Liver Flashcards
(150 cards)
1
Q
what are the 4 parts of the liver
A
4 lobes: right lobe, quadrate lobe, caudate lobe,and left lob.
2
Q
liver is the primary __ reservoir in the body
A
liver is the primary blood reservoir in the body
3
Q
what % of liver function is required for live
A
10—20% of function required for life
4
Q
what are the sources of blood in the liver?
A
- 1a. Arterial blood, which provides the liver’s O2 supply and carries blood-borne metabolites for hepatic processing, is delivered by the hepatic artery.
- 1b. Venous blood draining the digestive tract is carried by the hepatic portal vein to the liver for processing and storage of newly absorbed nutrients.
- Blood leaves the liver via the hepatic vein.
5
Q
what are kupffer cells?
A
macrophagic cells of liver
6
Q
which direction does bile flow in, relative to blood im hepatocyte lobules
A
in the opposite direction
7
Q
what is the primary liver’s mechanism for metabolizing drugs?
A
The liver’s primary mechanism for metabolizing drugs is via a specific group of cytochrome P-450 enzyme
8
Q
which blood vessles drains into vena cava? what is the role of vena cava?
A
hepatic vein
vena cava carries blood around the body
9
Q
liver role in protein metabolism?
A
- Liver is the site for both transamination and deamination of amino acids; liver repackages ammonia into urea through urea cycle which will go into kidney
- done by ALT and AST enzymes that stay in the liver
- Site for synthesis of proteins such as albumin and clotting-factors needed for blood coagulation
10
Q
albumin and liver problems consequences
A
albumin is a colloid and has an important role in maintaining blood pressure
blood coagulation is important in healing-> someone with liver problems might have problems with healing
11
Q
Liver function: Fat metabolism
A
- Liver receives triglycerides and redistributes via lipoproteins
- Cholesterol synthesis occurs in liver
- Site for fatty acid synthesis, ketone production, and fatty acid oxidation
12
Q
Liver function: Vitamins/Minerals
A
- Primary site for vitamin and mineral storage, transport, and activation.
- All fat-soluble vitamins as well as zinc, iron, copper, and magnesium are stored in liver.
- Liver is involved in conversion of Vit D into active form -> Cholecalciferol is hydroxylated in the liver to 25-hydroxycholecalciferol
13
Q
Liver function: Bile synthesis secretion
A
- Hepatocytes synthesize and secrete 600-1000ml bile/d
- Emulsifying agent
- Facilitates absorption of fatty acids, monoglycerides, cholesterol, and other lipids by forming micelles that are soluble in chyme.
- Without bile salts, a large percentage of ingested fats would be lost in feces.
14
Q
what is the primary site for bile salt reabsorption? what happens if this site is damaged?
A
ileum
damage/inflammation of the ileum-> loss of bile salts so they don’t get recycled-> diarrhea
15
Q
Liver function: Bile and heme metabolism
A
- When RBC degrade, Hgb released and broken down to heme and globin.
- Heme is converted to biliverdin and transformed into unconjugated bilirubin.
- Within the liver, bilirubin is conjugated and excreted in bile.
16
Q
What is the biochemical marker of liver functioning
A
Bilirubin is a biochemical marker of liver functioning
17
Q
Do we always make bile from scratch?
A
no
- Secreted bile salts consist of 95% old, recycled bile salts and 5% newly synthesized bile salts.
- 95% of bile salts are reabsorbed by the small intestine.
- Reabsorbed bile salts are recycled by enterohepatic circulation.
18
Q
how does live impact bile salt recycling
A
liver helps in bile salt recycling
liver problems-> no recycling
gallbladder can oversecreat, but only up ti a point
19
Q
Liver function in Carbohydrate metabolism
A
Glycogenesis, gluconeogenesis, oxidation via T C A cycle, glycogenosis, glycolysis
20
Q
Liver function in Lipid metabolism
A
Lipogenesis, lipolysis, saturation/desaturation, ketogenesis, esterification of fatty acids, fatty acid oxidation, uptake/formation/breakdown of phosphotides, synthesis/ degradation/ esterification/ excretion of cholesterol, formation of lipoproteins
21
Q
Liver function in protein metabolism
A
Synthesis of serum proteins, prothrombin, globin of hemoglobin, apoferritin, nucleoproteins, and serum mucoprotein; degradation of some proteins to peptides and amino acids; synthesis of urea
22
Q
Liver function in enzyme metabolism
A
Synthesis of alkaline phosphatase, monoamine oxidases (MAO’s), acetylcholine esterase, oxidases, cholesterol esterase, dehydrogenases, beta glucuronidase, aspartate transaminase (AST), and alanine transaminase (ALT)*
23
Q
Liver function in storage?
A
Storage of glycogen, fats, fatty acids, and fat-soluble vitamins
24
Q
Describe stages of liver damage
A
- Healthy liver
- Fatty liver: can happen in PN
- Liver fibrosis: functional cells start beiign replaced with scar tissue. 10-20% of functional cells
- Cirrhosis: irreversible, we can also manage symptoms
25
Biochemical test to assess liver function and what it reflects
```
Bilirubin,
Alanine aminotransferase (ALT)
Aspartate aminotransferase (AST)
Gamma-glutamyl transferase (GGT)
Alkaline phosphatase (ALP)
Prothrombin time
```
26
Normal levels for bilirubin test and what does it show?
DIrect: 2–9 μmol/L; total: 3–17 μmol/L
| Reflets ability of liver to conjugate and excrete bilirubin
27
Normal levels for ALT test and what does it show?
```
Alanine aminotransferase (ALT) 17–63 IU/L
Most sensitive to detect hepatocellular injury (esp. secondary to infectious hepatitis)
```
28
Normal levels for AST test and what does it show?
Aspartate aminotransferase (AST)
15–37 IU/L
Less specific enzyme to detect hepatic disease
29
Normal levels for GGT test and what does it show?
Gamma-glutamyl transferase (GGT)
5.0–55.0 IU/L (F)
15.0–85.0 IU/L (M)
Elevation indicative of hepatocellular injury secondary to alcohol abuse
30
Normal levels for ALP test and what does it show?
Alkaline phosphatase (ALP)
50–136 IU/L
Increased activity occurs in hepatic disease, but non-specific.
31
Normal levels for prothrombin time test and what does it show?
Prothrombin time
10–14 s
# of seconds for blood to clot; prolonged with hepatic disease
32
what are the common causes of cirrhosis?
Chronic HCV (hepatitis C virus) & Alcoholism
33
what are the 2 types of cirrhosis
* Compensated Cirrhosis: Cirrhosis without ascites (accumulation of fluid in peritoneal cavity) or encephalopathy.
* Decompensated Cirrhosis: Cirrhosis with ascites and/or encephalopathy (partially caused by accumulation of ammonia in the brain).
34
muscle status in cirrhosis patients? Why?
often muscle wasting is present
Decreased carbohydrate use and storage capacity, plus an increase in fat and protein
catabolism, which leads to a chronic catabolic state...depleting muscle reserves!
35
cirrhosis and glucose levels
Without adequate glycogen synthesis, cannot respond quickly to drop in BG → hypoglycemia
36
cirrhosis and blood pressure
Normal blood flow cannot occur within the liver if scar tissue is present → portal hypertension and esophageal varices
37
cirrhosis and oncotic pressure
Inadequate synthesis of serum proteins (e.g., albumin). Albumin maintains oncotic pressure. Reduced concentration of albumin in blood lowers oncotic pressure→ascites (fluid accumulates in peritoneal cavity)
38
cirrhosis and water retention due to water shifting
Blood volume drops (because fluid has shifted to “third spaces”), and stimulates kidneys to retain sodium and water → worsened ascites
39
cirrhosis and mental problems
Liver cannot metabolize products that are toxic to brain (e.g., ammonia)→ hepatic encephalopathy (HE)
40
Describe portal hypertension
Increased BP in hepatic portal vein which carries blood from digestive tract to the liver
Liver damage may result in blockage that leads to an increased blood pressure -> blood builds up and results in collateral circulation and enlarged veins e.g. esophageal varices that can lead to bleeding oesophagus-> risk of haemorrhage
41
signs of portal hypertension
- ascites caused by fluid leaking into abdominal cavity under high blood pressure
- gastrointestinal bleeding from varices (extremely dilated veins)
- encephalopathy (reduced mental capacity and consciousness)
42
CIRRHOSIS: Nutrition goals
reduce development of/ alleviate major complications such as encephalopathy and reduce development of/ alleviate manifestations of portal hypertension, such as ascites.
43
is malnutrition common in cirrhosis patients?
yes
| 60% of patients
44
what are common mineral and vitmain deficiencies in cirrhosis?
• Vitamin and mineral deficiencies commonly include: Thiamin, folate, vitamin A, D, zinc and selenium
45
Nutritional treatment in cirrhosis?
Tx involves maximizing oral intake (early satiety d/t ascites), avoiding hypoglycemia, correcting micronutrient deficiencies, and controlling physiological side effects of ascites with sodium and fluid restrictions.
46
How can we reduce encephalopathy?
• Prevent/correct malnutrition.
• Protect/Preserve muscle mass!
-providing sufficient protein is important to preserve muscle mass. Damaged liver will delegate its role of converting ammonia into urine to muscles
47
How can we reduce ascites?
we have both water and Na retention (Hypervolemic hyponatremia)
• Restrict Na to 2g/d
• Restrict fluids ONLY if neurologic symptoms or serum Na <125 mmol/L (some reference <120)
• The mainstay of therapy of hyponatremia in patients with cirrhosis is fluid restriction (1-1.5 L/d) to a level sufficient to induce a negative water balance.
Hypertonic IV is indicated only in symptomatic patients with profound hyponatremia (< 110 mmol/L), or within hours of liver transplantation.
48
What is the pathophysiology of Hypervolemic hyponatremia
• Observed secondary to advanced cirrhosis and portal hypertension.
• Water AND sodium retention, but water retention relatively greater than
Na retention (therefore serum Na appears low).
49
do we use hypertonic IV in cirrhosis patients?
Hypertonic IV is indicated only in symptomatic patients with profound hyponatremia (< 110 mmol/L), or within hours of liver transplantation.
50
```
Your patient with ascites and hyponatremia needs enteral, what formula is likely to meet the patient’s needs?
A. 1kcal/ml
B. 2kcal/ml
C. 1.5 kcal/ml
D. 1.2 kcal/ml
```
B. 2kcal/ml
51
Patient with cirrhosis, ascites and hyponatremia patient needs a PEG
True or False?
False
PEG will puncture the abdomen and start infusing formula into the stomach-> not gonna work as the abdomen is full of fluid
52
can we administer feed via a tube with varices?
if there is oesophageal varices, we can still feed the patient with the tube, but we want small tube- smallest French size that is compatible with the formula used
if there is bleeding-> stop the feed, wait for 48h until bleeding stops-> start again
53
what are esophageal varices
Esophageal varices are enlarged veins in the esophagus. They're often due to obstructed blood flow through the portal vein, which carries blood from the intestine, pancreas and spleen to the liver.
varices is not a counter-indication for EN, but bleeding is
54
Your patient has been on a 1.5L fluid restriction for 48 hours, but hyponatremia persists. What might you do?
2020-10-21
A. Check I/O
B. Provide patient with education to adhere to fluid restriction
C. Check to see if patient is eating out/family bringing food in
D. Check to see fluid restricted diet is ordered
E. Consider reduction to 1L/d.
F. All of the above.
F. All of the above.
water restriction is the last thing to consider
55
Details of an Anthropometric assessment in cirrhosis patients
• Weight....often inaccurate!
* ASPEN dry weight calculation, subtract:
* 3-5kg for mild ascites
* 7-9kg for moderate ascites
* 14-15kg for severe ascites
• IBW preferred over dry weight (ESPEN).
56
Details of an food assessment in cirrhosis patients
* Meal patterns (to see how often they eat to control hypoglycemia)
* Adequacy of intake
* Fluid and salt intake
* salt substitute use -i f yes, does it contain potassium (important in case pt takes potassium sparing diuretic)
57
Functional assessment in cirrhosis patients
• Aim for a measurement of muscle mass, such as mid-arm circumference and/or calf-circumference
• Aim for measurement of muscle function, such as handgrip (HG)
• Compare to population norms and compute a z-score: E.g., mean HG score for 80-year-old female is 20kg (SD 4.3)
• Calculate z-score: pt score – mean SD
= 13kg-20kg/4.3 = -1.6
58
Common meds in cirrhosis patients
• Tx: HE, lactulose: Don’t be alarmed by ++ diarrhea!
- stimulates ammonia release from body tissues via diarrhea
• Tx: Ascites, diuretics to correct fluid balance
- Furosemide = K+ wasting-> High K diet
• Spironolactone = K+ sparing
- Avoid excessive K intake, K supplements,
salt substitutes (contain potassium chlroide)
59
Physical exam in cirrhosis pts
* Subjective assessment of fat and muscle stores (e.g., temporalis muscle)
* Ascites (can measure abdomen) -> measuring tape around belly
* Micronutrient deficiencies
* Nutrition-impact symptoms
60
manual treatments of cirrhosis
* Paracentesis: draining fluid from abdomen' also results in protein loss
* TIPS (shunt): in case pt has oesophageal varices and portal hypertension- > reroutes their blood
61
CIRROHSIS: Diagnosis
• Related to malnutrition or inadequate intake:
- “inadequate oral intake”
- “inadequate energy protein intake”
- “severe chronic malnutrition”
• Specific to disease:
- Ascites – “excessive Na intake”
“excessive fluid intake”
- Esophageal varices – “swallowing difficulty” “disordered eating pattern”
62
Energy recommendations
• 30-35kcal/kg dry weight (ESPEN)
• ESPEN - Due to considerable inter-
individual variability, REE should be measured using indirect calorimetry, if available: 1.3 x REE. ASPEN 1.2-1.4 x REE
• Obese = 25kcal/kg IBW (ESPEN)
63
Carbohydrate recommendations
* Meals spaced evenly throughout the day to avoid hypoglycemia
* Emphasize breakfast and nighttime snack
64
Protein recommendations
• Don’t need to restrict – old!-> Don’t want to enhance ammonia
production, but don’t want muscles to waste away either!
• 1.2-1.5g/kg dry weight (ESPEN)
• 1.5 if malnourished or sarcopenic
• Obese 2-2.5g/kg IBW (ESPEN)
• Plant proteins may be better tolerated
• Dairy may be better tolerated.
• BCAA? No conclusive evidence-> thus no need
65
which weight shoud we use for energy/prot calculations
In cirrhotics without ascites, the actual body weight should be used for the calculations. In patients with ascites the ideal weight according to body height should be used - ESPEN
66
Nutritional recommendations for ascites
```
• Restrict Na to 2g/d
• Regular hospital diet provides 3-4g
Na/d
• If a patient is only eating 50% of
meals, Na restriction is redundant!
• restrict fluids if serum Na <125 mmol/L
```
67
Nutritional recommendations for esophageal varices
- soft food, no sharp edges
| - chew well
68
v & m supplementation recommendations
A, D, K, zinc, selenium, thiamin, folate may need to be supplemented
69
supplementation caution
Supplements that contain iron and copper should be avoided until hemochromatosis (Genetic disorder of iron overload; resultant Fe accumulation affects the liver) and Wilson’s disease (Genetic disorder of mutations affecting the biliary Cu transporter = reduced Cu exertion.) as a cause of cirrhosis have been ruled out
70
taste abnormalities reccs
* Associated with Mg and Zn deficiencies
* Oral care
* Mouth rinses
* Cold or room temp foods
71
early satiety reccs
* Correct ascites!
* Small, frequent meals
* Energy dense meals/snacks
* Avoid gas-producing foods
* Drink liquids at end of meal/between
* Distracted eating, E.g., in front of TV
* Motility agents before meals
72
nausea reccs
* Cold foods, no smells
* Small meals, frequently
* Avoid being full or hungry
73
anorexia recc
* Excessive restrictions of protein and salt? (bland food= non-desirable)
* Eat largest meal when feeling hungry
* Manage NIS that contribute to poor intake
74
ONS reccs in cirrhosis
Nutrient dense ONS
• Supplementation with ONS providing ~1000kcal and 40g protein/d reduced
hospitalization visits in one study.
75
when should en be given in cirrhosis
In cirrhotic patients, who cannot be fed orally or who do not reach the nutritional target through the oral diet, EN should be performed
76
which type of EN should be used?
* Small bore nasogastric (NG) placement is feasible in most patients, even those with recent GI bleeding and esophageal varies (hold EN for 48hrs if patients has bleeding esophageal varices)
* PEG placement is associated with a higher risk of complications, due to ascites-> do not use
77
which en formula is recommended?
• Standard calorie-dense, polymeric EN formulas are tolerated by most patients
78
when PN should be used? oil reccs?
Parenteral if PO or EN contraindicated
| • Try fish oil emulsions and aim for <1g/kg
79
What suggestions might you make to assist with compliance with the fluid and sodium restrictions?
Chew on ice chips when thirsty, educate, introduce more herbs and spices, cold foods, adding lemons to limited amounts of liquids can help to make it more refreshing.
80
is steatorrhea common in liver disease?
yes
| problems with bile recycling-> insufficient bile-> fat malabsorption-> steatorrhea
81
causes of maldigestion and malabsorption in cirrhosis
— Fat malabsorption due to cholestasis or chronic pancreatitis
— Water-soluble vitamin malabsorption related to alcohol abuse
— Calcium and fat-soluble vitamin malabsorption due to cholestasis
82
what are the common clinical manifestations of liver disease?
Hepatomegaly
Ascites
Jaundice
Esophageal varices - bleeding, kind like ulcer
Spider angiomas (burst blood vessels)
Encephalitis & coma- very sever complication of liver damage
Hepatorenal syndrome- kidney failure due to liver failure
Coagulopathies
83
How does cirrhosis lead to complications?
cirrhosis results in
1) portal HTN -> variceal hemorrhage; ascites that may lead to hepatorenal syndrome and bacterial peritonitis
2) liver insufficiency-> encephalopathy and jaundice
84
can u tell that a person has hepatomegaly by physical touch?
yes
85
what can jaundice be caused by?
o Excessive bilirubin production due to hemolysis
o Acute or chronic hepatocellular injury
o Obstruction of bile ducts
o Newborn or physiologic jaundice
86
what is portal hypertension
elevated blood pressure in the hepatic portal vein
87
how does ascites develop?
liver damage (alcohol or virus)- > cirrhosis-> decreased albumin production and resistance in portal vein-> decreased osmotic pressure and portal hypertension-> fluid accumulation-> ascites
88
complications of ascites
```
Respiratory distress syndrome (edema, metabolism)
Sepsis
Dilutional hyponatremia (seizure risk)
Renal dysfunction
- Hepatorenalsyndrome
- Overdiuresis
- Sepsis
Umbilical hernias
Decreased appetite
```
89
Treatment of ascites
o Dietary sodium/fluid restriction
o Use of diuretics
o Paracentesis: withdrawal of fluid from the abdomen via a catheter- has the largest impact
90
Which ascites treatment do we use when ascites is severe
once ascites is severe , the malnourishment is so bad, we cannot continue dietary restriction and have to rely on surgical methods-> paracentesis
91
how do Esophageal Varices get developed
Portal hypertension causes blood flow to be forced backward, causing veins to enlarge and varices to develop across the esophagus and stomach from the pressure in the portal vein.
92
What are the consequences of esophageal varices?
o Blood loss / bleeding
o Elevation of ammonia
o Pain with eating
o NPO for prolonged periods
93
Treatment for Esophageal Varices
Meds to decrease portal HTN
Banding: bands to tie off bleeding veins
TIPS: to shunt blood away from portal vein-> this is very invasive, so it is considered only after all other options have been tried
94
what is hepatic encephalopathy?
Syndrome of impaired mental status and abnormal neuromuscular function d/t consequences of liver failure
95
What are potential contributors of hepatic encephalopathy
```
o Liver failure
o Diversion of the portal blood through the
venous systemic circulation
o Bleeding from varices
o Infection / Sepsis
```
96
Pathogenesis of hepatic encephalopathy
o Multifactorial
o Inability of liver of the liver to metabolize
products that are toxic to the brain
o Elevation of serum ammonia
o Neurotoxin produced by intestinal bacteria
97
Symptoms of Encephalopathy
Signs and symptoms vary depending on the severity of HE
o Changes in mental status, behavior and personality
o Forgetfulness
o Neuromuscular changes
o Asterixis
o Coma
98
what does HE treatment focus on?
Treatment focuses on reducing circulating ammonia
99
name HE treatment options
lactulose, antibiotics, high protein provision
100
describe lactulose as HE treatment option
o Stimulates the passage of ammonia from body tissues into the gut lumen
o Inhibits intestinal ammonia production
o Lactulose titrated to several BM per day (GOAL IS DIARRHEA!)
101
describe antibiotics as HE treatment option
(neomycin, rifaximin, metrodinazole)
| o Decrease concentration of colonic ammonia-producing bacteria
102
describe high protein as HE treatment option
High protein provision with 1.2-1.5 g/kg/d dry weight
| o Lower protein intake will result in catabolism and further increases ammonia production
103
nutrition considerations in HE treatment
Swallowing eval and if intubated: EN
104
Methods of scoring liver disease
Child-Turcotte-Pugh Scoring System for Cirrhosis (CTP)
- To assess prognosis of pt with cirrhosis
Model for End-Stage Liver Disease (MELD)
- Previously used only to predict mortality post TIPS
- Now used to determine prognosis and prioritize pts waiting for Liver Tx
105
How is MELD score calculated? what do scores mean?
o Higher score correlates to the severity of the liver disease. Patients with higher scores are prioritized on the transplant list.
o Three blood tests: bilirubin, prothrombin time (PT) measured as international normalized ratio (INR) and creatinine (a measure of kidney function)
o The MELD score is calculated using the following equation:
3.8 x log (e) (bilirubin mg/dL) + 11.2 x log (e) (INR) + 9.6 log (e) (creatinine mg/dL)
106
what is the most common cause of hepatitis?
virus
107
describe HAV
Acute hepatitis A (HAV)
o Transmitted almost exclusively by the oral-fecal route
o Sources include contaminated drinking water, food, and sewage
108
describe HBV
o Transmitted via blood, blood-derived fluids, improperly sterilized medical instruments, or other skin-puncturing instruments
o Can be acute or chronic
o Complications include cirrhosis and hepatocellular malignancy (liver cancer)
109
describe HCV
o Exposure to blood or body fluids from an infected person
| o Associated with development of chronic liver disease, cirrhosis, HCC and need for liver transplant
110
describe HDV AND HEV
- Uncommon, requires HBV to replicate (often, its a mutation of HBV)
- Acute infection
111
Nutrition implications for Hepatitis
o N & V, fatigue, abd pain
o Anorexia with weight loss and nutritional
deficiency
o Hypoglycemia d/t decreased gluconeogenesis due to liver damage
o Fluid and electrolyte imbalance: serum Na
and K
112
Nutrition diagnosis for Hepatitis
o Inadequate oral food/beverage intake
o Inadequate protein and calorie intake
o Food-medication interaction
o Impaired nutrient utilization
113
Nutrition Intervention for Hepatitis
o Provide nutrients needed for liver regeneration
- ESPEN 2019: Stress factor 1.3 x REE
- NCM: 30-35 kcal/ kg , 1-1.2 g pro/kg
o High energy and high protein diet if patient is anorexic
o Frequent, small meals for hypoglycemia
o Adequate rest and fluid
o Avoid alcohol
o Food-medication interaction
o New medications for viral hepatitis treatment: Entavir (Baraclude), Tenofovir (Viread), Lamivudine (Epivir),
Adefovir (Hepsera), Telbivudine (Tyzeka)
o EN if indicated
o PN
114
What is Nonalcoholic Fatty Liver Disease
| NAFLD
Refers to a wide spectrum of liver disease ranging from steatosis to nonalcoholic steatohepatitis (NASH) and to cirrhosis
115
Medications for fatty liver
No fatty liver disease specific medication available
116
Symptoms of NAFLD
Usually asymptomatic
117
Goal for NAFLD treatment
goal to prevent cirrhosis which is scarring of the liver
118
Difference in occurrence of NAFLD across genders and ages
Increasing rate, ~men > women, age 50+
119
Fatty liver definition
could be due to alcohol or other factors. Greater than 5% by weight of liver is fat. Liver appears somewhat yellow.
120
NAFLD progression, types and definitions
Steatosis-> NASH-> fibrosis-> cirrhosis
NAFL: non-alcoholic fatty liver
1. Steatosis
- First hit (usually obese with or without DM2)
- Insulin resistance
- Deposition of lipids in hepatic parenchyma (impaired synthesis and export of VLDL)
2. NASH: non-alcoholic steatohepatitis - inflammation caused by fat accumulation in liver
- Second hit (~10-20% progress to this stage) - Oxidative stress
- DM nephropathy and proteinuria
4. Cirrhosis: a pathological l condition where fibrous connective tissue replaces healthy tissue in the liver, likely due to inflammation or injury
- Increased susceptibility to multiple injuries
- Progressive fibrosis
- Hepatic protein synthesis impaired
- Liver failure, hepatocellular carcinoma (HCC)
121
Conditions Associated with Fatty Liver
Alcoholism
Type 2 diabetes mellitus Metabolic syndrome
Obesity
Polycystic ovary syndrome Obstructive sleep apnea Dyslipidemia
Parenteral nutrition
Pancreato-duodenal resection
Hypopituitarism Hypogonadism Hypothyroidism
Iatrogenic Refeeding syndrome
Amiodarone
Methotrexate
Tamoxifen
Corticosteroids
122
Nutrition Intervention for NAFLD (ESPEN vs ASPEN vs NELMS)
o Intensive lifestyle intervention leading to weight loss (7-10%) and physical activity
o Abstinence from alcohol
o Use of vitamin E (800 IU alpha-tocopheral daily) in non-diabetic patients, probiotics or symbiotics to improve liver enzymes and histology
o Use of the Mediterranean dietary principles for creating a healthy dietary pattern
o ASPEN: Wt management, reduction of fats and simple sugars, Mediterranean diet, add PA
o NELMS: Same
123
Hepatotoxic alcohol threshold
40 g (4 drinks) and 20 g (2 drinks) daily for men and women respectively
124
3 liver disorders that are associated with ALD:
fatty liver (hepatic steatosis), alcoholic hepatitis and cirrhosis
125
Consequences of alcoholic liver disease
acetaldehyde toxicity, inflammation, metabolic competition, induced metabolic tolerance, cerebellar degeneration, malnutrition and malabsorption
126
Clinical Presentation of ALD: non-specific syndromes
```
o Fatigue
o Weakness
o Nausea
o Anorexia
o Malaise
o Low-grade fever
```
127
Clinical Presentation of ALD: LIVER DISEASE SPECIFIC SYMPTOMS
o Jaundice
o Hepatomegaly
o Ascites
o Portal hypertensive bleeding o Hepatic encephalopathy
128
Vitamin and mineral deficiencies in ALD
Metabolism of ethanol and the end products acetaldehyde increases the need for:
o B vitamins: folate, thiamin, pyridoxine (B6)
o Selenium
o Zinc
o Magnesium
129
Nutrition Implication of ALD
ALD often results in:
Anorexia and dysgeusia Intestinal maldigestion and malabsorption Hypermetabolism
Decreased protein synthesis and increased autophagy
Which leads to:
Malnutrition
Vitamin and mineral deficiencies
Sarcopenia
130
Common Nutrition Diagnoses
```
o Increased energy expenditure
o Inadequate energy intake
o Inadequate oral food/beverage intake
o Inadequate protein-energy intake
o Malnutrition
o Inadequate vitamin/mineral intake
o Excessive EtOH intake
o Impaired nutrient utilization
o Underweight
o Altered GI function
o Nutrition-related laboratory values
o Food-medication interactions
o Involuntary weight loss
```
131
Other Nutrition Intervention for ALD
- Correction of nutritional deficiencies as well as prevention or treatment of malnutrition
- Restriction of sodium, fluid and other substrates depending on comorbid conditions like renal failure or diabetes mellitus
- Ensure adequate energy and protein intake without increasing the risk of HE
132
causes of cirrhosis in the United States:
o Hepatitis C is most common
o Alcoholic liver disease (21%)
o Hepatitis C plus alcoholic
liver disease (15%)
o Cryptogenic causes (18%); many due to NAFLD
o Hepatitis B, which may be coincident with hepatitis D (15%)
133
Miscellaneous Causes of Cirrhosis
```
o Autoimmune hepatitis
o Primary biliary cirrhosis
o Secondary biliary cirrhosis (associated with chronic extrahepatic bile duct obstruction)
o Primary sclerosing cholangitis
o Hemochromatosis
o Wilson's disease
o Alpha-1 antitrypsin deficiency
o Granulomatous disease (sarcoidosis)
o Type 4 glycogen storage disease
o Drug-induced liver disease (methotrexate, alpha methyldopa, and amiodarone)
```
134
Cirrhosis manifestations: general symptoms
```
Fatigue
Weakness
Nausea
Poor appetite
Malaise
Vitamin and mineral deficiencies
```
135
Cirrhosis manifestations: LIVER-SPECIFIC SYMPTOMS
Jaundice
| Dark urine Light stools Steatorrhea Itching Abdominal pain Bloating
136
Major clinical complications of cirrhosis
```
o Portal hypertension
o Hepatic encephalopathy
o Ascites
o Hepatorenal syndrome
o Esophageal varices
```
137
Cirrhosis: Clinically Meaningful States- COMPENSATED
```
Cirrhosis without ascites or encephalopathy. May show beginnings of:
o Variceal hemorrhage
o Ascites
o Encephalopathy
o Jaundice
```
138
Cirrhosis: Clinically Meaningful States DECOMPENSATED
Cirrhosis with ascites and/or encephalopathy.
o Albumin < 30 g/L
o Total bilirubin > 2.5 mg/dl (normal < 0.9 mg/dL)
o Other clinical presentation: behavioural changes, reversal of sleep pattern, slurred speech, disorientation, coma
o High risk of death
139
Nutrition Assessment of Cirrhosis
o Should include attention to physical assessment and steps to identify sarcopenia.
o SGA,MUST, NUTRIC, and NRS2002 are used to screen for malnutrition risk
Anthro: MAC, MAMC
o Fxnal assessment: Handgrip, 6 min walk
o Nutrition Diagnosis similar to ALD, may relate to particular complication
o Ascites
o Esophageal varices
o Hepatorenal syndrome
o HE
140
Nutrition Implication of Cirrhosis
```
o Similar to ALD
o Increased energy expenditure related to acute complications, refractory ascites
o Malnutrition
o Sarcopenia
o Micronutrient deficiencies
o Early satiety from ascites
o Impaired nutrient digestion and absorption (eg Cholestasis, chronic pancreatitis, EtOH)
o Hypoglycemia
```
141
Nutrition Intervention for Cirrhosis
o Early assessment and f/u with Adequate energy and protein to replenish malnourished and sarcopenic cirrhotic patients:
- Frequent meals
o Replace vitamins and minerals as needed
o Sodium restriction in ascites (Fluid restriction if low serum Na: NCM)
o Soft diet for patients with esophageal varices
o Lifestyle interventions after improvement of conditions (post-discharge)
142
nutrient and energy requirement recommendations for cirrhosis
o Energy 30-35 kcal/kg/d (ESPEN)vs 35-40 kcal/kg/d (Nelms) vs 1.2-1.4 X REE (ASPEN)
o ASPEN: Protein: 1-1.5
o ESPEN, 2019:
- Protein for non-malnourished patients with compensated cirrhosis: 1.2 g/kg/d (ESPEN)
- Protein for malnourished and/or sarcopenic cirrhotic patients: 1.5 g/kg/d (ESPEN)
- For obese cirrhotic patients: Energy 25 kcal/kg/d IBW and protein 2.0-2.5 g/kg/d IBW (ESPEN)
143
Nutrition Support in cirrhosis (ESPEN 2019)
- Consider level of consciousness and symptoms of HE.
- Prioritize oral intake and the use of oral nutritional supplements (ONS) to achieve adequate energy and protein intake
- Patients with mild HE can be fed orally as long as cough and swallow reflexes are intact
- Acute LF patients and severe ASH patients who cannot achieve adequate intake via oral should receive EN via nasogastric/naso-jejunal tube.
- Esophageal varices are not absolute contraindication for positioning a nasogastric tube.
- PEG placement is associated with a higher risk of complications, due to ascites or varices, and thus, can only be used in exceptional cases.
144
PN reccs in cirrhosis -
- PN should be used as second line treatment in patients who cannot be fed by oral and/or EN.
- PN should be commenced immediately in moderately or severely malnourished patients with severe ASH who cannot be nourished sufficiently by oral and/or enteral route.
- PN should be considered in patients with unprotected airways and HE when cough and swallow reflexes are compromised or EN is contraindicated or impracticable.
ASPEN: Use EN as indicated- including supplemental EN; use PN for shortest time possible if warranted
145
when is liver transplant considered?
Considered in cases where effects of the disease have a higher potential to cause mortality than the complications of liver transplan
146
What is used to determine eligibility for liver transplant
Model for End-Stage Liver Disease (MELD) scoring system is used to determine eligibility.
147
Liver transplant nutritional implications
Malnutrition and ascites
| Need for early nutritional support after surgery Food-borne infections (post Tx)
148
Liver Transplant: Nutrition Diagnosis
Increased energy expenditure
Inadequate energy, oral food/beverage, or protein intake
Malnutrition
Inadequate vitamin/mineral intake
Altered GI function
Impaired nutrient utilization
Altered nutrition-related laboratory values
Food–medication interactions
Food- and nutrition-related knowledge deficit
Unintentional weight loss
149
Liver Transplant: Intervention
- Oral or enteral nutrition is preferred
- Patients should be managed according to ERAS to prevent malnutrition (ESPEN)
- Aim for daily energy intake of 30–35 kcal/kg/d and protein intake of 1.2–1.5 g/kg/d (ESPEN).
- For obese patients: energy 25 kcal/kg/d IBW, protein 2.0 – 2.5 g/kg/d IBW (ESPEN)
- Other nutrients are individualized based on immunosuppressant drug regimen
150
Monitoring and Evaluation in liver transplant
Post-transplant patients should be monitored regularly for:
Recovery and healing
Dietary intake
Tolerance to diet
Weight changes
Food safety guidelines
Nutrient-related complications associated with medications including steroids
