cardiac Cirrhosis ● Inherited Metabolic Liver Disease ○ Hemochromatosis ○ Wilson’s Disease ○ Alpha-1 antitrypsin deficiency ○ Cystic Fibrosis ● Cryptogenic Cirrhosis
  • 7. Chronic Liver Disease ● Cirrhosis is a leading cause of mortality and morbidity worldwide. 11th leading cause of death and 15th leading cause of morbidity ● Most common causes of prevalent diseases: ○ Nonalcoholic Fatty Liver Disease (59%) ○ Hepatitis B Infection (29%) ○ Hepatitis C Infection (9%) ○ Alcoholic Liver Disease (2%) ○ Others (1%) ● Others refers to Primary Biliary Cholangitis, Primary Sclerosing Cholangitis, Alpha-1-Antitrypsin Deficiency, Wilson’s Disease and Autoimmune Hepatitis
  • 9. Alcohol-Associated Cirrhosis ● Due to excessive chronic alcohol use ● Associated with various types of chronic liver disease ○ Alcohol Associated Fatty Liver ○ Alcoholic Hepatitis ○ Alcohol Associated Cirrhosis ● Alcohol use with the presence of other liver diseases can contribute to the development of liver cirrhosis ○ Hepatitis C ○ Hemochromatosis ○ Fatty Liver Disease related to obesity
  • 10.
  • 11. Alcohol-Associated Cirrhosis ● Ethanol intake increases intracellular accumulation of triglycerides ○ Increases fatty acid uptake ○ Reduces fatty acid oxidation ○ Reduces lipoprotein secretion ● Formation of reactive oxygen species causes oxidative damage to the hepatocyte membranes and also result in kupffer cell activation ○ Profibrogenic cytokines are produced and initiate stellate cell activation, creating excess collagen and extracellular matrix
  • 12. Alcohol-Associated Cirrhosis ● Connective tissues connect with the portal triads with the central veins forming regenerative nodules. ● Combination of hepatocyte loss and collagen deposition leads to contraction and decrease in size of the liver over a number of years.
  • 13.
  • 14. Cirrhosis due to Chronic Viral Hepatitis B or C
  • 15. Hepatitis C ● Noncytopathic Virus, therefore more likely immune related ● Portal-based fibrosis with bridging fibrosis and development of nodules. ● Liver is characterized as small and shrunken with micro and macronodular cirrhosis. ● Inflammatory infiltrates are seen in portal areas with interface hepatitis
  • 16. Hepatitis B ● Similar findings as with Hepatitis C
  • 17. Nonalcoholic Fatty Liver Disease ● Occurs when triglyceride synthesis leads to accumulation of fat within hepatocytes. ● Stimulated by obesity which reduces intestinal barrier function, stimulating liver cells and inflammatory mediators ● Adipose depots decreases insulin sensitivity, causing hyperinsulinemia, promoting lipid uptake, fat synthesis and fat storage, ultimately leading to hepatic triglyceride accumulation (steatosis)
  • 18.
  • 19. DIAGNOSIS You can enter a subtitle here. 03
  • 20. General Diagnosis for Cirrhosis ● Clinical Features ○ ○ May present with non-specific symptoms ■ Vague RUQ Abdominal Pain ■ Fever ■ Nausea/Vomiting ■ Diarrhea ■ Anorexia ■ Malaise
  • 21. General Diagnosis for Cirrhosis ● May present with more specific complications ○ Ascites ○ Edema ○ Upper GI Hemorrhage ○ Jaundice ○ Encephalopathy ● Physical Examination ○ Liver and spleen enlargement ■ Firmness of liver edge with possible nodules ○ Scleral Icterus ○ Palmar Erythema ○ Spider Angioma ○ Parotid Gland Enlargement ○ Digital Clubbing ○ Muscle Wasting ○ Edema
  • 22.
  • 23. General Diagnosis for Cirrhosis ● Laboratories ○ Anemia from GI blood loss ○ Hypersplenism ○ Platelet counts reduced early on in the disease ■ Reflective of hypertension with hypersplenism ○ Serum total bilirubin can be normal or elevated in advanced disease ○ Prothrombin time is often increased and isn’t decreased with administration of Vitamin K ○ Sodium levels can be decreased if patient presents ascites.
  • 24. Alcohol-Associated Cirrhosis ● Accurate history of amount and duration of alcohol intake/consumption ● Men ○ Decreased Body Hair ○ Gynecomastia ○ Testicular Atrophy ● Women ○ Menstrual Irregularities ○ Amenorrhea
  • 25. Alcohol-Associated Cirrhosis ● Laboratories ○ May be normal in early compensated alcohol-associated cirrhosis ○ Zieve’s Syndrome ■ Jaundice ■ Hemolytic Anemia ■ Hyperlipidemia ○ ALT/AST levels are elevated in active drinkers, with an AST:ALT ratio of 2:1
  • 26. Alcohol-Associated Cirrhosis ● Diagnosis is done based on the previously mentioned findings as well as the patient’s drinking history. ● Other causes of chronic liver disease should be ruled out or included as their presence may hasten the speed of disease development. ● Liver biopsy can help confirm diagnosis but is generally not performed. ● Patients who have complications of cirrhosis who continue to drink have <50% 5-year survival. ● Abstinent patients have significantly higher prognosis but may sometimes not improve
  • 27. Hepatitis C or B ● Present with the usual signs and symptoms of chronic liver disease ○ Fatigue, malaise, RUQ Abdominal Pain ● Hepatitis C ○ HCV RNA Testing ○ Analysis for HCV Genotype ● Hepatitis B ○ Serologies ■ HBsAg, anti-HBs, HBeAg, anti-HBe ○ Quantitative HBV DNA Levels
  • 28. Nonalcoholic Fatty Liver Disease ● Patients with nonalcoholic steatohepatitis can progress to increased fibrosis and cirrhosis. ● Generally presents with similar signs, symptoms and labs as the above-mentioned diseases ● NAFLD and FIB-4 Score can assess severity of liver fibrosis in NAFLD and NASH patients. ● Transient Elastography ○ Inexpensive ○ Rules out cirrhosis when the elasticity is low
  • 29.
  • 30. Diagnostic Imaging ● Ultrasound ○ Widely available ○ Operator dependent ○ Imprecise qualitative assessment of fat severity in mild steatosis ○ Initial screening test for suspected liver fat ● Transient Elastography ○ Requires specialized equipment and software ○ Good alternate screening test for suspected liver fat ○ Helps provide an indirect assessment of fibrosis and cirrhosis
  • 31. Diagnostic Imaging ● CT Scan ○ Rapid Assessment ○ Imprecise quantitative assessment of fat ○ Generally not recommended for clinical assessment of liver fat ● MRI ○ Direct assessment of liver fat ○ Highly sensitive and specific ○ Test of choice for quantitative assessment of liver fat
  • 32. Non-Invasive Methods of Assessing Hepatic Fibrosis and Cirrhosis Method Parameters Advanced Fibrosis Cirrhosis APRI AST, platelet count >1 > 1.5 ELF Age, hyaluronic acid, MMP-3, TIMP-1 >7.7 > 9,3 FIB-4 Age, AST, ALT, Platelet Count >1.45 > 3.25 Fibrotest Haptoglobin, Alpha 2-macroglobulin, apolipoprotein A1, gamma-GT, Total Bilirubin >0.45 >0.63 Transient Elastography Speed of a shear wave generated by vibration through liver tissue >7.3 kPa > 15 kPa Acoustic Radiation Force Impulse Speed of shear wave generated by acoustic radiation force through liver tissue > 1.3m/s >1.87 m/s
  • 33.
  • 34. MELD Score and PELD Score
  • 35. MANAGEMENT You can enter a subtitle here. 04
  • 36. Alcohol-Associated Cirrhosis and Alcoholic Hepatitis ● Abstinence is the cornerstone of therapy for patients with alcohol associated liver disease ● Nutrition and constant medical follow-ups ● Complications such as ascites, edema, variceal hemorrhage, portosystemic encephalopathy have specific management ● Glucocorticoids may be used in the absence of infection along with N-acetylcysteine. ● Acamprosate calcium and baclofen can be used to reduce the craving for alcohol.
  • 37. Cirrhosis due to Chronic Viral Hepatitis B or C ● Chronic Hepatitis B ○ Antiviral Therapy ■ Lamivudine ■ Adefovir ■ Telbivudine ■ Entecavir ■ Tenofovir ● Chronic Hepatitis C ○ Glecaprevir-Pibrentasvir ○ Sofosbuvir-velpatasvir ● Interferon-Alpha should not be used for cirrhotics
  • 38. Nonalcoholic Fatty Liver Disease ● Diet and Exercise ○ 3-5% weight loss improves steatosis and greater weight loss (>7%) improves steatohepatitis and hepatic fibrosis ○ Mediterranean-type diet with reduced fructose and increased coffee intake has been shown to lower risk of liver fibrosis ● Improve the risk factors of NAFLD and NASH ○ Insulin Resistance/Diabetes ○ Metabolic Syndrome ○ Dyslipidemia ● Incretin Mimetics have been used to optimise insulin and glucagon release which improved enzyme elevations ● Antioxidants such as Vitamin E have shown some improvements to the histologic features of NASH
  • 40. Portal Hypertension ● Elevation of the hepatic venous pressure (HVPG) to >5 mmHg ● Increased intrahepatic resistance of the passage of blood flow due to cirrhosis, regenerative nodules and microthrombi ● Increased splanchnic blood secondary to vasodilation in the splanchnic vascular bed ● Clinically Significant Portal Hypertension (HVPG >10 mmHg) has substantial risk of decompensation with variceal bleeding, ascites or hepatic encephalopathy ● CT and MRI can be used to detect nodular liver and other changes ● Measuring the HVPG via interventional radiology is rarely done.
  • 41. Esophageal Varices ● Common practice to screen known cirrhotics with endoscopy to look for varices ● Majority of patients with cirrhosis will develop esophageal varices over their lifetime. ● ⅓ of patients with varices are expected to develop bleeding ● Risk of bleeding depends on the severity of cirrhosis (Child-Pugh class, MELD score), height of wedged-hepatic vein pressure, size of varix, location of varix, red wale sign, hematocystic spots, diffuse erythema, white nipple spots, etc. ● Patients with tense ascites are also at risk for bleeding from varices
  • 42. Variceal Hemorrhage ● Patients with cirrhosis are encouraged routine surveillance by endoscopy ● Primary Prophylaxis ○ Nonselective Beta Blockade ■ Goal HR 55-60 beats/min ■ Systolic BP >90 mmHg ○ Variceal band ligation ■ Shown equal efficacy when compared to NSBB ● Fluid and RBC replacement to stabilize hemodynamics ● Vasoconstricting agents (somatostatin and octreotide) show improved initial bleeding control
  • 43. Variceal Hemorrhage ● Transjugular intrahepatic portosystemic shunt (TIPS) ○ If with endoscopic failure ○ If recurrent variceal bleeding occurs despite repeated band ligation and NSBB treatment
  • 44. Ascites ● Accumulation of fluid within the peritoneal cavity ● Mostly caused by portal hypertension related to cirrhosis ○ May also be caused by malignant, infectious and cardiac sources ● Increased production of splanchnic lymph ○ Increase in intrahepatic resistance, causing increased portal pressure ○ Increase in vasodilation of splanchnic arterial system causes increase in portal venous inflow ● Activation of Renin-Angiotensin-Aldosterone due to underfilling of arterial dilation of the vascular bed ○ Increased aldosterone and activation of sympathetic nervous system lead to Na retention ■ Fluid accumulation and expansion of extracellular fluid volume, causing peripheral edema and ascites
  • 45. Ascites ● Hypoalbuminemia from decreased synthetic function in cirrhotic liver results in reduced plasma oncotic pressure, contributing to loss of fluid from vascular compartment into the peritoneal cavity ● Clinical Features ○ Increased Abdominal Girth ○ Often accompanied with peripheral edema ○ Patients with massive ascites are often malnourished and have muscle wasting and excessive fatigue and weakness ● Diagnosis ○ PE Findings ■ Bulging Flanks, Fluid wave, Shifting Dullness
  • 46. Ascites ● Diagnostics ○ Diagnostic paracentesis should be performed to characterize the fluid ○ SAAG and Protein concentration should be calculated, along with blood cell counts and cultures.
  • 47. Ascites ● Treatment ○ Small amounts of ascites can be managed with dietary sodium restriction alone (Target only 2g of sodium per day), eating fresh or frozen foods, avoiding canned/processed foods. ● Diuretic therapy is indicated for moderate amounts of ascites ○ Spironolactone ○ Furosemide ● Refractory Ascites ○ Large amount of ascites despite diet and drug compliance ○ Large volume paracentesis may be indicated ○ TIPS procedure may also be done
  • 49. Hepatic Encephalopathy ● Alteration of mental status and cognitive function occurring in the presence of liver failure. ● Increased ammonia levels are present ● Brain edema can be seen with severe encephalopathy associated with swelling of the gray matter. ● In cirrhosis, often a result from hypokalemia, infection, increased dietary protein load or volume depletion. ● Patients may be uncooperative and violent, or very sleepy and difficult to rouse. ● Asterixis is often present
  • 50. Hepatic Encephalopathy ● Treatment ○ Management of the above-mentioned precipitating factors ■ Hypokalemia, Infection, Protein Load, Volume Depletion ○ Lactulose ■ Colonic acidification ■ Elimination of nitrogenous products in the gut ■ Promotion of 2-3 soft stools per day ○ Rifaximin ■ Lowers Bacterial Endotoxin and Ammonium Neurotoxins ○ Zinc Supplementation
  • 51. CREDITS: This presentation template was created by Slideshow, including icons from Flaticon, and infographics & images by Freepik. THANKS! Source: Harrisons, T.R., Fauci, A.S., Hauser, S.L., Jameson, J.L., Kasper, D.L., Longo, D.L., & Loscalzo, J. (2018). Harrison’s Principle of Internal Medicine 20th Edition. New York, NY. McGraw-Hill Education Cheemerla, S., &amp; Balakrishnan, M. (2021). Global epidemiology of chronic liver disease. Clinical Liver Disease, 17(5), 365–370. https://doi.org/10.1002/cld.1061
  • 53. AWESOME WORDS Mercury is the closest planet to the Sun and the smallest one in the Solar System—it’s only a bit larger than the Moon.
  • 54. ABOUT THE DISEASE Saturn is composed mostly of hydrogen and also helium. JUPITER Mars is full of iron oxide dust, which gives the planet its reddish cast. MARS It’s a gas giant and the biggest planet in the Solar System. JUPITER
  • 55. ABOUT THE DISEASE 01 02 03 04 Jupiter is a gas giant and the biggest. It’s composed of hydrogen and helium. Mars is a planet is full of iron oxide dust. Earth is the planet where we live on.
  • 56. YOU COULD USE TABLES DISEASES PATIENTS TREATMENT MERCURY 267 187 65% MARS 669 224 10%
  • 57. CONCEPTS AND TYPOLOGY Saturn is composed mostly of hydrogen and also helium. TYPE A It’s a gas giant and the biggest planet in the Solar System. TYPE B Mars is full of iron oxide dust, which gives the planet its reddish cast. GESTATIONAL
  • 58. PATHOLOGY The planet is full of iron oxide dust. Despite being red, Mars is a cold place. Saturn is the ringed one. It’s a gas giant. Jupiter is a gas giant and the biggest planet.
  • 59. SYMPTOMS OF THE DISEASE Despite being red, Mars is a cold place. It’s full of iron oxide dust. SYMPTOM 1 Jupiter is a gas giant and the biggest planet in the Solar System. SYMPTOM 2
  • 60. RISK FACTORS Despite being red, Mars is a cold place. The planet is full of iron oxide dust. JUPITER To modify this graph, click on them, follow the link, change the data and paste the new graph here. SATURN MERCURY VENUS 20% 15% 25% 40%
  • 61. Mercury is the closest planet. 50,000 Patients in the hospital. 20,000
  • 62. A PICTURE IS WORTH A THOUSAND WORDS
  • 63. 923,857 People have suffered from fatty liver disease.
  • 64. SOMEONE FAMOUS “This is a quote, words full of wisdom that someone important said and can make the reader get inspired.”
  • 65. DIAGNOSIS Mercury is the closest planet to the Sun. It is the smallest one in the Solar System. Despite being red, Mars is a cold place. The planet is full of iron oxide dust. Venus is the second planet from the Sun. It’s a gas giant and the biggest planet.
  • 66. PREVENTION Jupiter is the biggest of them all. The planet is full of iron oxide dust. It is the smallest one in the Solar System. Venus is the second planet from the Sun.
  • 67. TREATMENT Despite being red, Mars is a cold place. It’s full of iron oxide dust. TREATMENT 1 Jupiter is a gas giant and the biggest planet in the Solar System. TREATMENT 2
  • 68. ● Here you can describe what the patient shouldn’t do ● Here you can describe what the patient shouldn’t do ● Here you can describe what the patient shouldn’t do RECOMMENDATIONS ● Here you can describe what the patient should do ● Here you can describe what the patient should do ● Here you can describe what the patient should do
  • 69. PREVALENCE 25% - JUPITER 20% - SATURN 40% - MERCURY 15% - VENUS
  • 70. CONCLUSIONS Mercury is the closest planet to the Sun and the smallest one in the Solar System—it’s only a bit larger than the Moon. The planet’s name has nothing to do with the liquid metal, since it was named after the Roman messenger god, Mercury.
  • 71. OUR TEAM You can replace the image on the screen with your own. JENNA DOE You can replace the image on the screen with your own. JOHN DOE
  • 72. MOCKUP You can replace the image on the screen with your own work. Just delete this one, add yours and center it properly.
  • 73. REFERENCES ● AUTHOR (YEAR). Title of the publication. Publisher ● AUTHOR (YEAR). Title of the publication. Publisher ● AUTHOR (YEAR). Title of the publication. Publisher ● AUTHOR (YEAR). Title of the publication. Publisher ● AUTHOR (YEAR). Title of the publication. Publisher
  • 74. CREDITS: This presentation template was created by Slideshow, including icons from Flaticon, and infographics & images by Freepik. THANKS! Do you have questions? addyouremail@freepik.com +91 620 421 838 yourcompany.com Please keep this slide as attribution.
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  • 84. JANUARY FEBRUARY MARCH APRIL MAY JUNE PHASE 1 PHASE 2 Task 1 Task 2 Task 1 Task 2 JANUARY FEBRUARY MARCH APRIL PHASE 1 Task 1 Task 2
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