Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FNN 401 Final > Liver > Flashcards

Liver Flashcards

1
Q

____ returns deoxygenated blood from the liver to the heart

A

hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

____ supplies oxygen-rich blood from the heart to the liver

A

hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

____ carries nutrient-rich blood from the digestive tract to the liver

A

portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

_____ transport absorbed nutrients to the portal vein

A

GI tract veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 3 roles of hepatocytes?

A
  1. metabolism
  2. detoxification of drugs, vitamins, hormones
  3. biochemical oxidation reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The liver has a huge functional reserve - ___ % of liver cells must be injured before physiological dysfunction happens

A

80-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are 5 roles of the liver?

A
  1. flood filtration/detoxification
  2. glycogen storage and gluconeogenesis
  3. deamination and transamination of proteins
  4. cholesterol synthesis (makes cholesterol and bile)
  5. stores up to 400 mL of blood

Lipid, carb, protein metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the liver receives blood from:

A
  1. hepatic artery - gives the liver O2
  2. hepatic portal vein - venous blood goes to liver for nutrient processing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

blood leaves liver from:

A

the hepatic vein (it goes back to the heart for reoxygenation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

_____ takes deoxygenated blood back ot the heart

A

hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is biles main role?

A

it breaks down fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are 6 common causes of acute liver failure?

A
  1. trauma
  2. injury
  3. toxins (alcohol, poison)
  4. tylenol
  5. obesity (NAFLD)
  6. infection (viral - hep A)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is acute liver failure?

A

rapid deterioration of liver function in 26 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

there has been an increased prevalence of chronic liver disease due to 2 epidemics:

A

hep C
NAFLD/NASH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is hemochromoatosis?

A

body cant clear iron - you have too much of it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What types of tests are done to assess liver?

A
  1. ultrasound (most common)
  2. bloodwork (most common)
  3. fibroscan (for more severe)
  4. MRI
  5. CT
  6. elastography
  7. liver function test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what type of labs should be investigated for liver disease?

A
  1. serum bilirubin - this is produced during the normal breakdown of RBCs. it passes through the liver and gets excreted in stool.
  2. urine bilirubin - in liver disease, bilirubin can leak into the urine
  3. total protein with albumin - albumin is produced in the liver and can help us figure out nutrition parameters if someone is malnourished
  4. prothrombin time and international normalized ration - if the liver is impaired, it doesnt produce enough prothrombin. cant clot properly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are important reference ranges?

A

ALT < 63
AST < 37
ALP < 136
Bilirubin < 9
GGT < 85
INR (prothrombin time) < 1.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is hepatitis?

A

inflammation of the liver

it is caused by a virus, bacteria, toxin, obstruction, or parasite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are 5 causes of hepatitis?

A
  1. virus
  2. bacteria
  3. toxin
  4. obstruction
  5. parasite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

viral hepatitis is caused by 5 viruses:

A

A, B, C, D, E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 5 manifestations of hepatitis?

A
  1. jaundice
  2. dark urine
  3. anorexia
  4. fatigue
  5. fever
  6. enlarged liver/spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does hep b (HPV) get transmitted?

A

blood transfusion
blood
semen
saliva
bodily fluids
improper sterilization of instruments (dental drills)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the difference between acute and chronic HBV?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are common causes of Hep C (HCV)?

A
  1. cirrhosis
  2. hepatocellular cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the leading cause of liver transplantation?

A

hep c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are major risk factors of hep c?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the worldwide prevalence of hep c?

A

1-4% - there is no vaccine to prevent it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

75% of hep c infections will turn chronic - need medication

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are 5 major symptoms of hepatitis?

A
  1. fatigue
  2. nausea/vomiting
  3. ab pain
  4. loss of appetite
  5. dark urine
  6. clay-coloured poop
  7. join pain
  8. jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the primary nutrition concerns with viral hepatitis?

A
  1. weight loss
  2. nausea and anorexia
  3. drug / nutrient interaction (immunosuppresants, antivirals, ppis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are 4 nutrition interventions for viral hep?

A
  1. avoid alcohol
  2. energy dense foods for anorexia
  3. gi symptom management
  4. medical side effect management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

____ is a form of toxic livery injury associated with chronic ethanol consumption

A

Alcoholic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

alcoholic liver disease is a form of toxic liver injury associated with chronic ethanol consumption. It is made up of 3 disorders:

A
  1. fatty liver (hepatic steatosis)
  2. alcoholic hepatitis (more inflammation, scarring, reduced blood flow)
  3. cirrhosis (life threatening)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are clinical presentations of ALD?

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the threshold for alcoholic drinks at which people ALD may develop?

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are 3 stages of liver damage?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is steatohepatitis?

A

fatty liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are some signs of fatty liver (steatohepatitis)? aka stage 1 of ALD

A
  1. hepatomegaly
  2. increased GGT
  3. increased AST
  4. increased ALT

need to stop alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the cause of stage 1 of ALD (fatty liver)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

liver cell necrosis (cell death) and increased fibrous scar tissue begins at which stage of ALD?

A

stage 2 - alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how are the symptoms in stage 3 different than stage 2 of ALD?

A

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
Q

what 10 conditions are associated with steatohepatitis (advanced form of NAFLD)?

A
  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
Q

what is the primary nutritional considerations in ALD?

A

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
Q

what is the best nutrition intervention for ALD?

A

multivitamin
Thiamin (B4) - essential coenzyme in carb metabolism
folate
vit A
vit D

smokers or drinkers should have vitamin C

48
Q

thiamin deficiency in ALD leads to:

A
  • wernicke’s encephalopathy (neurological symptoms caused by brain lesions related to b vitamin deficiency)
49
Q

what is wernickes encephalopathy

A

neurological symptoms caused by brain lesions related to b vitamin deficiency

  • weak eye movements
  • ataxia
  • confused state
  • hypothermia
  • coma
50
Q

what is korsakoff syndrome?

A

caused by thiamin deficiency - caused by memory disturbances

51
Q

What is NAFLD?

A

refers to a broad spectrum of liver diseases including:
- steatosis
- fibrosis
- cirrhosis

52
Q

what is steatosis?

A

the accumulation of excess fat in liver cells (non-alcohol related)

53
Q

what is non alcoholic steatohepatitis?

A

NASh - a type of NAFLD

fat acccumulation associated iwth liverl cell inflammation and scarring = cell damage

54
Q

most patients with NAFLD are asymptomatic

A
55
Q

hepatomegaly is a common clinical sign of

A

NAFLD

56
Q

the most common cause of chronic liver disease is:

A

NAFLD

57
Q

1 in ___ Canadians will be affected by liver disease

A

1 in 4

58
Q

1 in ___ overweight children will be affected by liver disease

A

1 in 5

59
Q

100% of morbidly obese people experience NAFLD

76% of obese people experience it

A
60
Q

what are the 4 stages of liver damage?

A
  1. healthy liver
  2. fatty liver - NAFLD
  3. fatty liver - NASH
  4. liver cirrhosis
61
Q

when is NAFLD diagnosed?

A

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
Q

what are 3 risk factors for developing NASH?

A
  1. T2MD
  2. diet
  3. hyperplasia -increased # of cells in the liver - growth spurt, pregnancy, lots of obesity
63
Q

how do you diagnose NAFLD?

A
  1. hepatic steatosis (trigs accumulate in hepatocytes)
  2. no excessive alcohol intake
64
Q

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

A
65
Q

what is the difference between NASH and NAFLD?

A

both have hepatic steatosis (trigs build in in hepatocytes), but NASH includes inflammation, fibrosis, cirrhosis

66
Q

what are 3 current areas of research interest for NAFLD nutrition?

A
  1. keto diet
  2. bariatric diet
  3. antioxidant supplements
67
Q

what is currently the best diet for NAFLD?

A

medi diet

68
Q

if you have NAFLD, what type of weight loss do you want?

A

10% weight loss (0.5-1 kg/week)

rapid weight loss of > 1.5 kg/week is associated with worsening liver function

69
Q

things to avoid with NAFLD

A

green tea extract
milk thistle
supplements

70
Q

_____ is the replacement of functional hepatocytes by fibrotic cells

A

cirrhosis

healthy tissue is replaced by scar tissue in the liver - this blocks blood flow in the liver and decreases function

71
Q

often NASH, viral hep c, etc will end in

A

cirrhosis

72
Q

what are the most common causes of cirrhosis?

A

alcohol
hep c

73
Q

what are 5 general symptoms of cirrhosis?

what are 5 liver specific symptoms of cirrhosis?

A

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
Q

what vitamins and minerals are needed for cirrhosis?

A

thiamine
vitamin A
vitamin D

75
Q

4 major complications from cirrhosis include:

A
  1. portal hypertension
  2. ascites
  3. hepatic encephalopathy
  4. esophageal varices
76
Q

what is the difference between compensated and decompensated cirrhosis?

A

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
Q

what is the protein energy malnutrition prevalence for compensated and decompensated liver disease?

A

decompensated liver disease = 20 % prevalence of PEM

compensated liver disease = 60-100% prevalence of PEM

78
Q

what tool is used to determine who is a good candidate for a liver transplant?

A

MELD scoring - model for end-stage liver disease

79
Q

What does MELD scoring look like when assessing candidacy for liver transplant?

A
  1. serum bilirubin
  2. serum creatinine
  3. INR (for prothrombin)
80
Q

how does the scoring system work for MELD when assessing candidacy for liver transplant?

A

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
Q

what therapy is used for cirrhosis?

A
  1. abstain from alcohol
  2. treat complications
82
Q

what are 5 nutrition implications of cirrhosis?

A
  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
Q

How much energy is needed for cirrhosis management?

A

30-40 kcal/kg

84
Q

How much protein is needed for cirrhosis management?

A

1.2-1.5 g/kg - DONT RESTRICT PROTEIN, EVEN WITH ENCEPHALOPATHY

85
Q

what are 5 examples of nutrition for cirrhosis

A
  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
Q

elevated bp in the hepatic vein is called:

A

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
Q

______ is when some of the blood destined for the liver is shunted elsewhere

A

portasystemic shunting

88
Q

what are the primary symptoms/complications of portal hypertension?

A
  1. ascites
  2. GI bleed from varisces
  3. hepatic encephalopathy
89
Q

what is ascites?

A

accumulation of fluid in the peritoneal cavity

90
Q

what are 3 things that cause ascites?

A
  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
Q

what are 3 ways to treat ascites?

A
  1. diuretics (spironolactone, furosemide)
  2. low sodium diet (2 g/day)
  3. paracentesis
92
Q

What is varices?

A

extremely dilated (bulging) veins due to high pressure

93
Q

where does varices occur?

A

can occur anywhere in the GIT. but most common in stomach and esophagus

esophageal varices causes life threatening bleeding

94
Q

what are signs and symptoms of esophageal varices?

A
  1. bloody emesis (vomiting)
  2. black, tarry, bloody stool
  3. low bp

need emergency intervention!

95
Q

what causes esophageal varices?

A

portal hypertension

96
Q

what is hepatic encephalopathy?

A

impaired mental status and abnormal neuromuscular function resulting form liver failure

97
Q

what are signs and symptoms of hepatic encephalopathy?

A
  • change in mental status and personality
  • mild confusion –> lethargy –> coma
  • neuromuscular changes
98
Q

what are contributing factors to hepatic encephalopathy?

A
  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
Q

What is the pathogenesis of HE?

A

its debated - likely related to livers inability to eliminate products toxic to the brain

2 main hypotheses:
1. ammonia hypothesis
2. false neurotransmitter

100
Q

explain about the ammonia hypothesis for HE

A

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
Q

what is a tool to diagnose HE?

A

plasma ammonia levels - but there is a poor correlation between ammonia levels and HE

102
Q

explain the false neurotransmitter hypothesis for HE

A

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
Q

What is the primary treatment for HE?

A

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
Q

how prevalent is malnutrition in non-alcoholic cirrhosis? in alcoholic cirrhosis?

A

malnutrition in non-alcoholic cirrhosis: 27-87%
malnutrition in alcoholic cirrhosis: 34-82%

104
Q

what % of patients with cirrhosis experience skeletal muscle wasting?

A

40-60% (most severe sarcopenia is seen in alcoholic cirrhosis)

SUPPLEMENTAL NUTRITION DOES NOT IMPROVE CLINICAL OUTCOMES

105
Q

what are the 3 major causes of malnutrition in cirrhosis?

A
  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
Q

what is the etiology of skeletal muscle wasting?

A
  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
Q

what are the goals of nutrition therapy for cirrhosis?

A
  1. restore nutritional status
  2. promote liver regneration
  3. prevent exacerbaiton of metabolic abnormalities
  4. treat malnutrition

FNN 401 Final (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions