Liver Flashcards
1
Q
____ returns deoxygenated blood from the liver to the heart
A
hepatic vein
2
Q
____ supplies oxygen-rich blood from the heart to the liver
A
hepatic artery
3
Q
____ carries nutrient-rich blood from the digestive tract to the liver
A
portal vein
4
Q
_____ transport absorbed nutrients to the portal vein
A
GI tract veins
5
Q
What are 3 roles of hepatocytes?
A
- metabolism
- detoxification of drugs, vitamins, hormones
- biochemical oxidation reactions
6
Q
The liver has a huge functional reserve - ___ % of liver cells must be injured before physiological dysfunction happens
A
80-90%
7
Q
what are 5 roles of the liver?
A
- flood filtration/detoxification
- glycogen storage and gluconeogenesis
- deamination and transamination of proteins
- cholesterol synthesis (makes cholesterol and bile)
- stores up to 400 mL of blood
Lipid, carb, protein metabolism
8
Q
the liver receives blood from:
A
- hepatic artery - gives the liver O2
- hepatic portal vein - venous blood goes to liver for nutrient processing
9
Q
blood leaves liver from:
A
the hepatic vein (it goes back to the heart for reoxygenation)
10
Q
_____ takes deoxygenated blood back ot the heart
A
hepatic vein
11
Q
how much bile does the liver synthesize each day?
A
600-1000 mL (but the gall bladder can only store 40 mL of bile at a time)
12
Q
what is biles main role?
A
it breaks down fat
13
Q
what are 6 common causes of acute liver failure?
A
- trauma
- injury
- toxins (alcohol, poison)
- tylenol
- obesity (NAFLD)
- infection (viral - hep A)
14
Q
what is acute liver failure?
A
rapid deterioration of liver function in 26 weeks
15
Q
there has been an increased prevalence of chronic liver disease due to 2 epidemics:
A
hep C
NAFLD/NASH
16
Q
what is hemochromoatosis?
A
body cant clear iron - you have too much of it
17
Q
What types of tests are done to assess liver?
A
- ultrasound (most common)
- bloodwork (most common)
- fibroscan (for more severe)
- MRI
- CT
- elastography
- liver function test
18
Q
what type of labs should be investigated for liver disease?
A
- serum bilirubin - this is produced during the normal breakdown of RBCs. it passes through the liver and gets excreted in stool.
- urine bilirubin - in liver disease, bilirubin can leak into the urine
- total protein with albumin - albumin is produced in the liver and can help us figure out nutrition parameters if someone is malnourished
- prothrombin time and international normalized ration - if the liver is impaired, it doesnt produce enough prothrombin. cant clot properly
19
Q
What are important reference ranges?
A
ALT < 63
AST < 37
ALP < 136
Bilirubin < 9
GGT < 85
INR (prothrombin time) < 1.1
20
Q
What is hepatitis?
A
inflammation of the liver
it is caused by a virus, bacteria, toxin, obstruction, or parasite
21
Q
what are 5 causes of hepatitis?
A
- virus
- bacteria
- toxin
- obstruction
- parasite
22
Q
viral hepatitis is caused by 5 viruses:
A
A, B, C, D, E
23
Q
What are 5 manifestations of hepatitis?
A
- jaundice
- dark urine
- anorexia
- fatigue
- fever
- enlarged liver/spleen
24
Q
How does Hep A get transmitted?
A
fecal-oral route
contaminated drinking water
food
sewage
It rarely causes liver damage.
What do yo do for it? rest, nutrition, and fluid
25
How does hep b (HPV) get transmitted?
blood transfusion
blood
semen
saliva
bodily fluids
improper sterilization of instruments (dental drills)
26
what is the difference between acute and chronic HBV?
acute:
-1-2% will develop into chronic HBV
- some immunoglobulins can be given within 1st week
chronic
- 5% of cases
- medications
- development of cirrhosis, liver cancer (20%)
- irreversible, can lead to liver failure
can live a long life with hep b. slow to evolve
27
what are common causes of Hep C (HCV)?
1. cirrhosis
2. hepatocellular cancer
28
what is the leading cause of liver transplantation?
hep c
29
What are major risk factors of hep c?
1. blood transfusion before 1992
2. frequent exposure to blood products
3. injection drug use
4. tattoo
5. maternal-infant transmission
6. high risk sexual behaviour
30
what is the worldwide prevalence of hep c?
1-4% - there is no vaccine to prevent it
31
75% of hep c infections will turn chronic - need medication
32
what are 5 major symptoms of hepatitis?
1. fatigue
2. nausea/vomiting
3. ab pain
4. loss of appetite
5. dark urine
6. clay-coloured poop
7. join pain
8. jaundice
33
what are the primary nutrition concerns with viral hepatitis?
1. weight loss
2. nausea and anorexia
3. drug / nutrient interaction (immunosuppresants, antivirals, ppis)
34
what are 4 nutrition interventions for viral hep?
1. avoid alcohol
2. energy dense foods for anorexia
3. gi symptom management
4. medical side effect management
35
____ is a form of toxic livery injury associated with chronic ethanol consumption
Alcoholic liver disease
36
alcoholic liver disease is a form of toxic liver injury associated with chronic ethanol consumption. It is made up of 3 disorders:
1. fatty liver (hepatic steatosis)
2. alcoholic hepatitis (more inflammation, scarring, reduced blood flow)
3. cirrhosis (life threatening)
37
what are clinical presentations of ALD?
1. jaundice
2. hepatomegaly
3. ascites (fluid retention in ab cavity in advanced cases. body cant produce enough protein to regulate fluid levels)
4. hepatic encephalopathy (neuropsych abnormalities)
38
what is the threshold for alcoholic drinks at which people ALD may develop?
1. males - 4 drinks (40 g)
2. females - 2 drinks (20 g)
fatty liver (stage 1) can occur in most people who abuse alcohol for more than 6 days
39
what are 3 stages of liver damage?
1. fatty liver - deposits of fat lead to liver enlargement
2. liver fibrosis - scar tissues forms
3. cirrhosis - growth of connective tissue destroys liver cells
40
what is steatohepatitis?
fatty liver
41
what are some signs of fatty liver (steatohepatitis)? aka stage 1 of ALD
1. hepatomegaly
2. increased GGT
3. increased AST
4. increased ALT
need to stop alcohol intake
42
what is the cause of stage 1 of ALD (fatty liver)?
increased availability of fatty acids in the liver due to decreased degradation of fatty acids/decreased fatty acid oxidation
increased uptake of fatty acids from trigs
decreased lipoprotein biosynthesis and secretion
43
liver cell necrosis (cell death) and increased fibrous scar tissue begins at which stage of ALD?
stage 2 - alcoholic hepatitis
44
how are the symptoms in stage 3 different than stage 2 of ALD?
both stages have liver cell necrosis and fibrous scar tissue development
but stage 3 has:
1. portal hypertension
2. ascites
3. esophageal and gastric varices - increased pressure in hepatic portal vein
4. hepatic encephalopathy (detoxification pathway isnt working so things accumulate in brain)
5. hepatorenal syndrome (development of renal failure)
45
what 10 conditions are associated with steatohepatitis (advanced form of NAFLD)?
1. alcoholism
2. T2DM
3. metabolic syndrome
4. obesity
5. PCOS
6. obstructive sleep apnea
7. dyslipedmia
8. total parenteral nutrition
9. corticosteroids
10. refeeding syndrome
46
what is the primary nutritional considerations in ALD?
malnutrition
- poor diet quality
- duration of alcohol use
- anorexia
- intestinal maldigestion
- deficiencies: vitamins, A, C, D, K, folic acid, thiamin, b6, niacin
- hypermetabolism
- low sodium diet
- PROTEIN and cal intake can decrease during alcohol consumption
47
what is the best nutrition intervention for ALD?
multivitamin
Thiamin (B4) - essential coenzyme in carb metabolism
folate
vit A
vit D
smokers or drinkers should have vitamin C
48
thiamin deficiency in ALD leads to:
- wernicke's encephalopathy (neurological symptoms caused by brain lesions related to b vitamin deficiency)
49
what is wernickes encephalopathy
neurological symptoms caused by brain lesions related to b vitamin deficiency
- weak eye movements
- ataxia
- confused state
- hypothermia
- coma
50
what is korsakoff syndrome?
caused by thiamin deficiency - caused by memory disturbances
51
What is NAFLD?
refers to a broad spectrum of liver diseases including:
- steatosis
- fibrosis
- cirrhosis
52
what is steatosis?
the accumulation of excess fat in liver cells (non-alcohol related)
53
what is non alcoholic steatohepatitis?
NASh - a type of NAFLD
fat acccumulation associated iwth liverl cell inflammation and scarring = cell damage
54
most patients with NAFLD are asymptomatic
55
hepatomegaly is a common clinical sign of
NAFLD
56
the most common cause of chronic liver disease is:
NAFLD
57
1 in ___ Canadians will be affected by liver disease
1 in 4
58
1 in ___ overweight children will be affected by liver disease
1 in 5
59
100% of morbidly obese people experience NAFLD
76% of obese people experience it
60
what are the 4 stages of liver damage?
1. healthy liver
2. fatty liver - NAFLD
3. fatty liver - NASH
4. liver cirrhosis
61
when is NAFLD diagnosed?
when the total weight of the liver is made up of more than 5% fat (not related to alcohol)
(different than NASH, which is when liver cells get damaged)
62
what are 3 risk factors for developing NASH?
1. T2MD
2. diet
3. hyperplasia -increased # of cells in the liver - growth spurt, pregnancy, lots of obesity
63
how do you diagnose NAFLD?
1. hepatic steatosis (trigs accumulate in hepatocytes)
2. no excessive alcohol intake
64
majority of people with NALFD have no problems, but 2-6^ of adlts and 20% of obese adults progress to NASH, which is steatosis WITH inflammation, fibrosis, cirrhosis
65
what is the difference between NASH and NAFLD?
both have hepatic steatosis (trigs build in in hepatocytes), but NASH includes inflammation, fibrosis, cirrhosis
66
what are 3 current areas of research interest for NAFLD nutrition?
1. keto diet
2. bariatric diet
3. antioxidant supplements
67
what is currently the best diet for NAFLD?
medi diet
68
if you have NAFLD, what type of weight loss do you want?
10% weight loss (0.5-1 kg/week)
rapid weight loss of > 1.5 kg/week is associated with worsening liver function
69
things to avoid with NAFLD
green tea extract
milk thistle
supplements
70
_____ is the replacement of functional hepatocytes by fibrotic cells
cirrhosis
healthy tissue is replaced by scar tissue in the liver - this blocks blood flow in the liver and decreases function
71
often NASH, viral hep c, etc will end in
cirrhosis
72
what are the most common causes of cirrhosis?
alcohol
hep c
73
what are 5 general symptoms of cirrhosis?
what are 5 liver specific symptoms of cirrhosis?
general symptoms:
1. fatigue
2. weakness
3. nausea
4. poor appetite
5. malaise
liver-specific symptoms:
1. jaundice
2. dark urine
3. light stools
4. steatorrhea (fat)
5. itching skin
6. ab pain
7. bloating
74
what vitamins and minerals are needed for cirrhosis?
thiamine
vitamin A
vitamin D
75
4 major complications from cirrhosis include:
1. portal hypertension
2. ascites
3. hepatic encephalopathy
4. esophageal varices
76
what is the difference between compensated and decompensated cirrhosis?
compensated liver disease = person wont exhibit symptoms related to their liver disease
decompensated liver disease = person will present with symptomatic complications related to liver disease (jaundice, ascites, HE, esophageal varices)
77
what is the protein energy malnutrition prevalence for compensated and decompensated liver disease?
decompensated liver disease = 20 % prevalence of PEM
compensated liver disease = 60-100% prevalence of PEM
78
what tool is used to determine who is a good candidate for a liver transplant?
MELD scoring - model for end-stage liver disease
79
What does MELD scoring look like when assessing candidacy for liver transplant?
1. serum bilirubin
2. serum creatinine
3. INR (for prothrombin)
80
how does the scoring system work for MELD when assessing candidacy for liver transplant?
the higher the score = the higher the chance of mortality
40> = 70% mortality
30-40 = 50% mortality
20-30 = 20% mortality
10-20 = 5% mortality
<9 = 2% mortality
81
what therapy is used for cirrhosis?
1. abstain from alcohol
2. treat complications
82
what are 5 nutrition implications of cirrhosis?
1. early satiety from ascites (masks weight loss)
2. impaired nutrient digestion due to portal hypertension
3. increased energy expenditure
4. erratic serum glucose
5. hypoglycemia at 80% cell dysfunction
83
How much energy is needed for cirrhosis management?
30-40 kcal/kg
84
How much protein is needed for cirrhosis management?
1.2-1.5 g/kg - DONT RESTRICT PROTEIN, EVEN WITH ENCEPHALOPATHY
85
what are 5 examples of nutrition for cirrhosis
1. 30-40 energy
2. 1.2-1.5 g/kg protein - dont restrict
3. carbs spread out throughout the day
4. < 30% fat (may try MCTs)
5. restrict sodium in ascites < 2000 mg
6. might need enteral feeding with encephalopathy
7. soft diet for patients with esophageal varices
increase in energy, protein, and fat requirements
86
elevated bp in the hepatic vein is called:
portal hypertension
fibrosis forms resistance to blood flow through liver - which increases pressure in the portal vein - collateral circulation develops between portal vein and nearby veins to divert some blood into the systemic veins
portal hypertension causes blood flow to be forced backward, causing veings to enlarge and varices to develop across the esophagus and stomach from the pressure of the portal vein. the backup of pressure also causes the spleen to become enlarged
87
______ is when some of the blood destined for the liver is shunted elsewhere
portasystemic shunting
88
what are the primary symptoms/complications of portal hypertension?
1. ascites
2. GI bleed from varisces
3. hepatic encephalopathy
89
what is ascites?
accumulation of fluid in the peritoneal cavity
90
what are 3 things that cause ascites?
1. decreased osmotic pressure of plasma due to decreased albumin synthesis
2. increased sodium retention - renal excretion of fluid decreases due to loss of fluid from circulation - kidneys retain sodium
3. increased intrahepatic pressure with increased lymph obstruction and leaks into abdominal cavity
91
what are 3 ways to treat ascites?
1. diuretics (spironolactone, furosemide)
2. low sodium diet (2 g/day)
3. paracentesis
92
What is varices?
extremely dilated (bulging) veins due to high pressure
93
where does varices occur?
can occur anywhere in the GIT. but most common in stomach and esophagus
esophageal varices causes life threatening bleeding
94
what are signs and symptoms of esophageal varices?
1. bloody emesis (vomiting)
2. black, tarry, bloody stool
3. low bp
need emergency intervention!
95
what causes esophageal varices?
portal hypertension
96
what is hepatic encephalopathy?
impaired mental status and abnormal neuromuscular function resulting form liver failure
97
what are signs and symptoms of hepatic encephalopathy?
- change in mental status and personality
- mild confusion --> lethargy --> coma
- neuromuscular changes
98
what are contributing factors to hepatic encephalopathy?
1. degree of liver failure
2. diversion of portal blood through venous systemic circulation
3. bleeding from varices
4. exogenous factors (sepsis)
asterixix (flapping tremor of hands)
99
What is the pathogenesis of HE?
its debated - likely related to livers inability to eliminate products toxic to the brain
2 main hypotheses:
1. ammonia hypothesis
2. false neurotransmitter
100
explain about the ammonia hypothesis for HE
the colon produces ammonia, which is a product of protein.
typically, a healthy liver detoxifies ammonia into urea. but in a diseased liver, ammonia bypasses liver metabolism and gets metabolized to glutamine by the brain and muscle - this is why muscle wasting happens
so ammonia detoxification yields glutamine production --> too much glutamine can lead to swelling and dysfunction in the brain
101
what is a tool to diagnose HE?
plasma ammonia levels - but there is a poor correlation between ammonia levels and HE
102
explain the false neurotransmitter hypothesis for HE
usually, the ratio of BAA to aromatic AAs is 3:1.
damaged liver cant regulate this balance, so ratio becomes 1:1
increased AA metabolism in liver failure then results in:
- increased levels of aromatic AA in blood
--> phenylalanine, tyrosine, tryptophan
--> decreased plasma BCAA
--> isoleucine, leucine, valine
the hyptohesis is that increased AAA can worsen HE as they cross the blood-brain barrier acting as faulse neurotransmitters and increased inhibitory neurotransmitters
103
What is the primary treatment for HE?
goal is to reduce NH3
1. lactulose - stimulates passage of NH3 from body tissues into gut lumen --> inhibits intestinal NH3 production --> it is a potent laxative so need to be mindful of side effects
2. antibiotics - they decrease colonic concentration of bacteria that degrade protein and produce NH3
have 1.2-1.5 g/kg/d of protein (of dry weight) - better to have plant based proteins because they have less AAA
104
how prevalent is malnutrition in non-alcoholic cirrhosis? in alcoholic cirrhosis?
malnutrition in non-alcoholic cirrhosis: 27-87%
malnutrition in alcoholic cirrhosis: 34-82%
104
what % of patients with cirrhosis experience skeletal muscle wasting?
40-60% (most severe sarcopenia is seen in alcoholic cirrhosis)
SUPPLEMENTAL NUTRITION DOES NOT IMPROVE CLINICAL OUTCOMES
105
what are the 3 major causes of malnutrition in cirrhosis?
1. factors resulting in decreased oral intake
- anorexia, early satiety, ab discomfort, alcohol use, medications
2. physiological aberrations resulting in impaired digestion/absorption
- fat malabsorption due to cholestasis, water-soluble vitamin malabsorption
3. impaired nutrient metabolism
- glucose intolerance, reduced glycogen stores, increased protein metabolism, increased lipid metabolism, hypermetabolic state
106
what is the etiology of skeletal muscle wasting?
1. anabolic resistance
2. accelerated lipolysis
3. accelerated oxidation of AA
4. increased autophagy-mediated proteolysis in muscle
5. hyperammonia (perturbations in muscle signaling pathways)
107
what are the goals of nutrition therapy for cirrhosis?
1. restore nutritional status
2. promote liver regneration
3. prevent exacerbaiton of metabolic abnormalities
4. treat malnutrition
