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Clinical Nutrition 2 > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

___ Canadians may be affected by liver disease, including everyone from newborns and older adults

A

1 in 4

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2
Q

_____ is the most common liver disease in Canada

A

Non-alcoholic fatty liver disease

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3
Q

What us one of the fastest rising and deadliest forms of cancer in Canada?

A

Liver cancer

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4
Q

Costs for hepatitis C?

A

$20,000 - 70,000 per year

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5
Q

What are some key functions of the liver?

A
  • Storage of blood glycogen, synthesis
  • Detoxification and Metabolism
  • Excrete bile, bilirubin and urea
  • Macrophage storage
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6
Q

What happens when we bleed? How is the liver involved?

A
  • Clotting cascade, vitamin K
  • Where the liver is required to produce proteins to activate the clotting cascade and vitamin K
  • Those with liver diseases are at a very high risk of bleeding out
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7
Q

Which organ houses the most macrophages within the body?

A

The lover

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8
Q

How does the liver receive blood supply?

A
  • Through the hepatic artery (oxygen rich) and the portal vein (nutrient rich, deoxygenated)
  • two ports of entry
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9
Q

What does the portal vein supply?

A

-Intestine, spleen and pancreas

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10
Q

How does the portal vein and liver system act to protect us from toxins?

A

Is a “first-pass” system, where anything we eat will be shunted through the portal vein to the liver for detoxification

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11
Q

How much liver function is required for life? What % of function may we begin to see symptoms?

A
  • 10-20%

- 75-80%

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12
Q

Describe intermediary metabolism in the liver

A
  • Synthesis of protein
  • Storage of CHO
  • Synthesis of glucose
  • Cholesterol/lipid transport
  • Bioactivation of vitamins and minerals
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13
Q

Which blood supply to the liver will provide O2 and blood borne metabolites fo hepatic processing?

A

-Hepatic artery

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14
Q

Which blood supply to the liver is drained from the digestive tracts for processing and storage of newly absorbed nutrients?

A

-Hepatic portal vein

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15
Q

What does blood leave the liver through?

A

The hepatic vein

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16
Q

Discuss the flow of blood from the hepatic portal vein

A

Deoxygenated blood will flow from the intestine to the liver, where the nutrient rich blood will bathe the sinusoidal space. The sinusoids will aggregate into the hepatic vein, which will be delivered to the heart through the IVC for oxygenation

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17
Q

What are sinusoids?

A

Open system which the nutrient-rich blood from hepatic portal vein will drain into and eventually be returned to the heart

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18
Q

What is the space of disse?

A

The space between the sinusoids and the hepatocytes, which is lined with kupffer and stellate cells

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19
Q

What are kupffer cells?

A

Large macrophagic cells of the liver

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20
Q

What are stellate cells?

A
  • Store vitamin A
  • Produce fibrin and collagen
  • Key cells when we consider the fibrosis and damage of the liver
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21
Q

Discuss enterohepatic circulation

A

1) Secreted bile salts will consist of 95% old recycled bile salts and 5% newly synthesized bile salts
2) 95% of bile salts are reabsorbed by the small intestine, 5% are excreted in feces
3) Reabsorbed bile salts are recycled by enterohepatic circulation

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22
Q

What is important to consider in liver damage?

A

That the liver has over 500 functions, therefore will have many consequences - especially nutrition related as it is an intermediate of nutrient metabolism

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23
Q

What are the 8 key metabolic functions of the liver?

A

Metabolism of:

  • CHO
  • Lipids
  • Protein
  • Enzyme
  • Vitamins
  • Bile acid
  • Heme
  • Storage
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24
Q

CHO metabolism?

A
  • Glycogenesis
  • Gluconeogenesis
  • Oxidation via TCA cycle
  • Glycogenosis
  • Glycolysis
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25
Q

Lipid metabolism?

A
  • Lipogenesis
  • Lipolysis
  • Ketogenesis
  • FA oxidation
  • Formation of lipoproteins
  • Cholesterol metabolims
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26
Q

Vitamin metabolism?

A
  • Formation of Acetyl CoA from pantothenic acid
  • Hydroxylation of Vitamin D
  • Phosphorylation of pyridoxine
  • Formation of coenzyme B12
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27
Q

Bile acid metabolism?

A

Transformation of cholesterol to 7-hydroxycholesterol to cholic acid and chenodeoxycholic acid

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28
Q

Heme metabolism?

A
  • Heme is oxidized and reduced to bilirubin

- Bilirubin is transported to liver where it is converted to bilirubin diglucuronide to be excreted with bile pigments

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29
Q

Storage in the liver?

A

-Glycogen, fats, FA, fat-soluble vitamins?

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30
Q

What is going to happen to blood sugars with someone with liver disease?

A
  • May have hypoglycemia

- Less glycogen sotrage and synthesis

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31
Q

Protein metabolism?

A
  • Synthesis of serum proteins
  • Degradation of proteins to peptides and AA
  • Synthesis of urea
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32
Q

Enzyme metabolims?

A

-Synthesis of alkaline phosphatase, AST, and ALYT

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33
Q

Common diseases/conditions with livers?

A
  • Hepatitis
  • Alcoholic hepatitis and cirrhosis
  • NAFLD
  • NASH
  • Fibrosis
  • Cirrhosis
  • Liver failure (as we cascade down into the complications of fibrosis and cirrhosis)
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34
Q

_____ leads to NASH

A

NAFLD

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35
Q

What is hepatitis?

A

Severe inflammation in the liver, which can lead to severe liver disease

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36
Q

How is liver disease diagnoses?

A
  • CT scan
  • Liver biopsy
  • Liver function can be interpreted against hepatic enzymes
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37
Q

What are the 6 key liver enzymes?

A
  • AST/SGOT
  • ALT/SGPT
  • AST/ALT ratio
  • GGT
  • Alkaline phosphatase
  • Lactic dehydrogenase (LDH)
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38
Q

When AST and ALT are elevated, what is this most often an indication of?

A

Acute liver disease

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39
Q

(T/F) Both AST and ALT are very unspecific, and either come directly from the liver

A

F

ALT comes from the cytosol of the hepatocyte, and is more specific for liver injury

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40
Q

Where doe AST originate from? What is it elevated in?

A
  • Liver, skeletal or cardiac muscle, kidney
  • Increase in liver cell damage, especially viral hepatitis
  • Will also be elevated with severe cardiac and muscle damage
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41
Q

Where does ALT originate from? What is it indicative of?

A
  • Cytosol of hepatocyte

- Specific for liver injury

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42
Q

What is a normal ALT/AST ratio? When is it indicative of alcoholic liver disease?

A
  • 1

- >2

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43
Q

What does high GGT indicate?

A

-Hepatocellular injury secondary to ethanol abuse

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44
Q

What does high alkaline phosphatase indicate?

A

-Elevated in hepatic disease and in chronic obstruction of the biliary duct, but non-specific

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45
Q

Where does LDH originate from? What is it used to differentiate?

A
  • Liver, RBCm kidney and cardiac muscle
  • Differentiate hepatitis from other diagnoses such as mononucleosis
  • Not a sensitive marker
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46
Q

All types of _____ rise as liver function declines

A

Bilirubin

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47
Q

Which bilirubin is more toxic? What can elevated bilirubin cause?

A
  • Unconjugated

- Jaundice and dark urine

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48
Q

High conjugated/direct bilirubin is indicative of what?

A

Excretion impaired owing to disease, stress of injury or surgery

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49
Q

High unconjugated/direct bilirubin is indicative of what?

A

-Usually hemolysis or impaired liver capacity to conjugate with glucoronic acid, which makes it water soluble and possible to excrete

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50
Q

What is the normal amount of bilirubin detected in urine?

A
  • There should be no urine detected in the liver
  • If there is an presence, indicative of liver disease
  • Will also cause the “darkness” of the urine
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51
Q

What is prothrombin (PT) time? Why can it help us assess liver disease?

A
  • Number of seconds for blood to clot
  • Prolonged in liver disease, as liver is highly implicated in the clotting cascade
  • May be one of the best measures
  • Those with liver disease can be at a very high risk of bleeding out
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52
Q

Why is albumin decreased in liver disease?

A

The liver produces albumin

-Also likely in an inflammatory state

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53
Q

We can asses liver function in stool test, what can alterations in stool colours indicate?

A
  • Decrease or absence of urobilinogen

- Light brown if hepatocellular damage is present

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54
Q

What are other ways to assess liver function?

A
  • Total protein (decr.)
  • Ammonia (incr.)
  • Urea (decr)
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55
Q

What is the fecal fat test used for?

A

-To assess steatorrhea which may be present in hepatic diseases

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56
Q

What does light brown stool indicate?

A

-Hepatocellular damage because of decrease of urobilinogen

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57
Q

What does normal stool and dark urine indicate?

A
  • Bilirubin excretion in urine due to RBC breakdown/hemolysis
  • Liver function OK
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58
Q

Fecal fat test?

A

<7g fat within 72 hours or <60 droplets of fat/hpf

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59
Q

What are the 8 common clinical manifestations of liver disease?

A
  • Hepatomegaly
  • Ascites
  • Jaundice
  • Esophageal varices
  • Spider angiomas
  • Encephalitis & coma
  • Hepatorenal syndrome
  • Coagulopathies
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60
Q

Discuss hepatomegaly?

A

There will be an accumulation of fat and inflammation within the hepatocytes, liver will enlargen with these deposits
-Recall the role of stellate cells which will deposit fibrin and collagen

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61
Q

How does portal HTN arise?

A

The build up of collagen and inflammation/enlargement of the liver will impair the flow of nutrient rich blood through the portal vein, causing a shunting of blood flow back towards to GI tract –> damaging the delicate blood vessels

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62
Q

What is another word for Jaundice?

A

Icterus

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63
Q

What is a key nutritional intervention in liver disease?

A
  • Preventing, attenuating and treating malnutrition

- If there is malnutrition, the cirrhosis gets worse

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64
Q

What is jaundice?

A

Elevated concentration of bilirubin in extracellular fluid which causes a yellowish tint in body tissues

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65
Q

What can jaundice be caused by? (4)

A
  • Excessive bilirubin production due to hemolysis
  • Acute or chronic hepatocellular injury
  • Obstruction of bile dicts
  • Newborn or physiologic jaundice
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66
Q

What are other causes of jaundice? (4)

A
  • Hypoalbuminemia
  • Response to TPN (less binding of bilirubin)
  • Liver diseases
  • Trauma (excess and possible liver dysfunction)
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67
Q

What are the two key consequences of cirrhosis?

A
  • Portal HTN

- Liver insufficiency

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68
Q

What are the 3 main consequences of portal HTN?

A
  • Variceal hemorrhage
  • Ascites
  • Encephaopathy
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69
Q

What are the 2 main consequences of ascites?

A
  • Spontaneous bacterial peritonitis

- Hepatorenal syndrome

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70
Q

What are the two main consequences of liver insufficiency?

A
  • Encephelopathy

- Jaundice

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71
Q

What is portal hypertension?

A

Elevated blood pressure in the hepatic PORTAL vein

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72
Q

What is ascites?

A

Accumulation of fluid within the peritoneal cavity, a primary symptom and complication of portal HTN

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73
Q

Discuss the progression of liver to fluid transudation

A
  • Liver damage will progress to cirrhosis
  • The cirrhosis will decrease the livers ability to make albumin, and the fibrosis/inflammation will increase resistance to portal venous flow
  • The decrease serum albumin will lead to decreased colloid osmotic pressure
  • The increase in portal venous pressure will lead to increased capillary hydrostatic pressure
  • The combination of decreased colloid osmotic pressure and increased capillary hydrostatic pressure will result in fluid transudation
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74
Q

Discuss how fluid transudation will perpetuate the development of ascites (viscous cycle)?

A

It will result in ascites and decrease blood volume as fluid enters into peritoneal cavity. However, the low blood volume will elicit the RAAS system, increase aldosterone and renin which will result in further retention of Na+ and H2O, worsening the ascites

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75
Q

How is kidney failure related to liver failure?

A

-Due to the overcompensation of the RAAS system due to changes in colloid and hydrostatic pressures

76
Q

What are the 6 key complicaitons of ascites?

A
  • Respiratory distress syndrome
  • Sepsis
  • Dilutional hyponatremia
  • Renal dysfunction
  • Umbilical hernias
77
Q

What can increase seizure risk?

A

-Dilutional hyponatremia

78
Q

What kinds of renal dysfunction will ascites cause?

A
  • Hepatorenal syndrome
  • Over diuresis
  • Sepsis
79
Q

What is hepatorenal syndrome?

A

-Will cause many alterations in mental function, body function and will increase risk for seizures

80
Q

In severe ascites, how much fluid accumulation can their be? What is a key consequence?

A
  • 14-15 kg of fluid

- Issues with digestions, discomfort

81
Q

Nutritional treatment for ascites?

A
  • Sodium/Fluid restriction

- Note that many of these patients will be malnourished

82
Q

Medical treatment for ascites?

A
  • Use of diuretics

- Paracentesis

83
Q

What is paracentesis? What is the nutritional implication?

A
  • Withdrawal of fluid from the abdomen via the catheter
  • We lose a lot of protein when we drain these fluids, and these protein are lost in the fluid in the first place
  • Increase protein requirements
84
Q

What are esophageal varices?

A

-Caused by portal HTN, where blood flow is shunted back into the delicate veins of the esophagus (can also happen in the intestine, stomach)

85
Q

Consequences of esophageal varices?

A
  • Blood loss
  • Elevation of ammonia
  • Pain when eating
  • Eating patters
86
Q

2 surgical treatments of esophageal varices?

A
  • Transjugular Intrahepatic Portal Systemic Shunt (TIPS)

- Distal Splenorenal Shunt (DSRS)

87
Q

Describe the TIPS surgical procedure

A
  • A tunnel will be made through the liver, connecting the portal vein to one of the hepatic veins.
  • A metal stent is placed to keep the track open
  • This will help shunt blood to flow to the hepatic vein (and to the heart) instead of the liver
  • Will reduce portal HTN, allow for veins to shrink, help stop variceal bleeding
88
Q

Describe the DSRS surgery

A
  • Left gastric vein (from esophagus –> portal vein) is disconnected and tied off
  • The splenic vein (from stomach –> portal vein) is disconnected, and rerouted to the left renal vein
  • Redirects the blood flow to reduce portal HTN and vein size, ultimately reducing variceal bleeding
89
Q

What may appear on the skin?

A

Spider Angioma

-May be seen more in alcoholics, dilation of blood vessels

90
Q

What is encephalopathy?

A

Elevated ammonia levels in the blood, will result in impaired mental status and abnormal neuromuscular function

91
Q

Potential contributors to encephalopathy?

A
  • Liver failure
  • Diversion of the portal blood through the venous systemic circulation
  • Bleeding from varices
  • Sepsis
92
Q

Pathogenesis of encephalopathy?

A
  • Multi-factorial
  • Inability of liver and liver to metabolize products that are toxic to the brain-
  • Elevation of serum ammonia
  • Neurotoxin produces by intestinal bacteria
93
Q

Symptoms of encephalopathy?

A
  • Changes in mental status and personality
  • Forgetfulness
  • Neuromuscular changes
  • Asterixis
  • Coma
94
Q

What is asterixis?

A

Uncontrollable flapping of hand s

95
Q

What is used to stage encephalopathy?

A

West Haven Staging Scale

96
Q

At what stages of encephalopathy may modifications to nutrition intervention be needed?

A
  • At stage 3, may be lethargic, disorientated, inattentive
  • At stage 4, may be disorientated, confused
  • At stage 5, likely to be in Coma (nutrition support needed)
97
Q

Medical treatment for hepatic encephalopathy?

A
  • Lactulose

- Antibiotics

98
Q

Lactulose in HE?

A
  • Stimulates the passage of ammonia from body tissues into the gut lumen
  • Inhibits intestinal ammonia production
99
Q

Antibiotics in HE?

A

Decrease concentration of colonic ammonia-producing bacteria

100
Q

Nutritional intervention in HE?

A
  • High protein provision of 1.2-1.5 g/kg/day

- MUST use dry weight, caution w/ ascites

101
Q

What does lower protein intake result in HE?

A

-Catabolism an further increases in ammonia production

102
Q

In the rare case of a protein intolerant patient, what may be beneficial?

A

A vegetable protein diet

103
Q

What are the 3 assessment classification schemes for liver disease?

A
  • Child-Turcotte-Pugh Scoring System (CTP)
  • Model for End-Stage Liver Disease (MELD)
  • Glasgow Coma Scale (GCS)
104
Q

What does CTP consider?

A

-Evaluates encephalopathy and ascites with bilirubin, albumin and PT

105
Q

What is MELD initially used for? What else is it used for?

A
  • Predict the mortality rate after TIPS
  • Used to calculate patients likelihood of dying within three months from their liver disease
  • Higher score = more severe disease, and ay be prioritized for liver transplant
106
Q

What does the MELD consider?

A

-Bilirubin
-PT
Creatinine

107
Q

What is PT measured as in MELD?

A

international normalized ratio (INR)

108
Q

What does the glasgow coma scale consider?

A
  • Eye opening
  • Verbal response
  • Motor response
109
Q

What are the 5 types of hepatitis?

A
  • Hepatitis C
  • Hepatitis D and E
  • Hepatitis A
  • Hepatitis B (or serum hepatitis)
  • Fulminant Hepatitis
110
Q

What is Hep A?

A
  • Acute hepatitis
  • Transmitted almost exclusively through the oral-fecal route
  • Sources include contaminated drinking water, food and sewage
111
Q

What is serum Hep or Hep B?

A
  • Can be acute or chronic
  • Transmitted via blood, blood-derived fluids, improperly sterilized medical instruments
  • Complications include cirrhosis and hepatocellular malignancy
112
Q

Tx for serum Hep or Hep B?

A

-Oral antivirals for life

113
Q

What is Hep C?

A
  • Exposure to blood or body fluids from infected persons

- Associated w/ development of chronic liver disease, cirrhosis and need for liver transplant

114
Q

What is Hep D and E?

A
  • Acute infection

- Uncommon, and required HBV to replicate

115
Q

What is Fulminant Hepatitis (ALF)?

A
  • Acute liver failure, rare

- Characterized by the development of hepatic necrosis, coagulopathy and ecephalophathy

116
Q

50% of ALP cases are due to what?

A

-Acetaminophen and other drug toxicities (especially when combines with alcohol)

117
Q

Other causes of ALF?

A
  • Virus infection
  • Toxin
  • Metabolic disorder
  • Immune-mediated attack
118
Q

Treatment for ALF?

A

Liver transplant

119
Q

Nutritional implications ofr hepatitis?

A
  • N&V, fatigue, abdo pain
  • Anorexia, weight loss and nutritional deficiency
  • Hypoglycemia w/ decr. gluconeogenesis-
  • Fluid and electrolyte imbalance
  • Prolonged PT time event with adequate vitamin K
120
Q

Nutritional diagnosis in hepatitis?

A
  • Inadequate oral food/beverage intake
  • Inadequate protein and kcal intake
  • Food-med interaction
  • Impaired nutrient utlization
121
Q

Energy with Hepatitis?

A

30-35 kcal/kg

122
Q

Protein with Hepatitis?

A

1-1.2 g/kg/day

123
Q

If hypoglycemia is present in hepatitis, nutritional intervention?

A

-Frequent meals

124
Q

Other nutritional interventions for hepatitis?

A
  • Adequate rest/fluid
  • Avoid alcohol
  • High energy and high protein diets if patient is anorexic
125
Q

What is NAFLD?

A
  • refers to a wide spectrum of liver disease ranging from steatosis to non-alcoholic steato-hepatitis (NASH) and to cirrhosis
  • usually asymptomatic
  • More men than women
126
Q

What is fatty liver caused by?

A
  • Could be due to alcohol or other factors

- When greater than 5% of the weight of the liver is fat, we have fatty liver (may appear yellow0

127
Q

What does NASH stand for? What is it?

A

-Non-alcoholic steatotic hepatitis (inflammation caused by fat accumulation in the liver)

128
Q

What is cirrhosis?

A

-A pathological condition where fibrous connective tissue replace healthy tissue in the liver, likely due to inflammation or injury

129
Q

Discuss the progression of NAFLD

A

Steatosis –> NASH –> Cirrhosis

130
Q

What elicits steatosis? What does it result in?

A
  • May be obese, with or without DM
  • Insulin resistance, hyper TG
  • Deposition of lipids in the hepatic parenchyma, causing impaired synthesis and export of VLDL
131
Q

What elicits NASH? What does it result in?

A
  • Oxidative stress

- DM nephropathy and proteinuria

132
Q

What doe cirrhosis result in?

A
  • Increases susceptibility to multiple injuries
  • Progressive fibrosis
  • Hepatic protein synthesis impaires
  • Liver failure, hepatocellular carcinoma
133
Q

Name 5 conditions associated with fatty liver

A
  • Alcoholism
  • Type II DM
  • Metabolic Syndrome
  • PN (overfeeding)
  • Amiodarone (Heart md)
  • Corticosteroids
134
Q

Nutrition Intervention for NAFLD?

A
  • Weight loss of 7-10% and PA
  • Abstinence from alcohol
  • Med diet
135
Q

Which patients with NAFLD may benefit from vitamin E? how much? What else may benefit?

A
  • non-diabetic patients
  • 800 IU
  • probiotics or symbiotics to improve their liver enzymes and histology
  • results in a + interaction between gut-microbiome and obesity
136
Q

Alcohol abuse has a toxic effect on _____

A

all major organ systems

137
Q

What is the hepatotoxic alcohol threshold?

A

40 g (4 drinks) and 20 g (2 rinks) for men and women respectively

138
Q

What are the three liver disorders associated with ALD?

A
  • Fatty liver (hepatic steatosis)
  • Alcoholic hepatitis
  • Cirrhosis
139
Q

Consequences of ALD?

A

-Acetaldehyde toxicity, inflammation, metabolic competition, malnutrition, malabsorption

140
Q

Explain metabolic competition and micronutrient deficiencies in ALD

A

-The liver will prioritize the detoxification of alcohol over the activation of micronutrients

141
Q

Non-specific symptoms of ALD?

A
  • Fatigue
  • Weakness
  • N/V
  • Anorexia, Malaise
  • Low grade fever
142
Q

Liver disease specific symptoms of ALD?

A
  • Jaundice
  • Hepatomegaly
  • Ascites
  • Portal HTN bleeding
  • HE
143
Q

Minor alcohol withdrawal symptoms?

A
  • Gi upset
  • Anorexia
  • Headache
  • Diaphoresis
144
Q

Complications of alcohol withdrawal?

A
  • Micronutrient deficiencies
  • Alcoholic halluconosis
  • Delirium tremens
  • Seizures
145
Q

What does the metabolism of ethanol and end products of acetaldehyde increase the need for?

A
  • Folate, thiamin and pyridoxine
  • Selenium
  • Zinc
  • Magnesium

–> Incr. risk of deficiencies for these nutrients

146
Q

Tx of alcohol withdrawal?

A
  • Anti-anxiety and anti-seizure meds
  • Replacement of vitamins and electrolytes
  • Caution with RF
147
Q

Key nutritional concerns of ALD?

A
  • Anorexia and dysgeusia
  • Intestinal maldigestion and malabsorption
  • Hyper metabolism
  • Decreased protein synthesis and increased autophagu
148
Q

What are the implications of the nutritional concerns in ALD?

A
  • Malnutrition
  • Vitamin and mineral deficiencies
  • Sarcopenia
149
Q

Other nutritional interventions of ALD

A
  • Correct nutrient deficiencies, prevent malnutrition
  • Restrict sodium, fluid and other substrates depending on co-morbid conditions (renal failure, DM)
  • Ensure adequate E and P intake w/o increasing risk of HE
150
Q

What is the most common cause of cirrhosis?

A
  • Alcoholic liver diseases and hepatitis (95%)

- Hep C most common (26% of causes)

151
Q

What are the other 5% causes of cirrhosis?

A
  • Autoimmune
  • Biliary causes or cholangitis
  • Hemochromatosis
  • Wilson’s disease
  • Gene mutations
152
Q

What is Wilson’s disease?

A

Rare genetic disorder which causes the improper metabolism of copper

153
Q

Which gene mutation will cause alterations in lungs and kidney?

A

Alpha-1 antitrypsin deficiency

154
Q

General symptoms of cirrhosis?

A
  • N/V
  • Weakness, fatigue
  • Poor appetite
  • Malaise
  • Vit and min deficiencies
155
Q

Liver-specific symptoms of cirrhosis?

A
  • jaundice
  • dark urine
  • light stools
  • steatorrhea
  • abdo pain, bloating
156
Q

Clinical manifestations of cirrhosis?

A
  • Portal HTN
  • HE
  • Ascites
  • Hepatorenal sundrome
  • Varices
157
Q

What are the the two clinically meaningful states in cirrhosis?

A
  • Compensated

- Decompensated

158
Q

Compensated state of cirrhosis?

A
  • Cirrhosis without ascites or encephalopathy

- May start to show beginnings of variceal hemorrhage, ascites, encephalopathy, jandice

159
Q

Decompensated state of cirrhosis?

A
  • Cirrhosis with ascites and/or encephalopathy
  • Albumin <30
  • Total bilirubin >2.5
  • May have behavioural changes, reversal of sleep patterns, slurred speech
  • -> High risk of death
160
Q

What should nutritional assessment of cirrhosis include?

A
  • Attention to physical assessment to identify sarcopenia
  • MAC, MAMC, handgrip, 6 min walk
  • Consider complications including ascites, varices and hepatorenal syndrome
161
Q

Examples of nutrition implications in cirrhosis?

A
  • Increase EE
  • Malnutrition, sarcopenia
  • Micronutrient deficiencies
  • Early satiety from ascites
  • Impaired nutrient digestion/absorption
  • Hypoglycemia
162
Q

Theme of nutritional intervention in cirrhosis?

A

Adequate energy and protein to replenish malnourished and sarcopenic cirrhotic patients

  • Frequent meals
  • Replace vitamins and minerals
163
Q

Energy in cirrhosis?

A

30-40 kcal/kg

164
Q

Protein for non-malnourished patients w/ compensated cirrhosis?

A

1.2 g/kg/day

165
Q

Protein for malnourished and/or sarcopenic cirrhosis patients?

A

1.5 g/kg/day

166
Q

Energy for obese cirrhosis patients?

A

25 kcal/kg/day of IBW

167
Q

Protein for obese cirrhosis patients?

A

2.0-2.5 g/kg/day of IBW

168
Q

Diet for patients with esophageal varices?

A

Soft diet

169
Q

What are two diuretics which may have nutritional issue?

A
  • Furosemide

- Spironolactone

170
Q

Furosemide?

A
  • Incr. excretion of Na, K, Mg and Ca
  • Diet should be high in K, Mg and Ca
  • Avoid natural licorices
171
Q

Spironolactone?

A
  • Increases reabsorption of K
  • Avoid salt substitute
  • Caution w/ K supplements
  • Avoid excessive K in diet
172
Q

Other nutritional considerations in cirrhosis?

A
  • Consider pancreatic enzymes
  • Consider red. cooper if Wilson’s
  • consider red. iron if hemochromatosis
173
Q

When may nutritional support be indicated?

A
  • HE, based on level of consciousness

- Acute Liver Failure and severe ASH patients if they cannot meet adequate oral intake

174
Q

What should be prioritized to achieve adequate protein and E intake?

A

ONS

175
Q

When may patient with mild HE be fed orally?

A

When their swallowing and cough reflexes are intatc

176
Q

How should acute F and severe ASH patients be fed with NS/

A

EN via NG or NJ tube

177
Q

(T/F) Esophageal varices are an absolute contraindication to NG tubes

A

G

178
Q

What is PEG placement associated with?

A

-Higher risk of complications, due to ascites or varices and should only be used in exceptional cases

179
Q

When should PN be commenced immediately?

A

In mod or sever malnourished patents who cannot be nourished sufficiently by oral/EN route

180
Q

When should PN be considered?

A
  • unprotected airways
  • HE with compromised cough/swallow reflexes
  • EN contraindicated/impracticable
181
Q

When is liver transplant considered?

A

When the effects of liver disease have a higher potential to cause mortality than the complications of the liver transplant
-Considers MELD score

182
Q

Nutritional implications of liver transplant?

A

-Malnutrition, ascites
-Need for early NS after Sx
-Food-borne illness
(due to compromised immune system)

183
Q

Nutriton intervention in liver transplant?

A
  • Oral or En preferred

- ERAS protocol

184
Q

Energy in liver transplant?

A

30-35 kcal/kg/day

185
Q

Protein intake in liver transplant?

A

1.2-1.5 g/kg/day

186
Q

Obese kcal and pro requirements?

A
  • 25 kcal/kg/day IBW

- 2.0-2.5 g/kg/day IBW

Clinical Nutrition 2 (21 decks)

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