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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

0.3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

0.6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

0.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the stimuli for the cephalic phase of HCl secretion

A

Smelling, tasting, chewing, swallowing, & conditioned reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the stimuli for the Gastric phase of HCl secretion

A

Distention of the stomach & the presence of AAs and amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the stimuli for the Intestinal phase of HCl secretion

A

Products of protein digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When is HCl secretion inhibited

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do prostaglandins inhibit HCl secretion

A

By reducing cAMP to antagonize histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes Gastric ulcers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the components of pancreatic secretions

A

aqueous component (very high in bicarb)
enzymatic component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pancreatic secretion comprises how much of the pancreas

A

0.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the enzymatic component of pancreas secretions do

A

Digest major nutrients like carbs, proteins, & fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does the acinus of the exocrine pancrease secrete

A

Enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

Both secrete the aqueous portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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