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Clinical Dietetics 2 > Liver > Flashcards

Liver Flashcards

1
Q

Main functions of the liver (7)

A
  1. carbohydrate metabolism
    - glycogen storage
    - gluconeogenesis
  2. protein metabolism
    - utilisation of amino acids for protein synthesis and gluconeogenesis
  3. storage of vitamins and minerals
  4. detoxification
  5. immune function
  6. heamotoligcal function
  7. lipids and lipoproteins
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2
Q

what proteins does liver synthesise? (4)

A
  1. albumin
  2. prothrombin
  3. fibrinogen
  4. clotting factors - bleeds more if compromised
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3
Q

hat vitamins liver stores? (7)

A
  1. vitamin A
  2. B2
  3. B3
  4. B6
  5. B12
  6. vitamin K
  7. folate
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4
Q

hat vitamins liver stores? (7)

A
  1. vitamin A
  2. B2
  3. B3
  4. B6
  5. B12
  6. vitamin K
  7. folate
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5
Q

how does liver detoxification (2)

A
  1. oxidation of alcohol
  2. deactivation of drugs in the cytochrome P450 system
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6
Q

what roles does liver play in immune function (2)

A
  1. tumor necrosis alpha production - compromise = impaired immune function
  2. cytokine signalling production
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7
Q

what haematological function of liver (1)

A
  1. synthesis of haem iron metabolism - also clotting factors
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8
Q

role of liver in lipid production? what can indicate impaired liver function? (2)

A
  1. production of triglycerides from free fatty acids
  2. cholesterol formation => lower serum cholesterol levels are not an indication of CVD risk. Can give an idea of how poor liver function is
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9
Q

Role of impaired liver function on glycogen storage?

A

Normally store up to 72 hours

end stage liver failure = 10-12 hours only so patients lose glycogen from muscle stores (catabolism)

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9
Q

Role of impaired liver function on glycogen storage?

A

Normally store up to 72 hours

end stage liver failure = 10-12 hours only so patients lose glycogen from muscle stores (catabolism)

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10
Q

2 roles of protein metabolism in liver - what measure can indicate liver function?

A
  1. synthesis of albumin, prothrombin, fibrinogen and clotting factors
  2. utilisation of amino acids for protein synthesis and gluconeogenesis
  3. end stage ALWYAS LO ALBUMIN = the lower the albumin the poorer liver function is
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11
Q

3 main causes of liver disease

A

fatty liver disease

hepatitis

alcohol

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12
Q

Name 7 causes and their aetiology of liver disease

A
  1. infections; viral hepatitis; cytomegalovirus
  2. metabolic = NAFLD and NASH
  3. autoimmune = autoimmune hepatitis; primary billiary cirrhosis (celiac patients/ inherited condition affecting fat absorption)
  4. biliary tract disease = primary sclerosis cholangitis (linked with UC)/ affects fat absorption
  5. vascular disorders = budd chiari
  6. metabolic disorders = glycogen storage disease (always need NG); Wilson’s disease (copper excess); haemochromatosis (iron accumulation); Alpha-1-trypsin deficiency
  7. other; sarcoidosis (idiopathic); cryptogenic
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13
Q

Difference between compensated and decompensated liver disease

A

compensated = no symptoms

decompensated = symptoms

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14
Q

symptoms of decompensated liver disease

A
  1. jaundice because of high bilirubin
  2. hepatic encephalopathy
  3. portal hypertension
  4. vatical bleeds
  5. ascites
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15
Q

cause and consequence of hepatic encephalopathy

A

build up of toxins, when ammonia builds up can’t excrete properly = causes cognitive dysfunction. 4 levels 1= mild; 4=severe, go to ICU, intubated to help rid of toxins

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16
Q

cause and consequence of portal hypertension

A

high blood pressure in portal vein of liver. Give diuretics to drain if worried about kidney function

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17
Q

name 4 stages of liver disease

A
  1. healthy
  2. fatty liver
  3. liver fibrosis
  4. liver cirrhosis
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18
Q

describe fatty liver - causes, consequence and if reversible

A

reversible - liver can still regenerate from this.

regardless of cause = deposits of fat in the liver

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19
Q

describe liver fibrosis - causes, consequence and if reversible - how diagnosed

A

can still reverse

scarring on liver starts to harden. diagnosed via fibre scan that detects amount of fibrosis in liver

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20
Q

cause and consequence of cirrhotic liver - can it be reversed?

A

end stage liver disease = unable to regenerate

can be asymptomatic

needs to be considered for transplant

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21
Q

main causes of malnutrition in liver disease

A
  1. malabsorption
  2. increased energy needs b/c stress factor
  3. inadequate oral intake
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22
Q

is albumin a good indicator of nutrition status in liver patient?

A

no. poor indicator of nutritional status in any patient with liver disease.

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23
Q

what are signs and symptoms of portal hypertension

A

Ascites
1. discomfort
2. breathlessness
3. feel bloated

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24
Q

consequences of portal hypertension? medical management?

A

can cause viriceal bleeds = happens in oesophageal tract affecting anywhere from mouth to anus because the pressure gets too much, they burst and bleed out of mouth, nose of bum

causes inadequate nutrition => if actively bleeding, unable to place NG = often patient isn’t eating can cause days of not eating

can be managed with blood pressure lowering medication

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25
Q

hat does PEM mean

A

protein energy metabolism

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26
Q

Causes and consequences of PE
What percentage of liver disease patients are malnourished?

Why is malnourishment so common? And what are the implications of being malnourished on clinical outcome?

What complications does malnourishment increase the risk of?

By how much can calorie and protein needs be increased by?

A
  1. malnutrition = common in compensated (20-40%) and decompensated (>80%) cirrhosis
  2. protein and carbohydrate metabolism = affected
  3. nutrition requirements for calories and protein = increased up to 60%
  4. increased complication risk = susceptibility to infections, hepatic encephalopathy, ascites, worsening hepatic function, pre-surgical morbidity and lower survival in transplant
  5. loss of muscle mass = extreme - affects survival, length of hospital stay and recovery
  6. malnutrition significantly impacts quality of life, mobility and infection susceptability
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27
Q

what food restriction is needed in ascites?

A

salt - no added salt at table

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28
Q

why are PEM liver disease patients nutritional requirements +60%>

A

store glycogen in liver is compromised so breaks down glycogen stores in muscle and increase in gluconeogenesis occurs to meet needs

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29
Q

why do liver patients need close monitoring for dietetic management? what would you do?

A

can have very rapid decline (i.e. 20kg weight loss in 2 weeks).

if unsure about condition and think it may quickly deteriorate always put on ONS to be safe (can take it off at review if needed)

30
Q

definition of sarcopenia?

A

loss of muscle mass, strength OR physical function

31
Q

What symptoms can cause sarcopenia in end stage liver disease?

What lifestyle factors can increase sarcopenia and malnutrition risk?

A
  1. nausea and early satiety: ascites, delayed gastric emptying, impaired gut motility, small intestinal bacterial overgrowth
  2. low of appetite: up regulation of tumor necrosis factor alpha and leptin
  3. taste alteration; zine deficiency (metallic taste) recommend strong mint or lemon sherbet/slice to suck before eating.; oral thrush
  4. active alcoholism; poor and irregular feeding, low socioeconomic status (prioritises alcohol over food)
32
Q

Affect of ascites on nutritional status? symptoms? how severe?

A

can carry up to 20kg (20L) fluid => affects:
1. movement
2. breathing
3. delayed gastric emptying

causes vomiting and early satiety, puts people off eating.

Can also get up to 10kg oedema on legs.

33
Q

sarcopenia in liver disease: causes of metabolic disturbances and consequences?

A
  1. increased rate of gluconeogenesis; reduced liver storage of glycogen; breakdown of fat and muscle mass to meet needs
  2. hyper metabolic state; increased sympathetic nervous system activity; hyper dynamic circulation; gastrointestinal bacterial translocation; systemic inflammation in cirrhosis; sepsis.
34
Q

What info would you want in dietetic assessment?

A
  1. dietary intake history and ho it compares to what they used to eat
  2. symptoms
  3. subjective global assessment
  4. weight (estimate dry weight if ascites or oedema)
  5. height
  6. BMI (estimated with dry weight)
  7. anthropometry (MUAC, handgrip strength, tricep skin fold
  8. micronutrient deficiencies: zinc, vitamins, copper, selenium, vitamin D
35
Q

How do you measure ascites and oedema to calculate dry weight?

A

look at patient medical notes - could be visible in assessment (do not touch)

minimal = ~2.2 L ascities; 1L oedema (reduce actual weight by 5%)

moderate = ~6L ascites; ~5L oedema (reduced actual weight by 10%)

severe = ~14L or more ascites; 10L oedema (reduce actual body weight by 15%)

36
Q

Why liver disease/cirrhosis patients with ascites/oedema more susceptible to infection?

A

get infections in fluid by spontaneous bacterial peritonitis (SPB) => antibiotics can cause SIBO (small intestinal bacterial overgrowth)

antibiotics can = nausea and bowel movements

37
Q

should someone with sarcopenia and hepatic encephalopathy be on a low protein diet?

A

no. moderate protein.

sometimes dr will put someone on low protein to reduce ammonia build up in liver but it makes it worse because of muscle breakdown and increased effects of malnutrition

38
Q

when would you recommend using PERT?

A

in biliary disorders causing steatorrhea - most often in alcoholic fatty liver disease causing pancreatic issues.

if caused by PSC or PBC = recommend low fat diet

39
Q

if malabsorbing fats - what vitamins can be affected?

A

A, D, E, K

CHECK LEVELS - often vitamin d deficient because not storing + not getting as much sun because sick.

40
Q

what measures used for anthropometry? and why? how often repeated?

A

repeated monthly - detects long term changes

MUAC and TSF (tricep skin fold)

Handgrip dynamometry - weekly because can change quickly; compare patient score against previous because of inter-individual differences.

MAMC (mid arm muscle circumference) - independent predictor of mortality after liver transplant

CT scan (rarely because expensive)

Liver frailty index = sit/stand test, balance test and 6 min walk test

41
Q

describe sarcopenia obesity

name a cause

A

loss of skeletal and muscle mass and gain of adipose tissue

obesity does not rule out malnutrition

cause = after transplant on steroid = a lot of weight gain. also feeling better so tends to eat more.

42
Q

what would you ask about in sarcopenia obesity patient and what would you recommend for weight management outcomes.

A

rate of weight loss and have they lost any function in muscles

measure with hand grip strength

often told to lose weight = recommend moderate weight loss with a weight loss factor accounted into needs (-500-800. kcal/day) to prevent muscle loss.

No transplant if BMI >40 because risks

43
Q

how would you estimate kcal and protein requirements in liver disease? how much weight gain factor (kcal)? and weight loss (kcal)?

A

PENG or ESPEN guidelines for kcal and protein

no PENG guideline for compensated liver disease

weight gain factor = +400 - 1000 kcal (unless have acute infection) - often added because liver disease is chronic condition that won’t improve without transplant

weight loss = -500-800 kcal for steady weight loss

44
Q

kcal requirements for compensated liver disease ESPEN

A

25-35 kcal/kg (actual weight)

45
Q

kcal requirements for decompensated liver disease ESPEN

A

35-40 kcal/kg estimated dry weight

46
Q

ESPEN kcal requirements for post liver transplant

A

35 - 40 kcal/kg

47
Q

What equation would you use to calculate energy needs in obese liver disease patients?

A

Mifflin-St Joer equation + PAL

48
Q

protein requirements: compensated liver disease

A

1.2-1.3 g/kg

49
Q

protein requirements: decompensated L disease

A

1.2 - 1.5 g/kg (can go up to 2g/kg)

50
Q

protein requirements for obesity liver disease. How would you adjust protein requirements in people with BMA 30-50 kg/m2?

How would you adjust protein requirements in people with BMI >50 kg/m2

A

1.5g/kg for ideal body weight

OR

75% of req for BMI 30-50 kg/m2

OR

65% of req for BMI >50 kg/m2

51
Q

what are goals of nutrition support in liver disease (6)

A
  1. improve nutritional status
  2. maintain lean body mass
  3. minimise fluid retention
  4. reduce morbidity and mortality associated with malnutrition
  5. maintain muscle mass
  6. stabilise weight
52
Q

What specific dietetic advice would you recommend for people with liver disease? (4)

A
  1. 50g CHO rich bedtime snack is vital to reduce glycogenolysis and improves nitrogen balance
  2. regular meals and snacks because reduces fasting gluconeogenesis
  3. moderate to high protein even in hepatic encephalitis
  4. avoid skipping meals
53
Q

Why regular eating needed? Why does every meal and snack need to be rich in carbs?

A

to ensure adequate glucose circulating and reduce muscle break down.

54
Q

before ned snack - what supplement or supplement and snack would you recommend?

A

juice based ONS because higher in carbs than milk based.

if don’t like taste - a milk based supplement + an extra carbohydrate snack (i.e. a biscuit)

55
Q

What recommendations for nutritional management of ascites? (4)

A
  1. no salt added at the table - use other methods of flavouring. small pinch can be used in cooking
  2. avoid low nutritional content foods that are rich in salt i.e. soups, bacon, processed foods, crisps or salter snacks, no halloumi or feta
  3. can include small amounts oc cheese but not salty or processed cheese
  4. 80 - 120 mmol of sodium per day (4.6 - 6.9 g salt) = ~1 tsp salt
56
Q

If patient needs to use ready melas to eat hat recommendations would you make?

A

cooking may not be practical and ready meals better than nothing

educate patient on labelling and traffic light system to choose low salt options

57
Q

how quickly to progress from ONS to EN?

A

quickly. If not improving on ONS then move to EN fast.

NG = preferred but NJ can be used to help with nausea and side effects of NG.

NG or NJ can really improve patient condition and even liver condition.

if condition not improving, may need EN + ONS + food to meet requirements. In this instance risk of overfeeding is safer than not meeting requirements if continued weight loss.

58
Q

Why no gastronomy or jejunostomy in liver disease patients?

A

contraindicated because of varices, ascites, raised INR (blood clotting derangement) and therefore increased risk of bleeding.

59
Q

Why no gastronomy or jejunostomy in liver disease patients?

A

contraindicated because of varies, ascites, raised INR (blood clotting derangement) and therefore increased risk of bleeding.

60
Q

why not use fibre feeds?

A

patients often already feel bloated and on laxatives to keep bowels moving. Feed volume can also be difficult to manage because of ascites and the side effects of ascites. Therefore filling high fibre supplement is not helpful.

61
Q

How would you identify suitable feeds for liver disease? (4)

A
  1. high energy (1.5 kcal/ml or 2kcal/ml) and high protein
  2. low volume if ascitic
  3. all feeds are suitable for no added salt diet
  4. use MCT/low fat feeds for cholestatic liver disease or chylous ascites
62
Q

What are benefits of using MCT feed?

What symptoms would indicate the need for MCT feed? (2)

A

it is semi elemental and will help with bowel symptoms and discomfort.

Use MCT if have steatorrhea or high bilirubin

63
Q

when to have bedtime snack?

A

~1-2 hours before sleep to avoid fullness/discomfort

if unable to eat anything = have supplement

64
Q

recommendations for bedtime snack using ONS

A

milk based = fortisip compact or fortisip compact protein because they’re smaller and high protein, (can be filling) WITH ADDITIONAL CHO snack

because milk based supplement has ~40g CHO - need at least 50g

Juice based ONS has about 60g CHO

65
Q

If a patient has hepatic encephalopathy what protein recommendations would you make on amount and type

A

amount = don’t want to reduce too much because this will increase muscle breakdown, further increasing ammonia levels

type of protein = animal based proteins can increase frequency and severity of encephalopathies episodes. Encourage more plant based proteins in meals and snacks.

66
Q

how often should review patients?

A

every 1 - 2 weeks when more stable. When very unstable more frequently until on a steady plan.

67
Q

which biochemical marker influences the plan

A

bilirubin - if it is high = means patient doesn’t absorb well so low fat diet or supplements are preferred i.e. fortijuice or semi elemental feed or low fat food with adequate protein and CHO

68
Q

when would you consider PN?

A

for this eunable to tolerate EN feeding routes

there is increased infection risk

some PN feeds can have effect on LFTs but have improved recently

69
Q

What is MAFLD?

A

new term for NAFLD = metabolic associated fatty liver disease

most common cause of liver disease = closely associated with metabolic syndrome, insulin resistance and obesity but is more complex than previously thought because can happen in someone who has never been overweight/obese

70
Q

How is MAFLD diagnosed?

A

steatosis with any of the following:
1. obesity/overweight
2. diabetes
3. metabolic dysfunction

71
Q

what is NASH?

A

non-alcoholic steatohepatitis

72
Q

what are the three steps on spectrum of MAFLD

A
  1. fatty liver = fat accumulation in liver - no symptoms. treatment = weight loss or management of symptoms of metabolic syndrome
  2. NASH = fat and inflammation and scarring
    sometimes its symptoms
  3. Cirrhosis = scar tissue replaces liver cells = end stage liver disease and unable to recover
73
Q

MAFLD treatment principles? (7)

A
  1. lifestyle and diet modification
  2. target weight loss 5-10% can improve outcomes
  3. hypo caloric diet (500 - 1000 kcal deficit)
  4. physical activity (30 mins x3-4 days/week) include resistance training
  5. target components of metabolic syndrome:
    diabetes = HbA1c, medications, insulin (metformin can make liver disease worse so switch to insulin)

dyslipidaemia = diet change

hypertension = statins, DASH diet

Clinical Dietetics 2 (9 decks)

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