Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

T1 - Phase 1 - Integrated (II) > GI - Physiology - Barrier Function; Swallowing & Gastric Emptying; Motility; Saliva; Gastric Glands > Flashcards

GI - Physiology - Barrier Function; Swallowing & Gastric Emptying; Motility; Saliva; Gastric Glands Flashcards

1
Q

What are the three main functions of the GI tract?

A

Digestion

Absorption

Excretion

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

What are the names for the three cell layers of the esophagus?

A

Functional;

prickle;

basal

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

What two layers protect the gastric epithelium from acidic conditions?

A

The mucosal layer (superficial) and unstirred water (deep) layers

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

Does the esophagus have a mucus or unstirred water barrier?

A

Neither

(only a small amount of bicarbonate from swallowed saliva)

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

If the mucus and unstirred water layers are depleted, how can gastric epithelium protect itself against stomach acid?

A

H+ entry into the cell via cation channels is blocked via pH regulation of these channels

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

True/False.

Some H+ can slip past the tight junctions binding gastric epithelium.

A

True.

(This will be buffered by the bicarbonate-rich interstitium.)

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

What are the three buffers to counteract acidity within the gastric epithelium?

A

Proteins;

bicarbonate;

phosphate

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

Describe the cell and interstitial acidifier(s) of the gastric epithelium.

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

Describe the cell alkalinizer(s) of the gastric epithelium basolateral membranes.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The pH of what compartment will determine the intracellular pH of gastric epithelia?

A

The interstitial pH

(i.e. if the interestitial pH falls, the basolateral epithelial transporters cause a fall in pH in the cells.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the stomach pH at rest?

What is the stomach pH when eating?

A

~3

1 - 2

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

What is the stomach alkaline tide?

A

Parietal cells producing HCl also produce intracellular HCO3-;

this HCO3- then travels through the bloodstream to the surface epithelial cells to contribute to the surface mucosal protection

(A rise in acid leads to a rise in base)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

If the epithelium of the esophagus, stomach, or duodenum is damaged and the basement membrane is intact, how long will healing take?

If the epithelium of the esophagus, stomach, or duodenum is damaged and the basement membrane is destroyed, how long will healing take?

A

30 - 60 minutes (restitution by migration of adjacent cells);

days/weeks/months (regeneration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the two main types of repair for the esophagus, stomach, and/or duodenum?

A

Restitution (rapid migration of adjacent cells to cover injury);

regeneration (reparative mechanisms; new synthesis of proteins/basement membrane/cells)

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

True/False.

The mucosal/unstirred water layers in the stomach can entrap damaged epithelial and connective tissue contents, creating an extra buffering layer over ulcerations and damage.

A

True.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which prostaglandin is protective for the gastric mucosa?

Which enzyme produces it?

A

PGE2;

COX-1

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

What are the effects of PGE2 on the gastric mucosa?

A

Increased mucus/HCO3- secretion;

increased blood flow;

promotes epithelial restitution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do NSAIDs cause gastric upset?

A

By inhibiting PGE2 production by COX-1

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

COX-__ produces __, which has protective/regenerative effects on the gastric mucosa.

A

1;

PGE2

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

Do VIOXX or Celebrex cause gastric upset?

Why or why not?

Should they be prescribed for every day aches and pains?

A

No;

it only blocks COX-2 (leaving PGE2 production uninhibited);

no –> only blocking COX-2 leads to excess thromboxane production by COX-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Barrett’s esophagus is a metaplasia of __________ epithelium to _________ epithelium in the ___________.

A

Stratified squamous,

simple columnar;

esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a major risk of Barrett’s esophagus?

A

Adenocarcinoma development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the two main layers of the muscularis externa?

What lies between them?

A

The inner circumferential layer and the outer longitudinal layer;

the myenteric (Auerbach’s) plexus + connective tissue

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

Which layer of the muscularis externa is more responsible for GI tract shortening and which is more responsible for peristalsis?

A

Shortening - longitudinal layer;

peristalsis - circular layer

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

Which small intestine plexus is sensory?

Which is motor?

A

Meissner’s (submucosal);

Auerbach’s (myenteric)

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

What are the two main substances controlling muscle contraction in the gut?

(What does each do?)

A

Acetylcholine (activation);

nitric oxide (relaxation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How long does it typically take a bolus to travel down the esophagus?

And the stomach?

And the small intestine?

And the large intestine?

A

7 seconds;

3 - 4 hours;

2 - 3 hours;

2 - 3 days

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

What are the three phases of swallowing?

Which are voluntary?

A

Oral (voluntary),

pharyngeal (medulla control),

esophageal (medulla control)

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

What happens during the muscular contractions of the pharyngeal phase of swallowing?

A

Soft palate closure of the nasopharyngeal isthmus;

epiglottis closure of the larnyx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Via what nerve does the medullary swallowing center control pharyngeal and esophageal function?

A

The Vagus n.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What substance mediates cardiac sphincter relaxation in the lower esophagus?

A

Nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the three nuclei of the medullary swallowing center?

A

Nucleus solitarius (sensory);

nucleus ambiguus (skeletal muscle);

nucleus dorsal motor (smooth muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the state of the lower esophageal sphincter when one is not swallowing (i.e. ‘at rest’)?

A

Constricted

(smooth muscle locking mechanism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is the lower esophageal sphincter necessary under normal conditions?

A

Gastric pressures (positive abdominal p.) are higher than esophageal pressures (negative intrathoracic p.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is secondary peristalsis?

A

Stretch reflex for the stuck bolus (that wasn’t successfully moved by the primary peristalsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Primary esophageal peristalsis is caused by:

Secondary esophageal peristalsis is caused by:

A

Swallowing;

esophageal distention (stuck bolus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

For what purpose does the lower esophageal sphincter naturally relax in a transient manner?

A

Due to gastric distention to allow for gas release

(belch reflex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where does swallowed food initially collect?

A

The gastric fundus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What portion of the stomach has the pacemaker zone?

What is its basal electrical rhythym?

A

The upper body (corpus);

3 waves / min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What part of the stomach is the ‘storage’ portion immediately after eating?

Via what mechanism?

A

The fundus;

receptive relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Gastrin secretion increases following _________ distention.

A

Antral (of the gastric antrum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Distention of the gastric antrum causes an increase in __________ secretion.

A

Gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What size particles does the pyloric junction allow through to the duodenum?

A

≤ 2 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the purpose of enterochromaffin cells in the duodenum?

A

To regulate the chyme entering the duodenum

(via secretin, cholecystokinin, and the vagovagal reflex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Low pH in the duodenum is sensed by ____________ cells and ____________ is released.

A

Enterochromaffin;

secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

High osmolality in the duodenum is sensed by ____________ cells and the ____________ is activated.

A

Enterochromaffin;

vagovagal reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

High fat content in the duodenum is sensed by ____________ cells and ____________ is released.

A

Enterochromaffin;

cholecystokinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What effect do each of the following, respectively, have on gastric emptying?

Secretin

The vagovagal reflex

Cholecystokinin

A

Decrease

Decrease

Decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are secretin’s effects?

A

To neutralize acidity in the duodenum

  • increased pancreatic HCO3- secretion
  • increased Brunner’s glands secretion
  • decreased gastric emptying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are cholecystokinin’s effects?

A

To optimize digestion (especially of fat)

  • increased pancreatic enzyme secretion
  • increased gallbladder contraction
  • decreased gastric emptying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

True/False.

The larynx depresses during deglutition.

A

False.

The larynx rises during deglutition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Where is calcium absorbed in the small intestine?

Where is iron absorbed in the small intestine?

Where is vitamin B12 absorbed in the small intestine?

Where are bile salts absorbed in the small intestine?

A

The duodenum and proximal jejunum;

the duodenum and proximal jejunum;

the terminal ileum;

the terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What substance(s) is(are) absorbed in the terminal ileum?

A

Vitamin B12;

bile salts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

True/False.

Segmentation waves help push boluses down the small intestine in the process of peristalsis.

A

False.

Segmentation waves push chyme in both directions, mixing and churning it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the basal electrical rhythym in the duodenum?

What is the basal electrical rhythym in the jejunum?

What is the basal electrical rhythym in the ileum?

A

12 waves / min

10 waves / min

8 waves / min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

______________ causes smooth muscle contraction in the gut.

______________ causes smooth muscle relaxation in the gut.

A

Acetylcholine;

nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the ileo-colic reflex?

A

Upon gastric distention, the ileum empties its content into the colon to make room for incoming material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

When the colonic smooth muscle contracts, the ileocecal valve is ____________.

When the ileal smooth muscle contracts, the ileocecal valve is ____________.

A

Closed (acetylcholine);

open (nitric oxide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why is the ileocecal valve important?

A

To prevent regurgitation of fecal material and bacteria into the small intestine

60
Q

Describe the migrating motor complex.

When does it occur?

A

A peristaltic wave that passes from the gastric antrum to the ileocecal valve;

every two hours post-prandial

61
Q

You ate an hour ago. Is the migrating motor complex active in your small intestine?

A

No;

it begins 2 hours after eating and repeats every 2 hours of fasting

62
Q

How can objects larger than 2 mm get past the gastroduodenual junction?

A

Migrating motor complexes empty all stomach contents (starting 2 hours after eating and repeating every 2 hours)

63
Q

How much of the H2O present in the large intestine is absorbed?

A

~90%

64
Q

Does stool become softer or firmer as it spends time in the colon?

A

Firmer

65
Q

What is the large intestine equivalent of the segmentation waves found in the small intestine?

What is the term given to peristaltic waves found in the large intestine?

A

Haustration (colon mixing waves);

‘mass movements’

66
Q

How is mass movement in the colon different from small intestine peristalsis?

A

Large segments of colon can all contract simultaneously, pushing masses of fecal material to distal regions

67
Q

What is the defecation reflex?

A

Internal anal sphincter relaxation triggered by feces entering the rectum

68
Q

What two muscles are the major players in fecal continence?

A

External anal sphincter;

puborectalis

69
Q

What occurs if fecal material enters the anal canal (after triggering the defecation reflex and internal anal sphincter relaxation) and is inhibited for a period of time by the puborectalis and external anal sphincter?

A

Receptive relaxation in the rectum to accomodate more volume (taking the strain off the anal canal)

70
Q

What is the gastroileal reflex?

A

Food enters the stomach –> the ileum expels its contents into the colon

Food enters the stomach –> the colon expels its contents into the rectum

71
Q

What is the gastrocolic reflex?

A

Food enters the stomach –> the colon expels its contents into the rectum

72
Q

Which salivary gland secretes α-amylase?

Which salivary gland secretes lipase?

A

Parotid;

sublingual

73
Q

Which salivary gland(s) secrete(s) more viscous (less serous and more mucinous) fluid?

A

Sublingual, submandibular

74
Q

Describe the basic structure of a salivary gland acinus.

A
75
Q

How do salivary glands eject their contents?

A

Myoepithelial cells

76
Q

Salivary glands drain from small ________ ducts into larger ________ ducts and, finally, into ________ ducts.

A

Intercalated,

striated,

excretory (interlobular)

77
Q

What major protein type is secreted in serous salivary fluid?

What major protein type is secreted in mucinous salivary fluid?

A

Zymogens;

mucins

78
Q

Besides salivary transport, what effect do intercalated ductal cells have on the acinar fluid coming from the salivary glands?

A

Increased HCO3- and K+;

hypotonic fluid produced

79
Q

What are some of the roles of saliva?

A

Defense (antibacterial, acid neutralization, cleansing);

solvation (taste facilitation);

lubrication;

digestion

80
Q

Name the major chemicals found in saliva.

A

Water;

HCO3-

81
Q

Name the individual functions of the following three substances found in the saliva:

Lactoferrin

Muramidase

EGF

A

Lactoferrin - antibacterial; binds iron

Muramidase - antibacterial; hydrolyzes cell walls

EGF - stimulates cell growth and repair

82
Q

True/False.

Proton pump inhibitors can decrease risk of bacterial colonization of the small intestine.

A

False.

Proton pump inhibitors can increase risk of bacterial colonization of the small intestine (by neutralizing the acid defense).

83
Q

How does EGF selectively initiate growth and repair in damaged tissues around the mouth or stomach?

A

Damage to tissues allows EGF to bypass the epithelium and stimulate underlying proliferative cells

84
Q

Name the major defensive proteins found in saliva.

A

Mucins;

lactoferrin;

muramidase;

EGF

85
Q

Name the major digestive proteins found in saliva.

A

α-amylase;

lingual lipase;

R protein

86
Q

What does salivary R protein do?

A

Binds vitamin B12 –>

facilitates its binding to intrinsic factor

87
Q

What protein increases blood flow to the salivary glands?

A

Salivary kallikrein

88
Q

Saliva is which: isotonic, hypertonic, or hypotonic?

What decides its tonicity?

A

Hypotonic;

flow rate

(**slower flow = lower tonicity due to increased Na+ and Cl- reabsorption)

89
Q

Why is it important that saliva be hypotonic?

A

So ingesting food doesn’t cause it to be overly hypertonic and dehydrating for the rest of the GI tract

90
Q

When acinar fluid is first ultrafiltrated into the salivary glands, it is isotonic.

What happens next?

A

HCO3- and K+ are secreted

+

Na+ and Cl- are reabsorbed;

the fluid becomes hypotonic

91
Q

True/False.

The acinar cells of the salivary glands are similar to renal tubular cells in that they have various apical and basolateral transporters ferrying ions around the system.

A

True.

  • (NaCl reabsorption;*
  • KHCO3 secretion)*
92
Q

Identify which regulates salivary secretion: hormonal control, neural control, or both.

A

Neural control only

(mainly via sensory reception of chemoreceptors and pressure receptors)

93
Q

Which has a stimulatory effect on salivary glands, parasympathetic or sympathetic innervation?

Which has a much stronger effect?

A

Both;

parasympathetic

94
Q

Which causes an increase in salivary gland secretion of protein-rich (mucinous) saliva, parasympathetic or sympathetic innervation? (Via what intracellular signalling molecule?)

Which causes an increase in salivary gland secretion of protein-poor (serous) saliva, parasympathetic or sympathetic innervation? (Via what intracellular signalling molecule?)

A

Sympathetic (cAMP);

parasympathetic (Ca2+)

95
Q

Which nuclei trigger parasympathetic increases in salivation?

To what ganglia?

A

The superior and inferior salivary nuclei (via CNs VII and IX);

submandibular and otic

96
Q

Which salivary gland is only innervated by parasympathetic nerves?

A

Parotid

97
Q

T1-T2 sympathetic nerves run from the ___________________ ganglia to which salivary glands?

A

Superior cervical;

sublingual, submandibular

98
Q

What secondary messenger will norepinephrine trigger in salivary gland acinar cells?

What secondary messenger will acetylcholine trigger in salivary gland acinar cells?

A

cAMP;

IP3 + Ca2+

99
Q

What is ‘water brash’?

A

The clinical phenomenon of the body neutralizing heartburn by increasing parotid gland secretion

100
Q

What is ‘cotton mouth’?

A

Dry, mucinous mouth following sympathetic stimulation

101
Q

What is a common cause of xerostomia?

A

Sjogren’s disease

(dry eyes, dry mouth, arthritis)

102
Q

How much saliva does the average individual produce per day?

How much gastric acid does the average individual produce per day?

A
  1. 5 L
  2. 5 L
103
Q

Name the major sphincters of the GI tract.

A

Upper esophageal s.

Lower esophageal (cardiac) s.

Pyloric s.

Ileo-cecal valve

Internal + external anal s.

104
Q

True/False.

Substances ≤ 2 mm cannot pass through the pyloric sphincter.

A

False.

Substances > 2 mm cannot pass through the pyloric sphincter.

105
Q

Does any absorption happen in the stomach?

A

Yes

(of non-polar substances such as alcohol and NSAIDs)

106
Q

What type of epithelium are the surface mucus cells of the stomach?

A

Simple columnar

107
Q

What two cell types of the gastric glands stimulate acid secretion by the parietal cells?

Via what substances?

A

G cells (gastrin);

enterochromaffin cells (histamine)

108
Q

Name all seven cell types found in a gastric gland.

A
109
Q

Why do the mucus neck cells and surface mucus cells of the stomach secrete different types of mucus?

A

The surface cells secrete insoluble mucus (so the unstirred water layer will form beneath);

the neck cells secrete soluble mucus so the gland doesn’t become occluded

110
Q

What cell type of the gastric gland inhibits parietal cell secretion of gastric acid?

Via what substance?

A

D cells;

somatostatin

111
Q

Describe the general locations of D cells, G cells, chief cells, enterochromaffin-like cells, parietal cells, mucus neck cells, and surface mucus cells in the gastric glands.

A
112
Q

Enterochromaffin-like cells secrete ___________ to __________ gastric acid secretion by the parietal cells.

A

Histamine;

increase

113
Q

G cells secrete ___________ to __________ gastric acid secretion by the parietal cells.

A

Gastrin;

increase

114
Q

What two proteins are secreted by gastric chief cells?

A

Pepsinogen;

gastric lipase

115
Q

How is pepsinogen activated?

A

Low pH

(optimal 1.8 - 3.5)

116
Q

Increased flow rate of gastric acid secretion will lead to an ____________ (increase/decrease) of HCl secretion.

A

Increase

117
Q

When is the peak proton secretion in the stomach greatest?

A

3 hours post-prandial

118
Q

Gastric parietal cells are characterized by high concentrations of what organelles?

A

Mitochondria;

intracellular cannaliculi;

SER (fuse to form the cannaliculi)

119
Q

From an intracellular perspective, what happens when a gastric parietal cell is stimulated?

A

SER tubulovesicular membranes fuse to form intracellular cannaliculi;

increase in proton pumps;

increase in mitochondria

120
Q

Where do the protons secreted from parietal cells originate?

A

H2CO3 formation via carbonic anhydrase

121
Q

What is the main proton pump of the parietal cell apical membrane?

What two leak channels are also present?

A

The H+/K+ exchanger ATPase;

K+, Cl-

122
Q

H+ is secreted at the apical membrane of parietal cells in exchange for what other ion?

A

K+

123
Q

Upon formation of H+ and HCO3- (via carbonic anhydrase) in the gastric parietal cells, what happens to the HCO3-?

A

It is exchanged for Cl- at the basolateral membrane

(to join the alkaline tide)

124
Q

Describe the major ionic channels/transporters/enzymes of the gastric parietal cells.

A
125
Q

What three substances increase gastric acid secretion by parietal cells?

A

Histamine (from enterochromaffin-like cells);

acetylcholine (from vagal stimulation);

gastrin (from G cells)

126
Q

Describe the various parietal cell intracellular effects (membrane receptors and secondary messengers) stimulated by each of the following:

Histamine (from EC-L cells)

Acetylcholine (from vagal stimulation)

Gastrin (from G cells)

A
127
Q

What parietal cell receptor does gastrin bind?

And histamine?

And acetylcholine?

A

CCK receptors

H2

M3

128
Q

What parietal cell secondary messenger does gastrin stimulate?

And histamine?

And acetylcholine?

A

Ca2+, IP3 (via phospholipase C);

cAMP (via adenylyl cyclase);

Ca2+, IP3​ (via phospholipase C);

129
Q

Somatostatin and PGE2 stimulate the Ginhibitory subunit that blocks the effects of which substance on gastric parietal cell function?

A

Histamine (H2 receptors)

130
Q

What is parietal cell potentiation?

A

Intracellular cAMP and Ca2+ levels increase via different mechanisms, creating synergystic effects when both gastrin and acetylcholine are present

131
Q

What factors cause increased histamine release from enterochromaffin-like cells?

A

Vagal stimulation;

gastrin

132
Q

How does gastrin arrive at ECL and parietal cells?

A

Via the bloodstream

133
Q

Name the four phases of gastric acid secretion.

A
  1. Basal (baseline)
  2. Cephalic (thinking about food)
  3. Gastric (distention, amino acids)
  4. Intestinal (inhibits secretion)
134
Q

What four hormones inhibit gastric acid secretion (in the intestinal phase)?

A

Cholecystokinin;

glucose-dependent insulinotropic peptide (AKA gastric inhibitory peptide);

secretin;

somatostatin

135
Q

What is another name for glucose-dependent insulinotropic peptide?

A

Gastric inhibitory peptide

136
Q

What is the most common cause of peptic ulcer disease (~95% of cases)?

A

Helicobacter pylori

137
Q

What enzyme allows H. pylori to live in the stomach?

Via what enzymatic mechanism?

A

Urease;

converts urea to ammonia –> ammonia neutralizes the gastric acid

138
Q

The vast majority of cases of peptic ulcer disease is caused by H. pylori.

What are some other common causes?

A

NSAIDs;

alcohol abuse

139
Q

Where do Zollinger-Ellison syndrome gastrinomas most commonly arise?

A

The pancreas;

the duodenum

140
Q

How do drugs like cimetidine and ranitidine affect the stomach?

A

H2 inhibition –> decreased HCl secretion

141
Q

How do drugs like omeprazole affect the stomach?

A

Proton pump (H+/K+ exchanger) inhibition –> decreased HCl secretion

142
Q

How do anticholinergic drugs (e.g. diphenhydramine, atropine) affect gastric acid secretion in the stomach?

A

Block ACh receptors –> decreased HCl secretion

143
Q

Name three drug classes that can be used to treat hypersecretion of gastric acid.

A

Proton pump inhibitors (e.g. omeprazole);

anticholinergics (e.g. atropine, oxybutinin, diphenhydramine);

H2-blockers (e.g. cimetidine, ranitide)

144
Q

What is the technical term for dry mouth?

A

Xerostomia

145
Q

What percentage of cases of peptic ulcer disease are caused by H. pylori?

A

~95%

T1 - Phase 1 - Integrated (II) (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions