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FHB - GI/Metabolism - Exam 3 > Lecture 11 - Role of Liver in Excretion > Flashcards

Lecture 11 - Role of Liver in Excretion Flashcards

1
Q

Where is motility faster

Stomach or small intestine?

A 
Small intestine
(12 waves/min)

Stomach (3)

  • both have slow waves to set the basic rhythm
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2
Q

What is the blood supply to the liver?

A

Portal vein

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3
Q

What does the Hepatic Triad Consist of?

A
  1. Hepatic Artery
  2. Bile Duct
  3. Portal Vein
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4
Q

What are the major cells in the liver?

How are they arranged?

What is the blood supply to this area in the liver? (low resistance cavities)

A
  1. Hepatocytes
  2. Plates
  3. Sinusoids
    - supplied by portal vein & hepatic artery
    - low resistance
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5
Q

What are the 3 major functions of the liver?

A

Metabolism
Detoxification
Excretion

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6
Q

The Hepatic Triad defines 3 zones.

State which zone has:

  1. Most oxygen supply and is closest to triad
    - most active in detoxification and thus most likely to be affected by viral pathogens
  2. Closest to hepatic vein
    - most sensitive to ischemia
    - most active in BILE synthesis
A
  1. ZONE 1 –> Periportal Cells

2. Zone 3 –> Pericentral cells (near central vein)

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7
Q

What are the origination point of the biliary system?

What does the apical membrane of adjacent hepatocyte form?

A

Hepatocytes

  • form a channel called canaliculus
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8
Q

What do canaliculi drain?

A

Bile from liver

and transport to biliary ductules

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9
Q

What type of cells line the biliary ductules ?

specific name

A

Columnar epithelial Cells

= CHOLANGIOCYTES

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10
Q

Why is the endothelium of the liver fenestrated?

A

To allow for passage of large proteins

ex: ALBUMIN

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11
Q

What is the function of KUPFFER Cells?

A

Macrophage activity

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12
Q

Which cells produce collagen?

If these cells become hyper-active, what can occur?

A
  1. Stellate cells

2. Cirrhosis, Fibrosis

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13
Q

Describe the structure of the following:

  1. Classic Lobule
  2. Acinar Structure
A
  1. Classic Lobule:

2 portal triads and a central vein

  • blood from portal triad  central vein  hepatic vein  IVC
2.Acinar Structure:
2 central veins & 2 portal veins
**ZONES**
based on nutrient & oxygen supply
have various zones
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14
Q

Describe the structure from biliary ductules to common hepatic duct

A
  1. Biliary ductules
  2. Large bile duct
  3. Right and Left hepatic Duct
  4. Common hepatic Duct
    - bile then flows either to gall bladder via cystic duct
    - or to the intestine via common bile duct
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15
Q

______ participate in metabolism of major nutrients, carbs, lips, and proteins

A

Hepatocytes

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16
Q

What are the 2 main functions of the LIVER when it comes to glucose?

A
  1. Gluconeogenesis
    - conversion of sugars to glucose
  2. Glucose buffer function
    - liver stores excess glucose as glycogen and releases stored glucose in bloodstream when needed
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17
Q

What is the result of impaired liver function?

  1. During meals
  2. Between meals
A
  1. Hyperglycemia

2. Hypoglycemia

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18
Q

Hepatocytes:

  1. Rich store of enzymes for ________
  2. Convert products of carb metabolism into ___
  3. Produce (3)
  4. Convert cholesterol to ______
A
  1. Fatty Acid Oxidation
  2. Lipids
  3. Lipoproteins, cholesterol, and phospholipids
  4. Convert a significant portion of cholesterol to bile acids
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19
Q

What 2 important proteins are synthesized by the liver?

What does the liver convert?

A
  1. Non-essential amino acids
  2. Plasma proteins
    (including albumin) & clotting factors
  3. Ammonia to Urea
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20
Q

What do patients with liver failure develop?

What can this lead to?

A

Hypoalbuminemia

lead to PERIPHERAL EDEMA since the oncotic pressure is lost
- clotting disorder

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21
Q

What is the source of ammonia produced in the body?

A

Colonic bacteria

  • ammonia can cross the BBB
  • produce negative side affects

** liver is the only place that UREA cycle is present**

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22
Q

How does the liver protect the body from toxic substances?

A

Modifies them in “first pass metabolism”

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23
Q

What are the 2 phases of First pass metabolism?

A

Phase 1:

  • oxidation
  • hydroxylation
  • catalyzed by cytochrome P-450 enzymes

Phase 2:

  • conjugate the substances with glucuronide
  • sulfate
  • AA’s
  • glutathione
24
Q

What are the 2 general ways that the liver modifies substances?

A

2 ways to modify:
Macrophages/Kuppfer Cells:
engulf certain molecules

Chemical reactions –conjugate the substances w/ AA OR oxidation/hydroxylation

25
Q

Because large water soluble catabolites and molecules bound to plasma proteins, steered hormones, etc cannot be excreted through the kidney,

where will these be excreted instead (with the help of the liver)?

A

BILE

  • ultimately excreted in FECES
26
Q

Where is bile synthesized?

Which cells secrete bile?

Into which specific area?

A
  1. Hepatocytes
  2. Hepatocytes
  3. Bile Canaliculi
27
Q

What is the structure of BILE? (name 6 components)

What are the 3 major components?

A
  1. Bile acids (65%)
  2. Phospholipids
  3. Proteins
  4. Cholesterol
  5. Bile Pigments (bilirubin)
  6. Electrolytes (similar & isotonic to plasma)

MAJOR:

  1. Bile acids
  2. Cholesterol
  3. Bile pigments (bilirubin)
28
Q

What are the 2 primary bile acids synthesized by Hepatocytes?

In order to yield SECONDARY bile acids, what must act on these 2 primary acids?

What 3 secondary bile acids are produced?

A
  1. Cholic Acid
  2. Chenodeoxycholic Acid

** Colonic Bacterial Enzymes **

  1. Ursodeoxycholic Acid
  2. Deoxycholic Acid
  3. Lithocholic Acid
29
Q

In hepatocytes, only primary bile acids are conjugated with glycine or taurine.

True or false?

A

FALSE

BOTH primary and secondary bile acids are conjugated with glycine or taurine

30
Q

Why do bile acids need to be conjugated to produce conjugated bile acids or BILE SALTS?

What transported actively absorbs conjugated bile acids?

A

More water soluble!!

  • Conjugated bile acids are fully ionized in intestinal lumen
  • actively absorbed in terminal ILEUM via apical Na+ -dependent bile salt transporter (asbt)

ABST

[Some (that escape) are deconjugated by colonic bacterial enzymes – unconjugated forms reabsorbed passively in colonic epithelium]

31
Q

What distinguishes primary and secondary bile acids?

A

Whether colonic bacteria has acted on

  1. Cholic Acid
  2. Chenodeoxycholic
32
Q

What is the rate limiting enzyme for bile acid synthesis?

Under what type of feedback is bile synthesis regulated? How does this affect the synthesis?

Specifically during Ileal resection? What can ill resection lead to?

A

7 alpha hydroxelase

Under negative feedback, this means if more bile acids are produced, less will be recycled back!

Ileal resection:
Bile acids will not be recycled back and thus there is no feedback regulation
= MORE activity of 7alpha hydroxelase and thus more bile acids produced

BUT the synthesis is not very efficient, so these patients have a problem with lipid digestion leading to steattorhea

33
Q

Conjugated bile acids (bile salts) can passively cross the intestinal wall.

True or false.

A

FALSE

  • transported actively by ABST (Test)

** if UNconjugated, ABST will not transport Lithocholicacid back to the blood.

WILL BE LOST IN THE STOOL
* does not recycle back the toxic form of the bile acids

34
Q

How are the following levels during Ileal resection:

  1. Bile acid levels
  2. Bile acid synthesis

How can this problem be treated?

A
  1. bile acid levels DECREASE

BUT

  1. Bile acid SYNTHESIS increases (since none are recycled back, no negative feedback preventing the synthesis)
    - –losing the bile in the stool!
  • DECREASE synthesis by Feeding bile acids (to instigate negative feedback)
35
Q

How do the following levels change during Bile acid feeding:

  1. Bile acid secretion levels
  2. Bile acid synthesis
A
  1. Bile acid secretion INCREASES

2. LOW bile acid synthesis

36
Q
  1. Which circulation recycles the majority of the BILE ACID pool back to the liver?
  2. What happens to the small fraction of bile acids that enter the colon after passing the terminal ileum?
A

– via enterohepatic circulation.

  1. Become de-conjugated and is reabsorbed passively.
37
Q
  1. What cells (lining the biliary ductules) modify bile?
  2. What happens to Bile here?
  3. How does Bile become more alkaline? (through what channels specifically)
A
  1. Cholangiocytes
  2. Bile is diluted here
    - Secretin stimulate the formation of aquaporin channels
  • similar mechanism of secretion as the pancreas:
    1. Glucose, AA’s are reabsorbed
    2. CFTR channels activated
  • exchangers move Cl in and HCO3- out into the lumen
    BILE = MORE ALKALINE (and reduces acidic crystals)
38
Q

How is bile concentrated in the gallbladder (stored here)?

Which transporters?

A

In between meals, outflow of bile is blocked by constriction of sphincter of Oddi

  • gallbladder is relaxed
  • sphincter of do is closed
  • gallbladder fills with bile
    CONCENTRATED as a result of isosmotic absorption of solutes and H20

NHE –> Sodium Hydrogen exchanger
- a lot of water absorption in addition to sodium

39
Q

Where in the small intestine is there a Na-Bile acid cotransporter [ABST] (secondary active transport) that recirculates bile acids to the liver?

A

TERMINAL ILEUM

  • because bile acids are not recirculated until they reach the terminal ileum, bile acids are present for maximal absorption of lipids throughout the small intestine

(except during ill resection –> gone = fatty stool!)

40
Q

What are the 2 stimuli for contraction of gallbladder?

A
  1. CCK
    - relaxes gallbladder AND causs sphincter of do to relax
  2. ACh (vagal stimulation)
    - contracts gallbladder
41
Q

What causes the release of CCK?

What are the paracrine and endocrine effects of CCK?

A
  1. Amino acids, small peptides, fat acids (monitor peptide)
  2. paracrine: vagal efferents with CCK1 receptors
    endocrine: transported in circulation
42
Q

WHAT IS THE MAJOR STIMULUS FOR GALL BLADDER CONTRACTION & RELAXATION OF SPHINCTER OF ODDI?

A

CCK!!

43
Q

How are gall stones formed?

What is the consequence?

What normally inhibits the precipitation of agents that cause gall stones?

Prolonged storage of bile increases the chances of gall stones how?

What occurs if gall stones block the bile duct & sphincter of Odi?

A
  1. Composed of Cholesterol or Ca2+ Bilirubin
  2. Obstruct biliary flow
    - pain, poor tolerance of fatty food, biliary injury
  3. Anti-Nucleating proteins
  4. prolonged storage of bile increases the chance of NUCLEATION (ex: skipping breakfast might enhance this)
  5. PANCREATITIS!
44
Q

Heme is degraded in the _______ and first forms pigment ____ (green) and then _____ (yellow).

A
  1. RES (reticuloendothelial system)
  2. Biliverdin
  3. Bilirubin
45
Q

Bilirubin binding to albumin increases its ability for what?

What transporter is necessary for hepatocytes to take up Bilirubin- Albumin?

What conjugates bilirubin to glucoronic acid?

A
  1. Increases solubility and thus transported to the liver
  2. OATP
  3. UDP Glucoronyl transferase
46
Q

How does jaundice develop in newborns?

A

Lack UDP enzyme to conjugate bilirubin with glucoronic acid

  • thus it is NOT excreted in the urine and usually stays in the body (combines with albumin)
47
Q

What happens if the conjugated bilirubin is not excreted in urine, and instead is secreted in bile?

Where is it converted to urobilinogen? How?

A
  1. Travels to small intestine
  2. Deconjugated in the terminal ILEUM and colon by colonic bacteria
    - portion is absorbed by Enterohepatic circulation (to liver)
    - remainder is converted to urobilin and stercobilin = EXCRETED in feces
48
Q

Unconjugated or conjugated bilirubin levels in plasma - important tools for diagnosis of liver disease.

State what INCREASES in the following suggest:
1. UNConjugated Bilirubin in PLASMA (2)

  1. Conjugated Bilirubinemia = high amount in URINE (low in plasma)(2)
A
  1. Conjugate:
    a) loss or absence of UGT enzyme (as in newborns)
    b) Oversupply of HEME (ex: transfusion)
  2. Conjugated:

a) Defect in transporter that secretes conjugated Bilirubin in bile
b) blockage of BILE flow
= gallstones

49
Q

What is the major cause of Jaundice?

What are the clinical signs?

What is it usually accompanied with?

When is jaundice clinically manifest?

A
  1. Accumulation of FREE and CONJUGATED bilirubin in blood
  2. Pruritus: itching of the skin
    - increased levels of bile acids in serum
  3. plasma bilirubin > 2mg/dl
    = Hyperbilirubinemia
50
Q

What is the source of ammonia? (2)

What is a major function of the liver in terms of ammonia?

Which form is permeable: NH3 or NH4+?

A
  1. COLONIC bacteria
    - converts it to NH4+ since slightly acidic envi.
  2. Liver - via protein catabolism

LIVER’S MAJOR FUNCTION IS TO DETOXIFY AMMONIA

NH3 is membrane permeable

-liver converts the ammonia to UREA (soluble in water) and excreted in URINE

-if not excreted it is recycled back and converted back to ammonia by colonic bacteria
cycle continues

51
Q

If the metabolic activity of the liver is comprised, what can this lead to in terms of:

  1. Acute phase
  2. Chronic

What is the result of chronic liver disease?

A
  1. Acute phase
    - coma and death
  2. Chronic liver disease
    - gradual decline of mental function
    - ammonia and other toxins not cleared by the liver
  3. RESULT: Hepatic Encephalopathy
52
Q

If the liver is destroyed by way of injury, fibrosis, or tissue degradation, what will be the clinical term?

Causes?

What cells would be over-functional?

A
  1. Liver Cirrhosis
  2. Alcohol, poisons, drugs, hepatitis
  3. Stellate cells that produce too much collagen
53
Q

How does destruction of the hepatic parenchyma lead to portal hypertension?

Where does blood pressure increase?

A
  • stellate cells produce too much collagen, the elasticity of the vascular bed is REDUCED
  • the vascular resistance in the liver INCREASES

= PORTAL HYPERTENSION

  1. Increases in the Sinusoids!
    - this pressure backs up to the PORTAL VEIN (no valves) and other vascular beds
54
Q

What are the main consequences of portal hypertension?

How is this treated?

A
  1. Hepatic Encephalopathy
  2. Esphageal Varices
  3. Caput Medusae
  4. Spider Nevi
  5. Ascites
  6. Spleenomegaly
  7. Rectal Varices

Treated with a SHUNT: portal-caval anastomoses

  • shunt blood from portal vein to to the systemic system

THUS REDUCES hydrostatic pressure in the liver

55
Q

What is one aspect of Portal Hypertension as a result of liver cirrhosis that cannot be treated with portal-caval shunt?

A

HEPATIC ENCEPHELOPATHY

  • ammonia cannot be converted to urea
  • need to give antibiotics to reduce the level of ammonia!

FHB - GI/Metabolism - Exam 3 (21 decks)

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