Lecture 56 Flashcards

1
Q

List the steps for stimulation of HCl secretion by using the direct path of vagal stimulation

A

Vagus nerve sends a signal to the parietal cells
The parietal cells release Ach to then release HCl
OR
The vagus nerve activates GRP to stimulate G cells
The G cells will then release gastrin

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2
Q

What are the steps of the indirect path of vagal stimulation (for HCl secretion)

A

Gastrin from the G cells goes into systemic circulation
This then causes a release of HCl from Parietal cells

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3
Q

T/F: Atropine WILL block HCl secretion completely b/c it DOES have an effect on the direct paths of vagal stimulation

A

F

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4
Q

What percent of HCl comes from the cephalic phase of HCl secretion

A

0.3

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5
Q

What percent of HCl comes from the gastric phase of HCl secretion

A

0.6

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6
Q

What percent of HCl comes from the Intestinal phase of HCl secretion

A

0.1

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7
Q

What is the stimuli for the cephalic phase of HCl secretion

A

Smelling, tasting, chewing, swallowing, & conditioned reflexes

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8
Q

What is the stimuli for the Gastric phase of HCl secretion

A

Distention of the stomach & the presence of AAs and peptides

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9
Q

What is the stimuli for the Intestinal phase of HCl secretion

A

Products of protein digestion

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10
Q

What are the mechanisms of the Cephalic phase

A

Direct stimulation of parietal cells by the vagus nerve (Ach)
Indirect stimulation via gastrin

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11
Q

What are the mechanisms of the Gastric phase

A

Distension (causes vagal stimulation which stimulates parietal cells)
indirect stimulation via gastrin
Distension of the antrum causes gastrin
Aas and peptides stimulate gastrin
Caffeine and alcohol stimulates gastrin

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12
Q

When is HCl secretion inhibited

A

When it is no longer needed for the conversion of pepsinogen to pepsin

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13
Q

How can decreased pH of gastric contents inhibit HCl secretion

A

pH decreases when food enters the stomach (food does buffer the pH a little)
When food leave the pH falls more & starts to inhibit further gastrin release

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14
Q

How does somatostatin inhibit HCl releease

A

Can be a direct inhibition by binding to the parietal cells - this antagonizes the histamine pathway by decreasing cAMP
Can be indirect inhibition by inhibiting both histamine & gastrin release

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15
Q

How do prostaglandins inhibit HCl secretion

A

By reducing cAMP to antagonize histamine

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16
Q

Definition: “Ulcerative lesion of the gastric or duodenal mucosa. Is caused by a loss of mucus & an excessive amount of H & pepsin secretion. Can be b/c of other damaging factors like helicobacter pylori infection or stress”

A

Peptic ulcer disease

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17
Q

What causes Gastric ulcers

A

The mucosal barriers are defective & hydrogen ion penetrat/pepsin digest the mucosa

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18
Q

Why can H.pylori colonize & cause gastric ulcers

A

Because they make urease to increase the pH of the enviroment so that they can bind to cells
Urease allows H.pylori to survive in the stomach

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19
Q

Definition: “An enzyme that converts urea to NH3 to decrease the pH of the local enviornment

A

Urease

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20
Q

T/F: Most dogs & cats are positive for pylori but they rarely have ulcers

A

T

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21
Q

Why do duodenal ulcers occur

A

Because the H+ secretory rate is higher than normal (this overwhelms the buffering capacity of the pancreas)

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22
Q

What occurs in Gastrinoma (Zollinger-Ellison syndrome)

A

High rates of H+ secretion ocurs due to high amounts of gastrin
Delivery of the high rates of H+ to the duodenmen causes steatorrhea

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23
Q

What does gastrinoma cause steatorrhea

A

Because the decrease in pH of the intestine inactiv ates enzymes such as lipase so there is very little to no fat digested

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24
Q

What are the components of pancreatic secretions

A

aqueous component (very high in bicarb)
enzymatic component

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25
Q

Pancreatic secretion comprises how much of the pancreas

A

0.9

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26
Q

What is the enzymatic component of pancreas secretions do

A

Digest major nutrients like carbs, proteins, & fat

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27
Q

What are the important structures of the exocrine pancreas glands

A

Acinus lined w/ acinar cells
ducts lined with ductal cells & centroacinar cells

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28
Q

What does the acinus of the exocrine pancrease secrete

A

Enzymes

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29
Q

What does the centroacinar cells and duct cells of the exocrine pancrease secrete

A

Both secrete the aqueous portion

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30
Q

Where does SNS innervation for the exocrine pancreas come from & is it inhibitory or stimulatory

A

The celiac & superior mesenteric plexuses
Inhibits

31
Q

Where does PNS innervation for the exocrine pancreas come from & is it inhibitory or stimulatory

A

Vagus nerve
Stimulates

32
Q

What are the steps of forming the enzymatic component of pancreatic secretions

A

Enzymes are synthesized on the rough ER of the acinar cells
They will then be transferred to the golgi, put into vacuoles, & stored as zygomens (if protease)
(amylase & lipase are secreted as active enzymes)

33
Q

Definition: “inactive state of protease”

A

Zymogens

34
Q

What are the steps of forming the aqeous component of pancreatic secretions

A

centroacinary & ductal cells make initial secretion that is then modified by the transport process in the ductal cells

35
Q

Is the aqueous component of pancreatic secretions isotonic, hypotonic, or hypertonic (what compounds does it contain)

A

Isotonic
Na, Cl, K, & HCO3

36
Q

What transporters are on the luminal membrane of the exocrine pancreas

A

HCO3/Cl exchanger

37
Q

What transporters are on the basolateral membrane of the exocrine pancreas

A

Na/KATPas and Na/H exchanger

38
Q

What happens to HCO3, H, Cl, Na, & K during creation of the aqueous component of pancreatic secretions

A

HCO3 - goes into the lumen
H - goes into the blood
Na & K concentrations in the juice will be similar to plasma
HCO3 & Cl concentration depends on the flow rate

39
Q

T/F: the Na & K concentration of the juice stay constant no matter the flow rate

A

T

40
Q

What happens to HCO & Cl juice concentration during high flow rates

A

HCO3 concentration increase
Cl concentration decrease

41
Q

What happens to HCO & Cl juice concentration during low flow rates

A

HCO3 concentration decreases
Cl concentration increases

42
Q

Why does Cl concentration increase in the juice during flow rates & why during high flow rates the HCO3 concentration increase

A

At low flow rates the solution contains mostly Na,Cl, & water while at high flow rates the solution is mostly Na, HCO3, & water

43
Q

T/F: The aqueous & enzymatic portions of pancreatic secretion are regulated TOGETHER

A

F

44
Q

What stimulates the production of aqueous portion of the pancreatic solution

A

H+ in the duodenum

45
Q

What stimulates the production of enzymatic portion of the pancreatic solution

A

Products of digestion

46
Q

What initiates pancreatic secretion during the Cephalic phase & what happens

A

Initieated by smell, taste, & condition
sends to the vagus nerve (responsible for some enzymatic secretion)

47
Q

What initiates pancreatic secretion during the Gastric phase & what happens

A

Distention of the stomach
Vagus nerve (has the same responsibility as it did in the cephalic phase)

48
Q

During the intestinal phase what do Acinar cells have recptors for

A

CCK
Ach

49
Q

During the intestinal phase what stimulate CCK

A

AAs
Peptides
Fatty acids

50
Q

During the intestinal phase what do the ductal cells have receptors for

A

CCK
Ach
Secretin

51
Q

Why are the ductal cells important during the intestinal phase

A

they are important for aquous bicarb & hydrogen stimulation of secretin

52
Q

Which phase is the most important phase during regulation of pancreatic secretion and why

A

Intestinal phase b/c it makes up ~80% of pancreatic secretions

53
Q

Why is bile secretion needs

A

For digestion & absorption of lipids

54
Q

Definition: “A mixture of bile salts, bile pigements, cholesterol, phospholipids, ions, & water

A

Bile

55
Q

What do bile salts do

A

Emulsify lipids for digestion & solubilize products into micelles for absorption

56
Q

What does the biliary system consist of

A

Liver
Gallbladder
Bile duct
Duodenum
Ileum
Portal circulation

57
Q

What do hepatocytes do in bile secretion

A

Synthesize components of bile -> take them out of the bile duct & into the gallbladder

58
Q

What does CCK doe during Bile Secretion

A

Stimulates contraction of the gallbladder & relaxes the sphincter of oddi

59
Q

What happens to bile salts after lipid absorption

A

They are reabsorbed by the ileum and recirculated back to the liver

60
Q

What is the composition of Bile

A

50% of bile salts
2% bile pigments
4% cholesterol
40% phospholipids
resgt is ions & water

61
Q

What amino acids does the liver conjugate w/ bile acids

A

Glycine
Taurine

62
Q

What are the two primary bile acids made by hepatocytes

A

Cholic acid
Chenodeoxycholic acid

63
Q

T/F: Biles ARE amphipathic (have a hydrophilic & hydrophobic portions) & emulsify lipids

A

T

64
Q

the _____ charge on bile salts causes droplets to repel each other

A

Negative charge

65
Q

Bile salts bind to the products of lipid digestion to form _______ & assist in absorption of lipid products

A

Micelles

66
Q

What does the core of a micelle contain

A

The product from lipid digestion

67
Q

Definition: “Product of hemoglobin degradation”

A

Bilirubin

68
Q

What are the functions of the Gallbladder

A

Stores, concentrates, & ejects bile

69
Q

T/F: Bile is NOT produced continuously & stored

A

F

70
Q

What do the epithelial cells of the gallbladder absorb

A

Water & ions

71
Q

When does ejection of bile occur & what helps with ejection

A

Abt/ 30 mins afer a meal in ingested
CCK will contrant the gallbladder & relax the sphincter of oddi
Bile is ejected in spurts

72
Q

What type of circulation does bile salts use to return to the liver

A

Enterohepatic circulation

73
Q

What are the steps of enterohepatic circulation of bile salts

A

Bile salts are transported from the SI lumen into the portal blood by Na/bile salt co transporters
The portal blood cares the salts to the liver
The liver extracts the bile salts & adds them to the hepatic bile salt/bile acid pool

74
Q

Approx how much bile salt is lost in fecal a day

A

~600 mg/d