L3: Swallowing and Stomach Histology

Question 1

Peristalsis initiated by the swallow

Answer 1

Primary Peristalsis

Question 2

Peristalsis initiated by distention of the esophagus

Answer 2

Secondary Peristalsis

Question 3

During a swallow an initial _______ component leads to _______

Answer 3

Initial Voluntary component leads to involuntary swallow

Question 4

During a swallow upper oesophageal sphincter opens rapidly and then shuts quickly to prevent ________________ => ___________________ then kicks-in

Answer 4

Upper oesophageal sphincter opens rapidly and then shuts quickly to prevent reflux => Secondary peristalsis then kicks-in

Question 5

________________ can still occur after vagotomy

Answer 5

Peristalsis can still occur after vagotomy

Vagus nerve is important for physciological peristalsis, however lower esophagus can persist without vagal intervention. The Enteric Plexus is capable of coordinating persistalsis independently of autonomic innervation

Question 6

Normal swallowing involves the coordinated action of both the ____________ and ____________

Answer 6

Normal swallowing involves the coordinated action of both the ANS and the ENS

Question 7

During Peristalsis contraction behind the bolus is facilitated by release of _________ while relaxation in front of the bolus is facilitated by release of ________

Answer 7

Contraction behind the bolus (ACh)

Relaxation in front of the bolus (NO)

Question 8

The ________________________ co-ordinates peristaltic contractions

Answer 8

The Enteric Nervous System co-ordinates peristaltic contractions

Question 9

What happens during multiple rapid swallows?

What is this known as?

Answer 9

Peristalsis is inhibited until the last swallow

Known as Deglutitive Inhibition

Question 10

What is used to analyse Esophagus via X-Ray?

Answer 10

Normal Barium Swallow

Question 11

Esophageal Motility disorder associated with impaired or absent peristalsis

Apearance of Esophagus?

Answer 11

Esophageal Achalasia

Dilated Oesophagus showing tapering at distal part Distended oesophagus and 'Bird–beak' appearance

Question 12

Esophgeal Disorder associated w/ Diffuse spasms, Impaired motility, and Uncoordinated contractions

Apearance of Esophagus?

Answer 12

Corkscrew Esophagus

‘Corkscrew’ or Rosary bead appearance of disordered peristalsis

Question 13

Esophageal condition in which tone of lower esophageal sphincter impaired => acid leaks up damaging the mucosa of lower esophagus=> dysplasia (Barrett’s Esophagus)

Answer 13

Gastro Oesophageal Reflux Disease ( GORD)

Question 14

Anatomomical Regions (4)
Histological Regions (3)

Answer 14

Question 15

Part of the stomach primarily responsible for secretion of mucous and relaxation to accomodate a meal?

Function?

Answer 15

Fundus

Secretion of mucous rather than acid. Helps protect esophagus/small intestine

Question 16

Part of stomach that produces majority of Gastric Acid and Facilitates mixing of stomach contents?

Answer 16

Body/Corpus

Question 17

Part of stomach which is mainly mucus and highly muscular?

Answer 17

Pylorus

Question 18

Stomach cell that secretes mucus and bicarbonate?

Location/Role of this cell?

Answer 18

Surface Mucous Cell

Protects Stomach from Acid in Lumen

Question 19

Stomach cell present in neck or isthmus with an acidic secretion containing Mucin

Location/Characterisitics of this cell?

Answer 19

Mucous Neck Cell

Less columnar - rounded nuclei

Question 20

Stomach cell present in neck and deeper parts of gland that Secretes HCl and Intrinsic Factor?

Answer 20

Parietal cell

Strong eosinophilic staining

Question 21

Where are Chief Cells located and what do they Produce?

Answer 21

Lower region of the gastric gland
Produces Pepsinogens, Gastric lipase, Rennin

Pepsinogen: precursor of pepsin => converted by meeting of acid in lumen=> able to digest protein

Question 22

What is Pepsinogen

From where is it secreted?

Answer 22

Pepsinogen: precursor of pepsin => converted by meeting of acid in lumen=> Pepsin: Active protease that breaks down proteins into peptidesand amino acids

Released from Chief Cells (Response to ACh, Gastrin Secretin)

Question 23

Gastrin/5HT producing cells in pylous?

Answer 23

Enteroendocrine cells (G-Cells)

Question 24

What Pathogen exploit’s stomach’s protection from autodigestion?

Answer 24

H. Pylori embeds flagella into mucous layer, enabling it to avoid the stomach’s acid

Question 25

Process of Gastric Mucous Production?

Answer 25

Question 26

Mucous secretion is ____________ by prostaglandins

Answer 26

Mucous secretion is stimulated by prostaglandins ## Footnote NSAIDS can inhibit prostaglandins and thus limit surface mucous production

Question 27

What Macromolecule begins to be digested in stomach by Gastic Acid?

Answer 27

Proteins | Carbohydrates/Lipids primiarily digested later on

Question 28

How is protein Digested in stomach?

Answer 28

Denaturing of proteins by gastric acid ->Exposure of peptide bonds Acid converts Pepsinogen -> Pepsin protease that breaks down proteins into peptides + amino acids

Question 29

# Fundus/ Corpus Histology What are the folds called? What are the pright pink cells in middle of the glands? What are the purple tubular cells at bottom of gland?

Answer 29

Folds/Ruggae of stomach -> when it is empty Bright pink midle of glands=**Pareital cells** **Chief cells** near bottom of gland: produce pepsinogen/gastic lipase

Question 30

**Describe the process of HCl excretion from Parietal Cells** * CO2 Produced via normal activity encounters H2O and is converted via carbonic anhydrase to ______ and an ____ ion * ______transported to the intraluminal cell surface * _____ actively pumping hydrogen ion out into lumen in exchange for potassium * Loss of H+ on lumenal surface is compensated by exchanging Bicarbonate on the basal side in for____ * _____then participates on the lumenal surface in exchanged for potassium that is co-transported out with Cl- (H+ + CL- => HCl Acid) * ____ is exchanged for K+ on the basal surface

Answer 30

* CO2 Produced via normal activity encounters H2O and is converted via carbonic anhydrase to **Bicarbonate (HCO3-)** and an **H+** ion * **Hydrogen ions** transported to intraluminal cell surface * **Potassium Hydrogen ATPase** actively pumping hydrogen ion out into lumen in exchange for potassium * Loss of H+ on lumenal surface is compensated by exchanging Bicarbonate on the basal side in for **Cl- ions** * **Cl-** then participates on the lumenal surface in exchanged for potassium that is co-transported out with Cl- (H+ + CL- => HCl Acid) * **Na+** is exchanged for K+ on the basal surface

Question 31

Why do Parietal Cells have an abundance of mitochondira?

Answer 31

Huge number of mitochondria needed to push out H+ into lumen against a massive concentration gradient

Question 32

What is Intrinsic Factor Required for? | Where is it produced? Optimum pH?

Answer 32

Intrinsic Factor: Protein required for takeup of vitamin B12 | Parietal Cells - pH 7

Question 33

Process of Vitamin B12 Digestion: * Vitamin B12 (___________) initially binds _________________ in the stomach * ______________ is then broken down by pancreatic enzymes in duodenum releasing B12 which then binds __________________ in more pH appropriate environment * This complex is Endocytosed by cells in the _________________ * B12 then released and complexes with ___________________ in the cells before traveling to the liver | What is B12's Importance?

Answer 33

* Vitamin B12 (Cobalamin) initially binds **Haptocorrin (Transcobalamin I)** in the stomach * **Haptocorrin** is broken down by pancreatic enzymes in the duodenum releasing B12 which then binds **Intrinsic Factor** in more pH appropriate environment * This complex is endocytosed by cells in the **Terminal Ileum** * B12 then released and complexes with **Transcobalamin II** in the cells before traveling to the liver | B12 is required for erythropoiesis

Question 34

Clinical condiiton associated with loss of parietal cells?

Answer 34

Pernicious Anaemia | autoimmune disease ## Footnote Loss of Parietal Cells => Amount of intrinsic factor is compromised => cant absorb B12 as effectively in small intestine => deficiency of B12 => erythropoiesis is compromised

Question 35

What hormones trigger Chief Cells? What do they then release?

Answer 35

_Triggerrs:_ ACh, Gastrin Secretin _Releases_: Pepsinogen, Gastric Lipase, Rennin | Pepsinogen is a pro-enzyme released by Chief cells -> pepsin in stomach

Question 36

Enzyme Producing Cell of Stomach?

Answer 36

Chief Cells (Pepsinogen/ Gastric Lipase)

Question 37

Hormone Producing Cells of Stomach? ## Footnote Role of each?

Answer 37

**Enteroendocrine Cells** _G- cells_: Secrete gastrin into blood => Promote gastric acid secretion _D-cells_: Secrete Somatostatin => Inhibition of other G cells _Enterochromaffin (EC) Cells_: Secrete Serotonin and Substance P => Promotion of gut motility

Question 38

What do G-Cells do? | What Type of Cell are they?

Answer 38

Secretion of GASTRIN into the blood Gastrin is a hormone that promotes gastric acid secretion | Enteroendocrine cell

Question 39

What do D-Cells do? | What Type of Cell are they?

Answer 39

Secretion of Somatostatin Inhibition of other G cells | Enteroendocrine cell

Question 40

What do Enterochromaffin (EC) Cells do?

Answer 40

Secretion of Serotonin and Substance P Promotion of gut motility

Question 41

Oxyntic Glands vs. Pyloric Glands? | Region and cell types of each

Answer 41

**Oxyntic glands** have a prevalence of Pareital/Chief Cell **Pyloric Glands** have a greater presentation of Mucous Producing (Surface Mucous/ Mucous Neck Cells) and Endocrine cells (Enterochromaffin Cells, D cell, G cells) associated with regulation of acid production in the other acid producing regions | *Oxyntic Gland*- Fundus/Corpus *Pyloric*: Near small intestine