Liver Disease Flashcards
1
Q
___ Canadians may be affected by liver disease, including everyone from newborns and older adults
A
1 in 4
2
Q
_____ is the most common liver disease in Canada
A
Non-alcoholic fatty liver disease
3
Q
What us one of the fastest rising and deadliest forms of cancer in Canada?
A
Liver cancer
4
Q
Costs for hepatitis C?
A
$20,000 - 70,000 per year
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
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
7
Q
Which organ houses the most macrophages within the body?
A
The lover
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
9
Q
What does the portal vein supply?
A
-Intestine, spleen and pancreas
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
11
Q
How much liver function is required for life? What % of function may we begin to see symptoms?
A
- 10-20%
- 75-80%
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
13
Q
Which blood supply to the liver will provide O2 and blood borne metabolites fo hepatic processing?
A
-Hepatic artery
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
15
Q
What does blood leave the liver through?
A
The hepatic vein
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
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
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
19
Q
What are kupffer cells?
A
Large macrophagic cells of the liver
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
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
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
23
Q
What are the 8 key metabolic functions of the liver?
A
Metabolism of:
- CHO
- Lipids
- Protein
- Enzyme
- Vitamins
- Bile acid
- Heme
- Storage
24
Q
CHO metabolism?
A
- Glycogenesis
- Gluconeogenesis
- Oxidation via TCA cycle
- Glycogenosis
- Glycolysis
25
Lipid metabolism?
- Lipogenesis
- Lipolysis
- Ketogenesis
- FA oxidation
- Formation of lipoproteins
- Cholesterol metabolims
26
Vitamin metabolism?
- Formation of Acetyl CoA from pantothenic acid
- Hydroxylation of Vitamin D
- Phosphorylation of pyridoxine
- Formation of coenzyme B12
27
Bile acid metabolism?
Transformation of cholesterol to 7-hydroxycholesterol to cholic acid and chenodeoxycholic acid
28
Heme metabolism?
- 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
29
Storage in the liver?
-Glycogen, fats, FA, fat-soluble vitamins?
30
What is going to happen to blood sugars with someone with liver disease?
- May have hypoglycemia
| - Less glycogen sotrage and synthesis
31
Protein metabolism?
- Synthesis of serum proteins
- Degradation of proteins to peptides and AA
- Synthesis of urea
32
Enzyme metabolims?
-Synthesis of alkaline phosphatase, AST, and ALYT
33
Common diseases/conditions with livers?
- Hepatitis
- Alcoholic hepatitis and cirrhosis
- NAFLD
- NASH
- Fibrosis
- Cirrhosis
- Liver failure (as we cascade down into the complications of fibrosis and cirrhosis)
34
_____ leads to NASH
NAFLD
35
What is hepatitis?
Severe inflammation in the liver, which can lead to severe liver disease
36
How is liver disease diagnoses?
- CT scan
- Liver biopsy
- Liver function can be interpreted against hepatic enzymes
37
What are the 6 key liver enzymes?
- AST/SGOT
- ALT/SGPT
- AST/ALT ratio
- GGT
- Alkaline phosphatase
- Lactic dehydrogenase (LDH)
38
When AST and ALT are elevated, what is this most often an indication of?
Acute liver disease
39
(T/F) Both AST and ALT are very unspecific, and either come directly from the liver
F
ALT comes from the cytosol of the hepatocyte, and is more specific for liver injury
40
Where doe AST originate from? What is it elevated in?
- Liver, skeletal or cardiac muscle, kidney
- Increase in liver cell damage, especially viral hepatitis
- Will also be elevated with severe cardiac and muscle damage
41
Where does ALT originate from? What is it indicative of?
- Cytosol of hepatocyte
| - Specific for liver injury
42
What is a normal ALT/AST ratio? When is it indicative of alcoholic liver disease?
- 1
| - >2
43
What does high GGT indicate?
-Hepatocellular injury secondary to ethanol abuse
44
What does high alkaline phosphatase indicate?
-Elevated in hepatic disease and in chronic obstruction of the biliary duct, but non-specific
45
Where does LDH originate from? What is it used to differentiate?
- Liver, RBCm kidney and cardiac muscle
- Differentiate hepatitis from other diagnoses such as mononucleosis
- Not a sensitive marker
46
All types of _____ rise as liver function declines
Bilirubin
47
Which bilirubin is more toxic? What can elevated bilirubin cause?
- Unconjugated
| - Jaundice and dark urine
48
High conjugated/direct bilirubin is indicative of what?
Excretion impaired owing to disease, stress of injury or surgery
49
High unconjugated/direct bilirubin is indicative of what?
-Usually hemolysis or impaired liver capacity to conjugate with glucoronic acid, which makes it water soluble and possible to excrete
50
What is the normal amount of bilirubin detected in urine?
- 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
51
What is prothrombin (PT) time? Why can it help us assess liver disease?
- 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
52
Why is albumin decreased in liver disease?
The liver produces albumin
| -Also likely in an inflammatory state
53
We can asses liver function in stool test, what can alterations in stool colours indicate?
- Decrease or absence of urobilinogen
| - Light brown if hepatocellular damage is present
54
What are other ways to assess liver function?
- Total protein (decr.)
- Ammonia (incr.)
- Urea (decr)
55
What is the fecal fat test used for?
-To assess steatorrhea which may be present in hepatic diseases
56
What does light brown stool indicate?
-Hepatocellular damage because of decrease of urobilinogen
57
What does normal stool and dark urine indicate?
- Bilirubin excretion in urine due to RBC breakdown/hemolysis
- Liver function OK
58
Fecal fat test?
<7g fat within 72 hours or <60 droplets of fat/hpf
59
What are the 8 common clinical manifestations of liver disease?
- Hepatomegaly
- Ascites
- Jaundice
- Esophageal varices
- Spider angiomas
- Encephalitis & coma
- Hepatorenal syndrome
- Coagulopathies
60
Discuss hepatomegaly?
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
61
How does portal HTN arise?
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
62
What is another word for Jaundice?
Icterus
63
What is a key nutritional intervention in liver disease?
- Preventing, attenuating and treating malnutrition
| - If there is malnutrition, the cirrhosis gets worse
64
What is jaundice?
Elevated concentration of bilirubin in extracellular fluid which causes a yellowish tint in body tissues
65
What can jaundice be caused by? (4)
- Excessive bilirubin production due to hemolysis
- Acute or chronic hepatocellular injury
- Obstruction of bile dicts
- Newborn or physiologic jaundice
66
What are other causes of jaundice? (4)
- Hypoalbuminemia
- Response to TPN (less binding of bilirubin)
- Liver diseases
- Trauma (excess and possible liver dysfunction)
67
What are the two key consequences of cirrhosis?
- Portal HTN
| - Liver insufficiency
68
What are the 3 main consequences of portal HTN?
- Variceal hemorrhage
- Ascites
- Encephaopathy
69
What are the 2 main consequences of ascites?
- Spontaneous bacterial peritonitis
| - Hepatorenal syndrome
70
What are the two main consequences of liver insufficiency?
- Encephelopathy
| - Jaundice
71
What is portal hypertension?
Elevated blood pressure in the hepatic PORTAL vein
72
What is ascites?
Accumulation of fluid within the peritoneal cavity, a primary symptom and complication of portal HTN
73
Discuss the progression of liver to fluid transudation
- 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
74
Discuss how fluid transudation will perpetuate the development of ascites (viscous cycle)?
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
75
How is kidney failure related to liver failure?
-Due to the overcompensation of the RAAS system due to changes in colloid and hydrostatic pressures
76
What are the 6 key complicaitons of ascites?
- Respiratory distress syndrome
- Sepsis
- Dilutional hyponatremia
- Renal dysfunction
- Umbilical hernias
77
What can increase seizure risk?
-Dilutional hyponatremia
78
What kinds of renal dysfunction will ascites cause?
- Hepatorenal syndrome
- Over diuresis
- Sepsis
79
What is hepatorenal syndrome?
-Will cause many alterations in mental function, body function and will increase risk for seizures
80
In severe ascites, how much fluid accumulation can their be? What is a key consequence?
- 14-15 kg of fluid
| - Issues with digestions, discomfort
81
Nutritional treatment for ascites?
- Sodium/Fluid restriction
| - Note that many of these patients will be malnourished
82
Medical treatment for ascites?
- Use of diuretics
| - Paracentesis
83
What is paracentesis? What is the nutritional implication?
- 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
What are esophageal varices?
-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
Consequences of esophageal varices?
- Blood loss
- Elevation of ammonia
- Pain when eating
- Eating patters
86
2 surgical treatments of esophageal varices?
- Transjugular Intrahepatic Portal Systemic Shunt (TIPS)
| - Distal Splenorenal Shunt (DSRS)
87
Describe the TIPS surgical procedure
- 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
Describe the DSRS surgery
- 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
What may appear on the skin?
Spider Angioma
| -May be seen more in alcoholics, dilation of blood vessels
90
What is encephalopathy?
Elevated ammonia levels in the blood, will result in impaired mental status and abnormal neuromuscular function
91
Potential contributors to encephalopathy?
- Liver failure
- Diversion of the portal blood through the venous systemic circulation
- Bleeding from varices
- Sepsis
92
Pathogenesis of encephalopathy?
- 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
Symptoms of encephalopathy?
- Changes in mental status and personality
- Forgetfulness
- Neuromuscular changes
- Asterixis
- Coma
94
What is asterixis?
Uncontrollable flapping of hand s
95
What is used to stage encephalopathy?
West Haven Staging Scale
96
At what stages of encephalopathy may modifications to nutrition intervention be needed?
- 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
Medical treatment for hepatic encephalopathy?
- Lactulose
| - Antibiotics
98
Lactulose in HE?
- Stimulates the passage of ammonia from body tissues into the gut lumen
- Inhibits intestinal ammonia production
99
Antibiotics in HE?
Decrease concentration of colonic ammonia-producing bacteria
100
Nutritional intervention in HE?
- High protein provision of 1.2-1.5 g/kg/day
| - MUST use dry weight, caution w/ ascites
101
What does lower protein intake result in HE?
-Catabolism an further increases in ammonia production
102
In the rare case of a protein intolerant patient, what may be beneficial?
A vegetable protein diet
103
What are the 3 assessment classification schemes for liver disease?
- Child-Turcotte-Pugh Scoring System (CTP)
- Model for End-Stage Liver Disease (MELD)
- Glasgow Coma Scale (GCS)
104
What does CTP consider?
-Evaluates encephalopathy and ascites with bilirubin, albumin and PT
105
What is MELD initially used for? What else is it used for?
- 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
What does the MELD consider?
-Bilirubin
-PT
Creatinine
107
What is PT measured as in MELD?
international normalized ratio (INR)
108
What does the glasgow coma scale consider?
- Eye opening
- Verbal response
- Motor response
109
What are the 5 types of hepatitis?
- Hepatitis C
- Hepatitis D and E
- Hepatitis A
- Hepatitis B (or serum hepatitis)
- Fulminant Hepatitis
110
What is Hep A?
- Acute hepatitis
- Transmitted almost exclusively through the oral-fecal route
- Sources include contaminated drinking water, food and sewage
111
What is serum Hep or Hep B?
- Can be acute or chronic
- Transmitted via blood, blood-derived fluids, improperly sterilized medical instruments
- Complications include cirrhosis and hepatocellular malignancy
112
Tx for serum Hep or Hep B?
-Oral antivirals for life
113
What is Hep C?
- Exposure to blood or body fluids from infected persons
| - Associated w/ development of chronic liver disease, cirrhosis and need for liver transplant
114
What is Hep D and E?
- Acute infection
| - Uncommon, and required HBV to replicate
115
What is Fulminant Hepatitis (ALF)?
- Acute liver failure, rare
| - Characterized by the development of hepatic necrosis, coagulopathy and ecephalophathy
116
50% of ALP cases are due to what?
-Acetaminophen and other drug toxicities (especially when combines with alcohol)
117
Other causes of ALF?
- Virus infection
- Toxin
- Metabolic disorder
- Immune-mediated attack
118
Treatment for ALF?
Liver transplant
119
Nutritional implications ofr hepatitis?
- 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
Nutritional diagnosis in hepatitis?
- Inadequate oral food/beverage intake
- Inadequate protein and kcal intake
- Food-med interaction
- Impaired nutrient utlization
121
Energy with Hepatitis?
30-35 kcal/kg
122
Protein with Hepatitis?
1-1.2 g/kg/day
123
If hypoglycemia is present in hepatitis, nutritional intervention?
-Frequent meals
124
Other nutritional interventions for hepatitis?
- Adequate rest/fluid
- Avoid alcohol
- High energy and high protein diets if patient is anorexic
125
What is NAFLD?
- 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
What is fatty liver caused by?
- 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
What does NASH stand for? What is it?
-Non-alcoholic steatotic hepatitis (inflammation caused by fat accumulation in the liver)
128
What is cirrhosis?
-A pathological condition where fibrous connective tissue replace healthy tissue in the liver, likely due to inflammation or injury
129
Discuss the progression of NAFLD
Steatosis --> NASH --> Cirrhosis
130
What elicits steatosis? What does it result in?
- 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
What elicits NASH? What does it result in?
- Oxidative stress
| - DM nephropathy and proteinuria
132
What doe cirrhosis result in?
- Increases susceptibility to multiple injuries
- Progressive fibrosis
- Hepatic protein synthesis impaires
- Liver failure, hepatocellular carcinoma
133
Name 5 conditions associated with fatty liver
- Alcoholism
- Type II DM
- Metabolic Syndrome
- PN (overfeeding)
- Amiodarone (Heart md)
- Corticosteroids
134
Nutrition Intervention for NAFLD?
- Weight loss of 7-10% and PA
- Abstinence from alcohol
- Med diet
135
Which patients with NAFLD may benefit from vitamin E? how much? What else may benefit?
- 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
Alcohol abuse has a toxic effect on _____
all major organ systems
137
What is the hepatotoxic alcohol threshold?
40 g (4 drinks) and 20 g (2 rinks) for men and women respectively
138
What are the three liver disorders associated with ALD?
- Fatty liver (hepatic steatosis)
- Alcoholic hepatitis
- Cirrhosis
139
Consequences of ALD?
-Acetaldehyde toxicity, inflammation, metabolic competition, malnutrition, malabsorption
140
Explain metabolic competition and micronutrient deficiencies in ALD
-The liver will prioritize the detoxification of alcohol over the activation of micronutrients
141
Non-specific symptoms of ALD?
- Fatigue
- Weakness
- N/V
- Anorexia, Malaise
- Low grade fever
142
Liver disease specific symptoms of ALD?
- Jaundice
- Hepatomegaly
- Ascites
- Portal HTN bleeding
- HE
143
Minor alcohol withdrawal symptoms?
- Gi upset
- Anorexia
- Headache
- Diaphoresis
144
Complications of alcohol withdrawal?
- Micronutrient deficiencies
- Alcoholic halluconosis
- Delirium tremens
- Seizures
145
What does the metabolism of ethanol and end products of acetaldehyde increase the need for?
- Folate, thiamin and pyridoxine
- Selenium
- Zinc
- Magnesium
--> Incr. risk of deficiencies for these nutrients
146
Tx of alcohol withdrawal?
- Anti-anxiety and anti-seizure meds
- Replacement of vitamins and electrolytes
- Caution with RF
147
Key nutritional concerns of ALD?
- Anorexia and dysgeusia
- Intestinal maldigestion and malabsorption
- Hyper metabolism
- Decreased protein synthesis and increased autophagu
148
What are the implications of the nutritional concerns in ALD?
- Malnutrition
- Vitamin and mineral deficiencies
- Sarcopenia
149
Other nutritional interventions of ALD
- 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
What is the most common cause of cirrhosis?
- Alcoholic liver diseases and hepatitis (95%)
| - Hep C most common (26% of causes)
151
What are the other 5% causes of cirrhosis?
- Autoimmune
- Biliary causes or cholangitis
- Hemochromatosis
- Wilson's disease
- Gene mutations
152
What is Wilson's disease?
Rare genetic disorder which causes the improper metabolism of copper
153
Which gene mutation will cause alterations in lungs and kidney?
Alpha-1 antitrypsin deficiency
154
General symptoms of cirrhosis?
- N/V
- Weakness, fatigue
- Poor appetite
- Malaise
- Vit and min deficiencies
155
Liver-specific symptoms of cirrhosis?
- jaundice
- dark urine
- light stools
- steatorrhea
- abdo pain, bloating
156
Clinical manifestations of cirrhosis?
- Portal HTN
- HE
- Ascites
- Hepatorenal sundrome
- Varices
157
What are the the two clinically meaningful states in cirrhosis?
- Compensated
| - Decompensated
158
Compensated state of cirrhosis?
- Cirrhosis without ascites or encephalopathy
| - May start to show beginnings of variceal hemorrhage, ascites, encephalopathy, jandice
159
Decompensated state of cirrhosis?
- 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
What should nutritional assessment of cirrhosis include?
- Attention to physical assessment to identify sarcopenia
- MAC, MAMC, handgrip, 6 min walk
- Consider complications including ascites, varices and hepatorenal syndrome
161
Examples of nutrition implications in cirrhosis?
- Increase EE
- Malnutrition, sarcopenia
- Micronutrient deficiencies
- Early satiety from ascites
- Impaired nutrient digestion/absorption
- Hypoglycemia
162
Theme of nutritional intervention in cirrhosis?
Adequate energy and protein to replenish malnourished and sarcopenic cirrhotic patients
- Frequent meals
- Replace vitamins and minerals
163
Energy in cirrhosis?
30-40 kcal/kg
164
Protein for non-malnourished patients w/ compensated cirrhosis?
1.2 g/kg/day
165
Protein for malnourished and/or sarcopenic cirrhosis patients?
1.5 g/kg/day
166
Energy for obese cirrhosis patients?
25 kcal/kg/day of IBW
167
Protein for obese cirrhosis patients?
2.0-2.5 g/kg/day of IBW
168
Diet for patients with esophageal varices?
Soft diet
169
What are two diuretics which may have nutritional issue?
- Furosemide
| - Spironolactone
170
Furosemide?
- Incr. excretion of Na, K, Mg and Ca
- Diet should be high in K, Mg and Ca
- Avoid natural licorices
171
Spironolactone?
- Increases reabsorption of K
- Avoid salt substitute
- Caution w/ K supplements
- Avoid excessive K in diet
172
Other nutritional considerations in cirrhosis?
- Consider pancreatic enzymes
- Consider red. cooper if Wilson's
- consider red. iron if hemochromatosis
173
When may nutritional support be indicated?
- HE, based on level of consciousness
| - Acute Liver Failure and severe ASH patients if they cannot meet adequate oral intake
174
What should be prioritized to achieve adequate protein and E intake?
ONS
175
When may patient with mild HE be fed orally?
When their swallowing and cough reflexes are intatc
176
How should acute F and severe ASH patients be fed with NS/
EN via NG or NJ tube
177
(T/F) Esophageal varices are an absolute contraindication to NG tubes
G
178
What is PEG placement associated with?
-Higher risk of complications, due to ascites or varices and should only be used in exceptional cases
179
When should PN be commenced immediately?
In mod or sever malnourished patents who cannot be nourished sufficiently by oral/EN route
180
When should PN be considered?
- unprotected airways
- HE with compromised cough/swallow reflexes
- EN contraindicated/impracticable
181
When is liver transplant considered?
When the effects of liver disease have a higher potential to cause mortality than the complications of the liver transplant
-Considers MELD score
182
Nutritional implications of liver transplant?
-Malnutrition, ascites
-Need for early NS after Sx
-Food-borne illness
(due to compromised immune system)
183
Nutriton intervention in liver transplant?
- Oral or En preferred
| - ERAS protocol
184
Energy in liver transplant?
30-35 kcal/kg/day
185
Protein intake in liver transplant?
1.2-1.5 g/kg/day
186
Obese kcal and pro requirements?
- 25 kcal/kg/day IBW
| - 2.0-2.5 g/kg/day IBW
