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M2 GI > Liver Structure & Function > Flashcards

Liver Structure & Function Flashcards

1
Q

T/F A fibrous capsule surrounds the entire liver.

A

False. A fibrous capsule surrounds the liver, except for a “bare spot” on the posterior aspect, which is in continuity with the retroperitoneum.

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2
Q

What are the 4 ligaments that hold the liver in place?

A

Coronary ligaments

R/L triangular ligaments

falciform ligament (contains round ligament aka obliterated umbilical vein)

hepatoduodenal ligament (hepatic artery, portal vein, bile duct, nerves, and lymphatic vessels)

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3
Q

What divides the left and right lobes of the liver?

A

Falciform

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4
Q

What gives rise to the hepatic artery?

What gives rise to the portal vein?

A

hepatic: celiac
portal: spenic + SMV

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5
Q

Where does blood flow if the patient has portal HTN?

A

Collaterals (varices) are prone to rupture:

  • submucosa of the esophagus and stomach
  • less often in the colon and at colostomy sites, but can occur
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6
Q

Where does lymph form in the liver? (3)

Where are lymphatic vessels found?

Where does it drain to?

A
  • formed in space beneath the sinusoidal endothelial cells (space of Disse), portal tracts, and around hepatic veins
  • vessels found in portal tracts and around hepatic veins
  • drains to hilum and IVC
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7
Q

Why do pleural effusions present as a complication of end stage liver disease?

A

lymph flow in trans-diaphragmatic lymphatics (lymphatics in the liver capsule drain the bile duct & ligaments, the latter of which crosses the diaphragm to esophageal and xiphisternal nodes

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8
Q

What is the nerve supply to the liver? (4)

A

Lower thoracic ganglia

celiac plexus

vagus nerve

right phrenic nerve

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9
Q

What are the canals of Hering(CoH)?

What are they lined by?

A

intra-hepatic bile ductules that are found between the bile canaliculi and interlobular bile ducts (near the outer edge of a classic liver lobule).

lined by cholangiocytes and hepatocytes

FYI only - courtesey of wikipedia - CoH are destroyed early in biliary cirrhosis and may be the primary sites of scarring in MTX toxicity

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10
Q

The liver has parenchymal cells and non-parenchymal cells. What are examples of each?

What are the functions of these cells?

A

Parenchymal cells:
- hepatocytes - processes and redistributes metabolic fuels (glucose, FFA, hormones)

Non-parenchymal cells:

  • space of disse (endothelial cells with fenestrae of variable diameters)
  • Ito cells (stellate cells) - Vitamin A storage, synthesizes collagen + mediates fibrogenic response to liver injury
  • Kupffer cells - macrophages; mediates inflammatory response
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11
Q

The hepatic parenchyma is organized into acini, lobule, and Hepatic Microcirculatory Subunits. What does this all mean?

A

Acinus - blood supply of a small portion of parenchyma and the bile duct draining that parenchyma residing in that portal triad

Lobule - blood supply by several separate portal vein branches, each of which also supplies adjacent lobules

Hepatic Microcirculatory Subunit (HMS) - Blood supply from a single inlet venule to a structural unit that includes two functional compartments, the choleon and the hepaton, that reside in a common space

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12
Q

Zonal populations of hepatocytes exhibit different synthetic capabilities. What type of synthesis goes on in the peri-portal zone? What about the peri-central zone?

A

Peri-portal: urea cycle, a.a. metabolism

Peri-central zone: glutamine syntehtase (scavenges ammonium and converts it to glutamine

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13
Q

Where does bilirubin come from?

How do they get to the liver?

A

dying red blood cells, which release heme.

Heme is bound to haptogloben, and this is taken up by the splenic macrophages and converted into bilirubin.

Bilirubin is transported in blood bound to albumin (unconjugated, lipid soluble)

This complex is taken up by hepatocytes by simple and facilitated diffusion

In hepatocytes, bilirubin bound to glutathione-s-transferase (GST) and then conjugated by bilirubin UDP-glucuronosyltransferase (GT) and then released into the canaliculus (-> bile duct)

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14
Q

What is the transporter that transports conjugated bilirubin into the bile ducts?

A

ATP-dependent transporter called multidrug resistance associated protein 2 (MRP2)

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15
Q

What is the composition of bile? (4)

A

conjugated bilirubin

cholesterol

phospholipids (primary: lecithin)

bile salts (primary: cholic acid and chenodeoxycholic acid).

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16
Q

What is the purpose of bile?

A

absorption of lipids, fat soluble vitamins (DEAK)

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17
Q

How and where is bile reabsorbed?

How much is resorbed?

What happens if you don’t have bile?

A

Conjugated bilirubin in the intestine is converted by bacteria into urobilinogen which is able to be reabsorbed.
Thus 99% of bile is be re-absorbed and returned to the liver (enterohepatic circulation) for reutilization.

Since bile colors stools, no bile = ‘white stool’ steatorrhea

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18
Q

Why is your urine yellow?

Why is your crap brown?

A

Conjugated bilirubin and urobilinogen in blood can be excreted by the kidney if the liver does not reabsorb them and thus, giving urine its yellow color.

In the bowel, urobilinogen can be further metabolised into stercobilin, which gives feces its chacteristic nasty color.

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19
Q

What are the causes of Hyperbilirubinemia (conjugated + unconjugated)?

A

Unconjugated:
• liver cell damage (no uptake)
• increase production (hemolysis)
• decreased conjugation (congenital: Gilbert’s and Crigler-Najjar or acquired drug effect)
• vascular (decreased flow to liver), or starvation

Conjugated:
• liver cell damage
• obstruction (stone or tumor)
• congenital (Dubin-Johnson and Rotor)

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20
Q

How are drugs/toxins metabolized in the liver?

A

Phase I: cytochrome P-450 monooxygenase system (many)
• Oxidation, Reduction, Hydrolysis, Hydration, Decarboxylation, Isomerization
• Variability: drug-drug, host factors, environmental factors

Phase II: other enzymes
o Glucuronidation, Sulfation, Methylation, Acetylation, Glutathione conjugation

21
Q

Glyogen synthesis, fatty acid oxidation (via TCA/Krebs), and FA synthesis (via Pentose Phopshate Shunt) all have one common substrate. What is it?

A

Glucose-6-phosphate

22
Q

If you suddenly decided to go on a hunger strike, how long can your body glycogen stores sustain you?

A

2 days

23
Q

What yields the highest ATP?

A

Oxidation of fatty acids to carbon dioxide and water

24
Q

What happens to excess glucose in the liver?

A

excess glucose can be converted to fatty acid for future use and stored as triglycerides in distal sites such as adipose tissue and carried by lipoproteins.

25
Q

T/F Cholesterol from food or made by the liver is used as a fuel source

A

False. Cholesterol from food or made by the liver is not used as a fuel source but as a structural component of membranes and as precursors for steroid hormones.

26
Q

T/F Immunoglobulins are produced by hepatocytes

A

False. They are produced by plasma cells

27
Q

T/F - LFTs, as their name implies, reflect liver function.

A

False. LFTs have limited sens. + spec and do not all reflect liver function

28
Q

What is the basis of abnormal AST/ALT levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Leakage from damaged tissue into circulation (hepatocellular necrosis)

Associated liver dz: viral, autoimmune, toxic, Wilsons, ischemia, OH, NASH etc.

Extrahepatic sources:

  • ALT: relatively specific for hepatocyte necrosis
  • AST: muscle (skeletal and cardiac), kidney, brain, pancreas, RBC **IMPT to know this list**
29
Q

What is the basis of abnormal Alkaline phosphatase levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Overproduction and leakage into serum (rise is delayed due to need for induction of enzyme)

Associated liver dz: intra/extra-hepatic cholestasis, infiltrating disease (tumor/MAC), alcoholic hepatitis.

Extrahepatic sources:

  • Bone, placenta, intestines, tumor/lymphomas **IMPT to know this list**
30
Q

What is the basis of abnormal GGT levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Overproduction and leakage into serum (inducible by alcohol and dilatin)

Associated liver dz: intra/extra-hepatic cholestasis, infiltrating disease (tumor/MAC), alcoholic hepatitis.

Extrahepatic sources:

  • Kidney, spleen, pancreas, heart, lung, brain **IMPT to know this list**
31
Q

What is the basis of abnormal LDH levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Overproduction and leakage into serum

Associaetd liver disease: ischemic hepatitis, malignant infiltration of liver; may reflect hemolysis

Extrahepatic sources: skeletal or cardiac muscle injury, hemolysis, stroke, and renal infarction, in addition to acute and chronic liver disease. *IMPT*

32
Q

What is the basis of abnormal Total Bilirubin levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Decreased hepatic clearance

Liver diseaes: extra- and intrahepatic bile duct obstruction, alcoholic, drug-induced or viral hepatitis, inherited hyperbilirubinemia

Extra-hepatic sources: Increased breakdown of hemoglobin (hemolysis, ineffective erythropoiesis, resorption of hematoma)
 or myoglobin (muscle injury)
33
Q

What is the basis of abnormal PT/INR levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Decreased synthetic capacity

Liver diseases:

  • Acute or chronic liver failure (unresponsive to vitamin K)
  • Biliary obstruction (responsive to vitamin K administration)

Extrahepatic sources:

  • Vitamin K deficiency (secondary to malabsorption, malnutrition, antibiotics)
  • consumptive coagulopathy
34
Q

What is the basis of abnormal Albumin levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Decreased synthesis (increased catabolism?)

Liver disease: Chronic liver failure

Extrahepatic sources

  • Malnutrition
  • Nephrotic syndrome
  • Protein-losing enteropathy,
  • vascular leak
  • malignancy
  • inflammatory states
35
Q

What is the basis of abnormal Ammonia levels?

What disease are they associated with?

Are there any extrahepatic sources of this?

A

Decreased hepatic clearance

Liver disease: Chronic liver failure

Extrahepatic sources

  • Hepatocaval shunting
  • Protein metabolism defect
36
Q

High transaminases relative to alkaline phosphatase and gamma-GT indicates….

A

hepatitic pattern, tends to reflect predominantly damage to hepatocytes

37
Q

High alkaline phosphatase and gamma-GT relative to transaminases indicates…

A

cholestatic pattern, tends to reflect injury to bile ducts

38
Q

An acute enormous elevation of transaminases (5000-10000), 5 days later low (300-500) strongly suggests

A

ischemic liver injury (“shock liver”)

39
Q

An acute elevation of transaminases persistent for 2-3 weeks (2000-4000) and then coming down to 200-400 after 2 months completely normal indicates…

A

acute hepatitis A

40
Q

Patient age 72, with general malaise, fever and abnormal liver tests, pain in back:

ALT 76 AST 47 Alkaline phosphatase 760.

What test would you order next? Why?

What happens if it is elevated? What happens if this is normal?

A

Gamma-GT

elevated: liver/biliary tract problem (cholangitis, a malignancy of pancreas or bile ducts, etc)
normal: bone metastasis of malignancy, lymphoma, etc

41
Q

Jaundiced patient with bilirubin of 3.4

What if this person had abnormal LFTs?

What if this person had normal LFTs?

A

Liver test abnormalities: liver disease likely
Normal liver tests: Gilbert’s syndrome (not a disease but has increased unconjugated bilirubin) or potentially a hemolytic problem

42
Q

What are the 4 major imaging modalities used to image the liver?

A

US

CT

MRI/MRCP

ERCP

43
Q

What are the pros and cons of using US for imaging the liver?

When is it used?

A
  • nearly always the test for initial screening for hepatic disease and/or complications (liver shape, spleen size, collaterals, ascites, tumor)

Pros: Real time imaging, good test to assess biliary system, particularly in jaundiced patient: Is the biliary system compromised (obstructed, dilated, can a cause be assumed like stone or tumor?), doppler capability to demonstrate hepatic blood flow

Cons:: unable to penetrate bone, air, or see lesions less than 1cm, poor results in very obese patients, operator skills may vary

44
Q

What are the pros and cons of using CT for imaging the liver?

When is it used?

A

Provides axial sections of the liver anatomy and adjacent structures using X-rays

Pros:

  • Unenhanced: fat infiltration or iron deposition, and focal changes such as subtle calcification or hemorrhage
  • Contrast-enhanced imaging following intravenous (IV) administration of water-soluble contrast medium is widely used for the detection of focal lesions.

Cons: $$, radiation and i.v. contrast can cause nephrotoxicity

45
Q

What are the pros and cons of using MRCP for imaging the liver?

When is it used?

A

Axial section imaging generated from magnet signal measurements as field is created around the patient

Pros:

  • large array of contrast materials which can better characterize tumors and infiltration of liver with fat, iron, etc.
  • no radiation, non-nephrotoxic contrast, images can be generated in transverse, longitudinal, coronal and even oblique planes
  • non-invasive way to assess biliary system (= MRCP); often used to assess who might need more invasive, more risky procedure (infection, bleeding, perforation # ERCP)

Cons:

  • $$$
  • can’t use in patients with pacemakers and metal devices
  • quality of imaging is subject to motion - longer imaging acquisition leads to blurred images from breathing/movement
  • patient size limit (300 lbs); not good claustrophobic patients
46
Q

What are the pros and cons of using ERCP for imaging the liver?

When is it used?

A

Allows visualization of biliary tree and treatment of any obstructions with drains or stone removal

Pros: Tissue can be sampled
Cons: $$$$, radiation exposure, requires sedation, increased risk of complications (bleeding, perforation, pancreatitis, and cholangitis)

47
Q

The hepatocyte has 3 sides. What are they and what do they face?

A

Basal: sinusoidal space, microvilli
Apical: adjacent cells, enclose bile canaliculi
Lateral: bile canaliculi > Disse’s space

48
Q
A

M2 GI (41 decks)

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