Guyton GI And Hepatic Questions Flashcards

1
Q

What are the layers of the GI tract from outer to inner?

A

Serosa, longitudinal muscle,circular muscle,submucosa,mucosa

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2
Q

What kind of electrical activity occurs within the GI tract during the resting phase?

A

Slow waves - characterized by slow undulating changes in the resting membrane potential - most waves do NOT cause GI contraction except in the stomach

These undulating changes in the resting membrane potential result in sodium entry into cells, but not calcium, explaining why contractions are not stimulated

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3
Q

Slow waves of gastrointestinal contraction are regulated by which cells? They are also known as the electrical pacemakers of smooth muscle cells in the GI tract

A

Interstitial cells of cajal

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4
Q

What are spike potentials in reference to gastrointestinal contraction?

A

They occur during stimulation and are characterized by true action potentials (resulting in GI contraction)

This results in a small amount of sodium and large amounts of calcium entry. These cells, unlike neurons, are more dependent on slow calcium channels and therefore have a longer duration action potential by 10-40 fold compared to neurons

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5
Q

When does depolarization of GI smooth muscle occur?

A

Following stimulation by stretch, acetylcholine (from parasympathetic nerves) and specific GI hormones

It is characterized by an overall increase in membrane potential and results in increased in excitability of muscle fibers

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6
Q

When does hyperpolarization of GI smooth muscle occur?

A

Following stimulation by epinephrine and norepinephrine (fight or flight) and is characterized by overall decrease in membrane potential

Results in decreased excitability of muscle fibers

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7
Q

What are tonic contractions of the GI tract caused by?

A

Continuous contractions within the GI tract that operate differently

They are caused by: continuous repetitive spike potentials
Hormones or factors that cause continuous partial depolarization without causing an action potential
Continuous entry of calcium of unknown mechanism

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8
Q

What are the main components of the enteric nervous system?

A
  1. Myenteric or Auerbach’s plexus - found in between longitudinal and circular muscular layers. Controls GI movements (often throughout the entire length of the GI tract). When stimulated it: increases tonic contraction/ tone of the gut wall, increases intensity of rhythmical contractions, and increases the rate or rhythm of contraction. IT also increases the velocity of conduction of an excitatory wave along the GI wall (this results in more rapid movement of peristaltic waves)
  2. Submucosal or Meissner’s plexus - This is found in the submucosa, and controls GI secretion and local blood flow (often as small segments of the GI tract) \

Nervous plexuses can provide both excitatory and inhibitory effects

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9
Q

Name the neurotransmitter substances secreted by the GI tract

A
Acetylcholine - excite GI activity
Norepinephrine - inhibits GI activity (in addition to epinephrine which travels TO the GI tract via the blood as opposed to nerve endings)
ATP
dopamine
CCK
Substance P
Vasoactive intestinal peptide
Somatostatin
Leuenkephalin 
Metenkephalin
Bombesin
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10
Q

What role does the parasympathetic nervous system play in control of the GI tract?

A

Cranial parasympathetic division - (vagus nerve) - provides inner action to the esophagus, stomach, pancreas, small intestines and first half of the large intestines - found originating from the brain stem

Sacral parasympathetic division (pelvic nerve) - provides inner action to the distal large intestines and rectum - found originating from the 2nd to 4th sacral segments of the spinal cord

Post ganglionic neurons - stimulate parasympathetic nerves to increase GI activity - found in both plexuses

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11
Q

What role does the sympathetic nervous system play in inner action of the GI tract?

A

Sympathetic fibers of the GI tract provide inner action to the entire GI tract

Found originating from the T5- L2 segments of the spinal cord

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12
Q

How are afferent sensory nerve fibers of the GI tract activated?

A

Irritation of the gut mucosa
Excessive dissension of the gut
Presence of specific chemical substances in the gut

**They can cause excitation or inhibition of GI movements or secretions under different conditions

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13
Q

What is gastrin, what does it do, and where is it produced?

A

It is a GI hormone
Produced by G cells of the antrum (stomach), duodenum, and jejunum (in response to meal ingestion, dissension of the stomach and release of gastrin releasing peptide following vagal stimulation)
It functions to increase gastric acid secretion and promote gastrointestinal mucosal growth

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14
Q

What is cholecystokinin (CCK), what does it do and where it is produced?

A

GI hormone

It is produced by the I cells of the duodenum, jejunum and ileum (in response to fat, fatty acids, and monoglycerides in the small intestines).

It stimulates: pancreatic enzyme and bicarbonate secretion, stimulates gallbladder contraction, growth of the exocrine pancreas and inhibits gastric emptying. It also acts to inhibit appetite

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15
Q

What is secretin, what does it do and where is it produced?

A

It is a GI hormone

It is produced by the S cells of the duodenum, jejunum and ileum (in response to gastric acid within the small intestine)

If stimulates pepsin secretion, pancreatic bicarb secretion, biliary bicarb secretion, growth of the exocrine pancreas. It INHIBITS gastric acid secretion

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16
Q

What is gastric inhibitory peptide, what does it do and where is it produced?

A

GI hormone

AKA GIP or glucose dependent insulinotropic peptide

IT is produced by the K cells of the duodenum and jejunum (in response to fats, amino acids and to a lesser extent carbohydrates in the small intestines).

It acts to inhibit gastric motility and promote insulin secretion

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17
Q

What is motilin, what does it do and where is it produced?

A

GI hormone

It is produced by the M cells of the duodenum and jejunum (in response to fasting)

It stimulates the inter digestive myoelectric complexes every 90 minutes during fasting (I.e. increases gastrointestinal motility)

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18
Q

What are the two different functional types of movements within the GI tract?

A

Propulsive movement - aka peristalsis - moves food/ingesta forward. It is stimulated byt dissension of the GI tract, chemical or physical irritation to the tract lining OR a strong parasympathetic nervous signal. Propulsive movement is mediated by the myenteric plexus (must be active for peristalsis to occur). Relaxation occurs ABORAD to peristalsis (receptive relaxation) and unidirectional (orad to aborad) movement occurs

Mixing movements - occurs differently in different parts of the GI tract. There are two different types. 1) peristalsis (especially when food is propulsed against a closed sphincter), 2) local intermittent constrictive contractions (which can occur every few cm in the gut wall to chop or shear GI content)

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19
Q

List the direct of blood flow through the GI tract all the way back to the caudal vena cava (venous drainage)

A

Splanchnic circulation = blood flow through GI tract and spleen, pancreas, liver

Blood flows from GI to portal vein and into hepatic sinusoids. Blood has access to the reticuloendothelial system of the liver to clear pathogens and provide hepatocytes with nutrients from food.

Blood leaves the liver via the hepatic veins before entering the caudal vena cava.

**Almost all fats that are absorbed enter the lymphatic system and are sent into the blood via the thoracic duct, meaning that they bypass the liver and are not carried in portal blood at all.

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20
Q

How/why does blood flow to the GI tract increase?

A
  1. Following ingestion of food
  2. Release of vasodilatory hormones: CCK, vasoactive intestinal peptide, gastrin, secretin)
  3. Release of kinins (Kalinin and bradykinin) from the GI tract —> vasodilation
  4. Decreased oxygen concentration following increased metabolic rate —> compensatory vasodilation and increased blood flow for improved oxygen deliver

Within GI villi, oxygen is exchanged from the arteriole to the venule with minimal oxygen reaching the tip of the villi, explaining why billows blunting and GI sloughing can occur during periods of shock

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21
Q

How to the sympathetic and parasympathetic nervous systems regulate blood flow to the GI tract?

A

PNS - increase blood flow indirectly by secretion of hormones

SNS - directly by vasoconstriction of intestinal and mesenteric veins (this can provide lifesaver perfusion to other parts of the body during shock).

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22
Q

Which cranial nerve innervates the muscles of mastication?

A

CN V

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23
Q

Name the three stages of deglutition (swallowing)

A

Voluntary —> pharyngeal —> esophageal

24
Q

Which nerves are important in the swallow reflex?

A

Afferent nerves - trigeminal (CN V) and glossopharyngeal (IX) receive input from sensory receptors around the tonsil lab pillars —> swallowing/ deglutition center in medulla/ lower pons —> efferent nerves (trigeminal, glossopharyngeal, vagus, and hypoglossal)

25
Q

What kind of muscle is present within the esophagus of cats? Of dogs?

A

Cats - proximal 2/3 is striated, distal 1/3 is smooth muscle

Dogs - entire esophagus is striated muscle

26
Q

What is the migrating motility complex?

A

Infrequent waves of peristalsis that functions to sweep residual undigested material through the GI tract (aka inter digestive house keeper)

27
Q

List the factors that play a role in stomach emptying

A
  1. GAstric factors (less important) — 1) gastric distension (via activation of the myenteric plexus), 2) gastrin
  2. Small intestinal factors
    2a. Nervous/ enters gastric nervous reflex - via local enteric reflex arcs, prevertebral sympathetic ganglia and the brain stem — results from duodenal distension, duodenal mucosal irritants or acidity, duodenal chyme, hypo/hyperosmolar chyme, duodenal proteins, and fats (to a lesser extent)
    2b. Hormonal (CCK, secretin, and GIP) — duodenal fat (CCK and GIP), duodenal carbohydrates (GIP), duodenal mucosal irritants and acidity (secretin)
28
Q

What factors regulate small intestinal motility?

A

Nervous - gastroenteritis reflex

Hormonal —
Stimulatory — gastrin, CCK, insulin, motilin, serotonin

Inhibitory - secretin, glucagon

29
Q

What are the main functions of the colon?

A

Absorption of water and electrolytes to form feces — proximal colon

Storage of feces until they can be expelled - distal colon

30
Q

What are haustrations?

A

Mixing movements of the colon - mediated by concurrent segmental and Teniae coli (three longitudinal muscles along the length of the colon) contraction —> result in bulging of non contracted areas and mixing of colonic contents

31
Q

What are the types of secretory glands in GI tract?

A
Mucous/goblet cells
Specialized secretory cells — found within crypts of lieberkuhn of the small intestines
Tubular glands (e.g. oxyntic glands - found in stomach and proximal duodenum
Complex glands (salivary gland, pancreas, liver)
32
Q

What are the basic mechanisms of stimulation of the GI tract?

A
  1. Enteric NS - occurs via tactile stimulation, chemical irritation, distension of gut wall
  2. Parasympathetic stimulation - stimulation of most of upper GI
  3. Sympathetic stimulation - stimulation of secretion where there is not already parasympathetic stimulation (in which cause causes inhibition via vasoconstriction
  4. Hormones
33
Q

What are the phases of salivary gland secretion?

A
  1. Ptyalin and mucin production — occurs in acini of salivary gland
  2. Ionic modification — Occurs in collecting ducts
    2a. Low sodium - caused by active resorption of sodium (at higher rate that potassium excretion resulting in electrochemical concentration gradient)
    2b. High potassium - caused by active excretion of potassium (lower rate than sodium resorption resulting in electrochemical concentration gradient)
    2c. Low chloride - caused by passive resorption due to electrochemical concentration gradient
    2d. High bicarbonate - caused by passive Cl-HCO3 exchange and active excretion
34
Q

Where are oxyntic glands located and what do they produce?

A

Aka gastric glands

Located in the body and fundus of the stomach

Produce HCl, Pepsi oven, intrinsic factor, and mucus

Components: 1) mucous neck cell - produces alkaline mucous (Stimulated by ACh release)

2) parietal or oxyntic cell - produce HCl and intrinsic factor (DOGS ONLY) Stimulated by ACh, gastrin and histamine stimulation
3) Enterochromaffin like cell. - produces histamine (stimulated by gastrin)
4) Peptic aka chief cell - produces pepsinogen (stimulated by ACh release (via gastric enteric nervous plexus) and detection of stomach acidity )

35
Q

Where are pyloric glands located and what do they produce?

A

Produce mucus and gastrin

They are located in the antrum and the pylorus

Components:

1) mucous cell - produce alkaline mucous - stimulated by ACh release
2) Gastrin or G cell - produces gastrin (releases directly into the gastric lumen for enterochromaffin like cell stimulation) - these cells are stimulated by detection of amino acids in gastric lumen

36
Q

How is HCL produced in the stomach and by what cells?

A

Produced by parietal cells.

  1. Hydrogen excretion - 1a. Dissociation of water into H+ and OH- within the parietal cell. Active secretion of H+ occurs in exchange for K+ via an H//K ATPase pump in the apical membrane
    1b. There is active transport of K+ into the cell and Na out of the cell via Na/K ATPase pump in the basolateral membrane
    1c. This results in passive diffusion of K+ into the lumen and Na into the cell equaling out Na and K shifts
  2. Chloride excretion -
    2a. With excretion of H+, OH- accumulates and combines with CO2 to form HCO3- via carbonic anhydrase, which leaves the cell in exchange or Cl- on the basolateral membrane.
    2b. Cl- follows H+ into the gastric lumen by passive transport across the apical membrane
  3. Water secretion -
    3a. - With excretion of ions from the cell, water passes passively from the interstitial space to the lumen
37
Q

What are the excitatory phases of gastric secretion?

A
  1. Cephalic phase - following site, sound, smell or thought of food —> cerebral cortex, amygdala, and hypothalamus is stimulated, resulting in vagal Ly mediated up regulation of HCl (from parietal cells) and gastrin (from G cells)
  2. Gastric phase - occurs following distension of the stomach with food. Results in further HCl production from parietal cells through local enteric reflexes, vasovagal reflexes and gastrin (G cells) and histamine (Enterochromaffin like cell) production
  3. Intestinal phase - occurs when chyme enters duodenum, resulting in further HCL production through up regulation of gastrin (G cells in duodenum)
38
Q

What are inhibitor factors of gastric secretion?

A
  1. Presence of increased volume, acid, amino acids or irritation within the duodenum (reverse enterogastric reflex)
  2. Hormones: secretin, gastric inhibitory peptide (GIP), vsaoactive intestinal peptide,

somatostatin — (binds to parietal cells and inhibits Na/K ATPas pump), enterochromaffin cells (inhibit histamine release) and G cells (inhibit gastrin release)

Somatostatin is produced by D cells in glandular and natural sstomach in response to decreased pH

39
Q

What is the difference in anatomy between dog and cat pancreas?

A

Dogs - pancreatic duct (smaller duct) enters the duodenum adjacent to the common bile duct at the MAJOR duodenal papilla. The accessory pancreatic duct (larger duct) opens at the minor duodenal papilla and is the most important duct in the dog.

Cats - the pancreatic duct fuses with the common bile duct before entering the duodenum at the duodenal papilla (increasing cats’ predisposition to triad it is). There is NO ACCESSORY pancreatic duct in the cat

40
Q

What are the protein digesting enzymes released from the exocrine pancreas? What does each of them do?

A

Trypsin - hydrolyzes whole and partially digested proteins into peptides of various sizes (does NOT cause release of individual amino acids)

Chymotrypsin - hydrolyzes whole and partially digested proteins into peptides of various sizes (DOES NOT cause release of individual amino acids)

Carboxypolypeptidase - hydrolyzes some peptides into individual amino acids, completing digestion

41
Q

What are carbohydrate digesting enzymes released from the pancreas?

A

Pancreatic amylase - hydrolyzes starches, glycogen and most other carbs except cellulose to form most disaccharides

42
Q

What are the fat digesting enzymes released from the exocrine pancreas?

A

Pancreatic lipase - hydrolyzes neutral fat into FFA and monoglycerides

cholesterol esterase - hydrolyzes cholesterol esters

Phospholipase - hydrolyzes fatty acids from phospholipids

43
Q

How does the pancreas avoid self digestion?

A
  1. Secretes inactive enzymes (enzymes are made in their inactive rooms and become active only by being released into GI tract.

1a. Trypsinogen is activated by enterokinase (Secreted by SI mucosa when it comes into contact with chyme) when it reaches the SI
1b. Chymotrypsinogen - activated by trypsin to chymotrypsin
1c. Procarboxypolypeptidase. - activated by trypsin

  1. Trypsin inhibitor - inhibitor protein secreted simultaneously with proteolytic digestive enzymes
44
Q

How does the pancreas secrete bicarbonate?

A
  1. Diffusion of CO2 from blood and subsequent combination with water to form carbonic acid (via carbonic anhydrase)
  2. Bicarb is transported (from dissociated carbonic acid, and is actively transported into the cell by Na-HCO3 co transporter) into the lumen by active Cl-HCO3 exchanger
  3. Chloride leaks back into the lumen by passive diffusion
  4. Hydrogen ions (from carbonic acid dissociation) are removed by Na - H exchanger
  5. Sodium passively diffuses into the lumen - it “follows” bicarbonate to maintain electro neutrality
45
Q

What neurotransmitter stimulates pancreatic enzyme secretion?

A

Parasympathetic NS — Acetylcholine

46
Q

What hormones stimulate pancreatic enzyme secretion and what are their other effects? What part of the GI tract are they secreted from?

A
  1. CCK/ cholecystokinin - secreted by I cells of the duodenum and upper jejunum when food (Especially proteins and long chain fatty acids) enters the small intestines. CCK release results in 1. Pancreatic enzyme secretion, 2) contraction of the gallbladder, 3) relaxation of the sphincter of oddi (smooth muscle that surround the end portion of the common bile duct and pancreatic duct)
  2. Secretin - secreted by the S cells of the duodenal and jejunum mucosa when highly acidic chyme (pH 4.5) enters the SI. This results in water and sodium bicarb secretion
47
Q

What are the primary functions of bile?

A

Fat digestion (via emulsification of fats and Michelle mediated fatty acid absorption)

Excretion of waste products

48
Q

What are the stages of bile secretion?

A
  1. Bile acid and cholesterol secretion - performed by hepatocytes
  2. Bile accumulation and secretion - 2a. Bile flows directly from the canniliculi to the terminal bile ducts then on to the hepatic and common bile ducts or via the gall bladder (where bile acids are stored and concentrated via active transport of sodium) and cystic duct. 2b. Bile accumulation and secretion involves the addition of water and sodium bicarbonate by bile cells that line the ducts (bicarbonate and water are secreted in response to secretin)
  3. Enterohepatic recycling - performed by absorption of bile salts (94%) as I cells within the SI
49
Q

What are the types of secretory glands of the small intestine? What regulates their secretion?

A
  1. Brunner’s glands - compound mucous glands in the first few cm of the duodenum that secrete alkaline protective mucous. These glands are stimulated by tactile or chemical irritation of the duodenum, vagal stimulation or GI hormones (e.g. secretin)
  2. Crypts of lieberkuhn - small pits between villi along the entire surface of the SI containing mucous producing goblet cells and water-electrolyte producing enterocytes

**Many enzymes secreted within the SI (e.g. sucrase, Maltese, lactase) are not released into the lumen but rather act on the molecules as they are absorbed into enterocytes)

**the enteric NS regulates their secretion

50
Q

What types of secretory glands are present in the large intestine? What regulates their secretion?

A

Crypts of Lieberkuhn - small pits that contain mucous producing goblet cells

Regulation - Enteric NS and parasympathetic NS (pelvic nerve)

51
Q

Name the important components (enzymes) of carbohydrate digestion.

A
  1. Salivary amylase (alpha amylase) - hydrolysis of minority (20-40%) of starches into maltose. Made in salivary glands and is active in stomach until gastric acid secretion
  2. Pancreatic amylase (alpha amylase) - hydrolysis of the majority of starches (50-80%) into maltose rapidly (15 - 30 min). Produced by the pancreas
  3. Maltase and alpha dextranase - hydrolysis of maltose into glucose. Produced by enterocytes of the brush border and active on luminal surface of cell membrane
  4. Lactase - hydrolysis of lactose into galactose and glucose. Produced by enterocytes of Brush border
  5. Sucrase - hydrolysis of sucrose into fructose and glucose. Produced by enterocytes of brush border

Following complete hydrolysis into water soluble monosaccharides, these molecular are absorbed immediately

52
Q

Name the components of protein digestion and where they are secreted from.

A
  1. Pepsin - results in initial hydrolysis of proteins (esp collagen), produced by chief cells of the stomach. Requires highly acidic environment.
  2. Pancreatic proteolytic enzymes (trypsin, chymotrypsin, carboxylpeptidase and elastase) - results in further hydrolysis of proteins into polypeptides (and to a lesser extent amino acids)
  3. Intestinal proteolytic enzymes (aminopolypeptidases and dipeptidases) - results in hydrolysis of polypeptides into AA, dipeptides and Tripeptides. Produced by enterocytes of brush border and are active on luminal surface of the cell membrane
  4. Cytosolic peptidases - results in hydrolysis of dipeptides and tripeptides into AA. Produced within the cytosol of enterocytes of the brush border.

**following complete hydrolysis of AA, these molecules are then transported into the bloodstream

53
Q

Name the components of fat digestion and where they come from.

A
  1. Lingual lipase - inconsequential (<10%) hydrolysis of triglycerides. Produced by salivary glands
  2. Bile acids and lecithin - results in fat emulsification (detergent effect) allowing increased surface area for lipases to act on. This is possible due to the lipophilic and hydrophilic structure of bile acids and lecithin, which reduce the interfacial tension and allow for dispersion of fat globules. These are produced by the liver
  3. Pancreatic lipase - results in almost complete hydrolysis of triglycerides into FFA and 2 monoglyceride. Produced by the pancreas
  4. Enteric lipase - results in almost complete hydrolysis of triglycerides into FFA and 2 monoglyceride (redundant due to efficacy of pancreatic lipase. Produced by enterocytes of brush border.

**following hydrolysis into FFA and monoglyceride so ,these molecules are ferried by bile salt micelles which accelerate fat digestion by removal of reaction products from the lumen.

**Cholesterol esters (cholesterol combined to FFA) and phospholipids (contain FFA) are hydrolyzed by cholesterol ester hydrolase and phospholipase A2 made by the pancreas

54
Q

What is the liver lobule and what are its components?

A

Aka: basic functional unit of the liver

Components:
1. Central vein - central blood vessel of the liver lobule draining portal blood into the hepatic veins and vena cava
2. Cellular plates - groups of cells that radiate from the central vein with a bile canaliculi at their center
3. Bile canaliculi - duct uses that lie in the center of hepatic plates and transport bile to bile ducts
4. Portal venules - peripheral blood vessels that provide blood from the portal vein to the sinusoids
5. Sinusoids - flat, branching blood vessels that transport blood from the portal venules to the central vein
6. Hepatic arterioles - blood vessels that carry blood from the systemic circulation to the sinusoids
7. Endothelial cells - lining of sinusoids that have very large pores (allows free movement of large molecules into the space of disse)
8 .Kupffer cells - resident macrophages capable of phagocytizing bacteria and other foreign matter in hepatic sinus blood (filtration of >99% of bacteria that enter the liver)
9. Spaces of Disse - interstitial space between endothelium and hepatic cells that connect with lymphatic vessels and removes excess fluid

55
Q

How is liver regeneration stimulated?

A

Hepatocyte growth factor produced by mesenchymal cells (can regenerate as long as no ongoing infectious/ inflammatory stimulus)

Liver regeneration is terminated by TGF B made by hepatocytes

56
Q

What coagulation proteins does the liver synthesize?

A

Fibrinogen
Prothrombin
Vitamin K dependent factors — II, VII, IX, X

57
Q

How is bilirubin metabolized?

A

RBC destruction —> macrophages phagocytize hemoglobin and heme which is converted to iron and pyrole

Pyrole forms biliverdin —> reduced to unconjugated bilirubin —> unconjugated bilirubin travels on albumin to liver where it is conjugated

Conjugated bilirubin is released in the bile where approximately half is broken down by bacteria into urobilinogen —> urobilinogen is able to be reabsorbed into the blood stream and enterohepatically recycled or excreted via the kidneys

Urobilinogen that remains within the GI tract is oxidized into stercobilin

Urobilinogen that is renal excreted is oxidized into urobilin