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FHB - GI/Metabolism - Exam 3 > Lecture 5 & 6 - Integrated Response to a Meal > Flashcards

Lecture 5 & 6 - Integrated Response to a Meal Flashcards

1
Q

What are the major functions of the stomach?

Which is the most essential?

A
  1. Storage
  2. Secretion of H+
    - converts pepsinogen to pepsin
  3. Secretion of IF
    - reabsorb B12
  4. Secretion of mucus and HCO3- to protect the gastric mucosa
  5. Secretion of water
    - lubricate the bolus
  6. Motor Activity
    - mix secretions with bolus
  7. Coordination of motor activity
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2
Q

The regulation of motor & secretory responses of the stomach are via:

  1. Neural
  2. Paracrine
  3. Endocrine

What hormones are involved in paracrine and endocrine regulation?

A

Paracrine:

HISTAMINE

Endocrine:
Gastrin
Somatostatin

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3
Q

What are the main functions of the following

  1. Histamine
  2. Gastrin
  3. Somatostatin
A

Histamine:
powerful stimulator of H+ secretion

Gastrin:
stimulates gastric acid secretion
( + regulator)
- stomach and duodenum

Somatostatin:
INHIBITS gastric secretion
( - regulator)
-stomach duodenum and pancreas

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4
Q

What secretions are common ALL THROUGHOUT the stomach?

A

Mucus & Bicarbonate!

Found at LES & Cardia
Fundus and Body

Antrum & Pylorus

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5
Q

Which part of he stomach has the most secretions overall?

A

Fundus & Body

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6
Q

State the main luminal secretions & the function of the following:

  1. LES/Cardia
  2. Fundus & Body
  3. Antrum & Pylorus
A
  1. LES & Cardia
    - mucus & HCO3-
    - prevent reflux, entry of food, regulates belching*
  2. Fundus & Body
    - H+, Intrinsic Factor, Mucus, HCO3-, Pepsinogens, Lipase

FX: Reservoir, tonic force during emptying

  1. Antrum & Pylorus
    - Mucus & HCO3-

MIXING/ GRINDING/ SIEVING/ REGULATION of emptying

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7
Q

What are the 3 divisions of the stomach?

A
  1. Cardia
  2. Corpus (fundus/body)
  3. Antrum

also divided into proximal & distal part

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8
Q

What cells are found within the stomach?

What folds do these create?

What empties here?

A
  1. Columnar epithelium
  2. Gastric Pits
  3. Gastric glands empty into gastric pits
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9
Q

What are the 3 divisions of the GASTRIC MUCOSA?

A
  1. Cardiac Glandular region
    - mucus & HCO3-
  2. Oxyntic/Parietal Gland Region (Fundus)
  3. Pyloric Gland Region (antrum)
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10
Q

What are the 6 secretary cells in the FUNDUS and ANTRUM?

A
  1. Parietal/ Ocyntic Cells
  2. Mucous Neck Cells
  3. Peptic/CHief cells
  4. Enterochromaffin–like Cells (ECL)
  5. D Cells
  6. G cells
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11
Q

Describe secretions/functions of of the following:

  1. Parietal/ Ocyntic Cells
    (2)

ONE IS VERY ESSENTIAL

  1. Mucous Neck Cells
  2. Peptic/CHief cells
A
  1. Parietal/ Ocyntic Cells

a) HCl - kills bacteria & creates low pH for activation of Pepsin
b) IF : glycoproteins that bind B12 and make it absorbable by ileum mucosa

* ESSENTIAL

  1. Mucous Neck Cells
    - protect gastric mucosa w/ mucus

3.Peptic/Chief cells:
- pepsinogens cleaved to pepsins in ACIDIC environments
(pepsin only active at low pH)

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12
Q

Describe the secretions/functions of the following:

  1. Enterochromaffin–like Cells (ECL)
  2. D Cells
  3. G cells
A
  1. Enterochromaffin–like Cells (ECL)
  • HISTAMINE (paracrine)
  • most powerful stimulator of HCl secretion
  1. D Cells:

SOMATOSTATIN
(endocrine)
- inhibits HCl secretion

  1. G cells:
    GASTRIN (endocrine)
    - HCl secretagogue
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13
Q

What are the 4 major gastric secretions that are secreted by cells of gastric mucosa

“GASTRIC JUICE”

A
  1. HCl
    - activates pepsinogen to pepsin = protein digestion (20%) –> not essential
  2. Pepsinogen
    - inactive proenzyme of pepsin
  3. Bicarbonate + Mucus
    - protection of gastric mucosa against acidic & peptic luminal environment
  4. Intrinsic Factor
    - glycoprotein for absorption of B12 in ileum
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14
Q

What is the ONLY essential component of Gastric Juice in a healthy human?

A

Intrinsic Factor!

  • glycoprotein that facilitates absorption of B12 in the ILEUM
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15
Q

What happens when parietal cells are activated?
What fuses together?

What transporters increase in number?

What is open?

A
  1. Tubulovesicular membranes fuse with plasma membrane of secretory canaliculi
  2. Increase H-K antiprotons on SECRETORY CANALICULI
  3. Opens to the LUMEN of the gland
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16
Q

What is the main function of the tubulovesicular system? Where is this found?

A
  1. Transport proteins for secretion of H+ and Cl-

2. Parietal Cells

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17
Q

What produces H2CO3 from CO2 and H20 in the intracellular fluid of gastric acid secretion?

A

CARBONIC ANHYDRASE

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18
Q

What is secreted in the lumen? (apical membrane)

Via what transporters?

What drug can inhibit this?

A
  1. H+
  2. via H-K ATPase (active)
    - against gradient
  3. Drug OMEPRAZOLE

(for GERD and to treat ulcers by reducing H+ secretion)

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19
Q

Increased intracellular Calcium & cAMP increases the conduction of what 2 ions?

A

Cl - and K+

  • thus as H+ is increased, Cl follows into the lumen
    , K is reabsored via H-K transporter
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20
Q

How & where is HCO3- reabsorbed?

What is the term for the high pH in the gastric venous blood after a meal?

A
  1. Basolateral Membrane
  2. HCO3- - Cl- exchanger

ALKALINE TIDE due to the absorbed HCO3-

  • eventually secreted back into GI
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21
Q

What are the net secretions and absorptions in the Gastric Acid?

A
  1. HCl = net secretion

2. HCO3 - = net absorption

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22
Q

The venous blood is slightly acidic.

True or False?

A

FALSE

  • slightly alkaline because Bicarbonate is reabsorbed on the basolateral side

Pancreas will be secreting the bicarbonate back into the lumen

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23
Q

What concentrations are similar to plasma & which are higher than plasma?

A
  1. Na & Cl = similar to plasma

2. K+ and HCO3 = HIGHER than plasma

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24
Q

Where is the HCO3 - trapped?

A

Viscous mucus that coats the stomach lumen

  • forms mucosal barrier
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25
Q

Where are Mucins secreted?

What is 80% of their composition?

How are they formed?

Which portion is susceptible to proteolytic digestion by pepsins?

A
  1. Mucous Neck Cells
  2. CARBOHYDRATE
  3. Tetramer of 4 similar monomers
  4. Central Portion of mucin tetramer is susceptible to proteolytic digestion by pepsins

Proteolytic fragments do NOT form gels, they dissolve the protective mucus layer

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26
Q

What happens if the mucins do not form a tetramer?

A

No thick viscous layer to protect from gastric secretions

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27
Q

What 2 things protect the surface of the stomach from H+ and pepsins?

Where is the GASTRIC MUCOSAL BARRIER?

A

Mucus & HCO3-

LUMINAL SIDE
- traps alkaline secretions in the mucus layer

  • separates HCO3- rich secretions of the surface epithelial cells

FROM the acidic contents of the gastric lumen

28
Q

What are the two main functions of the gastric mucosal barrier?

A

Mucus:

  1. Protects cells from H+
  2. Inactivates Pepsins
29
Q

What happens if the mucus membrane of the luminal gastric epithelial cells is damaged?

A

the ph of 2 in gastric juice is able to penetrate the gastric epithelial cells

  • leads to GASTRIC ULCERS
    ex: H. Pylori damages mucosal barrier
30
Q

What specific gastric secretion gets inactivated by the high pH in the Mucosal Barrier?

A

Pepsin

31
Q

What is the strongest stimulant for H+ secretion?

What cells do the efferent fibers terminate on and thus stimulate?

A
  1. Parasympathetic stimulation
  2. Parietal cells, ECL cells, G cells
    - also secretes pepsinogen mucus, HCO3- and IF
32
Q

H+ secretion by PARIETAL cells are stimulated by which 3 substances?

A
  1. Acetylcholine
  2. Histamine
  3. Gastrin
33
Q

Describe the following for Acetylcholine:

  1. Where is it released
  2. Which receptors does it bind to on PARIETAL cells?
  3. What are the 2nd messengers
  4. What is the final affect?
  5. What inhibits this and how?
A
  1. released from VAGUS nerve innervating the gastric mucosa
  2. binds to muscarinic (M3) receptors on the parietal cells
  3. IP3/Ca++
  4. stimulates H+ secretion
  5. Atropine (inhibits muscarinic receptors) blocks Ach effects on parietal cells.
34
Q

Describe the following for Histamine:

  1. Where is it released?Endocrine or Paracrine affect?
  2. Which receptors does it bind to?
  3. What are the 2nd messengers
  4. What is the final affect? Which cells does it stimulate specifically?
  5. What inhibits this and how?
A
  1. gastric ECL cells (paracrine effect on parietal cells)
  2. Binds to H2 receptors
  3. cAMP
  4. Stimulates H+ secretion by parietal cells
  5. CIMETIDINE blocks H2 receptors & thus histamine affect (no H+ secreted by parietal cells)
35
Q

Which cells have an indirect affect on parietal cells?

A

ECL (paracrine) & G cells (endocrine)

36
Q

Describe the following for Gastrin:

  1. Where is it released? Endocrine or Paracrine affect?
  2. Which receptors does it bind to on PARIETAL cells?
  3. What are the 2nd messengers
  4. What is the final affect?
A
  1. stomach G CELLS (endocrine affect on parietal cells)
  2. Binds to CCKB (cholesystokinin B) on parietal cells
  3. IP3/ Ca2+ are the second messengers
  4. H+ secretion (direct affect)

Vagus via ENTERIC nervous system –> stimulates GRP –> stimulates G cells –> produce Gastrin

37
Q

What is potentiation? Which 3 substances are involved?

A

Rate of H+ secretion can be regulated by:
1. ACh
2. Histamine
3. Gastrin
by each independtanly as well as INTERACTIONS among the three
= potentiation

  • reason is unclear since each agent works via a different receptor (histamine a different second messenger)
38
Q

What are the potentiation consequences for Histamine & Ach? (i.e. which drugs block and what specifically)

A

Histamine:

1.potentiates the actions of Ach & gastrin:

CIMETIDINE:

a) blocks direct histamine affects
b) blocks histamine - potentiated effect of ACh and gastrin

  1. ACH potentiates the actions of histamine and gastrin:

ATROPINE will:

a) block direct effects of Ach
b) block Ach potentiated effects of histamine and gastrin

39
Q

Why does CIMETIDINE not reduce the acidity of gastric secretions?

How does omeprazole decrease H+ secretions?

A

blocks Histamine release via H2 receptors
- thus only ONE access point is blocked, and acid secretion is NOT completely inhibited

Omeprazole blocks the H-K ATPase itself!

40
Q

Describe the following for the mechanisms that promote HCl secretions:

  1. Which are direct or indirect
  2. Is this a neural, paracrine, or endocrine effect
  3. Which cells are stimulated?

3 cases

A

DIRECT:
- stimulation of PARIETAL cells by vagus via ACH (muscarinic receptors)

–> neural effect

INDIRECT:
1. stimulation of G cells by vagus via GRP to produce gastrin
= ENDOCRINE effect

  1. stimulation of ECL cells by vagus (Ach) and GASTRIN (CCKB) to produce histamine
    = paracrine effect!
41
Q

What are the stimuli for the gastric phase?

What do they stimulate the release of, specifically?

Which has the vasovagal reflex?

A
  1. Distension of stomach
    - activates VASOVAGAL reflex
    - gastrin is released*
  2. Presence of amino acids & Small peptides
    - works on G CELLS to stimulate Gastrin release
  3. Alcohol & Caffeine

INTESTINAL phase only has 10% of total HCl secretion & is mediated by products of protein digestion

42
Q

What initiates the negative feedback loop in the distal stomach to INHIBIT ACID secretion?

What is released when the pH of the lumen is below 3?

A

Presence of Acidic Chyme in distal stomach

Somatostatin (SS) is released by endocrine cells) via direct & indirect pathways

43
Q

What is the direct pathway of SS release when the pH of the lumen is below 3?

What is the indirect pathway?

A

Direct:

SS binds to receptors in PARIETAL cells and inhibits the stimulatory affect of histamine (inhibit cAMP)
- released via D cells (endocrine)

Indirect:
SS inhibits histamine release via ECL cells and gastrin release from G cells

44
Q

What is the function of prostaglandins?

How do NSAIDS affect them?

A

Protects the gastric mucosa
- inhibit the stimulatory effect of HISTAMINE

NSAIDS block the activity of the enzymes producing prostaglandins (cyclohexanase)
which usually inhibit cAMP

  • patients complain of bleeding
45
Q

Acid in the antrum stimulates the release of _____ to inhibit ____ post-meal.

A

SOMATOSTATIN

  • to inhibit gastrin secretion
46
Q

How does omeprazole and other proton pump inhibitors like prilosec affect the negative feedback of Gastric Acid?

A

pH drop does not occur since H+ is inhibited

  • negative feedback is not present so GASTRIN is produced long term
  • somatostatin cannot inhibit G cells if the pH is constantly higher than 3
  • prolonged HyperGastronemia
    w/ other complications like H.Pylori may lead to CANCER
47
Q

What digests proteins? Is it essential?

Is there amylase driven digestion in the stomach?

Where does the digestion of lipids begin?

When is this essential?

A
  1. Pepsin
    - not essential (20%)
  2. Some amylase digestion
    - inactive at low pH but not when the active site is occupied by CARBS
  3. Lipid digestion starts in the stomach –> gastric lipase attach to surface of lipid droplets
  4. Only essential in PANCREATIC disorders
48
Q

What are the 2 regions of the stomach that are divided based on MOTILITY?

Which of these is responsible for mixing the food?

A
  1. Orad (proximal)
    - contains fundus, proximal part of body, THIN WALLED
  2. Caudad (distal)
    - contains distal part of body & antrum = THICK walled
  3. Mixing the food by contracting the CAUDAD region
    - propelled to intestine

Proximal area is usually relaxed (low pressure) until it has to move through PYLORIS
(pressure & contraction increases here)

49
Q

What is receptive relaxation?

What relaxes specifically?

What reflex is responsible for this?

Which receptors detect the stimulus?

What NT is released from post-ganglionic peptidergic vagal fibers?

A
  1. Dissension of lower esophagus by food causes relaxation
  2. LES & ORAD stomach (upper)
  3. VAGOVAGAL reflex
  4. Mechanoreceptors detect stomach distension
    - relay to CNS, CNS sends efferent info to smooth muscle in orad stomach to RELAX
  5. NT = VIP & NO
50
Q

What is retropulsion?

A

Much of the chyme is propelled back to the stomach for further mixing & breakdown
- pylorus is still closed!!

51
Q

Describe what occurs in mixing and digestion

A

Caudad region- waves of strong contraction start in the mid portion of stomach – move distally towards pylorus, increasing in strength towards pylorus.

They mix the gastric contents and periodically propel a portion of these in the duodenum through pylorus
- followed by closure of pylorus.

52
Q

What 3 important functions are under the control of the Vagovagal reflex?

What innervation is excitatory?

A
  1. Acid secretion
  2. Distension of gastric wall
  3. Gastric Motility
    (controlled via intramural plexus)

Parasympathetic innervation is excitatory (ACh and substance P)

  • increases motility in lower stomach
  • magnitude of contraction is regulated by NEURAL input (by rate of astral contractions is set by gastric pacemaker)
53
Q

What is usually closed during the gastric phase?

A

Pylorus

  • antral contractions mix the gastric contents & reduce size
54
Q

How long does emptying of gastric contents to duodenum take?

What empties more rapidly: liquid or solids?
Isotonic or hypotonic/hypertonic

How big must solids be to enter duodenum?

A
  1. 3 hours –> SLOW
  2. Liquids = rapid
    ISOTONIC = more rapid than hypotonic/hypertonic
  3. Solids must be <1mm^3

(glucose empties faster than proteins

55
Q

What kind of cells are in the stomach?

A

Columnar Epithelia

  • have glands in the lamina propr. that secrete mucus & bicarbonate
56
Q

The chief cells, parietal cells, mucous cells, and stem cells are all found where?

A

Fundic Glands

57
Q

Where are the Mucous Neck cells found?

A

Body of the stomach

- on the gastric pits where all the secretions are released

58
Q

What are the main signs that a gastric ulcer is present?

A

show INTESTINAL metaplasia

  • do not see goblet cells in the stomach but once intestinal metaplasia occurs there are goblet cells present
59
Q

What is the pylorus made of?

How is contraction/relaxation coordinated?

What are the 3 main functions of the Pylorus?

A
  1. 2 ring like thickenings of circular smooth muscle
  2. Antrum contracts while the initial portion of the duodenum relaxes
    • filter large sized particles of food
      - empty gastric content at a rate consistent w/ duodenum’s ability to digest chyme
      - prevent reflux of bolus into stomach
60
Q

What are the controls for the Gastroduodenul Junction / Pylorus?

What are common pathologies?

A
  1. Hormonal
  2. Paracrine
  3. Nervous factors

Gastric Ulcerations
-sensitive to bile (basic pH) –> TOO ALKALINE

Duodenal ulcerations
- intestinal mucosa is sensitive to gastric secretion = acidic pH)

61
Q

Describe how the following affect pyloric smooth muscle tone & gastric emptying.

  1. Sympathetic fibers
    - state the hormone involved
  2. Parasympathetic & Vagal Excitatory Fibers
    - state the 4 hormones involved
  3. Vagal Inhibitory Fibers
    - state the 2 hormones involved
A
  1. Sympathetic fibers (NE)
    - slow gastric emptying
    - constrict pylorus
  2. Parasympathetic Excitatory Fibers (ACH)
    - CCK
    - Gastrin
    - GIP
    - Secretion
  • ALL SLOW GASTRIC EMPTYING and cause PYLORIC CONSTRICTION
  1. VAGAL INHIBITORY FIBERS:
    - VIP & NO
  • -> SPEED gastric emptying
  • RELAX PYLORUS
62
Q

Describe Peptic Ulcer Disease.

What is it caused by? (2 main things)

State the 3 causes

What is it based on?

A

Ulcerative lesion of gastric or duodenal mucosa

  1. Caused by erosive & digestive action of H+ & pepsin on mucosa

1) Loss of protective mucous barrier
2) Excessive H+ and pepsin secretion
3) combo of both

  1. Based on location
    - can be gastric or duodenal
63
Q

Describe the PRIMARY cause of Gastric Ulcers.

What bacteria is a major cause?

How does this bacteria affect the protective barrier?

How are net H+ secretory rates? Gastrin?

A
  1. because of defects in MUCOSAL barrier
    - allows H+ and pepsin to digest a portion of the mucosa
  2. H. Pylori
  3. H. Pylori release CYTOTOXIN to destroy the protective barrier & cells underneath
  4. H+ secretions = LOWER (surprising)

and GASTRIN secretion is HIGHER (lacks negative feedback)

64
Q

Describe the PRIMARY cause of Duodenal Ulcers.

How are net H+ secretory rates? Gastrin?

A
  1. more common*
    - excess H+ is delivered to the duodenum which overpowers the buffering capacity of PANCREATIC HCO3-
  2. EXCESS H+ secretion (less gastrin)
    - excess H+ combined w/ pepsin damages the duodenal mucosa

-too much acid produced or not enough HCO3

65
Q

What is the Zollinger-Ellison Syndrome? What is secreted in high amounts?

A

A tumor (gastrinoma) located in the pancreas that secretes HIGH quantities of gastrin?

66
Q
  1. What is the effect of high gastrin in Zollinger-Elison Syndrome? (2)
  2. What other pathology does it produce as a result?
  3. What is inactivated that leads to Steatorrhea?
  4. What happens to gastrin levels over time?
  5. What are the treatments?
A

1.
a). Increased H+ secretion by PARIETAL cells

b) . Increased parietal CELL MASS
2. excess H+ produces Duodenal Ulcer
3. Steatorrhea (fatty stool) since low duodenal pH inactivates the pancreatic LIPASE
4. no negative feedback from gastrin secretion of the tumor so GASTRIN LEVELS INCREASE!
- somatostatin only inhibits H+ secretions in the D cells, and thus no somatostatin receptors to stop Gastrin levels from increasing

  1. TX:
    Inhibitors of H+ secretion (cimetidine, omeprazole)
    Surgical removal of tumor

FHB - GI/Metabolism - Exam 3 (21 decks)

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