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LD Flashcards

1
Q

Causes of LIVER DISEASE

A

LIVER DISEASE CAUSES:
* Viral hepatitits
* Alcohol
* Genetics
* Fat build up
* Excess weight
* Immune system condition
* Herbal supplements

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2
Q

Stages of LIVER DISEASE

A
  • Hepatitis: inflammation of the liver (no scarring)
  • Steatosis :fatty deposits in the liver (fatty liver)
  • Fibrosis: increased stiffness and scarring of the liver (impairment of function begins)
  • Cirrhosis: IRREVERSIBLE SCARRING of the liver
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3
Q

What are the main function (s) of the liver?

A

Main LIVER functions:
* Key for metabolism of CHOs, fats & protein. Glucose, fatty acids, and amino acids are absorbed into the bloodstream and transported to the liver through the portal vein circulation system.
* CHOs: gluconeogenesis, glycogenesis, glycogenolysis.
* Fats: fatty acid synthesis, triglyceride synthesis, conversion of TAGs to VLDLs, cholesterol synthesis.
* Protein:
* Regulation of CHOs, fats (plasma NEFAs) & protein in the blood.
* Bile production
* Vitamins storage: A, B12, D, E, K
* Mineral storage: iron, copper.
* combating infections
* blood detoxification/filtration
* drug metabolism

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4
Q

In 2023 how many people were admitted to hospital due to LIVER DISEASE in ENGLAND?

A

In 2023 ~86000 people were admitted to hospital due to LIVER DISEASE in England

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5
Q

Hospital admissions due to ALCOHOL RELATED LIVER DISEASE in England have increased by ? since 2013

A

Hospital admissions due to ALCOHOL RELATED LIVER DISEASE in England have increased by 68% since 2013

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6
Q

What are 9 out of 10 cases of LIVER DISEASE related to?

A

9 out of 10 cases of LIVER DISEASE are related to:
* Alcohol
* Excess weight
* Viral hepatitis

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7
Q

What is “Non Alchoholic Fatty Liver Disease” (NALFD) now called?

A

“Non Alcoholic Fatty Liver Disease” is now known as “Metabolic Dysfunction Associated Steatotic Liver Disease” (MASLD)

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8
Q

What is a COMPENSATED LIVER?

A

COMPENSATED LIVER:
* No symptoms
* Liver is CIRRHOTIC but there is NO evidence of LIVER FAILURE

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9
Q

What is a DECOMPENSATED LIVER?

A

DECOMPENSATED LIVER:
* Liver is CIRRHOTIC
* Symptoms of liver disease are present
* Examples of symptoms: ascites, jaundice, varices, portal HTN, hepatic encephalopathy

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10
Q

How can LIVER DECOMPENSATION occur?

A

LIVER DECOMPENSATION can occur via:
* Disease progression
* Additional stress due to drugs, infections, alcohol, surgery

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11
Q

Can other organs be compensated or decompensated?

A

Yes, other organs can be compensated or decompensated.

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12
Q

Is it possible for the liver to shift between compensated and decompensated states?

A

Yes, it is possible for the liver to shift between compensated and decompensated states.

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13
Q

Symptoms associated with LIVER DISEASE

A

Symptoms associated with LIVER DISEASE
* Jaundice
* Varices
* Portal HTN
* Impaired synthetic function: coagulopathy, low albumin
* Ascites
* Hepatic Encephalopathy
* Steatorrhoea
* Belly pain and swelling.
* Swelling in the legs and ankles.
* Itchy skin.
* Dark urine.
* Pale stool.
* Constant tiredness.
* Nausea or vomiting.
* Loss of appetite.
* Bruising easily.

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14
Q

Name conditions which are associated with LIVER DISEASE

A

Conditions associated with LIVER DISEASE:
* Spontaneous Bacterial Peritonitis
* Cholangitis
* Hepatorenal syndrome
* Hepatic hydrothorac
* Pancreatitis
* Osteoporosi
* Wernicke’s encephalopathy: thiamine deficiency
* Korsakoff’s synfrome: thiamine deficiency

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15
Q

What can Wernicke’s encephalopathy & Korsakoff’s syndrome be caused by?

A

Wernicke’s encephalopathy & Korsakoff’s syndrome can be caused by:
* Thiamine deficiency
* Blood vessel damage

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16
Q

What are the key medications used with LIVER disease?

A

Key medications used with LIVER DISEASE
* Diuretics
* Laxatives
* Beta blockers
* Antibiotics
* Steroids
* Antiemetics
* PERT, treatment for itching, B vitamins, Vit D, Calcium, HAS, Antiviral

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17
Q

Why is maintainance of nutritional status important in LIVER DISEASE?

A

Adequate nourishment in LIVER disease is important because it can increase survival. A study found that in patients with cirrhosis, there was greater survival amongst those that were adequately nourished, this was statisitically significant (p=0.0005)

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18
Q

? synthesis is impaired in CIRRHOTIC patients

A

Glycogen synthesis is impaired in CIRRHOTIC patients

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19
Q

Is malnutrition more prevalent in compensated or decompensated cirrhosis?

A

Malnutrition is more prevalent in decompensated (60%) cirrhosis than compensated cirrhosis (40%)

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20
Q

What is paracentesis?

A

Paracentesis is the drainage of fluid from the abdomen (ascites) via a needle. The drainage occurs for up to 6 hours.

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21
Q

Nutrition considerations of Paracentesis

A

Nutrition considerations of Paracentesis
* Protein losses during drains: 13g pro/l of ascites =** net pro loss of 6g/ L of ascites as some is replaced with HAS**
* Patients receive ~7g albumin/ L of ascites
* Adjust patient’s weight based on drainage
* Consider the effect of ascites on appetite: reduced appetite, abdo pain/discomfort, nausea,

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22
Q

ENERGY Requirements LIVER DISEASE (PENG)

A

ENERGY Requirements LIVER DISEASE (PENG)
* BMI: <18.5: 25-30kcal/kg +PAL. (Add 400-1000kcal for repletion, but initiation of repletion depends on the phase the patient is in)
* NAFLD (MASLD) steatosis BMI >30: 18kcal/kg
* BMI >30: Mifflin St Jeor + PAL
* Liver cirrhosis all causes (BMI18.5-29.9): 22kcal/kg+ PAL (19-27)
* ARLD with cirrhosis (BMI18.5-29.9): 28kcal/kg+ PAL (27-29)
* ARLD non abstinent steatosis/fibrosis (BMI18.5-29.9):27kcal/kg+ PAL (26-27)
* Viral ACUTE hepatitis (BMI18.5-29.9): 27kcal/kg+PAL (26-27)
* Viral CHRONIC hepatitis (BMI18.5-29.9): 21kcal/kg+PAL (19-22)
* Hepatocellular carcinoma (BMI18.5-29.9): 23kcal/kg+PAL (22-25)
* Other liver conditions (BMI18.5-29.9): 20-25 kcal/kg + PAL

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23
Q

ENERGY REQUIREMENTS: LIVER DISEASE BMI: <18.5

A

ENERGY REQUIREMENTS: LIVER DISEASE BMI: <18.5
* : 25-30kcal/kg +PAL. (Add 400-1000kcal for repletion)

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24
Q

ENERGY REQUIREMENTS:NAFLD (MASLD) steatosis BMI >30

A

ENERGY REQUIREMENTS:NAFLD (MASLD) steatosis BMI >30
* 18kcal/kg

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25
Q

ENERGY REQUIREMENTS: LIVER DISEASE BMI >30

A

ENERGY REQUIREMENTS: LIVER DISEASE BMI >30
* Mifflin St Jeor + PAL

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26
Q

ENERGY REQUIREMENTS:Liver cirrhosis all causes
(BMI 18.5-29.9)

A

ENERGY REQUIREMENTS:Liver cirrhosis all causes (BMI18.5-29.9):
* 22kcal/kg+ PAL (19-27)

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27
Q

ENERGY REQUIREMENTS: ARLD with cirrhosis
(BMI 18.5-29.9)

A

ENERGY REQUIREMENTS: ARLD with cirrhosis (BMI18.5-29.9):
* 28kcal/kg+ PAL (27-29)

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28
Q

ENERGY REQUIREMENTS:ARLD non abstinent steatosis/fibrosis
(BMI18.5-29.9)

A

ENERGY REQUIREMENTS:ARLD non abstinent steatosis/fibrosis (BMI18.5-29.9):
* 27kcal/kg+ PAL (26-27)

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29
Q

ENERGY REQUIREMENTS: Viral ACUTE hepatitis
(BMI18.5-29.9)

A

ENERGY REQUIREMENTS: Viral ACUTE hepatitis (BMI18.5-29.9):
* 27kcal/kg+PAL (26-27)

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30
Q

ENERGY REQUIREMENTS: Viral CHRONIC hepatitis (BMI18.5-29.9)

A

ENERGY REQUIREMENTS: Viral CHRONIC hepatitis (BMI18.5-29.9):
* 21kcal/kg+PAL (19-22)

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31
Q

ENERGY REQUIREMENTS: Hepatocellular carcinoma (BMI18.5-29.9)

A

ENERGY REQUIREMENTS: Hepatocellular carcinoma (BMI18.5-29.9):
* 23kcal/kg+PAL (22-25)

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32
Q

ENERGY REQUIREMENTS: Other liver conditions
(BMI18.5-29.9)

A

ENERGY REQUIREMENTS: Other liver conditions (BMI18.5-29.9):
* 20-25 kcal/kg + PAL

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33
Q

What is <21.5kcal/day associated with in severe alcoholic steatohepatitis?

A

In severe alcoholic steatohepatitis <21.5kcal/day is associated with worst outcomes (Moreno et al., 2016)

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34
Q

Why should caution be used when using MIFFLIN?

A

Caution should be used when using MIFFLIN because:
* illneses were not considered during its creation. The population it is based on are healthy subjects
* population were primarily caucasian
* doesn’t account for fat/muscle composition
* adjusted body weight recommended to avoid overestimation of requirements however caution to be used when individual is acutely unwell

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35
Q

What is the advice for liver disease prevention?

A

Advice for liver disease prevention:
* Healthy balanced diet
* Healthy weight
* Good diabetes control
* Physical activity
* Alcohol within government guidelines

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36
Q

ESPEN guidance for: Metabolic dysfunction–associated steatotic liver disease (MASLD) without cirrhosis

A

ESPEN guidance for: Metabolic dysfunction–associated steatotic liver disease (MASLD) without cirrhosis:
* Exercise and diet can treat MASLD - diet + exercise is the most effective approach
* Obese/overweight: Weight loss, 7-10% target
* Obese/overwit: hypoclaoric diet irrespective of macronutrient content
* No single diet better than others: should be individualised for each person
* Normal wt: increased physical activity to improve insulin resistance & steatosis (not based on evidence implied from overwt/obese)
* Normal wt: reduction in fructose rich drinks (no evidence cited)
* **Mediterranean diet **without alcohol: improve steatosis & insulin sensitivity
* Identify and treat co-morbidities – coeliac, diabetes as these contribute to poor liver function
* Vitamin E supplementation: NASH and probiotics + prebiotics may be helpful: LFT improvement
* Not enough evidence for omega-3 supplementation

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37
Q

Study cited by ESPEN PROBIOTIC use for MASLD without cirrhosis:

A

Study cited by ESPEN PROBIOTIC use for MASLD without cirrhosis:
* An Iranian double blind RCT of 72 patients aged 23-63.
* Compared the use of yoghurt enriched with lactoacidophilus La 5 & Bifidobacterium Lactis B12 with a conventional yoghurt.
* The intervention group had statistically significant decreases in liver function markers, total cholesterol & LDL. An increased intake of protein was also reported.
* The risk of bias in this trial was reduced due to the double blinding and use of same packaging and branding of the yoghurts given to participants.
* However, the diet histories of participants were only for 3 days at the beginning and end of the study provided as a 24H recall which makes it vulnerable to error.
* Also, by only analysing the diet on those 6 days out of 8 weeks, it is not clear whether the observed changes were due to intake of the yoghurt.
* Small study

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38
Q

Consequences of malnutrition

A

Consequences of malnutrition
* Increased mortality
* Infections
* More days in ICU
* More days on a ventilator
* More days in hospital
* Delayed wound healing
* Encephalopathy
* Variceal bleeding
* Ascites
* Worse quality of life
* Osteoporosis

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39
Q

Biochemistry associated with liver disease

A

Biochemistry associated with liver disease
* Alanine aminotransferase (ALT) ↑
* Aspartate aminotransferase (AST) ↑
* Alkaline phosphatase (ALP) ↑
* y-Glutamyltransferase (GGT) ↑
* Bilirubin ↑
* Albumin ↓
* Blood clotting tests: Prothrombin time (PT) ↑, International normalised ratio (INR) ↑
* CRP ↑

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40
Q

What are the:
UKELD- United Kingdom End Stage Liver Disease & MELD- The Model of End Stage Liver Disease?

A

UKELD- United Kingdom End Stage Liver Disease & MELD- The Model of End Stage Liver Disease:
* Scoring system used to predict mortality among patients waiting for a liver transplant
* A UKELD score of 49 or more is required for liver transplant unless there is another indication, such as hepatocellular carcinoma.
* Score of 49 or more: possible benefits of a transplant are estimated to be greater than the possible risks.

41
Q

What is TIPS (Transjugular intrahepatic portosystemic shunt)?

A

TIPS (Transjugular intrahepatic portosystemic shunt):
* Placement of a stent in the blood vessels which feed and drain the liver.
* Performed if there is a block of flow of blood through the liver, leading to high pressure.
* The high blood pressure can lead to varices.
* Risk of worsening hepatic encephalopathy

42
Q

What is a liver resection?

A

Liver resection:
* Treatment for liver cancer.
* Removal of a section of the liver where a tumour is growing.
* The part of the liver removed will grow back after a few weeks.
Nutrition Considerations:
Good nutrition post surgery
Low phosphate as liver regenerates

43
Q

Nutrition considerations for a liver resection

A

Nutrition Considerations for a liver resection:
* Good nutrition post surgery
* Low phosphate as liver regenerates ???

44
Q

Key Medications used in Liver Disease

A

Key Medications used in Liver Disease:
* Diuretics: Spironolactone (K sparing), Furosemide (K/Mg wasting)
* Laxatives: Lactulose - reduces ammonia production + absorption, Senna or Movicol
* Beta blockers: Propanolol or Carvedilol
* Antibiotics: Ciprofloxacin, Tazocin, Rifaximin - treats HE, Rifampicin - to treat itch
* Steroids: Prednisolone, likely to be on bone protection (Vit D/Ca)
* Antiemetics: Cyclizine, Metoclopramide - prokinetic, Ondansetron
* Other: Cholesytramine - to treat itch, Pancreatic Enzyme Replacement Therapy (PERT) - Creon, Pancrex, Nutrizym, Thiamine
, Vitamin B compound strong, Ursodeoxycholic acid (PBC), Vitamin D +/- calcium, Human Albumin Solution (HAS)
Penicillamine / Trientine - Wilson’s Disease
Antiviral e.g. tenofovir (hep B)

45
Q

Which factors contribute to malnutrition in Liver Disease?

A

Factors that contribute to malnutrition in Liver Disease:
* Decreased energy intake: ascites, salt restriction, micronutrients deficiency, loss of appetite despite increased ghrelin, portal HTN
* Malabsorption & nutritional losses: Impaired bile acid production, PEI, SIBO, Paracentesis protein losses, medication
* Altered protein, fat and CHO metabolism: Decreased BCAAs /Increases AAAs, Insulin resistance, Increased protein breakdown, decreased protein sythesis, inreased ketogenesis, decreased glucogenolysis> accelerated state of starvation> increased gluconeogenesis

46
Q

Pathogensis of malnutrition in liver cirrhosis

A

Pathogensis of malnutrition in liver cirrhosis:
Alcohol/Fasting periods lead to:
* gut microbiome dysbiosis
* altered nutrient metabolism
* hypermetabolism
* malabsorption
* hormones
* inflammation

47
Q

Cirrhotic livers have ? glycogen synthesis

A

Cirrhotic livers have impaired glycogen synthesis

48
Q

Decompensated livers ? to make enough glycogen. ~ ?h worth

A

Decompensated livers struggle to make enough glycogen. ~3h worth

49
Q

What is frailty?

A

Frailty:
* A biological syndrome of decreased reserve and resistance to stressors, resulting from cumulative decline across multiple physiological systems, and causing vulnerability to adverse outcomes”

50
Q

What is Sarcopenia?

A

Sarcopenia:
Low muscle mass & low strength/low physical performance

51
Q

Components of frailty

A

Components of frailty:
* Sarcopenia
* Malnutrition
* Functional decline
* Deconditioned/ poor fitness
* Impaired cognition

52
Q

What is important to remember about muscle mass and BMI?

A

It is important to remember that low muscle mass is possible at any BMI

53
Q

What is Cachexia?

A

Cachexia:
Cachexia is a complex syndrome associated with an underlying illness, causing ongoing weight loss, muscle loss that is not entirely reversed with nutritional supplementation.
* Characterized by:
- loss of skeletal muscle
- loss of fat
- loss of muscle strenght
- fatigue
- anorexia
- low fat free mass index
- abnormal biochemistry

54
Q

Diagnosis of Cachexia

A

Diagnosis of Cachexia (3 out of 5):
- Wt loss of at least 5% in 12m or less
- Decreased muscle strength
- Fatigue
- Anorexia
- Low fat free mass index
- Abnormal biochemistry: Increased inflammatory markers (CRP, IL-6), Anaemia (Hb<12g/dL), Low serum albumin(<3.2g/dL)

55
Q

Considerations for ANTHROPOMETRIC measures in liver disease

A

Considerations for ANTHROPOMETRIC measures in liver disease:
* BMI & weight may be unreliable due to ascites
* Upper arm anthropometry: TSF, MUAC, MAC might be useful
* MUAC tends not to be affected by oedema

56
Q

A prospective cohort study of patients with decompensated cirrhosis

A

A prospective cohort study of patients with decompensated cirrhosis found:
* Mid arm circumference may be an indicator of nutritional status
* A low MAC predicted mortality independently

57
Q

Estimating dry weight

A

Estimating dry weight:
* Dry weight= wet weight- estimated weight of ascites or oedema
* Advised to consider patient’s weight history prior to ascites/oedema
* Compare wt before and after drainage but don’t rely on wt post-drainage (fluid may still be present)
* Estimation of dry wt: use Mendenhall (1992) or EASL

58
Q

Mendenhall (1992)/ Madden & Wicks 1994 (PENG) Ascites & Oedema estimation

A

Mendenhall (1992)/ Madden & Wicks 1994 (PENG) Ascites & Oedema estimation:
Ascites
* Mild: 2.2kg
* Moderate: 6kg
* Severe: 14kg

Oedema
* Mild: 1kg
* Moderate: 5kg
* Severe: 10kg

Limitations:
* Unable to access paper to judge if based on evidence
* Patients tend to have more fluid than estimated.
* From 1992: how relevant to current population
* Based on visual opinion of fluid retention, subjective
* There will be great variability between patients. Very unlikely all will have same amount of fluid.

59
Q

EASL (2019) Ascites & Oedema estimation

A

EASL (2019) Ascites & Oedema estimation
Ascites
* Mild: 5%
* Moderate: 10%
* Severe: 15%

Oedema
* 5%

Advantages:
* In comparison to Mendenhall/ Madden & Wicks 1994 (PENG) this takes into account the patient’s own body weight and is more individualised as it is a percentage instead of just a value

Limitations:
* Not based on evidence: cited sources are just others who use the values
* Not validated
* How can a general percentage of fluid be assumed by grading of oedema/ascites?
* Not based on evidence: cited sources are just others who use the values

60
Q

LIVER disease dry weight estimation my choices

A

LIVER disease dry weight estimation my choices:
* Wt history, pre & post paracentesis weights, scans preferred to estimate dry wt
* Otherwise: EASL instead of Mendenhall (PENG, 1991)
* Assumed that Mendenhall is based on a study however, unable to locate.
* Mendenhall is just based on values, less individualised than EASL where percentages allow for different values based on the patient’s dry weight, more individual
* However: EASL’s values are not validated, nor are they based on evidence they are based on what other clinicians do. How likely is it that the values they suggest are reflective of different grades of ascites and of oedema?

61
Q

Biochemistry markers for Liver Disease

A

Biochemistry markers for Liver Disease:
* Sodium
* Potassium
* Magnesium
* Phosphate
* Adjusted Calcium
* Creatinine, urea and eGFR/AKI stage
* Liver function tests – bilirubin, alkaline phosphatase (ALP), alanine transaminase (ALT), albumin
* (Ammonia): doesn’t tell much likely to be high
* Blood glucose
* HbA1c
* CRP

62
Q

Clinical Considerations for LD

A

Clinical Considerations for LD:
* Aetiology of liver disease
* Stage of liver disease
* Decompensated or compensated?
* Refeeding risk
* Admission reason
* Current medical treatment
* Past medical history
* Nausea and vomiting
* Stool symptoms - malabsorption?

63
Q

Stool symptoms to consider

A

Stool symptoms to consider:
* Frequency
* Consistency
* Colour
* Signs of malabsorption: smell, oily, pale, orange, yellow, floaty, undigested food

Think about:
* What is normal for patient (before illness)
* Medication, e.g. laxatives, antibiotics, iron supplement, opioids
* Risk factors for malabsorption, e.g. alcohol related liver disease and pancreatic enzyme insufficiency, PBC/PSC
* Any dietary adjustments needed?

64
Q

Dietary considerations of LD

A

Dietary considerations of LD:
* Refeeding risk?
* CHO & Pro: Frequency (most important) & QTY
* Fluid
* Fat
* Food groups
* Alcohol
* Salt
* Changes to appetite?
* Eating pattern?
* Overall adequacy
* Restrictions?
* Allergies/intolerances
* Nutritional requirements vs intake
* Eating pattern (>3H with no intake and bedtime snack?)
* Contigency plans when not feeling well?

65
Q

Vitamin & mineral levels: Liver Disease

A

Vitamin & mineral levels: Liver Disease
* Risk factors for deficiencies, e.g. cause of liver disease, co-morbidities & treatment – influence on micronutrient absorption, metabolism or requirements.
* Identify deficiencies with available blood test results
* Look for overt signs of deficiency such as fatigue, impairment in wound healing
* Check for potential deficient intake
* Liaise with medical team for supplementation as sometimes this will be due to a medical cause i.e. variceal bleeding so this will be medically corrected
Common deficiencies:
B vitamins
Fat soluble vitamins, including vitamin D
Iron deficiency anaemia
Zinc, selenium, copper

66
Q

Protein Energy Malnutrition exists in what percentage of patients with decompensated cirrhosis?

A

Protein Energy Malnutrition exists in 80-100% of patients with decompensated cirrhosis (PENG)

67
Q

What are the main reasons for malnutrition in liver disease?

A

Main reasons for malnutrition in liver disease:
* decreased dietary intake
* poor quality diet
* impaired postprandial glucose storage
* increased energy expenditure
* altered substrate demands
* maldigestion and malabsorption

68
Q

How does altered metabolism cause malnutrition in liver disease?

A

How altered metabolism causes malnutrition in liver disease:
* Glycogen stores are small in comparison to healthy subjects
* Gluconeogenesis from body protein provides glucose for short-term energy needs: leads to muscle wasting

69
Q

Novel Approach for Ascites estimation

A

Novel approach for ascites estimation: abdominal girth may be a novel approach to the estimation of dry weight in patients with ascites.
1. Lamarti & Hickson conducted a study in 24 white british, liver disease patients with ascites.
2. A statistically significant relationship was found between the weight of the ascites and pre-paracentesis girth,
3. an equation was formulated based on this.
4. This method is not yet validated and will need to be assessed in a higher number of patients & with other ethnicities
5. however it was found that the values listed in PENG may underestimate the amount of ascites fluid in patients.
6. A validated equation would allow for greater individuality.

70
Q

Why is a 50g late evening snack beneficial in liver disease?

A

50g CHO late evening snack is beneficial in liver disease because:
* increases CHO oxidation
* decreases lipid & protein oxidation rate
* improves N balance and reduces fasting periods overnight

71
Q

Eating Patterns: Liver Disease

A

Eating Patterns: Liver Disease
* 50g CHO bedtime snack
* “Cirrhotic Eating Pattern”

72
Q

Patients with ? enter the starved state quicker than healthy controls.

A

Patients with cirrhosis enter the starved state quicker than healthy controls.

73
Q

Examples of 50g CHO snacks

A

Examples of 50g CHO snacks:
* 300ml milk & 3 plain biscuits
* ONS volume equivalent to 50g CHO
* 5 plain biscuits
* 2 thick slices toast w jam

74
Q

The “Cirrhotic” Eating Pattern

A

The “Cirrhotic” Eating Pattern
* Helps to reduce accelerated starvation due reduced glycogen stores
* At least 3-4 portions of protein per day
* Protein source with each meal
* Protein included with as many snacks as possible
* Protein rich drinks
* Reduces fasting gluconeogenesis & muscle catabolism

75
Q

50g bedtime CHO snack

A

50g bedtime CHO snack
* reduces amount of gluconeogenesis and muscle breakdown at night due to reduced glycogen stores
* increases CHO oxidation
* decreases lipid & protein oxidation rate
* improves N balance and reduces fasting periods overnight
* Patients with early satiety/poor appetite may find carbohydrate dense options more manageable
* Starchy is better but low GI is best
* Ideally include a good source of protein too
* Mindful of diabetes – more starchy snacks, monitor blood glucose: LOW GI foods

76
Q

Evidence for “Cirrhotic” Eating Pattern (Owen et al. 1983)

A

Evidence for “Cirrhotic” Eating Pattern (Owen et al., 1983)
* Various studies indicate that the cirrhotic eating pattern is beneficial
* A study investigating energy metabolism in patients with alcoholic cirrhosis using indirect calorimetry and tracer analysis found that:
* Despite normal basal metabolic rates after an overnight fast, the fuels oxidized by cirrhotic patients resembled those of healthy individuals after 36-72 hours of starvation,
* There was a higher reliance on fat and lower use of carbohydrates.
* These findings suggest that patients with alcoholic cirrhosis enter a starvation-like catabolic state more rapidly, potentially contributing to cachexia.

77
Q

Evidence for 50g CHO snack (Tsien et al., 2012)

A

Evidence for 50g CHO snack (Tsien et al., 2012)
* Systematic review to evaluate the efficacy of a late evening snack (LES) to improve substrate utilization, nutritional indices (including increase in skeletal muscle mass), and clinical outcomes in cirrhosis.
Findings:
* LES: the change in substrate utilization from glucose to fat is delayed
* Long-term LES = increase in lean mass with >50g CHO
* Can be food or ONS
* LES may be valuable in early compensated cirrhosis to preserve existing skeletal muscle mass.

78
Q

Cirrhosis is a state of ? resistance

A

Cirrhosis is a state of anabolic resistance

79
Q

50g bedtime CHO snack pros and cons (Tsien et al., 2012)

A

50g bedtime CHO snack pros and cons (Tsien et al., 2012)
Pros
* Cheap
* Easy
* Increases glucose oxidation and reduces fat & protein oxidation

Cons
* Higher amounts may be needed to have a difference on skeletal mass
* May exacerbate acid reflux
* May cause sleep disturbances
* May worsen glucose intolerance
* Poor compliance as outpatients

80
Q

We know that when someone has liver cirrhosis, not eating from evening meal until breakfast is like someone with a healthy liver not eating for ?-? days!

A

We know that when someone has liver cirrhosis, not eating from evening meal until breakfast is like someone with a healthy liver not eating for 2-3 days!

81
Q

Advice for malnourished

A

Advice for malnourished:
* High energy food and drink
* Little and often
* Add extra to the small portions managed
* Nourishing drinks
* High protein?
* Food fortification?

82
Q

Why are Gastrostomies contrainindicated in liver disease?

A

Gastrostomies are contrainindicated in liver disease because of ascites

83
Q

Nutrition support for LD

A

Nutrition support for LD
* Food
* Oral nutritional supplements
* Nasogastric feeding
* Nasojejunal feeding
* Gastrostomies are contraindicated
* Parenteral nutrition

84
Q

Nutritional intervention: Liver disease without malnutrition or obesity (Community/Non specific LD)

A

Nutritional intervention: Liver disease without malnutrition or obesity (Community/Non specific LD)

  • Individually tailored – comorbidities, risk of malnutrition, patient-preferences & desires

Cirrhosis
* Balanced diet with regular meals
* Good & frequent sources of protein
* Physical activity
* ?Add in bedtime 50g CHO snack +/- snacks between meals only if needed
* Achieve a cirrhotic eating pattern with healthy snacks – yogurt, fruit, whole nuts
* Prevention of malnutrition, sarcopenia and frailty

Fibrosis & Steatosis
* Remove the cause of liver damage if diet-related
* Alcohol abstinence
* Healthy balanced diet
* Good diabetes control

85
Q

What can rapid weight loss in obese patients with compensated cirrhosis cause?

A

Rapid weight loss in obese patients with compensated cirrhosis can cause the liver to decompensate

86
Q

What are branched chain amino acids?

A

Branched chain amino acids: essential nutrients that help support muscle metabolism and are important for building muscle tissue protein.

87
Q

Formulas for NS in LD

A

Formulas for NS in LD
* High protein
* High energy
* Low volume (concentrated)
* Patient preference and tolerance
* Reduced fat
* Medium chain triglycerides
* Feed for improved tolerance

88
Q

Liver disease with obesity

A

Liver disease with obesity

89
Q

What is hepatic encephalopathy?

A

Hepatic encephalopathy: a condition that occurs when the liver is too diseased or damaged to properly process ammonia, leading to a buildup of ammonia in blood that travels to the brain

90
Q

Why was protein previously restricted in hepatic encephalopathy?

A

Protein previously restricted in hepatic encephalopathy because the condition is caused by build of ammonia that travels to the brain & ammonia is produced by dietary proteins

91
Q

Hepatic encephalopathy & diet

A

Hepatic encephalopathy & diet
* Do not protein restrict
* Cordoba et al (2004) - no difference in outcome for hepatic encephalopathy for patients on low protein and normal protein diets. Low protein diet showed greater catabolism and muscle loss
* Skeletal muscles contribute to ammonia metabolism … if a patient has muscle wasting, the skeletal muscles have less capacity to metabolise ammonia, worsening HE
* Meet energy and protein requirements to reduce catabolism
* Continuous protein to keep ammonia levels steady
* Patients with severe HE may be protein intolerant
* Severe HE & high ammonia, not resolving: may protein restrict to a minimum of 1g/kg for a short period and monitor HE.
No improvements after a short period (1-2 weeks): protein restriction would be lifted.
Improvement: protein would be reintroduced gradually to tolerance.
* BCAAs could be an option for patients with protein intolerance and HE but this is not yet available in the UK,

92
Q

Dietary management for ascites

A

For patients with ascites:
* Restrict to ~5 g (~80 mmol sodium) per day
* Individual assessment and support
* Avoid adding salt at the table
* Reduce salt in cooking, e.g. lower salt stock, use herbs, garlic and lemon to add flavour.
* Avoid high salt foods
* Avoid salt alternatives, e.g. LoSalt, PanSalt, Solo.
* Ensure the restriction is not excessive
* Food label education

93
Q

Fat restriction LD

A

Fat restriction LD
* For symptomatic control
* More likely to be required in biliary conditions
* Not appropriate for treating Pancreatic Enzyme Insufficiency (PEI)

94
Q

Diabetes management LD

A

Diabetes management LD
* Monitor blood glucose. Good control is important. Perfect control may not be possible.
* HbA1c may not be an accurate measure of glycaemic control (neither accurate nor reliable in patients with cirrhosis due to the various kinds of anemia common in liver disease)
* Complex carbohydrates, wholegrain if appropriate
* Low GI foods
* Small carbohydrate snacks between meals, with fat and protein
* If supplements are needed consider their effect on blood glucose
* Collaborate with diabetes specialists. Diabetes medication may need to be adjusted to enable a cirrhotic eating pattern

95
Q

Why might HbA1c be unsuitable for monitoring blood glucose in diabetic cirrhotic patients?
(Sehrawar, 2018)

A

HbA1c is neither accurate nor reliable in patients with cirrhosis due to the various kinds of anemia common in liver disease (Sehrawat, 2018)

96
Q

Liver Disease nutrition before transplant

A

Liver Disease nutrition before transplant
* Good nutrition support to optimise for major surgery
* Treat malnutrition
* Prevent/minimise decline in nutritional status whilst waiting
* For some patients, controlled weight loss may be required to reduce the risk of the surgery
* Gradual weight loss
* Monitoring for malnutrition and sarcopenia

97
Q

Liver Disease nutrition after transplant

A

Liver Disease nutrition after transplant
* Some patients are tube fed post-transplant.
* Patients are gradually upgraded from sips water > normal diet.
* Short-term: High energy and protein diet to meet elevated nutrition requirements post-transplant, treat malnutrition and aid recovery.
* Long-term these patients are at increased risk of weight gain and cardiovascular disease, so when nutritional status is (almost) recovered they should be supported to stop ONS and transition to healthy eating.
* Exercise is important, walking is great!
* Due to being on immunosuppressant medication, patients are at higher risk of food-borne infections. Advice is given on foods to avoid reduce this risk.
* Certain foods interfere with immunosuppression. Advice is given on these.
* Avoid soft cheeses made from unpasteurized milk such as blue-veined cheeses, Brie, Camembert, feta, goat cheese, queso fresco/blanco

98
Q

Dietary advice following liver transplant with immunosuppressant use

A

Dietary advice following liver transplant with immunosuppressant use
* AVOID grapefruit,
pomegranate, pomelo, blood orange, and black licorice: increase amount of medication available
Ensure all food is properly cooked
 Do NOT eat any raw or undercooked meats,
proteins, dairy or egg products; this includes
sushi, raw cookie dough/cake batter, over-easy
eggs
 Reheat all leftovers
 Microwave or cook all lunch meats
 Avoid buffets
 Do not use wooden cutting boards
 Use separate cutting boards/utensils for raw
meats
 Make sure all products are pasteurized
 Wash all fruits and vegetables thoroughly
 Only eat at safe, clean, trusted restaurants
 Do not eat food that has been sitting out or exposed to direct sunlight, such as at picnics

99
Q

Other liver conditions dietary interventions
* Alcohol Related Liver Disease
* Wilson’s Disease
* Haemochromatosis
* Ascites without cirrhosis

A

Alcohol related liver disease
* Refeeding risk increased by alcohol
* Do not always lose weight due to ‘empty calories’ from alcohol
* Likely to require a broad spectrum multivitamin mineral with trace until diet adequate

Wilson’s Disease
* Dietary copper restriction may be required - often needs to be stricter in the early period of treatment

Haemochromatosis
* Consider iron restriction / avoidance of vit C products
* Standard feeds/ONS are used in end stage liver disease.

Ascites without cirrhosis
* No added salt diet
* High protein likely if having paracentesis
* Cirrhotic eating pattern not needed if good liver function

CCD (16 decks)

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