liver cirrhosis and medical nutrition therapy for the same.

1. Liver
cirrhosis
Presented by- Ruchika
Sharma

2. 01
INTRODUCTION
02
ETIOLOGY & PATHOPHYSIOLOGY
03
SIGNS AND SYMPTOMS
04
DIAGNOSIS
05
06
DIETARY GUIDELINES
MEDICAL NUTRITION THERAPY

3. INTRODUCTION
● Chronic state of liver disease in which
the liver is damaged beyond repair
with scar tissue and fatty infiltration.
● Cirrhosis of the liver is the end stage
of chronic liver disease.
● Serious and irreversible

4. ● Alcoholism
● Chronic Hepatitis C
● Non-alcoholic fatty
liver disease
(NAFLD)- most
common.
These are the common
causes in western
countries.
Chronic hepatitis B is the
primary cause of liver
cirrhosis in Asia-Pacific
regions
Other causes
● Inherited diseases like-
hemochromatosis and
wilson’s disease
● Galactosemia
● Blocked bile ducts
● Drugs and toxins
● Autoimmune hepatitis
● Primary biliary cirrhosis
● Primary Sclerosing
Cholangitis
ETIOLOGY
Multifactorial and varies
geographically

5. Fibrosis- precursor of cirrhosis
When fibrous scar tissue replaces
functional liver tissue → no circulation in
liver → portal hypertension
Ammonia load ↑ → ammonia intoxication
and hepatic encephalopathy
Portal HTN → esophageal varices →
rupture enlarged veins ( with hemorrhage)
→ death. FIBROSIS - Precursor of cirrhosis
PATHOPHYSIOLOGY

6. Pathophysiology
Liver cells
Parenchymal cells Non- parenchymal cells
Hepatic stellate
cells
Liver sinusoidal
endothelial cells
(LSECs)
Kupffer cells (KCs)

8. Contd.
LSECs
KCs HSCs
Fat-storing cells
Multiple injuries → inflammation
Cytokines → transition from
quiescent to activated state →
initiation and progression of
hepatic fibrosis → collagen
deposition.
Endothelium
Structural characteristic -
fenestrae(pores) on the
surface
Fenestrae act as dynamic
filter.
Chronic alcoholism →
defenestration and ↓
number of fenestrae
Stellate macrophages
Present in linings of walls of
the sinusoids of the liver
Viral infection
Alcohol
High-fat diet
Fe deposition
Activation of
KCs
Activated Kcs → activation of HSCs → fibrosis

9. Pathological characteristics
▪ Degeneration and necrosis of
hepatocytes
▪ Replacement of liver parenchyma
▪ Regeneration of nodules
▪ Loss of liver function
Hepatocytes
Target for hepatotoxic agents
Damaged hepatocytes → ROS
and fibrogenic mediators
Also induces activation of HSCs
and stimulate fibrogenic action of
myofibroblasts.

10. Signs and symptoms
▪ G.I Disturbance
▪ Anorexia
▪ Nausea
▪ Vomiting
▪ Pain and distension
▪ Disease progresses →
● Jaundice,
● Ascites,
● Lymphatic obstruction

11. Ultrasonography
● Inhomogeneity of hepatic
tissue
● Irregularity of the hepatic
surface
● Enlargement of caudate
lobe
DIAGNOSIS
Laboratory
● Low conc of albumin (< 3.4g/dL)
● ↑ international normalized ratio (
INR)
● Impairment of detoxification
function of liner → ↑ bilirubin
● ↑ Hyaluronic acid conc
Liver biopsy
If etiology of liver disease is
unclear and if the stage can’t be
determined from the findings of
the tests. Then biopsy is
performed
Esophagogastroduodenoscop
y
Diagnose - esophageal
varices and assess the risk
of bleeding

12. Diagnostic algorithm for chronic liver disease
Screening measures Step 1:General laboratory
testing
Step 2:Specific laboratory testing Step 3:Molecular and
invasive studies
History (identification of
risk constellations)
ALT, AST, GGT, AP,
bilirubin
Hepatitis serology(HBsAg, anti-
HCV)
Ceruloplasmin, copper in
24-hour urine sample,
genetic testing for Wilson
disease
Physical examination Complete blood count,
platelet count, routine
coagulation studies
Autoantibody testing(ANA, SMA,
LKM, SLA, p-ANCA, AMA)
HFE mutation
Serum ALT and GGT Total protein, albumin,
serum electrophoresis
Quantitative immunoglobulins(IgA,
IgG, IgM)
A1-antitrypsin genotype
(PIZZ)
Ultrasonography Cholesterol, triglycerides,
glucose
Ferritin, transferrin saturation, iron Liver biopsy, MRCP, ERC
(for suspected PSC)

13. Determined by Resting
metabolic rate (RMR),
120% to 140% of the REE
Approximately- 25 to 35
calories per kilogram body
weight
MEDICAL NUTRITION THERAPY
CARBOHYDRATES
ENERGY
Half of the calories
should come from
carbohydrates..
PROTEINS
High protein, 1 to 1.5
g/kg of ideal weight per
day.
FATS
Fat should not exceed
30% of total
kilocalories.
(In patients with severe
steatorrhea, use of MCT
oil could be considered)
FLUIDS
Restricted in case of
ascites
SODIUM
500-800 mg sodium diet
is prescribed ( ascites +)

14. ● Undernourished - 40 calories per
kilogram for underweight patients. (
Ideal body weight should be taken
to avoid overfeeding)
● Overnourished- 20 calories per
kilogram for obese patients
● Overweight and Pt. suffering from NASH,
→ calorie (but not protein) restriction.
● Avoiding fructose and sugary beverages,
trans fats and limiting saturated fats→
prevent weight gain
● Smaller portion size is also important
ENERGY

15. It is important to emphasize that
patients with cirrhosis generally
should not be on a low-protein diet;
recommending low-protein diets is
one of the most common errors
that health providers make.
High protein, why?
Sufficient protein is needed to
correct severe malnutrition, to heal
liver tissue, and to restore plasma
proteins.
In cirrhotic pt.
▪ Rapid muscle proteolysis
▪ ↓ Synthesis of protein
▪ ↓ Clearance of liver
PROTEIN
But if patient shows the signs
of impending hepatic coma -
Protein intake ↓
( Plasma AAA ↑ & isoleucine,
leucine, valine ↓ )
● Higher intake of BCAA helps to improve
cognitive status and is also ass. with ↓ed
frequency of hepatic failure.

16. Fats
Omega-6 fatty acids (which are found in corn
oil, for example)- RESTRICTED (patients
with alcohol-related liver disease).
It can lead to toxic lipid metabolites.
↑omega-6 F.A - ↓ omega -3 F.A
Omega-3 F.A - anti-inflammatory and have a
beneficial effect on the liver.

17. Cirrhotic patients often have multiple micronutrient deficiencies-
Micronutrients
Micronutrient Deficiency Signs/Symptoms
Magnesium Insulin resistance, muscle cramps
Selenium Myopathy, cardiomyopathy
Vitamin B1/thiamine Wernicke-Korsakoff syndrome, neurologic symptoms
Vitamin B2/riboflavin Glossitis, cheilitis, lingual papillae atrophy
Vitamin A/retinol Abnormal dark adaptation, rough skin
Vitamin C Scurvy with purpura and petechiae
Vitamin D Altered bone metabolism, altered gut barrier/immune function
Vitamin E Oxidative stress
Niacin Skin photosensitivity, confusion, pellagra
Folate, s-adenosylmethionine Anemia, altered methylation, epigenetic effects

18. Micronutrients
Supplementation should be considered
Because of the essential role of the liver in
nutrient transport, storage, and metabolism, in
addition to the presence of nutrient depletions
due to drugs.
Water-miscible forms of fat-soluble vitamins
are required Intravenous or intramuscular
vitamin K - 3 days - ↓ vitamin K deficiency -
↓prothrombin time

19. Probiotics
Probiotics provide a health benefit to humans
with cirrhosis is not well studied
Some of the in- vivo studies suggests that
probiotics are beneficial in case of liver disease,
1. Including stabilizing the gut barrier
function,
2. Improving the gut flora,
3. Decreasing endotoxin levels, and
4. Improving liver enzymes.
Whether all of these benefits will translate
into humans is not known,.

20. Dietary guidelines
▪ Avoid substances that are hepatotoxic (e.g., alcohol, drugs, toxins).
▪ Consume 4 to 6 small meals per day
▪ Consume a diet that is adequate in energy, macronutrients, and micronutrients.
▪ Vitamin and mineral supplementation and/or enteral or parenteral nutrition support may be
necessary to meet these needs.
▪ Cirrhosis patients are also commonly deficient in vitamins A, D, and E as well.
Supplementation of the fat soluble vitamins must be handled with care in order to avoid
toxicity.
▪ To treat hypoalbuminemia, eggs, cottage cheese, yogurt can be provided.
▪ As fat absorption is impaired, MCT fats (coconut oil, palm oil) are recommended.
▪ Ensure that fruits and vegetables should be washed and well cooked before eating.
▪ Direct tap water should be avoided.
▪ Fried foods, processed and canned foods(soups/juices/noodles/sauces), soft
drinks/caffeinated beverages, bakery foods should be completely avoided.

21. REFERENCES
● Raymond, J.L. and Morrow, K., Krause and Mahan’s Food & The Nutrition care Process, 15th
Edition, 2021, Elsevier Inc. ISBN 978-0-323-63655-1
● Williams, S. R. (2017). Nutrition and diet therapy (No. Ed. 15). CV Mosby Co..
● McClain, C. J. (2016). Nutrition in patients with cirrhosis. Gastroenterology & hepatology, 12(8), 507.
● Zhou, W. C., Zhang, Q. B., & Qiao, L. (2014). Pathogenesis of liver cirrhosis. World journal of
gastroenterology: WJG, 20(23), 7312.
● Ruiz-Margáin, A., Macías-Rodríguez, R. U., Ríos-Torres, S. L., Román-Calleja, B. M., Méndez-
Guerrero, O., Rodríguez-Córdova, P., & Torre, A. (2018). Effect of a high-protein, high-fiber diet plus
supplementation with branched-chain amino acids on the nutritional status of patients with
cirrhosis. Revista de Gastroenterología de México (English Edition), 83(1), 9-15.
● Wiegand, J., & Berg, T. (2013). The etiology, diagnosis and prevention of liver cirrhosis: part 1 of a
series on liver cirrhosis. Deutsches Ärzteblatt International, 110(6), 85.