Digestion And Absorption

Front 1

What is ascites?

Back 1

Accumulation of fluid in the peritoneal cavity

Front 2

What is assimilation?

Back 2

Overall process of digestion and absorption

Front 3

What is the biliary system?

Back 3

Liver, bile ducts, and gallbladder

Front 4

What is cholelithiasis?

Back 4

Gallstones

Front 5

What is cirrhosis?

Back 5

Deposition of excess collagen in the liver

Front 6

What is emulsification?

Back 6

Conversion of fat mass into fine droplets

Front 7

What is hypolactasia?

Back 7

Lactose intolerance

Front 8

As an exocrine gland, what does the pancreas primarily secrete?

Back 8

Digestive enzymes
Bicarbonate

Front 9

What do acinar cells of the pancreas secrete?

Back 9

Digestive enzymes

Front 10

What do centroacinar and duct cells do for the pancreas?

Back 10

Dilute pancreatic enzymes and render alkaline (HCO3)

Front 11

What are pancreatic enzymes packaged into?

Back 11

Zymogen granules

Front 12

As the flow rate increases, what changes in the pancreatic juice in regards to Cl and HCO3?

Back 12

Cl decreases and HCO3 increases

Front 13

In what phase do you see the greatest release of enzymes and volume from the pancreas?

Back 13

Intestinal phase

Front 14

What is the main regulator of duodenal cluster unit?

Back 14

Cholecytokinin (CCK)

Front 15

What effect does CCK have on gall bladder?

Back 15

Causes contraction

Front 16

What effect does CCK have on pancreas?

Back 16

Causes acinar secretion

Front 17

What effect does CCK have on the stomach?

Back 17

Causes reduced emptying

Front 18

What effect does CCK have on the Sphincter of Oddi?

Back 18

Relaxation

Front 19

Ultimately, what does CCK cause?

Back 19

Protein/Carb/Lipid absorption and digestion

Matching of nutrient delivery to digestive and absorptive capacity

Front 20

What promotes exocytosis in acinar cells?

Back 20

CCK and vagal stimulation (through ACh and GRP)

Front 21

What second messenger plays a critical role in acinar cells for the release of zymogens?

Back 21

Calcium

Front 22

What occurs during cephalic and gastric phases?

Back 22

Vagal stimulation causes release of pancreatic enzymes and monitor peptide

Front 23

What happens during the intestinal phase?

Back 23

Amino acids and fatty acids cause release of CCK-RP

Front 24

What causes the release of CCK? And from what cells?

Back 24

CCK-RP and monitor peptide cause release of CCK from I cells into the blood

Front 25

What effect does CCK have on monitor peptide and pancreatic enzymes?

Back 25

Increases both

Front 26

How does CCK-RP and monitor peptide get turned off?

Back 26

Pancreatic enzymes digest them

Front 27

What cleaves trypsinogen to trypsin? Where does this occur?

Back 27

Enzyme is enteropeptidase and it is found at the duodenal brush border membrane

Front 28

At what pH do the enzymes released from the pancreas work at (optimally)?

Back 28

Neutral pH

Front 29

What effect would a proton pump inhibitor have on duodenal bicarbonate secretion post-prandially?

Back 29

Decreased secretion

Front 30

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

Back 30

Secretin

Front 31

How is CFTR regulated?

Back 31

By secretin activation of cAMP

Front 32

Would loss of CFTR effect acinar secretion of enzymes?

Back 32

No

Front 33

Would loss of CFTR effect ductal cell secretion of bicarb?

Back 33

Yes, decreased secretion

Front 34

Would the secreted pancreatic enzymes be active if CFTR function was lost?

Back 34

No, too low of pH in duodenum

Front 35

How might you manage the condition of CFTR loss?

Back 35

Do something to increase pH, such as give PPI

Front 36

What might lead to pancreatic insufficiency?

Back 36

Activation of pancreas proteases inside the pancreas ducts = destruction of self

Front 37

What are the signals for acinar cells to release their zymogens?

Back 37

ACh CCK

Front 38

What are the causes of pancreatitis?

Back 38

1) occlusion of the pancreatic duct by gallstones or malignancy
2) hereditary trypsin mutation preventing trypsin from cleaving itself which is normal way to inactivate itself
3) Alcohol can be metabolized into product that cause hyperstimulation of acinar cells resulting in intracellular trypsin activation and cell death

Front 39

What are the effects of pancreatitis?

Back 39

1) Upper abdomen pain from autodigestion of pancreatic tissue
2) Enzymes spill over into circulation elevated serum amylase and lipase levels
3) Malabsorption of fat and fat-soluble vitamins (A,D,E,K) steathorrea
4) Infection

Front 40

What are the major functions of the liver?

Back 40

1) Metabolism of carbs, fats and proteins
2) Buffering of glucose
3) Detox, removal of bacteria (Kupffer cells)
4) Synthesis of factors important for the circ system
5) Bile formation

Front 41

What is included in the hepatic triad?

Back 41

Portal vein, hepatic artery, and the bile duct

Front 42

What type of cell are Kupffer cells?

Back 42

Type of macrophage in the liver

Front 43

What are Stellate cells?

Back 43

Produce collagen and store lipids like Vitamin A

Front 44

What are the effects of cirrhosis?

Back 44

Jaundice
Abdominal ascites
Esophageal varices
Hepatic encephalopathy
GI bleeding

Front 45

What is hepatic encephalopathy?

Back 45

Where toxins enter blood stream

Front 46

Where are bile acids synthesized? What are they synthesized from?

Back 46

Made in liver from cholesterol

Front 47

Reabsorbed bile acids exert negative feedback on which enzyme?

Back 47

7alpha-hydoxylase

Front 48

Explain what effect bile sequestrant cholestyramine would have on serum cholesterol levels?

Back 48

Leads to decreased bile acid recycling and thus decreased serum cholesterol

Front 49

How are bile acids converted to bile salts?

Back 49

They are conjugated to amino acids (either taurine or glycine)

Front 50

How are bile salts turned back to bile acids?

Back 50

They are deconjucated by bacteria in the intestine making them less effective

Front 51

Which of the following are bile salts or bile acid?
Cholic Acid
Glycocholic Acid
Taurocholic Acid

Back 51

Cholic Acid = bile acid
Glycocholic Acid = bile salt
Taurocholic Acid = bile salt

Front 52

After leaving the canaliculi, where does bile go?

Back 52

Enters the Canals of Hering lined with cholangiocytes

Front 53

If bile acid were to pool and be stored in the small intestine, what might be the consequences?

Back 53

1) Can't store as much bile which is problem for processing fats
2) More bacteria are present in the small intestine which leads to more deconjugation (turning primary bile acids into secondary bile acids)

Front 54

During intestinal phase, how does CCK effect gallbladder and secretion?

Back 54

Activates gallbladder contraction and relaxation of the sphincter of Oddi

Front 55

How are bile salts taken up within the intestinal epithelial cells?

Back 55

Uptake of conjugated bile salts by apical sodium-dependent bile salt transporter (found only in the ileum) is coupled to sodium intake

Front 56

What is primary biliary cirrhosis?

Back 56

Destruction of cholangiocytes

Front 57

What is primary sclerosing cholangitis?

Back 57

Inflammation of bile ducts

Front 58

What are the effects of cholestasis?

Back 58

1)Bile accumulates in liver leading to metabolic dsfxn
2) Itching associated with bile regurgitate into the plasma bile salts can be excreted into the urine
3) Hypercholesterolemia
4) Deficiency of fat soluble vitamins

Front 59

What are the primary causes of cholelithiasis?

Back 59

Cholesterol stones
Pigment stones (bilirubin-hemolysis)

Front 60

What are the symptoms of cholelithiasis?

Back 60

Upper abdomen pain
Fever
Jaundice
Many people lack symptoms

Front 61

In the gut, what does SGLT-1 take up?

Back 61

Sodium-glucose cotransporter

Front 62

In the gut what does GLUT5 take up?

Back 62

Fructose

Front 63

When monosacchraides leave the basolateral membrane of an intestinal epithelial cell, they all go thru which transporter?

Back 63

GLUT2 (where they then go to the liver)

Front 64

What is the name of the peptide transporter in the gut?

Back 64

PEPT1 (cotransport with H+)

Front 65

How are amino acids contransported in the gut?

Back 65

With Na

Front 66

Which cells take up proteins which are transferred to lymphocytes as antigens?

Back 66

M Cells

Front 67

Why do genetic disorders of apical amino acid transporters not result in amino acid deficiencies?

Back 67

Because of peptide transport

Front 68

What are olestra and orlistat?

Back 68

They are inhibitors of fat assimilation

Front 69

What is required for lipase activity in the presence of bile?

Back 69

Colipase (Bile acid binding displaces pancreatic lipase from fat droplets--colipase binds bile acids recruiting lipase to cleave fatty acids)

Front 70

What organ produces phospholipase A2? What type of enzyme is it?

Back 70

Produced by the pancreas, it is an esterase which converts phospholipids into fatty acids and lysophospholipids

Front 71

How do lipids enter enterocytes?

Back 71

1) nonionic diffusion
2) collision with the membrane
3) carrier mediated transport