The Liver & NAFLD Flashcards

1
Q

How is the liver involved in protein metabolism?

A

Synthesis of serum proteins
synthesis of blood clotting factors
deamination/transamination to produce non-essential amino acids
removal and detoxification of ammonia through urea synthesis

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2
Q

How is the liver involved in lipid metabolism?

A

Synthesis of cholesterol, phospholipids, triglycerides
Breakdown of fatty acids for energy production

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3
Q

What vitamins are stored in the liver?

A

B vitamins
Fat soluble vitamins

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4
Q

What minerals are stored in the liver?

A

Iron, Copper, Magnesium, Zinc

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5
Q

How does the liver assist in digestion?

A

Bile production which assists in fat and fat soluble vitamin absorption
Conjugation and excretion of bilirubin which is a breakdown product of red blood cells

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6
Q

What is jaundice?

A

Jaundice is a build up of bilirubin (not being excreted by the liver). Leads to yellowed skin and a build up of bilirubin can also lead to extremely uncomfortable itchy skin. try to give medications that normalize the bile pool

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7
Q

How does the liver aid in hormonal detoxification?

A

conjugation and excretion of aldosterone & alcohol dehydrogenase hormone
enzymes in the liver detoxify alcohol, drugs, poisons

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8
Q

What are the signs and symptoms of liver disease?

A

Mild abdominal pain and generalized fatigue - most common sign
Anorexia
Muscle wasting
weight loss
jaundice - end stage
Hypo or hyperglycemia
Anemia
portal hypertension - which can lead to swollen arteries that connect to the stomach or esophagus which can bust open and bleed esophageal varices
Ascites
Hypoalbuminemia

Encephalopathy - liver fails to detoxify waste products such as ammonia into urea (breakdown product of amino acids). pH goes up dramatically, proteins can denature

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8
Q

What is billiary atresia?

A

A condition in which the bilde ducts outside and inside the liver are scarred and blocked, bile can’t flow into the intestine so builds up in the liver and damages it.
***Problems with absorption of fat soluble vitamins (D and K) and supplement with MCT because it doesn’t need bile to abosrb MCT.

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9
Q

Which bile salts are toxic?

A

Non-polar bile salts

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10
Q

What do AST and ALT tell us?

A

Liver function tests but are very sensitive and can jump and down
ALT very sensitive to hepatic damage or if you injure yourself

Can go up with liver disease **ESPECIALLY if patients are being fed TPN

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11
Q

What is ascites?

A

Build up of acidic fluid related directely to the lack of albumin synthesis (Hypoalbuminemia)

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12
Q

What two liver biomarkers DECREASE in the liver disease states?

A

Albumin - not a good marker for visceral protein status, more a sign of how well your liver is making protein
BUN (can also be normal)

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13
Q

What would elevated ammonia, low albumin and a delayed Prothrombin time (PTT) indicate?

A

Liver disease/malfunction

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14
Q

What is ALP indicative of?

A

Non specific - can also be elevated during periods of growth (reflects bone function) however elevations in the presence of a liver diagnosis usually mean billiary flow is poor

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15
Q

What is Hepatitis A?

A

Viral infection that is extremely contagious
Associated with contaminated water (sewage, natural disaster etc.)
usually resolves in a few months
Vaccinations available
Does not tend to cause permanent liver damage

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16
Q

What is Hepatitis B?

HBV

A

Transmitted through bodily fluids through infected needles or blood, sexual activity
More serious chronic illness can result (Liver cancer), can lead to liver failure
vaccinations available

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17
Q

What is hepatitic C?

HCV

A

Transmission through blood
Chronic illness can result - fatty liver, liver cancer
Vaccine available

18
Q

What is something to keep in mind for end stage liver disease? Supplements? Meds?

A

Can’t give too much protein or else it will contribute to encephalopathy but need enough to prevent lean body mass wasting

Supplementation of Fat soluble vitamins (careful with A due to potential liver toxcitiy)

Anti viral meds for hepatitis

Avoidance of toxins

19
Q

What are other causes of Cirrhosis?

A

Alcoholism
Birth defects (Billiary Atresia)
Advanced Hepatitis
Wilson’s disease - excess copper accumulation
Toxin’s Chemotheraputic agents
Hemochromatosis

20
Q

Characterize the amino acids in a patient with Liver Disease

A

Higher levels of aromatic amino acids

Lower levels of BCAAs - likely due to increased uptake into the muscle as they can be oxidized as an energy substrate (leucine)

21
Q

What are considerations for energy guidelines in Liver Cancer Patients?

What would you keep in mind when choosing their kcals/kg etc.

A

Need high energy to prevent catabolism and spare protein but need to be careful with obesity
25-35kcal/kg dry bodyweight
40-50kcal/kg dry weight for acute hepatitis
Avoid fasting to prevent catabolism
consider the use of late evening snacks

*not hypermetabolic until end stage

22
Q

What are considerations for carbohydrate guidelines in Liver Cancer Patients?

A

Increase CHO to prevent catabolism and spare protein - around 300g-400g/day
May require insulin
consider lower GI snacks to avoid postprandial hyperglycemia and minimize gluconeogenesis

23
Q

What are considerations for Fat guidelines in Liver Cancer Patients?

A

As tolerated - malabsorption may be present
25/40% of kcal
MCT oil more easily absorbed - doesn’t require bile
give fat soluble vitamin supplementation *** optimizing vitamin D status is a big focus

24
Q

What are considerations for protein guidelines in liver disease patients?

A

1g/kg of protein for Adults minimum
Mild to moderate liver disease around 1.3g/kg
End stage liver failure with liver encephalopathy 0.8-1g/kg

25
Q

What are considerations for other nutrition care (not fat, protein, carbs) in liver patients?

A

Restrict sodium to 2-3g/day when ascites/edema present, need to carefully assess

Optimize bone health - need vitamin d and K, patients often have increased risk of fracture

Total absitence from alcohol required

Fluid restriction if ascites/edema present
1000-1500ml/d restriction
or 500-800ml output

Thiamin and Folate decrease in alcoholism

B12, and Zinc - decreased absorption with hepatic damage

Vitamin K - malabsorption

26
Q

What are the long term health outcomes of NAFLD?

A

Increased risk for liver cirrhosis
Increased risk for liver failure
Signficaint co-morbidity in patients with viral hepatitis and influences long term prognostic outcome

27
Q

How do we charactarize heptatic steatosis?

A

Fat more than 5% weight by volume

28
Q

What is hepatic steatosis?

A

Fatty liver

29
Q

How is NASH different from Hepatic Steatosis

A

NASH = the liver experiences more damage related to fibrosis and inflammation. Can eventually lead to Cirrhosis

30
Q

What can be done for NASH?

A

No specific treatment but weightloss and lifestyle are the best course of action

31
Q

What contributes to fatty liver?

A

HFCS
Processed food with High GI/GL - particularly fructose
High simple sugar intake
High intakes of sat. fats found in processed food, low intake of PUFA

32
Q

What stage of NAFLD is reversible?

A

Hepatic Steatosis - can be done with lifestyle and diet however at NASH, unsure what can be done and if reversible

33
Q

What are thought to be contributing factors to advances from hepatic steatosis to NASH?

A

Oxidative stress - diets (high fat, sugar) contributes to ongoing changes mitochondrial changes

Excess of substrate that needs to be oxidized - overwhelms glutathione antioxidant capactiy of the liver resutling in increased cytokine production

Stellate cell activation and adipocytokine imbalance - play a big role in insulin resistance

Defecits in LCPUFA

34
Q

What is acanthosis nigracans?

A

darkening of the skin - around the neck due to NAFLD

35
Q

What ethnicities is NAFLD more common in?

A

South Asian, Asian, Hispanic

Less common in Caucasian and Black

36
Q

What are common anthropometric and biochemical features in individuals with NAFLD?

A

Central obesity/overweight

Hyperinsulinemia with normal blood sugars

Acanthosis nigricans

Dislipidemia - hypertriglyceridemial + or - hypercholesterolemia
usually reduced HDL

Depressed adiponectin/erythryocyte glutathione and increased markers of oxidative stress and inflammation

Patients may have mild elevations in ALT and AST but could still be normal - cut off for ALT is 40, you can still have above 20, be classified as normal but be at increased risk

37
Q

What are the lifestyle guidelines for treatment of NAFLD?

A

Weight loss - generally reduces hepatic steatosis - either hypocaloric diet or in conjunction with physical activity
loss of at least 3-5% of body weight to improve severity - greater loss of 10% may be needed if at NASH

*no info about the best way to achieve weight loss for NAFLD

May be easier to do an isocaloric diet but focus on whole grains, fruits and vegetables

38
Q

What are some other treatments (outside of diet and exercise) that have been considered in for treatment of NAFLD?

A

Antioxidants - Vitamin D, daily at 800 IU/d does improve liver histology in non-diabetic adults but not better than weight loss
Lipid lowering agents
Orlistat
Bariatric surgery

39
Q

What evidence is there for exercise as a treament for NAFLD?

A

High impact aerobic exercise has an independent effect on reducing intrahepatic
Lower intensity exercise is less effective but may depend on type of exercise and duration of intervention - resistance training may be eaiser to adhere to

40
Q

What is a eating pattern that has been thought to help reduce NAFLD?

A

Mediterranean diet:
high consumption of fruits and vegetables
Red wine
Olive oil
MUFA
Omega 3 Fatty acids

41
Q

What are screening guidelines for patients 9-12 years of age with potential for NAFLD?

A

Obese (>95th percentile on growth charts for age and gender)
Overweight with risk factors (dyslipidemia, insulin resistance, central obesity, T2D)
Earlier screening for patients who have risk factors or have a family history
consider screening for siblings

42
Q

How do we diagnose pediatric NAFLD?

A

Consider patient history
ALT greater than 22 for girls and 26 for boys
If greater than 2x upper limit of normal - Can consider NAFLD

43
Q

What strategies are preferred for pediatric NAFLD?

A

Weight stabilization rather than loss - as they will continue to grow heigh and weight wise - isocaloric approach with a fructose reduction strategy
Important to have the family involved with sustainble lifestyle changes