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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
What are considerations for protein guidelines in liver disease patients?
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
What are considerations for other nutrition care (not fat, protein, carbs) in liver patients?
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
What are the long term health outcomes of NAFLD?
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
How do we charactarize heptatic steatosis?
Fat more than 5% weight by volume
28
What is hepatic steatosis?
Fatty liver
29
How is NASH different from Hepatic Steatosis
NASH = the liver experiences more damage related to fibrosis and inflammation. Can eventually lead to Cirrhosis
30
What can be done for NASH?
No specific treatment but weightloss and lifestyle are the best course of action
31
What contributes to fatty liver?
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
What stage of NAFLD is reversible?
Hepatic Steatosis - can be done with lifestyle and diet however at NASH, unsure what can be done and if reversible
33
What are thought to be contributing factors to advances from hepatic steatosis to NASH?
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
What is acanthosis nigracans?
darkening of the skin - around the neck due to NAFLD
35
What ethnicities is NAFLD more common in?
South Asian, Asian, Hispanic Less common in Caucasian and Black
36
What are common anthropometric and biochemical features in individuals with NAFLD?
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
What are the lifestyle guidelines for treatment of NAFLD?
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
What are some other treatments (outside of diet and exercise) that have been considered in for treatment of NAFLD?
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
What evidence is there for exercise as a treament for NAFLD?
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
What is a eating pattern that has been thought to help reduce NAFLD?
Mediterranean diet: high consumption of fruits and vegetables Red wine Olive oil MUFA Omega 3 Fatty acids
41
What are screening guidelines for patients 9-12 years of age with potential for NAFLD?
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
How do we diagnose pediatric NAFLD?
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
What strategies are preferred for pediatric NAFLD?
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

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