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GI Term 4 > 5.1- Liver and pancreas > Flashcards

5.1- Liver and pancreas Flashcards

1
Q

What happens in the duodenum?

A
  • the stomach empties chyme, 3 burts per minute into the duodenum
  • Chyme is highly acidic, hypertonic and partly digested
  • therefore the chyme needs to be neutralised
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2
Q

Describe the conditioning of chyme’s acidity and hypertonicity

A
  • Acidity corrected by HCO3- secreted from pancreas, liver and duodenal mucosa
  • Hypertonicity is corrected by osmotic movement of water across the permeable duodenal wall

-As chyme enters the duodenum, it draws water from ECF and dilutes it down; it lots of water leaves ECF and enters gut

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3
Q

What are the pancreas’ endocrine and exocrine functions?

A
  • Endocrine function: Islets of Langerhans secrete insulin, glucagon and somatostatin ie regulation of blood sugar
  • Exocrine function: have acini that secrete proteases, lipases, amylases
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4
Q

What is the exocrine function of the pancreas?

A

exocrine gland with acini and ducts:

1) Acini secrete enzymes
2) Ducts secrete alkaline juice

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5
Q

Describe how acinar secretions are formed in the pancreas?

A
  • acini secrete enzymes in a neutral isotonic fluid
  • enzymes are synthesised on ribosomes as inactive precursors eg trypsinogen
  • packaged into condensing vacuoles by golgi complex
  • form zymogen granuoles secreted by exocytosis
  • these are activated in intestine by enzymatic cleavage to form trypsin
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6
Q

How do enzymes cause pancreatitis?

A
  • happens when peptidases are inappropriately activated in pancreatic ducts and cause inflammation
  • In pancreatitis, these enzymes, especially amylase find their way into the blood stream producing a clear diagnostic sign.
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7
Q

What stimulates acinar secretions?

A

CHOLECYSTOKININ (CCK): signal to secrete enzymes at the right time ie the intestinal phase

  • secreted from I cells in the duodenum in response to hypertonicity and presence of peptides in lumen
  • acinar cells are also stimulated by ACh from postganglionic parasympathetic nerves activated via the vagus
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8
Q

What do duodenal APUD cells do?

A

DNES cells act on D cells to release somatostatin; antagonist of gastrin ie turns off acid secretion

  • Somatostatin inhibits gastrin
  • decreases acid secretions
  • therefore decreases HCl
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9
Q

What is CCK stimulated by?

A
  • hypertonicity
  • fats
  • gastrin
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10
Q

How does duct secretion from the exocrine pancreas work?

A
  • stimulated by secretin, released from S cells in jejunum
  • in response to low pH, to neutralize acid

NEGATIVE FEEDBACK: more acid gets pushed out of the stomachh, more HCO3-

action of secretin is facilitated by CCK

together CCK and secretin neutralise chyme

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11
Q

What are the functions of the liver?

A

1) Metabolism & Endocrinology: -energy metabolism
- makes clotting factors
- components of blood proteins
2) Exocrine function: -makes bile and contains alkaline juice to neutralize stomach acid
- secretes bile pigments and bilirubin

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12
Q

What ducts surround the liver?

A
  • 2 main lobes, both made up of 8 segments (containing lobules)
  • lobules are connected to small ducts which connect w larger ducts to form the COMMON HEPATIC DUCT

this transports bile made by liver cels to gallbladder and duodenun via the COMMON BILE DUCT

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13
Q

What are the two sources of blood supply to the liver?

A

Hepatic artery: oxygenated blood flows in from here

Hepatic Portal Vein: Nutrient-rich blood flows in from the HPV

Blood from HPV enters sinusoids lined with hepatocytes

Drains into central vein

Bile secreted into canaliculi

Bile flows to branch of bile duct

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14
Q

What is the meaning of a portal triad?

A
  • Hepatic Portal Vein
  • Hepatic Artery
  • Bile Duct
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15
Q

What are the two components of bile?

A

1) Bile acid dependent:

  • secreted into canaliculi by hepatocytes
  • contains bile acids and pigments

2) Bile acid-independent:

  • secreted by duct cells
  • alkaline HCO3-, controlled by secretin
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16
Q

What are the 2 main functions of bile?

A

1) Elimination of bilirubin, cholesterol and non-water soluble wastes
2) Bile salts promote emulsification and absorption of dietary fat

17
Q

What are bile acids?

A

critical for digestion and absorption of fat

-Related to cholesterol

  • cholic acid
  • chenodeoxycholic acid
  • conjugated to amino acids

-travel in bile as micelles; bile acids, cholesterol, phospholipids

18
Q

How does digestion of fats occur?

A

lipid digestion is hard bc of the hydrophobic nature of fats

form large globules as stomach acid breaks down natural emulsionlow

  • surface area for enzymes to act ( bc of globules)
  • bile acids emulsify fat into much smaller globules
  • increases SA for lipases to cleave FA’s and glycerol
  • colipase links bile acids and lipases to spread them over surface
19
Q

What is the purpose of micelles in fat emulsification?

A
  • they serve as a vehicle to carry hydrophobic molecules, after lipases and bile acids have acted on fat, through aqueous luminal contents
  • carry them into “unstirred layer” of mucous next cells next to epithelial cells
  • fatty acids are released slowly and enter cells by diffusion
20
Q

How are fatty acids processed in epithelial cells?

A

happens after micelles carry hydrophobic molecules into unstirred layer next to epithelial cells

  • fatty acids are used to re-synthesis lipids in epithelial cells
  • lipids get exported to lymphatics as chylomicrons
  • exist as a lipid with polar protein and phospholipid coat( protective covering)
  • get transported in blood and tissues
21
Q

How are bile acids recovered?

A
  • released into the lumen after fatty acids are absorbed
  • continue to terminal ileum
  • absorbed actively by epithelium of terminal ileum
  • return in hepatic portal blood to hepatic sinusoids
  • hepatocytes take up actively and re-secrete into canaliculi
22
Q

What is the entero-hepatic circulation?

A
  • substances are metabolised in the liver and excreted into bile and passed into intestinal lumen.
  • they are reabsrobed across the mucosa and returned to the liver via portal circulation.
23
Q

What is the meaning of a bile acid pool?

A
  • bile acids remain in gut ie most are recovered, absorbed in the terminal ileum and returned to the liver via the portal vein, from which they are re-secreted.
  • but some are unconjugated by bacterial action, in gut and lost
  • enterohepatic circulation preserves a pool of bile acids. Losses are replaced by hepatic synthesis. ( in hepatocytes)
24
Q

What problem can the bile acid pool cause?

A
  • Bile acids return to the liver and are secreted into bile between meals.
  • The bile acid dependent fraction of bile therefore, must be stored in the GB till the next meal
  • secreted by cannalicular cells well before needed next
  • volume stored is reduced by removal of salts and water( transport across GB epithelium)

Concentration process increases risk of precipitation ie GALL STONES

25
Q

What can gall stones present as?

A
  • often asymptomatic
  • but move into the neck of the gall bladder or the biliary tree
  • causing very painful biliary colic or even obstruction
  • often followed by inflammation and infection.
26
Q

How is bile secreted from storage in GB?

A

-CCK is secreted by the duodenum in response to gastric emptying

  • stimulates contraction of GB muscle
  • ejects concentrated bile acids together w enzymes from pancreas and alkali from pancreas and liver

IN RESPONSE TO SECRETIN ( ie secretin makes HCO3- neutralise the HCl)

27
Q

What is steatorrhoea?

A
  • if bile acids or pancreatic enzymes are not secreted in adequate amounts
  • fat appears in the faeces:
  • pale
  • floating
  • foul smelling
28
Q

What are the bile pigments and what do they do?

A

bilirubin is a bile pigment

  • breakdown product of Hb
  • conjugated in the liver
  • secreted into bile
  • excreted in faeces

accumulates in the blood if it cannot be excreted in the bile, leading to JAUNDICE

29
Q

What are the three types of Jaundice?

A
  1. Pre-Hepatic Jaundice ( hemolytic jaundice)
  2. Hepatic Jaundice ( hepatocellular jaundice)
  3. Post-Hepatic ( obstructive jaundice)
30
Q
A

GI Term 4 (7 decks)

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