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GI- Week 4 > Prunuske: Internal Digestion > Flashcards

Prunuske: Internal Digestion Flashcards

1
Q

Exocrine Pancreas

A

90% of cells

Secretes digestive enzymes and bicarb (to neutralize acidic chyme) into DUO

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2
Q

What contributes to exocrine pancreas secretions (1L/day)?

A

Acinar cells- secrete digestive enzymes

Centroacinar and duct cells

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3
Q

What is the difference between acinar cells and centroacinar cells?

A

Acinar cells- secrete digestive enzymes

Centroacinar and duct cells- dilute pancreatic enzymes and make it alkaline (HCO3)

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4
Q

What indicates an in-active form of a pancreatic enzyme?

A

-ogen or -pro

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5
Q

Pancreatic enzymes are synthesized w/ an N terminal signal peptide. Why is this important? which targets them for the secretory path

A

It targets them for the secretory pathway where they are packaged into zymogen granules and prevents them
from being exposed to the cytosol

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6
Q

What are the primary ionic components of pancreatic juice?

A

Na

Bicarb

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7
Q

As pancreatic flow rate increases, what changes in pancreatic juice?

A 
Cl decreases (more Cl exchange)
Bicarb increases
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8
Q

What is pancreatic exocrine secretion like in the cephalic/gastric phase?

A

30% mostly enzyme, low volume

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9
Q

What activates acinar cells?

A

Para efferents (ACh, GRP) from vagal centers in the brain

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10
Q

What is pancreatic exocrine secretion like in the intestinal phase?

A

70% increased enzyme, high volume

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11
Q

What happens to acinar cells, I cells and S cell during hte intestinal phase?

A

Acinar cells- activated by the vago-vagal reflex and by fat/AA in the duodenum

I cells relase CCK

H ions cause S cells to release SECRETIN activating ductal cell secretion of bicarb

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12
Q

What promomtes compound exocytosis in acinar cells?

A

Secretagogues:

CKK and vagal stimulation (ACh and GRP)

Ca signaling (most impt w/ cAMP signaling playing modifying role)

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13
Q

What is CCK regulated by?

A

CCK-Releasing peptide and Monitor peptide

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14
Q

When is Monitor Peptide release?

A

During cephalic and gastric phases, vagal stimulation causes release of pancreatic enzymes (Monitor Peptide)

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15
Q

When is CCK-RP released?

A

during the intestinal phase AA and FA cause release of CCK-RP

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16
Q

The presence of CCK-RP and Monitor Peptide cause…

A

release of CCK from I cells into the blood

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17
Q

What increase the release of monitor peptide and pancreatic enzymes?

A

CCK

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18
Q

What turns off CCK secretion?

A

Pancreatic enzymes digest the luminal nutrients, CCK-RP and MOnitor peptide (this turns CCK OFF)

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19
Q

What is a master regulator of the duodenal cluster unit?

A

Fat and protein in the duodenum>

CCK

  1. Gall bladder contraction> secrete bile salts
  2. Pancrease > acinar secretion
  3. Stomach > reduced emptying
  4. Sphincter of Oddi > relaxation

*also decreases food intake/promotes satiety

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20
Q

What is an enteropeptidase?

A

From the duodenal brush border (activates enzymes)

Cleaves trypsinogen to active trypsin (converts other enzymes)

*activating trypsin prematurely can cause problems

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21
Q

What does trypsin do?

A

activates lipases, endopeptidases, chymotrypsin and elastase

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22
Q

Where does trypsinogen autolysis occur?

A

Low Ca environment of the acinar cells

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23
Q

What causes hereditary pancreatitis?

A

mut in the tyrpsinogen PRSS1 gene that prevents trypsin elimination (more stable) and causes activation of digestive enzymes in the pancreas (can start eating away at your pancreatic tissue)

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24
Q

What happens when dudoenal pH < 4.5?

A

S cells release SECRETIN which raises pH by increasing bicar secretion from the pancreatic ducts, biliary ducts, and duodenal mucosa.

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25
Q

Will a pt on a PPI have increased or decreased duodenal bicarbonate secretion postprandially?

A

Decreased

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26
Q

What initiates secretion of bicarb solution by pancreatic duct cells?

A

Secetin

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27
Q

How is bicarb solution formed and secreted by pancreatic duct cells?

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 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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28
Q

What sxs might you see in a pt w/ cystic fibrosis?

A

Defect in Cl channel of CFTR>

Less effective at acid neutralization

enzymes won’t work as well at a lower pH> defect in activation of digestive enzymes

Thicker pancreatic juice that you can’t wash out into the lumen

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29
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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30
Q

What physical sxs are associated w/ pancreatitis?

A

Upper abdominal pain from autodigestion of pancreatic tissue

Malabsorption of fat and fat-soluble vitamins (A,D,E,K) steatorrhea

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31
Q

What enzymes are indicative of pancreatitis?

A

Enzymes spill over into circulation elevated serum AMYLASE and LIPASE levels.

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32
Q

What other conditions are associated w/ pancreatitis?

A

Malignancy, Diabetes, and Infections

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33
Q

What is the role of the exocrine pancreas?

A

Provide enzymes to promote digestion

Secrete bicarb to neutralize gastric acid

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34
Q

When is pancreatic secretion induced and when does maximal secretion occur?

A

Cephalic and gastric phases

Max during intestinal phase d/t release of CCK and secretin

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35
Q

What do the acini and ducts of the exocrine pancreas do?

A

acini- secrete inactive enzymes

ducts- secrete fluid and bicarb to neutralize acid from the stomach

36
Q

What activates enzymes from the exocrine pancreas?

A

brush border enteropeptidases

37
Q

What do intestinal L cells secrete? What does this do?

A

Incretin GLP-1

Increases insulin, decreases glucagon

38
Q

Does oral or IV glucose lead to higher insulin? Why?

A

Oral glucose

Oral glucose leads to higher insulin than IV glucose since glucose causes a release of glucagon-like peptide-1 (GLP-1) from L cells and glucose-dependent insulinotropic peptide (GIP) from K cells

39
Q

How do diabetes drugs work?

A

Gliptins: Increase GLP-1 stabiliy

Exenatide: GLP-1 agonists

40
Q

What stimulates insulin secretion of pancreatic B cells in the islets of Langerhans?

A

GLP-1
Gastrin
CCK
ACh

41
Q

What are negative regulators of pancreatic B cells?

A

Somatostatin

NE

42
Q

What acts as satiety signals at the hypothalamus decreasing food intake and increasing energy expenditure?

A

GLP1
CCK
Insulin
Leptin

43
Q

How does lack of sleep affect leptin? What does this cause?

A

LOWERS leptin

Hyperphagia (overeating)

44
Q

What is ghrelin?

A

Produced in stomach during FASTING

Stimulates appetite and DECREASES energy expenditure thorugh neuropeptide Y and agouti related peptide

45
Q

What would be hte consequence of giving grhelin prior to eating at a buffet?

A

Overeating

46
Q

What is the largest gland/organ in the body?

A

Liver

47
Q

What are the major functions of the liver?

A

Processing of all ingested nutrients and substances- detoxifies drugs (FIRST PASS metabolism) and bacteria

Metabolism of carbohydrates, fats, and proteins

Buffering of glucose within normal limits

Synthesis of proteins important for the circulatory system

Bile Formation enables lipid uptake and excretion of lipophilic molecules

48
Q

What are hepatocytes?

A

80% of total cells in the liver

Metaobolic factories able to regenerate and produce BILE

49
Q

What is the hepatic triad?

A 
portal vien (blood from intestines)
hepatic artery (off aorta)
bile duct-- bile is secreted continulously
50
Q

What happens in the liver AFTER a meal?

A

Increased blood enters the SINUSOIDS maximizing exposure of hepatocytes to blood contents

51
Q

Blood leaving hte liver enters what vein?

A

central brain (branch of IVC)

52
Q

What are Kupffer cells?

A

type of mphage that scavenge for bacteria in the liver

53
Q

What is the space of Dissse?

A

The sinusoidal endothelium of hte liver lacks a BM and has perforated fenestra.

Forced sieving by RBC promotes passage of molecules like chylomicron remnants into the SPACE OF DISSE

54
Q

What do stellate cells do?

A

Produce collagen

Store lipids like Vit A

55
Q

What is cirrhosis?

A

Hardening of the liver d/t irreversible deposition of excess collagen

56
Q

What are the effects of cirrhosis?

A

Jaundice, Abdominal ascites (swelling), Esophageal varices, Hepatic encephalopathy, GI bleeding

57
Q

What is the pathology of Cirrhosis?

A
  • Oxidative stress (alcohol) causes Kupffer cells to release cytokines inducing production of collagen by stellate cells. Accumulation of collagen results in compression of sinusoids increasing resistance to blood flow and decreasing number of functional hepatocytes.
  • Portal hypertension: elevated hepatic resistance and upstream venous pressure resulting in abdominal ascites and esophageal varices.

Hepatic encephalopathy- toxins enter blood stream

58
Q

What do bile salts do?

A

facilitate excretion of hydrophobic molecules (cholesterol) and uptake of long chain fatty acids and fat soluble vitamins

59
Q

How do bile salts act as emulsifiers?

A

amphipathic nature

facilitate excretion of hydrophobic molecules (cholesterol) and uptake of long chain fatty acids and fat soluble vitamins

60
Q

Describe enterohepatic circulation.

A

Bile is secreted into bile duct, concentrated in the gall bladder, passes into duodenum and is reabsorbed from the ileum into portal vein to return to liver.

Bile salts may “circulate” 4-5 times during intestinal processing of a fatty meal.

Recycling is critical since operates by MASS ACTION rather than catalytically

61
Q

How are primary bile acids synthesized? How do reabsorbed bile acids affect this process?

A

Primary bile acids (chenodoxycholic and cholic acid) are synthesized from cholesterol (7a-hydroxylase) and contain hydroyxl groups by

Reabsorbed bile acids exert negative feedback on 7α-hydroxylase

62
Q

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

A

decrease cholesterol

more conversion of cholesterol to bile salts

63
Q

How are bile acids conjugated to form bile salts?

A

Bile acids are conjugated to the amino acids, GLYCINE OR TAURINE, to generate bile salts

64
Q

How do bile salts differ from bile acids in terms of pKA and solubility?

A

Increased aqueous solubility

decreased pKA (prevents formation of gallstones)

65
Q

What are secondary bile acids?

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

66
Q

What is Lithocholic acid?

A

cytotoxic

Can be sulfated leading to its excretion (so that its not recycled)

67
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, high bicarbonate-containing solution secreted by bile duct cells.

68
Q

What happens to bile after leaving the canaliculi?

A

bile enters the canals of Hering lined w/ cholangiocytes

69
Q

What happens in the canals of Hering?

A

Glucose and amino acids are actively reabsorbed from the bile (prevents overgrowth of bacteria which could lead to deconjugation)

IgA and mucus are added

70
Q

How does the gallbladder store and concentrate bile between meals?

A

“Tight junctions” preclude water movement between epithelial cells

Active sodium pumping into the lateral spaces with chloride following produces an osmotic gradient that pulls water along

71
Q

How is filling of the gallbladder promoted between meals?

A

hepatic secretion pressure, high pressure at the sphincter of Oddi, and receptive relaxation of gallbladder smooth muscle

72
Q

What happens to the GB during the intestinal phase?

A

CCK activates GB contraction and relaxation of the sphincter of Oddi

73
Q

How is bile taken up by intestinal epithelial cells?

A
  • Uptake of conjugated bile salts by apical sodium-dependent bile salt transporter (found only in the ileum) is coupled to sodium uptake.
  • Organic solute transporter on basolateral membrane transports bile acids to portal circulation.
  • Bile acid are nonionized at luminal pH and can be taken up by passive diffusion from the jejunum and ileum and colon.
74
Q

What happens to bile taken up by portal hepatocytes?

A

Reconjugation and Resecretion

75
Q

How processing of conjugated vs unconjugated bile acids differ?

A
  1. The Na+-dependent taurocholate transporter, NTCP, takes up conjugated bile salts from sinusoids. Other transporters are involved with unconjugated bile acids
  2. Unconjugated bile acids are reconjugated in the hepatocyte with glycine or taurine
76
Q

What is Cholestasis?

A

Imparied bile secretion

77
Q

What is primary billiary cirrhosis?

A

descruction of cholangiocytes

78
Q

What is primary sclerosing cholangitis?

A

inflammaiton of bile ducts

79
Q

How does pregnancy affect hte GB?

A

progesterone REDUCES GB smooth muscle tone

80
Q

What are the effects 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

81
Q

A pt presents upper right quadrant abdomen pain, fever. Dx?

A

Cholelithiasis

82
Q

What are the two types of Cholelithiasis?

A
  1. CHOLESTEROL STONES

2. Pigment stones

83
Q

Choelsterol stones

A

D/t increased cholesterol or decreased bile salts

84
Q

How do you tx cholesterol stones?

A

bile acid (ursodeoxycholic acid)

85
Q

Pigment stones

A

Less commmon

Ca salts of unconjugated bilirunbin

86
Q

What can cause pigment stones (deconjugation)?

A

Hemolytic anemia

infection of the biliary tract

87
Q

What are the outcomes of cholelithiasis?

A

Depends on where blockage is:

Jaundice
Steatorrhea
Bleeding disorders (vit K)

GI- Week 4 (12 decks)

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