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GI Week 4 > Hormonal Control of Nutrient Assimilation: Pancreas and Gallbladder physiology > Flashcards

Hormonal Control of Nutrient Assimilation: Pancreas and Gallbladder physiology Flashcards

1
Q

Why can you say the GI system does NOT maintain a state of homeostasis?

A

because it generally assimilates everything presented to it in the diet

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2
Q

So where does the level of regulation come from in terms of nutrient assimilation?

A

the hypothalamus regulates energy homeostasis by maintaining ablance between food intake and energy expenditure - balancing satiety and hunger

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3
Q

What percentage of pancreatic cels are involved in the exocrine function of the pancreas?

A

90%

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4
Q

In general, what does the pancreas secrete as an exocrine gland?

A

bicarbonate and digestive enzymes

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5
Q

Specifically what cels secrete the digestive enzymes and which secrete the bicarb?

A

acinar cells secrete the digestive enzymes

centroacinar and duct cells secrete the bicarb

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6
Q

Enzymes are synthesized with a what to target them for the secretory pathway where they are packaged into xymogen granules?

A

N-terminal signal peptide

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7
Q

Which digestive enzyme is secreted in an active form, not a zymogen?

A

lipase - but it’s kept inactive by bile until procolipase is cleaved and activated

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8
Q

Which digestive enzyme is the key lynch pin in the cascade of activation of the other digestive enzymes?

A

trypsinogen to trypsin

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9
Q

What happens to the concentration o chloride and bicarb as the flow rate of pancreatic juice increases?

A

bicarb will increase and Chloride will decrease - makes sense teleologically because you’ll secrete at fast rates after a meal in order to neutralize the acidic chyme

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10
Q

During the cephalic and gastric pahses of digestion what percentage of maximum is pancreatic secretion at?

A

30%

and it’s mostly enzyme - not bicarb

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11
Q

What will stimulate the acinar cells during the cephalic and gastric phase?

A

parasynpathetic efferents from the vegal centers in the brain using ACh and GRP

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12
Q

During the intestinal phase, what in addition to the vago-vagal reflex will triger the pancreas to secrete bicarb and digestive enzmes?

A

CCK will increase digestive enzyme secretion and secretin will icnreased bicarb secretion

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13
Q

What are the 4 main secretagogues that promote compound exocytosis in acinar cells?

A

CCK, ACh and GRP (vagal stimulation)

Ca2+ is the most important signaling molecule with cAMP playing amodifying role

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14
Q

During the cephalic and gastric phases, vagal stimulation will cause release of a pancreatic enzyme that’s involved in CCK secretion. What is it?

A

Monitor peptide

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15
Q

During the intestinal phase, amino acids and fatty acids cause release of what additional enzyme that’s reuqired for CCK secretion?

A

CCK-releasing peptide

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16
Q

What cells are activated to secrete CCK by costimation with CCK-RP and Monitor peptide?

A

The I cells in the duodenum

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17
Q

How does the CCK signal get turned off?

A

pancreatic enzymes that were triggered by CCK will digest luminal nutrients including CCK=RP and monitor peptide, thus turning off CCK secretion. neat

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18
Q

What are the four general functions of CCK?

A
  1. contraction of GB
  2. increased acinar secretion in GP
  3. Relaxation of sphincter of oddi
  4. slowed gastric emptying

(also alters brain to promote satiety)

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19
Q

What will cleave trypsinogen to trypsin?

A

enteropeptidase from the duodenal brush border

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20
Q

What does the low calcium enviornment of the acinar cells do to trypsinogen if it’s not secreted by the pancreas?

A

Will cause trypsinogen to autolyse itself

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21
Q

Describe the pathophysiology of hereditary pancreatitis?

A

it’s a mutation in the trypsinogen PRSS1 gene which prevents trypsin elimination in the acinar cells causing activation of digestive enzymes in the pancreas

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22
Q

What will trigger S cell secretion of secretin?

A

H+ - when duodenla pH is below 4.5

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23
Q

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

A

decrease- no acid signal to trigger secretin release

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24
Q

How exactly does secretin trigger bicarb release?

A

secretion activates cAMP production, which then activates the CFTR channel that supplies the Cl for the HCO3/Cl exchanger

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25
Q

So what pancreatic-related ysmptoms do you see with cystic fibrosis?

A

You don’t have the necesary CFTR for the provision of Cl, so you don’t get bicarb exchange into the lumen. This means the duodenum stays acidic and digestive enzymes aren’t activated appropriate so you get digestion issues

also leads to thickened pancreatic juice which can cause blockage in the duct and extrvasation of digestive enzymes into the pancreas parenchyma leading to autodigestion of the pancreas

26
Q

What are the effects of pancreatitis then?

A

upper abdominal pain, enzymes spill over into circulation, malabsorption of fat and fat-soluble vitamins, steatorrhea

increased risk for malignancy, diabetes and infections

27
Q

What hormone is secreted by intestinal L cells to increase insulin release and decrease glucagon release?

A

GLP-1

28
Q

Why does oral glucose lead to higher insulin release than IV glucose?

A

because oral glucose causes a release of the forementioned GLP-1

29
Q

What hormone is secreted by K cells to increase insulin release?

A

glucose-dependnet insulinotropic peptide (GIP)

30
Q

How does diabeties pharmacotherapy release to GLP-1?

A

Some diabetes drugs work by increasing GLP-1 stability to increase insulin release (gliptins) and others are GLP-1 agonists (exenatide)

31
Q

What are four molecules that stimulate insulin secretion frmo pancreatic Beta cells in the islets of langerhans?

A

GLP-1, gastrin, CCK and ACh

32
Q

What are two molecules that will inhibit insulin secretion?

A

somatostatin and norepinephrine

33
Q

What are four hormones that act as satiety signals in the hypothalamus?

A

GLP-1, CCK, insulin and leptin

34
Q

What neurons do they modulate to produce satiety?

A

the neuropeptide Y and agouti-related peptide neurons

35
Q

What does lack of sleep do to satiety signals and why?

A

it decreases satiety signals and promotes overeating because lack of sleep will lower leptin levels

36
Q

What hormone will stimulate appetite thorugh the neuropeptide Y and agouti-related peptid eneurons of the hypothalamus?

A

ghrelin

37
Q

Where is ghrelin secreted?

A

in the fundus of the stomach during fasting

38
Q

In the liver, what happens to blood flow in the sinusoids after a meal?

A

it will increase to maximize the exposure ot hepatocytes to blood contents in order for filtration

39
Q

Describe the pathophysiology of cirrhosis.

A

hardening of the liver due to irreversible deposition of excess collagen

oxidative stress causes the kupffer cells to release cytokines which induces production of collagen by stellate cells. the collagen results in compression of sinusoids increasing resistnace to blood flow and decreasing the number of functional hepatocytes

40
Q

What about the structure of bile salts allow them to act as emulsifiers?

A

they have an amphipathic nature; there is a polar hydrophilic side that interacts with the aqueous environment and a non-polar hydrophobic side that interacts with lipids

41
Q

What about the way bile salts work make recycling via enterohepatic circulation so necessary?

A

they operate by mass action rather than catalytically, so there needs to be a lot - the body would’t be able to make enough on demand

42
Q

What type of bile acids (and two examples) are synthesized de novo in the liver from cholesterol?

A

primary bile acids

chenodoxycholic

cholic acid

43
Q

What enzyme promotes the formation of primary bile acids? What inhibits it?

A

7 alpha-hydroxylase

inhibited via negative feedback by reabsorbed bile acids

44
Q

What effect do the bile acid sequestrants have on cholesterol levels? An example?

A

cholestyramine

they bind the bile acids such that they’re excreted instead of recycled

this means more cholesterol needs to be taken up by the liver for bile acid production, lowering serum cholesterol

45
Q

What happens to the bile acids to make bile salts?

A

conjugated to amino acids - especially glycine ot taurine

46
Q

What makes the bile salts more effective than bile acids?

A

tey have higher solubility and decreased pKa which means they will be less likely to form gallstones

47
Q

What effect will bacteria have on the bile salts?

A

they deconjugate and dehydroyxylate primary bile acids to generate less effective secondary bile acids

48
Q

What secnodary bile acids is cytotoxic and thus sulfated in order for it to be excreted?

A

lithocholic acid

49
Q

What canals does the bile enter after leaving the canaliculi?

A

canals of hering lined with cholangiocytes

50
Q

What happens to the bile when it’s in the canal of hering?

A

glucose and amino acids are actively reabsorbed form the bile to prevent overgrowht of bacteria hwich could lead to deconjugation

IgA and mucus are also added

51
Q

How does the gallbladder concentrate the bile between meals?

A

there are tight junctions that stop water form moving between the pithelial cell sinto the GB lumen

active sodium pumping into the lateral spaces between cells will ahve chloride follow. this makes an oxmotic gradient such that water is pulled out of the lumen, concentrating the bile

52
Q

What promotes gallbladder filling between meals?

A
  1. hepatic secretion pressure
  2. high pressure keeping the sphincter of oddi closed
  3. receptir relaxation of the GB smooth muscle (with NO,VIP)
53
Q

Why is the ileum the only place int he small intestine that will take up conjugated bile salts?

A

it’s the only place where the apical sodium-dependent bile salt transporter is located

54
Q

why is is possible to take up bile acids from the jejunum, ileum and colon via passive diffusion?

A

because they will be non-ionized at luminal pH

55
Q

During the intestinal phase, what will vagal efferents release on the gall bladder to cause contraction? How about on the sphincter?

A

ACh on the GB and VIP/NO on the sphincter

all of this occurs in response to CCK

56
Q

What is cholestasis and what are some causes

A

impaired bile secretion

causes include primary biliary cirrhosis, primary sclerosing cholangitis and pregnancy

57
Q

What are the effects of cholestasis?

A
  1. bile accumulates in the liver leading to metabolic dysfunction
  2. itching associated with bile regurg into plasma
  3. bile salts in urine
  4. hypercholesterolemia because you don’t secrete your cholesterol in the bile
  5. deficiency of fat soluble vitamins
58
Q

What are the size ranges for cholelithiasis?

A

sand to golf ball

59
Q

what are the symptoms of choleithiasis?

A

RUQ pain, fever, but many are asymptomatic

60
Q

What’s the most common stone for cholethiasis?

A

cholesterol stones - due to increased cholesterol or decreased bile salts

61
Q

How can you treat cholesterol gall stones then?

A

you give a bile acid called ursodeosycholic acid

62
Q

What stones are less common?

A

pigmented stones - calcium salts of unconjugated bilirubin

GI Week 4 (11 decks)

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