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GI Week 3 - WLB > Pancreas and Gallbladder Physiology - Prunuske > Flashcards

Pancreas and Gallbladder Physiology - Prunuske Flashcards

1
Q

T/F Amino acids enter enterocytes along with Na+ ions, using five different co-transporters that are selective for neutral, aromatic, imino, positively charged and negatively charged amino acids.

A

True

(peptides are co-transported with H+)

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2
Q

T/F Monosaccharides leave the enterocyte by means of a Na+-coupled transporter protein on the basolateral surface of the cell.

A

False

(on apical side)

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3
Q

What regulating enzymes effect the action of the pancreas?

A
  • H+ in duodenum activate => Secretin => travels to pancreas => release bicarbonate
    • inhibit gastric motility
    • inhibit secretion
  • AA’s/Fat => CCK => pancreas
    • inhibit gastric motility
    • inhibit secretion
    • relaxation of sphinter of Oddi
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4
Q

What is the function of the Pancreas exocrine secretion?

A

(~90% of cells)

  • Release digestive enzymes and bicarbonate into the duodenum
    • Acinar cells secrete digestive enzymes
    • Centroacinar and duct cells dilute pancreatic enzymes and make rich in sodium and bicarbonate
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5
Q

What is the total amount of exocrine pancreas secretions per day?

A

Exocrine pancreas secretions = 1.5 L/day

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6
Q

What are the Pancreatic Acinar Cell Secretory Products?

A
  • Proteases
    • Trypsinogen
    • Chymotrypsinogen
    • Proelastase
    • Procarboxypeptidase A/B
  • Amylolytic enzymes
    • Amylase
  • Lipases
    • Lipase
    • Nonspecific esterase
    • Phospholipase A2
  • Nucleases
    • Deoxyribonuclease
    • Ribonuclease
  • Others
    • Procolipase
    • Trypsin Inhibitors
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7
Q

How do pancreatic acinar enzyme products get delivered to the correct place?

A

Enzymes are synthesized with an N-terminal signal peptide (Rough ER), which targets them for the

secretory pathway where they are packaged into zymogen granules (Golgi) and prevents them

from being exposed to the cytosol.

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8
Q

What amount of Pancreatic Exocrine Secretion occurs during the Cephalic/Gastric phase?

A
  • 30% of pancreatic enzyme volume secreted
    • low volume
  • Acinar cells activated by parasympathetic efferents (ACh) from vagal centers in the brain and secondary to gastrin release
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9
Q

What amount of Pancreatic Exocrine Secretion occurs during the Intestinal phase?

A
  • 70% of pancreatic enzyme volume secreted
    • increased enzyme, high volume
  • Acinar cells are activated by vago-vagal reflex and by fat/amino acids in duodenum
    • I cells release CCK
    • H+ ions cause S-cells to release secretin activating ductal cell secretion of bicarbonate.
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10
Q

What major stimuli promote compound exocytosis in acinar cellspromote compound exocytosis in acinar cells?

A
  • CCK and vagal stimulation (acetylchoine, GRP)
  • Ca2+ signaling most important with cAMP signaling playing modifying role
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11
Q

How is the release of CCK regulated?

A
  • CCK-Releasing Peptide and Monitor Peptide
    1. During cephalic and gastric phases, vagal stimulation causes release of pancreatic enzymes (Monitor Peptide).
    2. During intestinal phase, amino and fatty acids cause release of CCK-RP.
    3. CCK-RP and Monitor Peptide causes release of CCK from I cells into the blood.
    4. CCK increases release of Monitor peptide and pancreatic enzymes.
    5. Pancreatic enzymes digest luminal nutrients, CCK-RP, and Monitor peptide turning off CCK secretion.
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12
Q

What effects does the release of CCK have on the Stomach, Pancreas, Gallbladder, and Sphincter of Oddi after it is stimulated by fat and protein in the duodenum?

A
  • Promotes gastric emptying
  • Stimulate pancreatic secretion
  • Promotes gallbladder contraction
  • Causes relaxation of the Sphincter of Oddi
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13
Q

How are the pancreatic enzymes activated?

A
  • Enteropeptidase from duodenal brush border membranes cleaves trypsinogen to its active forms trypsin.
    • Trypsin then activates lipases and endopeptidases chymotrypsin and elastase.
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14
Q

Hereditary pancreatitis occurs due to a mutation in the trypsinogen PRSS1 gene causes activation of digestive enzymes in the pancreas which can lead to inflammation

Would this be autosomal dominant or recessive?

A

Autosomal Dominant

(mutations involving only one allele produces a phenotype)

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15
Q

When duodenal pH < 4.5, S cells release secretin, which raises the pH by increasing bicarbonate secretion from the pancreatic ducts, biliary ducts, and duodenal mucosa.

Do you predict a patient on a proton pump inhibitor will have increased or decreased duodenal bicarbonate secretion postprandially?

A

Decreased

(less secretin released from the duodenum, decreased signal to the pancreas to release bicarb)

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16
Q

What enzyme initiates secretion of bicarbonate solution by pancreatic duct cells?

A

Secretin

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17
Q

How is bicarbonate produced and released by the pancreas?

A
  • Na+/K+ ATPase on basolateral membrane generates the “power” in the form of a steep sodium gradient.
  • Carbonic anhydrase promotes formation of H+ and HCO3- and some bicarbonate from the alkaline tide (stomach) is taken up from the bloodstream by NBC in response to depolarization.
  • CFTR supplies the Cl- for the HCO3-/Cl- exchanger and is regulated by secretin activation of cAMP.
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18
Q

What would be the consequence in pancreas with cystic fibrosis?

A

decreased bicarbonate release

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19
Q

What are the causes of pancreatitis?

A
  • Cystic fibrosis
  • Occlusion of pancreatic duct:
    • gallstones
    • malignancy
  • Alcohol can be metabolized into products that cause hyperstimulation of acinar cells resulting in intracellular trypsin activation and cell death.
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20
Q

What are the consequential effects in the pancreas after pancreatitis develops from CF, gallstones, malignancy, or alcohol?

A
  • Upper abdominal pain from autodigestion of pancreatic tissue
    • can lead to vomiting and sympathetic activation
  • Enzymes spill over into circulation
    • elevated serum amylase and lipase levels.
  • Malabsorption of fat and fat-soluble vitamins (A,D,E,K) => steatorrhea
    • no lipase released
  • Malignancy, Diabetes, and Infections
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21
Q

What part of your brain is important in regulating energy homeostasis by maintaining a balance between food intake and energy expenditure?

A

Hypothalamus

22
Q

What two hormones are important in the GI Hormonal Control of Nutrient Assimilation?

A
  • GLP-1 and GIP
    • GLP-1 is an incretin > increase insulin and decrease glucagon
    • Oral glucose leads to higher insulin than IV glucose since glucose causes a release of glucagon-like peptide-1 (GLP-1) from intestinal L cells and glucose-dependent insulinotropic peptide (GIP) from K cells
23
Q

What things stimulate insulin secretion of pancreatic β-cells in the islets of Langerhans?

A
  • GLP-1
  • amino acids
  • cholecystokinin
  • acetylcholine
24
Q

What things are negative regulators of insulin secretion by the pancreatic β-cells in the islets of Langerhans?

A
  • Somatostatin (D cells)
  • Norepinephrine
25
Q

What four things act as satiety signals at the hypothalamus decreasing food intake and increasing energy expenditure?

A
  • GLP-1
  • CCK
  • Insulin
  • Leptin (adipose tissue)
26
Q

What peptide hormone produced in the fundus of the stomach during fasting stimulates appetite (orexigenic) and decreases energy expenditure through neuropeptide Y and agouti-related peptide?

A

Ghrelin

27
Q

Individuals with gastric bypass have relatively flat ghrelin levels. What would be the consequence of giving ghrelin prior to eating at a buffet?

A

OVEREAT!

28
Q

What are the major functions (5) of the liver?

A
  • Detoxifies drugs (first-pass metabolism) and bacteria
  • Metabolism of carbohydrates, fats, and proteins
  • Store glycogen, fats, vitamin B12, A and K
  • Synthesis of factors important for circulatory system
  • Bile Formation enables lipid uptake and excretion of lipophilic molecules
29
Q

80% of the total cells in the liver are what?

A

Hepatocytes

(Metabolic factories able to regenerate and produce bile)

30
Q

What three things make up the Hepatic Triad?

A

portal vein + hepatic artery + bile duct

31
Q

What is the function of the Hepatic Triad?

A
  • After a meal, increased blood enters the sinusoids (via hepatic vein) maximizing exposure of hepatocytes to blood contents
  • Blood leaving the liver enters central (portal) vein which is a branch of the inferior vena cava
  • Bile is secreted continuously into the right and left hepatic ducts
32
Q

What are Kupffer cells?

A

macrophages in the liver

33
Q

What are Stellate cells?

A

Cells in the liver that produce collagen and store lipids like vitamin A.

34
Q

What is the underlying pathophysiology of Cirrhosis as it pertains to Kupffer cells and Stellate cells?

A
  • Oxidative stress (alcohol, infection) causes Kupffer cells to release cytokines inducing collagen production by stellate cells.
  • Accumulation of collagen:
    • increases resistance to blood flow (portal hypertension)
    • reduces hepatocyte function (hepatic encephalopathy)
35
Q

How much bile is produced every day?

A

0.5 L

36
Q

What is the path that bile takes from synthesis to reabsorption for recycling?

A
  • Bile is produced by hepatocytes
  • secreted into bile duct
  • concentrated in the gallbladder
  • enters duodenum
  • finally reabsorbed from the ileum
37
Q

Why is your poop brown?

A
  • RBC hemolysis => releases Bilirubin (unconjugated)
  • Unconjugated bilirubin (yellow) => Conjugated bilirubin (green)
    • in liver
  • Secreted into bile
  • Bile enters intestines
  • Degraded into Urobilinogen
    • can be absorbed by urine (urobilin)
  • Urobilinogen degraded => Stercobilin (brown)
38
Q

How are bile acids synthesized?

A
  • Bile acid synthesis in the liver
  • Primary bile acids (chenodoxycholic and cholic acid) are synthesized from cholesterol and contain hydroyxl groups to make them amphipathic.
  • Bile acids can be conjugated to the amino acids, glycine or taurine, to generate bile salts
  • Reabsorbed bile acids exert negative feedback on 7α-hydroxylase
39
Q

What effect does a bile acid sequestrant (cholestyramine) have on serum cholesterol levels?

A

More cholesterol used to make bile salts which can be excreted in wastes.

40
Q

How are Secondary Bile Acids synthesized and reabsorbed?

A
  • Bacteria can deconjugate and dehydroxylate primary bile acids generating less effective secondary bile acids.
  • Secondary bile acids can be reabsorbed and conjugated in the liver
  • The secondary bile acid lithocholic acid is cytotoxic; can be sulfated leading to its excretion
41
Q

What are the components of Bile?

A
  • 61% bile salts
  • 3% phospholipids (lecithins)
  • 9% cholesterol
  • 3% conjugated bilirubin
  • 7% protein, inorganic ions especially cations (tight association, isosmotic)

***These products mix with a watery, bicarbonate-containing solution secreted by bile duct cells.

42
Q

After leaving the canaliculi, bile enters what area to undergo more modification?

A

Canals of Hering lined with cholangiocytes

  • Glucose and amino acids are actively reabsorbed from the bile
    • (prevents overgrowth of bacteria which could lead to deconjugation)
    • IgA and mucus (goblet cells) are added
43
Q

What promotes the filling of the gallbladder between meals?

A
  • hepatic secretion pressure
  • high pressure at the sphincter of Oddi
  • receptive relaxation of gallbladder smooth muscle
44
Q

What signals gallbladder contraction and relaxation of the sphincter of Oddi during the intestinal phase?

A

CCK + vagal efferents

45
Q

How does bile uptake by intestinal epithelial cells occur?

A
  • Uptake of conjugated bile acids by apical sodium-dependent bile salt transporter (ASBT) through secondary active transport.
  • Organic solute transporter (OST) on basolateral membrane transports bile acids to portal circulation.
  • Bile salts unionized at luminal pH and can be taken up by passive diffusion.
46
Q

What is Cholestasis?

A

impaired bile secretion

47
Q

What conditions may cause Cholestasis?

A
  • Primary Biliary Cirrhosis (destruction of cholangiocytes)
  • Primary Sclerosing Cholangitis (inflammation of bile ducts)
  • Pregnancy- progesterone reduces gallbladder smooth muscle tone
48
Q

What are the consequences of Cholestasis?

A
  • Bile accumulates in liver leading to metabolic dysfunction
  • Itching associated with bile regurgitate into the plasma bile salts can be excreted into the urine
  • Hypercholesterolemia = cholesterol aggregation “lipoprotein X”
  • Deficiency of fat soluble vitamins
49
Q

What are the most common types of stones in Cholelithiasis?

A

Cholesterol stones

(due to increased cholesterol or decreased bile acids, treat with bile acid = ursodeoxycholic acid)

50
Q

What factors could contribute to poor lipid digestion and absorption resulting in steatorrhea?

A
  • Cholelithiasis
  • Choledocholithiasis (blockage of bile duct)
  • Cholangitis (blockage at Ampulla of Vater)
  • Status post cholecystectomy
  • Cirrhosis
  • Surgical resection of ileum
    • decreased recycling of bile acids
  • Pancreatic duct blockage
  • Cystic Fibrosis
  • Decreased chylomicron formation

GI Week 3 - WLB (8 decks)

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