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GI Week 3 > Phys: Gallbladder Pancreas > Flashcards

Phys: Gallbladder Pancreas Flashcards

1
Q

What controls the relaxation of the Sphincter of Oddi?

A

CCK

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2
Q

What forms the Ampulla of Vater?

A

Pancreatic duct and common bile duct

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3
Q

What cells of the pancreas secrete digestive enzymes?

A

Acinar cells

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4
Q

What duodenal enzyme activates pancreatic enzymes?

A

Enteropeptidase

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5
Q

What do centroacinar and duct cells do to the enzymes produced by acinar cells?

A

Dilute them and make them rich in sodium and bicarbonate!

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6
Q

What is the target of enteropeptidase?

A

Trypsinogen

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7
Q

What is triggering activation of acinar cells during cephalic and gastric phases?

A

Parasympathetics via dorsal motor nucleus of vagus…release of acetylcholine on muscarinic receptors of acinus

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8
Q

During what phase is most of the pancreatic enzyme release happening?

A

Intestinal phase

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9
Q

What cells release CCK?

A

I cells

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10
Q

H+ ions cause S cells to release what during the ___________phase.

A

Secretin

Intestinal

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11
Q

What does secretin do?

A

Activates pancreatic duct cells to secrete bicarbonate

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12
Q

Where are the CCK receptors?

A

Acinar cells…trigger further fusion of zymogens

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13
Q

What triggers CCK-RP release from pancreas?

A

Amino acids

Fatty acids

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14
Q

What does CCK increase the release of in the pancreas?

A

Monitor peptide and pancreatic enzymes

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15
Q

What do pancreatic enzymes do to CCK and Monitor protein?

A

Digest them! Turning off CCK secretion

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16
Q

What does CCK do to gall bladder?

A

Contraction

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17
Q

Where does enteropeptidase come from?

A

Brush border of Duodenum

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18
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…..Autosomal dominant or recessive?

A

Dominant!

Alteration of one allele is enough to change the phenotype

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19
Q

What does the duodenal pH need to be in order to secrete secretin?

A

(I can’t think of it at the moment) but its acidic :/

Ooooo! Its

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20
Q

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

A

Decreased!

There won’t be an acid signal to induce secretin release

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21
Q

What does secretin do?!

A

Initiates secretion of bicarbonate solution by pancreatic duct cells!

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22
Q

What second messenger does secretin operate through?

A

cAMP

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23
Q

What second messenger does CCK operate through?

A

Ca++

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24
Q

Where was the alkaline tide generated? (organ)

A

Stomach

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25
Q

What would be a consequence on bicarbonate secretion in a pancreas with cystic fibrosis?

A

Decreased bicarbonate

**Pancreatic insufficiency–90 % reduction in amount of enzymes reaching intestine

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26
Q

What can alcohol do to acinar cells?

A

Hyperstimulate them…premature activation of trypsin…this can lead to cell death

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27
Q

Why would you see malabsorption of fat with pancreatitis?

A

Because we aren’t going to have sufficient colipase and lipase in the duodenum…won’t be able to cleave TAG to have fatty acids packaged into micelles to be absorbed!

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28
Q

What part of the brain is important in regulating energy homeostasis?

A

Hypothalamus

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29
Q

What cells release GLP-1? *Glucagon-like peptide

A

L cells

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30
Q

What cells release GIP? *Glucose-dependent insulinotropic peptide

A

K cells

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31
Q

What does GLP-1 do to levels of insulin and glucagon?

A

Increases insulin, decreases glucagon

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32
Q

What are the positive regulators of insulin secretion?

A

GLP-1
Amino acids
CCK
ACh

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33
Q

What are the inhibitors of Insulin secretion?

A

Somatostatin

NE

34
Q

What things act as satiety signals to decrease food intake and increase energy expenditure?
Act at hypothalamus

A

GLP1
CCK
Insulin
Leptin

35
Q

If someone has low Leptin, what would you expect?

A

Don’t get satiety signal…always eating! Likely obese

36
Q

What peptide hormone stimulates appetite? Where is it produced?

A

Ghrelin

Fundus of stomach

37
Q

What peptides are involved in the Ghrelin pathway?

A

Neuropeptide Y

Agouti-related peptide

38
Q

What cells of the pancreas does gastrin activate during cephalic/gastric phases?

A

Acinar cells

39
Q

Name some of the cool stuff our liver does! 5 general categories

A

Detoxifies drugs & bacteria

Metabolizes carbs, fat, protein

Stores glycogen, fat, V B12, A, K

Synthesizes good stuff for our circulatory system

Makes bile! Enables lipid uptake and excretion of lipophilic molecules

40
Q

Why is there a lot of Smooth ER in the liver?

A

Because it makes cholesterol!

41
Q

Hepatic triad

A

Portal vein
Hepatic artery
Common bile duct (reverse direction of the other 2)

42
Q

How does blood leave the liver?

A

Via central vein…enters IVC

43
Q

Major workforce cell of liver

A

Hepatocyte

44
Q

What type of cells are Kupffer cells?

A

Macrophage

45
Q

What enters the Space of Disse?

A

Sieving by RBCs to allow passage of chylomicron remnants into this space!

46
Q

What do stellate cells do?

A

Produce collagen and store lipids like Vitamin A

47
Q

What causes Jaundice?

A

Unconjugated bilirubin

48
Q

Cirrhosis

A

Hardening of liver due to irreversible deposition of excess collagen

49
Q

Describe the pathology of liver cirrhosis

A

Oxidative stress causes Kupffer cells to release cytokines inducing collagen production by stellate cells. Accumulation of collagen increases resistance to blood flow (portal hypertension) and reduced hepatic function (hepatic encephalopathy)

50
Q

What cells make bile?

A

Hepatocytes

51
Q

What is bilirubin conjugated to to promote excretion?

A

Glucuronic acid (via glucoronidase)

52
Q

Sx of unconjugated bilirubin build up

A

Abdominal pain
Pruritis
Jaundice

53
Q

Yellow pigment in urine

A

Urobilin

54
Q

Green color of bile

A

Conjugated bilirubin

55
Q

Yellow contributing to jaundice

A

Unconjugated bilirubin

56
Q

Brown color in poop

A

Stercobilin

57
Q

Amphipathic

Which molecules are amphipathic?

A

Hydrophobic on one side.
Hydrophilic on the other side.
Helps make it soluble in aqueous environment

*Primary bile acids

58
Q

What amino acids can bile acids be conjugated to to generate bile salts?

A

Glycine

Taurine

59
Q

Reabsorbed bile acids exert a negative feedback on what enzyme so you aren’t synthesizing as many bile acids?

A

7-alpha hydroxylase

60
Q

What does bile acid sequestrant (cholestyramine) do to serum cholesterol levels?

A

Decrease because more cholesterol is being diverted to produce bile acids

61
Q

Why are glucose and amino acids reabsorbed from bile in the cholangiocytes of the canals of Hering?

A

To prevent bacteria overgrowth that could lead to deconjugation

62
Q

What transporter uptakes conjugated bile acids in the lieum?

A

sodium-dependent bile salt transporter (ASBT) through secondary active transport!

63
Q

What transporter transports bile acids to portal circulation?

A

Organic solute transporter (OST)

64
Q

Cholestasis

A

Impaired bile secretion…creates a higher risk of forming stones

65
Q

What hormone reduces gallbladder smooth muscle tone?

A

Progesterone (makes it more likely for things to precipitate because it can’t contract as good!)

66
Q

2 types of cholelithiasis

A

cholesterol (most common)

Pigment stones

67
Q

Tx for cholesterol stones

A

increase bile acids–to promote solubilization of cholesterol

68
Q

Why might you have a bleeding disorder associated with gall stone blockage?

A

Decreased vitamin K absorption

69
Q

Explain the CCK regulation stuff

A

Monitor peptide is released during cephalic and gastric phases from the pancreas

CCK-RP is released from the pancreas in intestinal phase

When monitor peptide and CCK-RP hook up, they cause the release of CCK from I cells into the blood!

CCK increases the release of monitor peptide and other pancreatic enzymes.

Pancreatic enzymes digest luminal nutrients, CCK-RP and monitor peptide to turn of CCK secretion

70
Q

Who is the master regulator of the duodenal cluster unit?

A

CCK!!!

71
Q

What does CCK do to gallbladder, pancreas, stomach, sphincter of oddi, brain?

A 
Gallbladder: contraction
Pancreas: increase acinar secretion
Stomach: Reduce emptying
Sphincter of Oddi: relax
Brain: decrease food intake
72
Q

What happens if someone has a PRSS1 gene mutation?

A

Hereditary pancreatitis…trypsinogen gene mutation that causes activation of enzymes IN THE PANCREAS rather than the duodenum….serious inflammation

73
Q

How can alcohol cause pancreatitis?

A

Can be metabolized into products that cause hyperstimulation of acinar cells –> Intracellular trypsin activation prematurely–>cell death!

74
Q

Why is pancreatic exocrine activity highest in intestinal phase?

A

Due to secretion of CCK and secretin!

75
Q

Where is CCK released from?

A

Duodenum (I cells)

76
Q

Why may a baby be jaundiced?

A

Delayed expression of Glucoronidase!! Can’t conjugate bilirubin to glucoronic acid

77
Q

What is added to bile in the canals of Herring?

A

IgA and mucus

78
Q

What opens the Sphincter of Oddi?

A

CCK (I know I’ve over done this…but you should know it!)

79
Q

Cause of cholesterol stones?2

A

Too much cholesterol

Too little bile

80
Q

How can ZE syndrome cause steatorrhea?

A

H+ makes lipase not as active…poop out the fat!

GI Week 3 (13 decks)

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