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T1 - Integrated (Full Review) > Physiology - Gastrointestinal Block > Flashcards

Physiology - Gastrointestinal Block Flashcards

1
Q

What are the three main functions of the GI tract?

A

Digestion

Absorption

Excretion

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2
Q

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

A

Functional;

prickle;

basal

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3
Q

What two layers protect the gastric epithelium from acidic conditions?

A

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

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4
Q

Does the esophagus have a mucus or unstirred water barrier?

A

Neither

(only a small amount of bicarbonate from swallowed saliva)

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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

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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.)

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7
Q

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

A

Proteins;

bicarbonate;

phosphate

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8
Q

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

A
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9
Q

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

A
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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.)

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11
Q

What is the stomach pH at rest?

What is the stomach pH when eating?

A

~3

1 - 2

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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)

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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)

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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)

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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.

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16
Q

Which prostaglandin is protective for the gastric mucosa?

Which enzyme produces it?

A

PGE2;

COX-1

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17
Q

What are the effects of PGE2 on the gastric mucosa?

A

Increased mucus/HCO3- secretion;

increased blood flow;

promotes epithelial restitution

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18
Q

How do NSAIDs cause gastric upset?

A

By inhibiting PGE2 production by COX-1

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19
Q

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

A

1;

PGE2

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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

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21
Q

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

A

Stratified squamous,

simple columnar;

esophagus

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22
Q

What is a major risk of Barrett’s esophagus?

A

Adenocarcinoma development

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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

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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

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25
Q

Which small intestine plexus is sensory?

Which is motor?

A

Meissner’s (submucosal);

Auerbach’s (myenteric)

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26
Q

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

(What does each do?)

A

Acetylcholine (activation);

nitric oxide (relaxation)

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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

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28
Q

What are the three phases of swallowing?

Which are voluntary?

A

Oral (voluntary),

pharyngeal (medulla control),

esophageal (medulla control)

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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

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30
Q

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

A

The Vagus n.

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31
Q

What substance mediates cardiac sphincter relaxation in the lower esophagus?

A

Nitric oxide

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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)

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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)

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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.)

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35
Q

What is secondary peristalsis?

A

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

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36
Q

Primary esophageal peristalsis is caused by:

Secondary esophageal peristalsis is caused by:

A

Swallowing;

esophageal distention (stuck bolus)

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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)

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38
Q

Where does swallowed food initially collect?

A

The gastric fundus

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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

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40
Q

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

Via what mechanism?

A

The fundus;

receptive relaxation

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41
Q

Gastrin secretion increases following _________ distention.

A

Antral (of the gastric antrum)

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42
Q

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

A

Gastrin

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43
Q

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

A

≤ 2 mm

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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)

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45
Q

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

A

Enterochromaffin;

secretin

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46
Q

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

A

Enterochromaffin;

vagovagal reflex

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47
Q

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

A

Enterochromaffin;

cholecystokinin

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48
Q

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

Secretin

The vagovagal reflex

Cholecystokinin

A

Decrease

Decrease

Decrease

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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
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50
Q

What are cholecystokinin’s effects?

A

To optimize digestion (especially of fat)

  • increased pancreatic enzyme secretion
  • increased gallbladder contraction
  • decreased gastric emptying
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51
Q

True/False.

The larynx depresses during deglutition.

A

False.

The larynx rises during deglutition.

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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

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53
Q

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

A

Vitamin B12;

bile salts

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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.

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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

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56
Q

______________ causes smooth muscle contraction in the gut.

______________ causes smooth muscle relaxation in the gut.

A

Acetylcholine;

nitric oxide

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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

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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)

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59
Q

Why is the ileocecal valve important?

A

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

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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

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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

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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)

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63
Q

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

A

~90%

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64
Q

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

A

Firmer

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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’

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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

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67
Q

What is the defecation reflex?

A

Internal anal sphincter relaxation triggered by feces entering the rectum

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68
Q

What two muscles are the major players in fecal continence?

A

External anal sphincter;

puborectalis

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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)

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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

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71
Q

What is the gastrocolic reflex?

A

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

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72
Q

Which salivary gland secretes α-amylase?

Which salivary gland secretes lipase?

A

Parotid;

sublingual

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73
Q

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

A

Sublingual, submandibular

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74
Q

Describe the basic structure of a salivary gland acinus.

A
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75
Q

How do salivary glands eject their contents?

A

Myoepithelial cells

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76
Q

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

A

Intercalated,

striated,

excretory (interlobular)

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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

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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

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79
Q

What are some of the roles of saliva?

A

Defense (antibacterial, acid neutralization, cleansing);

solvation (taste facilitation);

lubrication;

digestion

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80
Q

Name the major chemicals found in saliva.

A

Water;

HCO3-

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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

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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).

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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

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84
Q

Name the major defensive proteins found in saliva.

A

Mucins;

lactoferrin;

muramidase;

EGF

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85
Q

Name the major digestive proteins found in saliva.

A

α-amylase;

lingual lipase;

R protein

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86
Q

What does salivary R protein do?

A

Binds vitamin B12 –>

facilitates its binding to intrinsic factor

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87
Q

What protein increases blood flow to the salivary glands?

A

Salivary kallikrein

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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)

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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

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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

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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)*
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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)

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93
Q

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

Which has a much stronger effect?

A

Both;

parasympathetic

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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+)

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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

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96
Q

Which salivary gland is only innervated by parasympathetic nerves?

A

Parotid

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97
Q

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

A

Superior cervical;

sublingual, submandibular

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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+

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99
Q

What is ‘water brash’?

A

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

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100
Q

What is ‘cotton mouth’?

A

Dry, mucinous mouth following sympathetic stimulation

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101
Q

What is a common cause of xerostomia?

A

Sjogren’s disease

(dry eyes, dry mouth, arthritis)

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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
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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.

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104
Q

True/False.

Substances ≤ 2 mm cannot pass through the pyloric sphincter.

A

False.

Substances > 2 mm cannot pass through the pyloric sphincter.

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105
Q

Does any absorption happen in the stomach?

A

Yes

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

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106
Q

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

A

Simple columnar

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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)

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108
Q

Name all seven cell types found in a gastric gland.

A
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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

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110
Q

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

Via what substance?

A

D cells;

somatostatin

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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
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112
Q

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

A

Histamine;

increase

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113
Q

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

A

Gastrin;

increase

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114
Q

What two proteins are secreted by gastric chief cells?

A

Pepsinogen;

gastric lipase

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115
Q

How is pepsinogen activated?

A

Low pH

(optimal 1.8 - 3.5)

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116
Q

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

A

Increase

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117
Q

When is the peak proton secretion in the stomach greatest?

A

3 hours post-prandial

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118
Q

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

A

Mitochondria;

intracellular cannaliculi;

SER (fuse to form the cannaliculi)

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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

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120
Q

Where do the protons secreted from parietal cells originate?

A

H2CO3 formation via carbonic anhydrase

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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-

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122
Q

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

A

K+

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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%

146
Q

What are the two main goals of pancreatic exocrine secretions?

A

Neutralize acidic chyme (via HCO3-);

promote digestion (via zymogens)

147
Q

Make the diagnosis.

A

Acute pancreatitis

148
Q

What are the two main cell types of the exocrine pancreas?

A

Acinar;

ductal

149
Q

Via what intracellular messenger do vagal stimulation and cholecystokinin cause increased pancreatic enzyme exocytosis?

A

Increased [Ca2+]

153
Q

What intestinal hormone causes increased pancreatic HCO3- secretion?

What intestinal hormone causes increased pancreatic enzyme secretion?

A

Secretin;

cholecystokinin

154
Q

What channel allows for Cl- return to the pancreatic lumen after it is exchanged for HCO3- and enters ductal cells?

A

The CFTR channel

155
Q

An increase in intracellular [Ca2+] in the pancreatic acinar cells will cause what results?

A

Increased enzyme secretion;

increased Na+, Cl-, and H2O secretion

156
Q

An increase in pancreatic fluid flow rate has what effect on HCO3- and Cl- levels in the fluid?

A

More [HCO3-];

less [Cl-]

157
Q

Which portion of the exocrine pancreas secretes enzymes, NaCl, and H2O?

Which portion of the exocrine pancreas secretes HCO3-?

A

Acinar cells;

ductal cells

158
Q

Describe the activation of pancreatic zymogen proteases.

A

Enteropeptidase (enterokinase) on duodenal brush border –>

activates trypsin –>

activates the others

159
Q

Pancreatic acinar cells secrete ______________ in response to _______________ stimulation.

Pancreatic duct cells secrete ______________ in response to _______________ stimulation.

A

Enzymes, NaCl, H2O;

cholecystokinin, vagal stimulation

HCO3-;

secretin

161
Q

What percentage of pancreatic fluid is made up of acinar secretions (enzymes, H2O, NaCl)?

What percentage of pancreatic fluid is made up of ductal secretions (HCO3-, H2​O)?

A

25%

75%

163
Q

Name some of the digestive enzymes secreted by pancreatic acinar cells.

A

α-amylase;

pancreatic Lipase;

various proteases (pepsin, trypsin, chymotrypsin, carboxypeptidases, elastase)

165
Q

How is auto-activation of trypsin within the pancreatic acinar cells avoided?

A
  1. Pancreatic enzymes exist as zymogens while in the pancreas
  2. Trypsin inhibitors can block any existing activity within the pancreas
    (e. g. trypsin inhibitory peptide and α-1 antitrypsin)
166
Q

What is the stimulating factor that increases secretin secretion by S cells of the duodenum?

What is the stimulating factor that increases cholecytokinin secretion by I cells of the duodenum?

A

Gastric acid in the duodenum;

fatty acid and amino acids in the duodenum

167
Q

How are secretin and cholecystokinin secretion potentiated?

A

Vagal stimulation

168
Q

______ cells secrete secretin.

______ cells secrete cholecystokinin.

______ cells secrete glucose-dependent insulinotropic peptide.

A

S

I

K

169
Q

What are the three stimulatory phases of pancreatic exocrine secretion?

A

Cephalic (minor role - vagus);

gastric (minor role - vagus/gastrin);

intestinal (vagus/secretin/cholecystokinin)

170
Q

Name the two most common causes of acute pancreatitis.

For what percentage does each account?

A

Alcohol abuse (40%);

gallstones (40%) (often associated with hyperlipidemia);

genetic diseases (e.g. cystic fibrosis);

hyperparathyroidism

171
Q

What bloodwork will you find in a paient with acute pancreatitis?

A

Elevated serum α-amylase and lipase;

decreased total cholesterol, HDL, and LDL

172
Q

What is the likely diagnosis?

What is the primary cause?

A

Cholecystitis;

gallstones

173
Q

What three organs are very commonly affected in patients with cystic fibrosis?

A

Lungs,

liver,

pancreas

174
Q

What digestive complications do patients with cystic fibrosis face?

A

Malabsorption,

acute pancreatitis,

obstruction,

etc.

175
Q

True/False.

Hepatocytes are a single layer of epithelial cells.

What type of junctions connect them?

A

True;

tight junctions

176
Q

Describe the bile cannaliculi and apical / basolateral sides of a hepatocyte.

A

Cannaliculi and apical sides = between cells

Basolateral sides = sides facing space of Disse

177
Q

Does gastrin potentiate pancreatic acinar secretions (via CCK) or ductal secretions (via secretin)?

A

Acinar

(to digest the proteins the stomach has sensed and responded to by secreting gastrin)

178
Q

What cell is here described:

change fluid in bile duct lumen to make bile

A

Cholangiocytes

179
Q

Describe the function of cholangiocytes.

A
180
Q

Presence of fatty acids in the duodenum causes increased ___________ (hormone) secretion.

Presence of gastric acid in the duodenum causes increased ___________ (hormone) secretion.

A

Cholecystokinin;

secretin

181
Q

What test can you use to help confirm a diagnosis of acute pancreatitis?

A

Blood work –> elevated serum α-amylase and lipase

182
Q

What test can you use to help confirm a diagnosis of cystic fibrosis?

A

Sweat test

184
Q

What percentage of hepatic circulation comes from the portal vein?

What percentage of hepatic circulation comes from the hepatic artery?

A

75%

25%

185
Q

What is a hepatic lobule?

A

The hepatocytes around a central vein and several associated portal triads

188
Q

What are the main components of bile?

A

Water (82%),

bile acids (12%),

phospholipids (4%),

cholesterol (1%)

bilirubin (<1%)

189
Q

Describe bile acid circulation.

A
192
Q

Describe the changes in pH and electrolytes from hepatic bile to gallbladder bile.

A

Increase:

Sodium

Bile acid (pH decreases initially until Cl-/HCO3- exchange catches up)

Decrease:

Bicarbonate (pH decreases until Cl-/HCO3-​ exchange catches up)

Chloride

193
Q

How are bilirubin and cholesterol excreted?

A

Through bile

194
Q

What are the purposes of bile?

A

Fat emulsification

Antibacterial

Neutralize gastric acid

195
Q

True/False.

Bile acids are amphipathic and form chylomicrons.

A

False.

Bile acids are amphipathic and form micelles.

196
Q

Bile acids are the end product of __________ metabolism.

What enzyme is responsible for cholesterol synthesis?

What enzyme is responsible as the rate-limiting step of bile acid synthesis?

A

Cholesterol;

HMG-CoA reductase,

7α-hydroxylase

197
Q

Describe the GALT.

A
198
Q

Why can statins cause cramps and neurological symptoms?

A

Changes in myelin (due to decreased cholesterol synthesis)

199
Q

Primary bile acids are formed in the _______.

Secondary bile acids are formed in the _______.

A

Liver;

colon

200
Q

Secondary bile acids (formed in the colon) are conjugated with:

A

Glycine or taurine

201
Q
A

2.

202
Q

How are secondary bile acids reabsorbed by the colon?

A

Na+-dependent cotransport

204
Q

What sphincter is relaxed by CCK?

A

The sphincter of Oddi

205
Q

What substances are released secondary to CCK action at the gallbladder and common bile duct?

A

VIP and NO (relaxation of Oddi);

ACh (further gallbladder contraction)

206
Q

______ ________ turns heme into iron and bilirubin.

A

Heme oxygenase

207
Q

Unconjugated bilirubin is transported in the blood via ________.

A

Albumin

208
Q

Describe the vessels found within a single intestinal villus.

A
209
Q

Which sex is at a greater risk of gallbladder disease?

Why?

A

Women;

oral contraceptives, estrogen

(effects on cholesterol, I think)

210
Q

What surface has the largest surface area of the body in potential direct contact with immunogenic/toxic substance?

A

The GI tract

211
Q

Describe the histological differences between the small intestine and large intestine.

A
212
Q

___% of Ig-secreting cells are in the GI tract.

A

80%

214
Q

True/False.

The enteric NS has the same number of neurons as the spinal cord (100,000,000)

A

True.

215
Q

Describe the function of histamine and somatostatin as paracrine factors.

A

Histamine – secreted by ECL cells and stimulates HCl release

Somatostatin – secreted by D cells in response to decreased GI luminal pH

216
Q

The action of histamine at H2-receptors in the stomach is blocked by what endogenous hormone?

A

Secretin

218
Q

Gastrin is secreted by what type of cell?

CCK is secreted by what type of cell?

Secretin is secreted by what type of cell?

Glucode-dependent insulinotropic peptide is secreted by what type of cell?

A

G cells;

I cells (duodenum and jejunum);

S cells (duodenum);

K cells (duodenum and jejunum)

219
Q

What are the stimuli for secretion of gastrin?

What are the stimuli for secretion of CCK?

What are the stimuli for secretion of secretin?

What are the stimuli for secretion of glucose-dependent insulinotropic peptide?

A

Amino acids, distention, vagal stimulation;

lipids and amino acids;

gastric acid and fatty acids;

oral glucose, fatty acids, and amino acids

220
Q

What are three substances that directly inhibit gastric acid secretion?

A

Somatostatin;

secretin;

glucose-dependent insulinotropic peptide (aka gastric inhibitory peptide)

221
Q
A

B.

222
Q

Cystinuria or Hartnup?

A

Cystinuria

223
Q

Gastrin is directly blocked by:

A

Secretin

224
Q

Gastrin causes increased secretion of:

CCK causes increased secretion of:

Secretin causes increased secretion of:

Glucose-dependent insulinotropic peptide causes increased secretion of:

A

HCl;

pancreatic enzymes, pancreatic HCO3-;

pancreatic HCO3-; biliary HCO3-;

insulin

225
Q

Gastrin’s non-secretory effects include:

CCK’s non-secretory effects include:

Secretin’s non-secretory effects include:

Glucose-dependent insulinotropic peptide’s non-secretory effects include:

A

Growth of gastric and intestinal mucosa, increased gastric motility;

gallbladder contraction, sphincter of Oddi relaxation, growth of pancreas and gallbladder, slowed gastric emptying;

inhibits gastrin/histamine, slowed gastric emptying;

inhibits glucagon, slowed gastric emptying

227
Q

What structural feature of the GI tract lends the highest increase in surface area to the tract (plicae circularis, villi, crypts of Lieberkuhn, microvilli)?

A

Microvilli

(600x increase)

228
Q

True/False.

GI stem cells are mostly found between the microvilli.

A

True/False.

GI stem cells are mostly found at the bottom of the crypts of Lieberkuhn.

230
Q

Describe the differences in breakdown and absorption between protein, carbohydrates, and lipids.

A

Proteins: broken down into oligopeptides or amino acids –> oligopeptides then digested within enterocytes

Carbohydrates: broken down into monomers

Lipids: broken down into fatty acids –> resynthesized into triglycerides in the enterocytes

231
Q

What is the main carbohydrate we eat?

What is the main carbohydrate of dietary fiber?

A

Amylopectin (plant starch);

cellulose

232
Q

Describe how a branched carbohydrate is broken down in the GI tract.

A
  1. α-amylase cuts branched structures (such as amylopectin) into monomers
  2. Disaccharides and limit-dextrans are then cut down by further brush border hydrolases (isomaltase, sucrase, lactase, etc.)
233
Q

Describe the cellular mechanism of calcium absorption in the GI tract.

A
234
Q

While carbohydrate/protein/lipid absorption happens in each portion of the small intestine, where does the majority occur?

A

The duodenum (then jejunum, then ileum)

(Graph A.)

235
Q

In what portion(s) of the small intestine does calcium absorption occur?

A

All three

(Graph B.)

236
Q

What transporter allows for apical glucose uptake in the GI tract?

What transporter allows for apical fructose uptake in the GI tract?

A

SGLT1

GLUT5

237
Q

What transporter allows for basolateral glucose uptake in the GI tract?

What transporter allows for basolateral fructose uptake in the GI tract?

A

GLUT2

GLUT2

238
Q

Where are bile acids absorbed in the gut?

A

Mostly the ileum

239
Q

Is protein uptake in the GI tract sodium-dependent at either the apical or basolateral sides?

A

Apical only

(secondary active transport)

240
Q

What type of diarrhea can a lactase deficiency cause?

Why is there excess gas production?

A

Osmotic diarrhea;

the bacteria turn the excess sugar into H2 and CO2

241
Q

What is Hartnup disease?

To what disorder does it lead?

A

A disorder (renal and intestinal) of oligopeptide and tryptophan absorption;

pellagra (niacin defiiency leading to dermatitis + diarrhea + dementia)

242
Q

What is cystinuria?

What is the common result?

A

Improper gut cysteine absorption;

renal stones

245
Q

Virtually all dietary lipids are __________ (90%).

A

Triglycerides

246
Q

Name a few luminal substances necessary for proper fat digestion and absorption by the GI tract.

A

Lipases, bile acids, and phospholipids

247
Q

Children with low sun exposure may be at-risk for what disorder of vitamin D?

A

Ricketts

248
Q

Name three lipases and a cofactor released into the proximal duodenum.

A

Glycerol ester hydrolase, cholesterol ester hydrolase, phospholipase A2;

colipase

249
Q
A

2.

250
Q
A

4.

251
Q
A

1.

252
Q

Describe the cellular mechanism of iron absorption in the duodenum.

Specifically, what is the apical transporter and other protein regulating the pathway?

A

DCT1;

hephaestin

253
Q

In what ways is absorption of glucose and amino acids in the gut similar to reabsorption in the kidneys?

A

Secondary active transport (Na+-linked) at the apical membrane;

Na+/K+ ATPases at the basolateral membrane

254
Q

Describe post-prandial sodium absorption in the duodenum, jejunum, and ileum.

A

Na+-linked secondary active transport;

Na+/H+ exchangers

255
Q

Describe sodium absorption during the inter-digestive phase in the ileum and colon.

A

Na+/H+ and Cl-/HCO3- exchangers;

Na+ leak channels

256
Q

Where does passive Cl- absorption predominate in the GI tract?

Where do Cl-/HCO3- exchangers predominate in the GI tract?

A

Jejunum, distal colon;

ileum, proximal colon

257
Q

Describe the mechanism of NaCl secretion in the crypts of Lieberkuhn.

A

CFTR transporters;

paracellular Na+ leakage

258
Q

Describe the changes in K+ absorption and secretion from the small intestine to the large intestine to the distal colon.

A
259
Q

Describe some of the mechanisms of NaCl absorption and K+ secretion by the colon.

A

Na+-linked cotransporters;

Na+/H+ exchangers;

Cl-/HCO3- exchangers;

K+ leak channels

260
Q

Malfunction/deficiency of the DRA / AE1 channels in this diagram of a colonic cell would result in what effects?

What is the name of this condition?

A

Alkalosis and osmotic diarrhea

(due to HCO3- retention and Cl- secretion);

congenital chloridorrhea

261
Q

In relative terms, describe the pHs of the following GI tract segments:

Salivary glands

Stomach

Biliary tree

Pancreas

Jejunum

Ileum

Colon

A

Alkaline

Highly acidic

Alkaline

Highly alkaline

Alkaline

Alkaline

Acidic

262
Q

What is colipase?

A

An amphipathic molecule that anchors lipases to lipid droplets

263
Q

Name some of the secretagogues increasing ion secretion in the intestines.

A

Acetylcholine,

nitric oxide,

VIP,

histamine,

prostaglandins,

bile acids,

gastrin,

long-chain FAs

264
Q

Name some of the absorbtagogues increasing ion secretion in the intestines.

A

Opioids,

norepinephrine,

somatostatin

265
Q

What effect do cAMP, cGMP, and Ca2+ have on intestinal anion secretion?

And NaCl absorption?

A

Increase;

inhibition

266
Q

What intracellular mediator(s) increase(s) intestinal anion secretion and inhibit(s) NaCl absorption?

A

cAMP, cGMP, Ca2+

267
Q

Do micelles contain triglycerides?

A

No;

free fatty acids

268
Q

How are the fat-soluble vitamins (ADEK) absorped?

A

They diffuse into micelles and then into enterocytes and then into chylomicrons

269
Q

Which is larger: chylomicrons or micelles?

Which contains triglycerides: chylomicrons or micelles?

A

Chylomicrons;

chylomicrons

270
Q

Which of the following are formed within enterocytes:

Triglycerides

Cholesterol

Micelles

Chylomicrons

A

Triglycerides;

chylomicrons

271
Q

Which macromolecules are digested within enterocytes as well as in the GI lumen?

Which macromolecules are reformed within enterocytes after being digested in the GI lumen?

A

Oligopeptides;

triglycerides

275
Q

Where is folate absorbed in the gut?

A

Duodenum and jejunum

276
Q

Where is iron absorbed in the gut?

A

The duodenum

278
Q

The ileum is specifically responsible for the absorption of what two substances?

A

B12;

bile acids

279
Q

About how much fluid is secreted into the gut every day?

About how much of that fluid is reabsorbed by the small intestine?

About how much of that fluid is reabsorbed by the large intestine?

A
  1. 5 L
  2. 5 L
  3. 9 L
280
Q

What is the basic mechanism of fluid reabsorption in the gut?

A

Solute reabsorption

(fluid follows solutes)

281
Q

What two types of junctions are responsible for water reabsorption in the gut?

With what two different tonicities?

A

Leaky junctions –> isosmotic absorption

Tight junctions –> absorption across gradients

282
Q

The small intestine absorbs net amounts of water and what electrolytes?

The small intestine secretes net amounts of what electrolytes?

A

Na+, K+, Cl-;

HCO3-

283
Q

The large intestine absorbs net amounts of water and what electrolytes?

The large intestine secretes net amounts of water and what electrolytes?

A

Na+, Cl-;

K+, HCO3-

284
Q

What causes congenital chloridorrhea?

What pH change is expected?

A

A deficiency of the gut Cl-/HCO3- exchanger;

metabolic alkalosis (HCO3- retention)

285
Q

What pH effect can secretory diarrhea have?

What pH effect can severe vomiting have?

A

Metabolic acidosis (HCO3- loss);

metabolic alkalosis (HCl loss)

286
Q

How can diarrhea be classified according to the reason for fluid moving to the vessel lumen?

A

Osmotic;

secretory

287
Q

True/False.

Diarrhea can be caused by either blocking gut solute absorption or increasing gut solute secretion.

A

True.

296
Q

In which locations does most Na-linked cotransport occur in the gut?

A

Duodenum > Jejunum >> Ileum

297
Q

In which locations does most Na+/H+ exchange occur in the gut?

A

Jejunum, ileum, proximal colon

298
Q

In which locations does most passive Cl- absorption occur in the gut?

A

Jejunum, distal colon

299
Q

In which locations does most K+ secretion occur in the gut?

A

Distal colon

300
Q

In which locations does most Cl-/HCO3- exchange occur in the gut?

A

Ileum, proximal colon

301
Q

What transporter in the duodenum allows for Fe3+ uptake?

What transporter in the small intestine allows for glucose​ uptake?

A

DCT1

SGLT1

302
Q

What transporter in the colon allows for short-chain fatty acid uptake?

What transporter in the colon allows for Cl-​ (uptake) and HCO3- exchange?

A

SMCT1

DRA/AE1

303
Q

A deficiency of what transporter in the colon leads to congenital chloridorrhea?

A

DRA/AE1

(a Cl-/HCO3- exchanger)

309
Q

What is the main controlling factor for intestinal ion transport?

A

Chemical mediators: absorbtagogues and secretagogues

314
Q

What sections of the stomach have parietal cells?

A

Body + fundus

315
Q

What section of the stomach is the primary location of G cells?

A

The antrum

316
Q

Which of the three factors that increase gastric acid secretion (histamine, gastrin, acetylcholine) increase intracellular Ca<strong>2+</strong> in the parietal cells they bind?

Which of the three factors that increase gastric acid secretion (histamine, gastrin, acetylcholine) increase intracellular cAMP ​in the parietal cells they bind?

A

Gastrin (CCKR), acetylcholine (M3);

histamine (H2)

317
Q

Name that respective intracellular messenger that each of the following utilizes to stimulate increased HCl secretion by parietal cells:

Gastrin

Histamine

Acetylcholine

A

Ca2+

cAMP

Ca2+

318
Q

Which is more likely to cause ulcer formation, acute or chronic NSAID use?

A

Acute

(chronic does increase risk though)

319
Q

How does a urease breath test work?

A

A patient ingests labeled urea;

labeled CO2 being breathed out is then measured to see if urease is present in the stomach;

if so, this indicates H. pylori infection

320
Q

H. pylori uses urease to turn ________ into ________.

A

Urea;

NH3 + CO2

321
Q

What is the mechanism of H. pylori-induced ulcer formation?

A

Urease creates ammonia –> neutralizing HCl so the H. pylori can approach the epithelium;

the H. pylori inhibit somatostatin at the epithelium –> causing increased HCl production

322
Q

Why can ulcer pain decrease after eating?

A

Food acts as a buffer

323
Q

True/False.

The mucus and unstirred water layers of the stomach contain high concentrations of HCO3-.

A

True.

324
Q

How is H. pylori infection treated?

A

Triple therapy:

a PPI (omeprazole)

+ 2 antibiotics

325
Q

What mnemonic can be used to remember the causes of pancreatitis?

A

I GET SMASHED

Idiopathic

Gallstones EtOH Trauma

Steroids Malignancy/Mumps Autoimmune Scorpion sting Hypertriglyceridemia/Hypercalcemia ERCP Drugs

326
Q

Use the mnemonic I GET SMASHED to list some major risk factors for pancreatitis.

A

Idiopathic

Gallstones EtOH Trauma

Steroids Malignancy/Mumps Autoimmune Scorpion sting Hypertriglyceridemia/Hypercalcemia ERCP Drugs

327
Q

What cofactor does the pancreas secrete to aid lipase in digesting lipids?

What does the pancreas secrete to inhibit trypsin activity?

Why?

A

Colipase;

trypsin inhibiting protein (TIP),

to prevent pancreatic autodigestion

328
Q

Name two proteins that the duodenum secretes.

One is solely to decrease gastric acid secretion, and one is to aid in protein digestion.

A

Urogastrone;

pepsinogen

329
Q

What is urogastrone?

A

A duodenal peptide that inhibits the action of gastrin

330
Q

Where are bile acids reabsorbed in the GI tract?

A

The ileum

331
Q

Why might a patient present with diarrhea following resection of the terminal ileum?

A

Secretory diarrhea

(bile acids remain in lumen and Cl- secretion is increased)

332
Q

Which is more soluble, bile salts or bile acids?

A

Bile salts (better able to emulsify fat)

333
Q

How are bile acids reabsorbed in the ileum?

Where do they go?

A

Via Na+-linked cotransport;

the portal vein

334
Q

What is chenodeoxycholic acid?

A

A primary bile acid

(can be used to dissolve gallstones)

335
Q

What is the rate-limiting enzyme for bile acid production?

A

7α-hydroxylase

336
Q

What three products does α-amylase produce?

A

Maltose,

maltotriose,

α-limit dextrans

337
Q

What bonds can α-amylase cleave?

A

Non-terminal α-1,4 bonds

(forming maltose, maltriose, and α-limit dextrans)

338
Q

Name the substrate each of the following enzymes acts upon:

Isomaltase

Lactase

Sucrase

A

Maltose, maltotriose, α-limit dextrans;

lactose;

sucrose

339
Q

After α-amylase cleaves amylopectin α-1,4 bonds to produce maltoses, maltrioses, and α-limit dextrans, what enzyme further degrades these products?

What bonds can it cleave?

A

Isomaltose;

α-1,4 (maltose, maltriose) and α-1,6 (α-limit dextrans)

340
Q

How are gut amino acid transporters classified according to their nomenclature?

A

Upper case letter (e.g. B): Na-dependent

0 Superscript (e.g. B0): neutral amino acids

Lower case letter (e.g. b): Na-independent

+ Superscript (e.g. b+): charged amino acids

341
Q

What type of gut amino acid transporter is missing in Hartnup disease?

A

Na-dependent for neutral amino acids

(B0)

342
Q

Are patients protein-deficient in either Hartnup’s disease or cystinuria?

A

No

351
Q

True/False.

Apical transport of amino acids into the enterocytes is bidirectional.

A

False.

Basolateral transport of amino acids into the enterocytes is bidirectional.

352
Q

What cotransporter allows for glucose uptake in the gut?

What cotransporter allows for glucose uptake in the kidneys?

A

SGLT1

SGLT2

T1 - Integrated (Full Review) (29 decks)

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