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Digestive System Physiology > Pancreas and Liver > Flashcards

Pancreas and Liver Flashcards

1
Q

The pancreas contains 2 types of tissue. What are these, and what are they involved in?

A

EXOCRINE tissue
ENDOCRINE tissue

Both involved in metabolism of nutrients, BUT:

  • have different functions
  • under different regulation
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2
Q

What type of cells make up exocrine tissue?

A

DUCT CELLS

ACINAR CELLS

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3
Q

What type of cells make up endocrine tissue?

A

ISLETS OF LANGERHANS

release glucagon [a cells] and insulin [b cells]

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4
Q

What is released from DUCT cells?

A

AQUEOUS ALKALINE SOLUTION
(sodium bicarb. rich)

–largest component of pancreatic juice

–neutralises chyme!
.secrete aqueous NaHCO3- [into lumen]
.absorb H+ [into blood]

(Acid-Base balance of body not altered by digestion)

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5
Q

What is released from ACINAR cells?

A

PANCREATIC ENZYMES

  • Proteolytic enzymes
  • Pancreatic Amylase
  • Pancreatic Lipase
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6
Q

What is the function of proteolytic enzymes?

A

PROTEIN digestion

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7
Q

What is the function of pancreatic amylase?

A

CARB. digestion

  • hydrolyses polysaccharides into disaccharides (maltose)
  • can be secreted in ACTIVE from as secretory cells don’t contain polysaccharides
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8
Q

What is the function of pancreatic lipase?

A

FAT digestion

  • hydrolyses triglycerides into monoglycerides & free fatty acids
  • secreted in ACTIVE from as triglycerides are not the structural component of pancreatic cells
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9
Q

What are the 3 main pancreatic proteases?

What happens when these enzymes are released into the duodenum?

A
  1. Trypsinogen
  2. Chymotrypsinogen
  3. Procarboxypeptidase

Trysinogen —(*Enterokinase)—> Trypsin
*expressed on epithelial cells

Chymotrysinogen —(Trypsin)—> Chymotrypsin
Procarboxypeptidase —(Trypsin)—> Carboxypeptidase

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10
Q

What protective mechanisms are in place to ensure the cells of the pancreas & duodenum (S.I.) aren’t digested by these proteolytic enzymes?

A
  • 3 main pancreatic enzymes are all stored in INACTIVE form
  • Trysinogen —(*Enterokinase)—> Trypsin
  • Pancreas produces TRYPSIN INHIBITOR
  • Duodenum secretes mucus
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11
Q

What is pancreatic insufficiency?

A

Pancreas not able to secrete sufficient enzumes

THUS, digestion of food incomplete/not possible

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12
Q

What is the main outcome of pancreatic insufficiency?

A

STEATORRHEA

=excess fat in faeces (~70%)

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13
Q

How are exocrine secretions regulated?

A

BY HORMONES

  • secretion
  • CCK
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14
Q

What happens when ACIDIC chyme is released into the duodenum?

A

SECRETIN release from enteroendocrine cells of duodenal wall (duod. mucosa) –>

Pancreatic DUCT cells –>

Increase secretion of aqueous NaHCO3 solution into duodenal lumen

THUS, this NEUTRALISES the acidic chyme

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15
Q

What happens when FAT & PROTEIN-RICH chyme is released into the duodenum lumen?

A

CCK release from enteroendocrine cells of duodenal wall (duod. mucosa) –>

Pancreatic ACINAR cells –>

Increase secretion of pancreatic digestive enzymes into duodenal lumen

THUS, this DIGESTS the fat & protein in chyme

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16
Q

SECRETIN

A

Secretion of ENZYME-rich pancreatic juice

17
Q

CCK

A

Secretion of BICARB.-rich pancreatic juice

18
Q

What is the pancreas innervated by?

A

Predominant stimulation is during intestinal phase!

Small amount of stim. in response to VAGAL (cephalic phase) & GASTRIN (gastric phase)

-causes a limited release of pancreatic juice

19
Q

What is the major DIGESTIVE role of the Liver?

A

SECRETION OF BILE SALTS

20
Q

Discuss blood flow to and from the liver.

A

Liver RECEIVES blood from 2 sources:

  1. arterial blood from AORTA (via hepatic artery)
  2. venous blood from DIGESTIVE TRACT (via hepatic PORTAL vein

Blood flow FROM liver:
-via hepatic vein
(leads to INFERIOR VENA CAVA)

21
Q

Discuss blood flow in a single liver lobule

A

Blood flows from periphery –>
Sinusoids (lined by Kupffer cells) –>
Central vein
[central veins converge to become hepatic vein!]

22
Q

Discuss the bile secretion pathway in the liver

A

Bile secreted from hepatocytes –>
Bile canaliculus –>
Peripheral bile duct
[bile ducts converge to become the common bile duct]

23
Q

What are the components of bile?

A

-Bile salts
(derivatives of cholesterol)

-Cholesterol

-Lecithin
(phospholipid)

-Bilirubin
(waste product from old RBCs)

-Aq. alkaline fluid
(from duct cells)

24
Q

What is the function of the GALLBLADDER?

A

STORAGE OF BILE BETWEEN MEALS
(as the liver secretes bile continuously)

CONCENTRATES BILE (5-10x)
-actively transports salt (Na+) out, THUS H20 follows!)

–Holds 50mL of concentrated bile (so can accommodate larger volumes from the liver)

25
Q

How does bile travel to the duodenum?

A

Ducts from LIVER - merge to form COMMON HEPATIC DUCT

Gallbladder - CYSTIC DUCT

–CYSTIC DUCT & COMMON HEPATIC DUCT merge to form BILE DUCT & sphincter

26
Q

How do bile salts facilitate fat digestion & absorption?

A
  1. EMULSIFICATION [digestion]

2. MICELLES [absorption]

27
Q

How do bile salts facilitate emulsification?

A

Triglycerides are INSOLUBLE in H20
THUS, aggregate in aq. S.I.

Bile salt molecules absorb on the surface of lipid droplets
THUS, provides a larger surface area on which the enzyme pancreatic lipase can act to digest the fats into fatty acids and glycerol.

28
Q

What is the structure of a bile salt molecule?

A

LIPID-SOLUBLE PORTION
(derived from non-polar cholesterol)

NEGATIVELY CHARGED H20-SOLUBLE PORTION
(polar hydroxyl & carboxyl groups all located on 1 side)
( (-) charge causes electrical repulsion between lipid droplets)

THUS, bile salt molecules absorb on the surface of lipid droplets

29
Q

How do bile salts facilitate micelles?

A
  • The formation of micelles facilitates FAT ABSORPTION
  • 3-10nm
  • Bile salts & lecithin aggregate in small clusters, with fat soluble parts forming a hydroPHOBIC core

-Are H20-soluble thanks to hydroPHILIC shell
(But are able to dissolve lipid soluble molecules in the core. e.g. monoglycerides, FFA, vitamins & cholesterol)

30
Q

Discuss cholesterol’s ability to dissolve in the core of a micelle

A

The amount of cholesterol that can be carried depends on relative amount of bile salts & lecithin

If cholesterol secretion is out of proportion -->
MICROCRYSTALS FORM (cholesterol gallstones)
31
Q

What is a form of treatment for cholesterol gallstones?

A

Ingestion of bile salts –>
THUS, increases bile salt pool –>
THUS, dissolves cholesterol!

32
Q

What is enterohepatic circulation?

A

BILE SALT RECYCLING
Following their role in fat digestion + absorption, most bile salts are reabsorbed by active transport in the terminal ileum! (approx. twice)

-they are returned via the HEPATIC PORTAL SYSTEM to liver, the re-secreted

33
Q

What is bile secretion regulated by?

A

CHOLERETICS

=substances that increase bile secretion

34
Q

What are the types of choleretics that regulate bile secretion?

A

–CHEMICAL
BILE SALTS stimulates their own secretion when returned to liver during meal digestion

–HORMONAL
SECRETIN stimulates an aq. NaHCO3 bile secretion to neutralise chyme

–NEURAL
VAGAL stimulation of liver to increase bile flow during cephalic phase plays minor role

35
Q

What is Bilirubin?

A

-2nd major component of bile!
(not involved in digestion, instead a waste product excreted in bile)

-Derived from degradation of HEME (iron-containing) part of haemoglobin in RBCs

–bilirubin is a yellow pigment, makes bile yellow
–in intestines, bilirubin is modified by bact. enzymes (makes faeces brown)
–some modified bilirubin is reabsorbed & can be excreted in urine (unmodified can’t pass kidneys)
[makes urine yellow]
–patients w. jaundice have a yellow colour as bilirubin accumulates in body (haemolytic, hepatic, obstructive)

36
Q

What is hepatitis?

A

Inflammatory disease of liver!

37
Q

What are the causes of hepatitis?

A

MULTIPLE CAUSES:

  • viral
  • obesity
  • toxic agents
38
Q

What are the outcomes of hepatitis?

A

Repeated or prolonged inflammation
(most commonly associated w. alcoholism leads to CIRRHOSIS!)

-Active liver tissue is reduced (replaced by CT!) & eventually leads to liver failure

Digestive System Physiology (6 decks)

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