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SMP - GI > Lecture 9 - Overview of the Liver > Flashcards

Lecture 9 - Overview of the Liver Flashcards

1
Q

7 functions of liver? What 3 groups can they be made into?

A

METABOLIC:
1. Regulation of carbohydrate and protein metabolism
2. Beta-oxidation of fatty acids
SECRETORY/EXCRETORY:
3. Regulation of cholesterol excretion through bile
4. Bile production and secretion
VASCULAR:
5. Degradation of hormones and detoxification and excretion of drugs and toxins into bile
6. Vitamin storage
7. Synthesis of blood plasma proteins: albumin, globulins, clotting factors

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2
Q

Where does the hepatic vein drain? What is the pressure in it?

A

IVC

Around < 1 mmHg

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3
Q

What % of lymph does the liver produce? What % of lymph in thoracic duct is produced by liver?

A

50%

25-50%

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4
Q

What are the Kupffer cells of the liver? Role?

A

Big fixed phagocytotic cells (aka macrophages) that line the liver sinusoids

Roles:

  1. Cleanse the blood rapidly
  2. Take care of ~ 99 % of the bacteria entering the portal blood from the intestines
  3. Metabolize old red blood cells (NOT BILIRUBIN) once they have been eliminated in the spleen and some antigens
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5
Q

Describe the 4 roles of the liver with regards to carb metabolism. Overall?

A

1) conversion of galactose and fructose to glucose
2) gluconeogenesis
3) glycogen storage (used during fasting (~18 hr supply)
4) formation of chemical compounds from intermediates of carbohydrate metabolism

OVERALL: maintain blood glucose levels

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6
Q

Describe the 4 roles of the liver with regards to lipid metabolism. Overall?

A

1) has a high rate of beta-oxidation of FAs
2) forms most lipoproteins
3) synthesizes lots of cholesterol and phospholipids
4) converts unused carbohydrates and proteins to FAT!!!!

Overall: provides another energy source, provides the building blocks for membranes, intracellular structures, as well as steroid hormones, and can bulk up your fat stores

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7
Q

Describe the 4 roles of the liver with regards to protein metabolism.

A

1) deamination of amino acids
2) forms urea to remove ammonia from body fluid (excreted in urine)
3) forms 90% of the plasma proteins
4) interconversion among different AAs via transamination

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8
Q

What vitamins does the liver store?

A

A, D, B12

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9
Q

Liver role with coagulation?

A

Formation of blood coagulation products: fibrinogen, prothrombin, factor VII

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10
Q

Liver role with regards to iron?

A

Stores it in ferritin pools (Fe2+) as free iron is toxic

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11
Q

What are the bile acids formed from in the liver?

A

Cholesterol backbone

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12
Q

What are the 2 primary bile acids formed by the liver? Are these hydrophilic or hydrophobic?

A
  1. Cholic acid
  2. Chenodeoxycholic acid

Both hydrophobic

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13
Q

What are primary conjugated bile acids? Purpose?

A

Primary bile acids conjugated with taurine or glycine => makes them amphipathic (polar), which increases their water solubility to be able act on lipids by getting through the water layer

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14
Q

What are bile salts?

A

Bile acids with NaCl and HCO3- (which is almost always the case)

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15
Q

What are secondary bile salts? Where are these produced? Are these hydrophilic or hydrophobic or amphipathic? What does this mean?

A

Bile salts produced in the intestines when bacteria can dehydroxylate the primary bile salts and DECONJUGATE THEM:

  1. Deoxycholic bile salt
  2. Lithocholic bile salt

Mainly in the colon

Hydrophobic => harder to reabsorb them into enterocytes

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16
Q

What is bilirubin? What does build up cause? Describe the excretion pathway and whether the bilirubin is hydrophilic or hydrophobic.

A

Major end-product of hemoglobin degradation => carried to liver by albumin (HYDROPHOBIC) => uptook at sinusoidal membrane by organic anion transporters => transported/stored in liver => conjugated with 1 or 2 glucuronide (80%) or sulfate (10%) (HYDROPHILIC) => excreted into bile canaliculi by MRP2/ABCC2 and into the intestines as a “bile pigment” => bacterial deconjugation and degradation forms: urobilinogen reabsorbed into portal circulation (90%) (HYDROPHOBIC) WITH CONJUGATED BILE ACIDS (HYDROPHILIC) => portion of urobilinogen is converted to stercobilin (HYDROPHOBIC) and excreted in feces (10%) => a portion of urobilinogen (2%) is filtered at the kidneys and excreted into the urine, making the urine yellow, the rest (CONJUGATED AND NOT) is reabsorbed by the kidney

Build-up in the blood (eg, from obstructive liver disease) associated with jaundice

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17
Q

What can bilirubin levels be used for?

A

As diagnostic criterion for hemolytic blood diseases and liver disease

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18
Q

Normal pressures of liver capillaries and veins?

A

VERY low

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19
Q

What do we call the capillary net of the liver?

A

Sinusoids of the liver

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20
Q

What are liver cells called?

A

Hepatocytes

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21
Q

What is hepatic cirrhosis? What is it due to?

A

Chronic degenerative disease in which normal liver parenchyma is damaged and then replaced by scar tissue due to repeated toxic insults to liver (e.g. alcoholism, viral hepatitis) => obstruction of blood flow + decrease in functional hepatocytes

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22
Q

Where are lymphatics found in the liver?

A

EVERYWHERE

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23
Q

Role of production of lymph in liver?

A

Removes fluid and proteins from the Space of Disse to drain it into the venous blood

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24
Q

What is the Space of Disse in the liver?

A

Interstitial space between liver sinusoids and hepatocytes

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25
Q

Other name for Kupffer cells?

A

Littoral cells

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26
Q

Describe the formation of ascites.

A

Portal hypertension => pooling of blood and lymph in liver sinusoids => increased hydrostatic pressure => increased transudation of fluid (since liver capillaries already have a high permeability) AND proteins from the plasma and space of Disse into peritoneal cavity = ascites

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27
Q

What would happen if there was increase hydrostatic pressure in other peripheral organs of the body? Difference between this and process of ascites?

A

Edema in interstitial space

Ascites do not accumulate in interstitial space, they go in the peritoneal cavity and also they include proteins which edemas do not

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28
Q

Does the liver normally leak?

A

Yes, a little which is absorbed by the greater omentum

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29
Q

What is hepatomegaly?

A

Increase in liver size usually due to fluid retention (400 mL to 1 L)

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30
Q

Can you have ascites without hepatomegaly?

A

YUP

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31
Q

Can you have hepatomegaly without ascites?

A

NOPE

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32
Q

What is jaundice?

A

Yellowing of skin, nail beds, whites of eyes etc due to an increased bilirubin in the blood

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33
Q

4 types of jaundices? Provide multiple names when appropriate.

A
  1. Obstructive jaundice = posthepatic jaundice
  2. Hepatic jaundice
  3. Hemolytic jaundice = prehepatic jaundice
  4. Neonatal jaundice
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34
Q

What is obstructive jaundice? Examples?

A

Results from obstruction of the bile ducts (e.g. cirrhosis, gallstones, biliary atresia, cancer). In each case, the bilirubin that is usually incorporated into bile enters the blood, instead.

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35
Q

What is hepatic jaundice? Examples?

A

Results from acute or chronic hepatitis, drug hepatotoxicity or cirrhosis causing a reduced ability of the hepatocytes to metabolize bilirubin

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36
Q

What is hemolytic jaundice? Examples?

A

Results from anything that increases hemolysis of RBCs (eg, malaria, sickle cell anemia, spherocytosis), and increases bilirubin production faster than bile can excrete it (normally RBCs last 3 months)

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37
Q

What is neonatal jaundice? Examples?

A

Usually is not pathologic, but results from metabolic changes, as the liver starts to function appropriately after birth:

  1. Immature hepatic 2 UDP-glucuronosyl transferase enzyme causing them to not appropriately conjugate bilirubin
  2. Impaired ligandins to uptake the bilirubin in the hepatocytes
  3. High rate of RBC turnover aka hemolysis right after birth

Congenital pathologic conditions such as G6PD deficiency and spherocytosis can also cause neonatal jaundice.

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38
Q

Is acute jaundice damaging?

A

NOPE

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39
Q

Is chronic jaundice damaging?

A

YUP => causes irreversible neurological issues because the bilirubin settles in the gray matter of the brain = kernicterus

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40
Q

What differentiates acute from chronic hepatitis?

A

6 months + duration

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41
Q

Treatment of neonatal bilirubin?

A

Put babies under UV light (phototherapy) which conjugates the bilirubin in the blood vessels so that the kidneys can excrete it

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42
Q

What is an example of an obstructive liver disease?

A

Cirrhosis

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43
Q

What enzyme in the liver converts excess blood glucose to glycogen?

A

Glucokinase

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44
Q

What hormones stimulate the release of glucose from liver glycogen stores? How?

A

Epinephrine and glucagon stimulate phosphorylase to release glucose

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45
Q

Describe gluconeogenesis by the liver.

A

AAs and glycerol from tryacylglycerol are converted to glucose

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46
Q

Through what mechanism does the liver uptake glucose? What other organs use this?

A

GLUT2 transporters which are insulin-independent and allow for high capacity transport

GLUT2 also found in brain, kidneys, pancreas, and basolateral side of enterocytes

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47
Q

Can the liver use galactose and fructose to enter the glycolytic and glycogenesis pathways?

A

YES, by using ATP

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48
Q

What other chemical compounds can the liver make through carbohydrate metabolism? Purpose?

A
  1. Pyruvic acid
  2. Lactic acid
  3. Succinic acid
  4. Acetyl CoA

Purpose: feed into energy producing metabolic pathways

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49
Q

What are the 3 monosaccharides absorbed by the GIT?

A
  1. Glucose
  2. Galactose
  3. Fructose
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50
Q

What would happen to blood glucose without the liver after a meal?

A

Would be 3 x as high

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51
Q

Describe the beta oxidation of FAs by the liver.

A

Tryacylglycerols are hydrolyzed to FAs and glycerol and beta oxidation is conducted in the mitochondria to produce acetyl CoA, which then enters the TCA

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52
Q

Describe the 3 types of lipoproteins formed by the liver and their contents.

A
  1. VLDLs: high tryacylglycerol content, some cholesterol and phospholipids, very little proteins
  2. LDLs: high cholesterol and phospholipid content with low tryacylglycerol, some proteins
  3. HDLs: 50% protein, less cholesterol and phospholipids (formed in the liver, and circulates around the vasculature collecting cholesterol)
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53
Q

Which lipoproteins contribute to atherosclerosis and plaque formation?

A

LDLs

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54
Q

How are fats (triacylglycerides) transported from the small intestine to target cells and then the liver? 8 steps

A
  1. Bile salts emulsify TAGs so that they can access the more aqueous environment
  2. Pancreas secretes lipases to degrade TAGs into FAs and glycerol
  3. Mucosa takes up FAs + glycerol, re-esterifies them into TAGs, and packages them into chylomicrons
  4. Chylomicrons travel through the lymph and bind to target tissues
  5. Liver collects excess chylomycrons and chylomycron remnants and repackages them with TAGs and cholesterol into VLDLs (very low density lipoproteins)
  6. TAGs in VLDLs are broken down and taken up by tissues => half of VLDLs remnants are taken up by tissues and half are sent to liver to be converted to LDLs
  7. Extrahepatic tissues send cholesterol back to the liver via HDLs
  8. Liver collects HDLs
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55
Q

What is the main form of circulating cholesterol targeted for extrahepatic tissues?

A

LDL

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56
Q

Why is HDL is considered good cholesterol in comparison to LDL?

A

Because HDL means there is more cholesterol transported back to the liver rather than to the periphery: you are getting rid of the cholesterol within your cells (presupposing you had too much in them though)

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57
Q

What does the liver do with unused carbs other than store it as glycogen?

A

Glucose => glycolysis => acetyl CoA => forms tryacylglycerole using malonyl CoA and NADPH => packaged into VLDLs to be transported to adipose tissues

58
Q

How does the liver form cholesterol?

A

Acetyl CoA molecules combine to form a sterol nucleus + side chains are added => cholesterol

Reaction catalyzed by HMG-CoA reductase

59
Q

What enzyme is the target of statin drugs?

A

HMG-CoA reductase used by liver to make cholesterol

60
Q

How does the liver conduct the deamination of AAs? Purpose?

A

Aminotransferases remove the amino group to an acceptor substance, which can be transferred again or released as NH3

Buffer the amount of acid ingested after having metabolized the proteins it needed from the diet

61
Q

How is excess NH3 removed from body?

A

Production of urea in the liver by combining NH3 with CO2 to form urea

62
Q

What % of plasma proteins is synthesized by the liver?

A

90%

63
Q

3 examples of plasma proteins?

A
  1. Albumin
  2. Globulins
  3. Fibrinogen
64
Q

Where does the liver dump plasma proteins produced? Why?

A

Lymph in Space of Disse

Too large to enter sinusoids

65
Q

9 symptoms of liver failure? Explain each.

A
  1. Ascites (explained)
  2. Jaundice (explained)
  3. Portal hypertension (explained)
  4. Bleeding/bruising: lack of blood coagulation products
  5. Confusion/cognition problems which can lead to hepatic encephalopathy: liver cannot adequately remove toxins from the blood => causes a buildup of toxins in the bloodstream, which can lead to brain damage
  6. Weakness: hypoglycemia
  7. Nausea: increase in toxic material in the blood
  8. Cholestasis: obvious
  9. Acidosis: liver cannot buffer diet AAs
66
Q

What does cholestasis mean? Consequence for the liver?

A

Reduced/blocked bile flow causing irritation of the liver => bile duct proliferation

67
Q

How long after eating will blood glucose levels increase? When will they peak?

A

15-20 min

Peak: 25-60 min

68
Q

When does GIP begin to rise?

A

5 min into meal

69
Q

Does the portal vein transport chylomicrons to the liver?

A

NOPE, they travel through lymphatics and bypass the liver

70
Q

Why is the lymph produced by liver different from lymph from other sites?

A

Because it is rich in plasma proteins

71
Q

What is liver cirrhosis characterized by?

A
  1. Hepatocellular necrosis
  2. Hepatocellular regeneration: nodularity
  3. Fibrosis with lipocyte activation
72
Q

What is liver cancer often associated with?

A

Viral hepatitis

73
Q

What % of dead liver cancer patients have hepatic metastasis?

A

30-50%

74
Q

Effect of the ampulla of Vater angling obliquely before it enters duodenum?

A

Helps prevent reflux of duodenal contents

75
Q

How does bile accumulate in the gallbladder?

A

Between meals the sphincter of Oddi is closed and bile backs up through the cystic ducts to collect in the gallbladder for storage

76
Q

What is scleral icterus?

A

Yellowing of white of eyes due to jaundice

77
Q

Insulinoma? Potential symptom?

A

A form of cancer involving the beta cells of the islets of the pancreas; these tumors may be functional which results in unregulated insulin hypersecretion and symptoms of hypoglycemia

78
Q

What is spherocytosis?

A

Auto-hemolytic anemia characterized by the production of spherocytes, i.e. erythrocytes that are sphere-shaped rather than biconcave disk shaped

79
Q

Purpose of urea?

A
  1. Buffer blood AAs

2. Remove excess NH3 via kidney excretion

80
Q

What is the unstirred water layer of the small intestine?

A

Water and chyme flow slower the closer to the surface of the intestinal tube + intestinal cells secrete mucus and bicarbonate to protest the lining which further slows the flow of fluids => there is a constant layer of water near the tube surface

81
Q

What nutrients have trouble accessing the intestinal lining? How is this solved for?

A

Lipids because of the unstirred water layer

Bile emulsify fats (duodenum) to create micelles (jejunum) which taxi the lipids through the unstirred water layer so that they can diffuse into the enterocytes

82
Q

Where does cholesterol to make bile come from?

A
  1. Dietary

2. De novo synthesis

83
Q

Does bile digest lipids?

A

NOPE

84
Q

Are all of the primary bile acids conjugated with taurine/glycine in the hepatocytes?

A

YUP

85
Q

What does it mean for bile to be an osmotic agent?

A

It pulls water as it is secreted into the bile caniliculi => this exerts solvent drag, pulling solutes with it and making a great buffer

86
Q

In what part of the intestine is the bile reabsorbed? In what form?

A

Absorbed at binding sites on the terminal ileum (primary conjugated bile salts)

87
Q

Effects of vagus stimulation on bile?

A
  1. Stimulates bile production

2. Mildly relaxes the sphincter of Oddi at the beginning of digestion

88
Q

Are there multiple cycles of bile release and reabsorption during each meal or just one?

A

Multiple

89
Q

Consequence of lacking of terminal ileum?

A
  1. Bile reabsorption is impeded on => loss of bile salts => liver will need to upregulate its production
  2. Loss of vitamin B12
90
Q

Why do chylomicrons travel through the lymph and not the blood?

A

They are too large to enter blood capillaries

91
Q

Describe the composition of chylomicrons.

A

TAGs (95%), PLs (4%), and cholesterol (1%) + beta-lipoprotein coat

92
Q

Which parts of the small intestine are most active in lipid absorption?

A

The duodenum and jejunum (most ingested fat is absorbed by mid-jejunum)

93
Q

Mechanisms of bile reabsorption in terminal ileum? Explain.

A

Through active and passive absorption:

  1. Active: secondary active transport with Na+ (same direction) of conjugated bile acids (with H2O of course)
  2. Passive: simple diffusion of SECONDARY unconjugated bile acids (represents a small portion of bile acids being reabsorbed)
94
Q

Once absorbed into the cell, how do bile salts enter the portal blood?

A

Simple diffusion

95
Q

Does he liver extracts the bile acids in one pass?

A

YUP

96
Q

What are the 2 sources of bilirubin? Describe the pathway.

A

Hb from aged RBCs (its heme) + heme from cytochrome containing enzymes => heme broken down by heme oxygenase => Fe + CO + biliverdin => bilirubin (from biliverdin with biliverdin reductase and NADPH)

97
Q

3 organs that breakdown heme?

A
  1. Spleen
  2. Liver
  3. Red bone marrow
98
Q

What enzyme liver conjugates glucoronide and bilirubin?

A

2 UDP-glucuronosyl transferase

99
Q

Enzymes responsible for transporting and storing the bilirubin in the liver? 2 names

A

Glutathione S-transferases = ligandins

100
Q

Bacterial enzymes that deconjugates and degrade bilirubin in bile?

A

Beta-glucoronidases and others

101
Q

Effect of bilirubin glucuronidation?

A

It interrupts internal H-bonding and increases solubility

102
Q

4 different blood types? Describe each. Why is this relevant here?

A
  1. A: antibodies for B
  2. B: antibodies for A
  3. AB: no antibodies
  4. O: antibodies for A and B

If pregnant mother has antibodies against baby’s blood type = ABO incompatibility => hemolysis

103
Q

What is the issue if a baby cannot pass it’s first poop (meconium)?

A

Cystic fibrosis, which can cause liver disease

104
Q

If patient has jaundice, how can you tell if the bilirubin is conjugated or not?

A

Urine! If brown: conjugated

If clear: unconjugated

105
Q

What form of bilirubin can the kidneys excrete?

A

Conjugated bilirubin

106
Q

How can breastfeeding affect bilirubin metabolism?

A
  1. Breast milk inhibits the liver’s UDP-glucuronyl transferase
  2. Breast milk contains enzyme called beta-glucuronidase that deconjugates bilirubin in the intestines
  3. Breast milk promotes binding of unconjugated bilirubin to intestinal cells => increased reuptake
107
Q

What hormones does UDP-glucuronyl transferase need to function?

A

Thyroid hormones

108
Q

Other name for UDP-glucuronyl transferase?

A

UGT

109
Q

What are 4 hereditary disorders associated with bilirubin transport/metabolism?

A
  1. Crigler-Najjar syndrome I and II
  2. Gilbert’s syndrome
  3. Dubin-Johnson syndrome
  4. Rotor syndrome
110
Q

Crigler-Najjar syndrome II:

  1. Defect?
  2. Bilirubin levels?
  3. Clinical findings?
A
  1. Severely defective UGT
  2. High unconjugated bilirubin
  3. Profound jaundice
111
Q

Gilbert’s syndrome:

  1. Defect?
  2. Bilirubin levels?
  3. Clinical findings?
A
  1. Reduced UGT activity
  2. Moderately high unconjugated bilirubin
  3. Very mild jaundice during illnesses and stress
112
Q

Dubin-Johnson syndrome:

  1. Defect?
  2. Bilirubin levels?
  3. Clinical findings?
A
  1. Impaired canalicular export of conjugated bilirubin
  2. High conjugated bilirubin
  3. Moderate jaundice + liver pigmentation
113
Q

Rotor syndrome:

  1. Defect?
  2. Bilirubin levels?
  3. Clinical findings?
A
  1. Impaired canalicular export of conjugated bilirubin
  2. High conjugated bilirubin
  3. Moderate jaundice
114
Q

Crigler-Najjar syndrome I:

  1. Defect?
  2. Bilirubin levels?
  3. Clinical findings?
A
  1. NO UGT => cannot live without liver transplant!!!!
  2. High unconjugated bilirubin
  3. Profound jaundice
115
Q

Is kernicterus treatable?

A

NOPE

116
Q

What is hepatic encephalopathy due to?

A

High plasma NH3 and other toxins

117
Q

Duration of physiologic jaundice?

A

First few days of life

118
Q

What is neonatal hepatitis?

A

Congenital hepatitis that is passed on genetically

119
Q

Normal total plasma bilirubin levels? Level to notice the jaundice in babies and adults?

A

0-1.4 mg/dL

Adults: 2.5
Babies: 5

120
Q

How to diagnose SCD?

A
  1. Hb/hematocrit

2. Blood smear to look at RBC shape

121
Q

Based on bilirubin values, how do you know if there is a conjugated hyperbilirubinemia?

A

If conjugated bilirubin levels are over 1/3rd of the total plasma bilirubin

122
Q

What do AST and ALT levels indicate?

A

They are both liver enzymes that indicate hepatocyte damage and measure the HEALTH of the liver:

  1. ALT = alanine transaminase: protein metabolism
  2. AST = aspartate transaminase: same but not as specific because found in other tissues
123
Q

What do alkaline phosphatase levels indicate? What to note?

A

Indicate biliary tree function or can indicate metastatic cancer lesions in bones (also found there) => enzyme found in all tissues, but is especially concentrated in the liver, bile duct, kidneys, bone and placenta. It catalyzes the dephosphorylation of molecules.

124
Q

What does the reticulocyte count tell you?

A

Tells you how fast the body is trying to replace hemolytic RBCs

125
Q

What does the prothrombin time tell you? Other name for this? When is this measure super important?

A

Measures function of clotting factors = liver function

= INR

After a liver transplant because AST and ALT are not a good indication as they will be super high

126
Q

2 ways of classifying a hyperbilirubinemia?

A
  1. Increased production or decreased clearance

2. Extra or intrahepatic causes

127
Q

Causes of increased production of bilirubin?

A
  1. Hemolysis
  2. Ineffective erythropoiesis: thalassemia, polycythemia
  3. Internal bleed
128
Q

Causes of decreased clearance of bilirubin?

A
  1. Impaired hepatic uptake: hepatitis or metabolic diseases
  2. Impaired conjugation: Crigler-Najjar, Gilbert’s
  3. Impaired bilirubin secretion: Dubin-Johnson or Rotor’s syndrome
129
Q

Causes of intrahepatic cholestasis?

A
  1. Altered sinusoidal/canalicular function
  2. Decreased hepatic perfusion
  3. Bile duct obstruction (e.g. biliary atresia or Aligiles’)
  4. Hepatocellular Destruction
130
Q

Causes of extrahepatic cholestasis?

A
  1. Bile duct obstruction (e.g. biliary atresia)

2. Choledochal cyst

131
Q

What is biliary atresia? Cause? What can it lead to?

A

Inflammatory damage to the intra- and extrahepatic bile ducts with sclerosis and narrowing or even obliteration of the biliary tree

Cause is unknown

Untreated, this condition leads to cirrhosis, fibrosis, portal HT, and death within the first years of life

132
Q

Treatment for biliary atresia?

A

Kasai procedure = hepatoporto-enterostomy directly connecting liver to duodenum until waiting for a liver transplant

133
Q

What is Aligiles’?

A

No normal intra-hepatic ducts

134
Q

What do CRP levels indicate? What is it produced by? What is it a risk factor for?

A

C-reactive protein (CRP) is an indicator of inflammation. It is produced by liver and adipose cells in response to elevated plasma IL-6, has been shown to enhance phagocytosis of damaged cells by macrophages.
Elevated plasma CRP is considered a risk factor for development of diabetes, hypertension and CVD

135
Q

What is non-alcoholic fatty liver disease? What causes it? Complications? What can exacerbate the damage? What does it look like on a CT scan? Treatment?

A

Diagnosis: fat in liver is normal (e.g. Ito cells), butif the fat content accounts for over 5-10% of total liver weight => fatty liver

Causes: many, like diabetes and high cholesterol but pathologic process is not clear: it has been postulated that fat metabolism in the liver is compromised + the ability to remove the TAGs to adipose tissues is reduced + shuttling of fatty acids from adipose tissue is increased = fat buildup

Complications: fatty liver alone may not produce complications, but it can cause inflammation, leading to steatohepatitis and scarring (cirrhosis).

Exacerbations: cirrhosis (from another stressor such as bacterial infection, oxidative stress or hormonal imbalances) can exacerbate the damage

CT: Liver is a darker shade (lower density) than the spleen (they are supposed to be the same shade)

Treatment: Treating the underlying causes (e.g. diabetes and hyperlipidemia) can reduce the symptoms including pain and jaundice, and fat deposits; if caught early enough, liver function may recover. If diagnosed late or untreated, can result in liver failure and may necessitate a transplant

136
Q

Other name for non-alcoholic fatty liver disease

A

Non-alcoholic steatohepatitis (NASH)

137
Q

3 potential causes of elevated liver enzymes?

A
  1. Liver damage (e.g. NSAIDs, statins, hepatitis)
  2. Diabetes
  3. Hyperlipedemia
138
Q

Can fatty liver lead to fat vacuoles and hepatomegaly?

A

YUP

139
Q

Can liver damage decrease plasma oncotic pressure?

A

YUP (liver produces most of the plasma proteins!)

140
Q

Is fatty liver irreversible?

A

NOPE

141
Q

Complication of low plasma oncotic pressure?

A

Peripheral edema

SMP - GI (21 decks)

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