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Sem3: PHYS30240 GI and Renal Physiology > L3: Swallowing and Stomach Histology > Flashcards

L3: Swallowing and Stomach Histology Flashcards

1
Q

Peristalsis initiated by the swallow

A

Primary Peristalsis

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2
Q

Peristalsis initiated by distention of the esophagus

A

Secondary Peristalsis

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3
Q

During a swallow an initial _______ component leads to _______

A

Initial Voluntary component leads to involuntary swallow

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4
Q

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

A

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

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5
Q

________________ can still occur after vagotomy

A

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

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6
Q

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

A

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

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7
Q

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

A

Contraction behind the bolus (ACh)

Relaxation in front of the bolus (NO)

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8
Q

The ________________________ co-ordinates peristaltic contractions

A

The Enteric Nervous System co-ordinates peristaltic contractions

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9
Q

What happens during multiple rapid swallows?

What is this known as?

A

Peristalsis is inhibited until the last swallow

Known as Deglutitive Inhibition

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10
Q

What is used to analyse Esophagus via X-Ray?

A

Normal Barium Swallow

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11
Q

Esophageal Motility disorder associated with impaired or absent peristalsis

Apearance of Esophagus?

A

Esophageal Achalasia

Dilated Oesophagus showing tapering at distal part Distended oesophagus and 'Bird–beak' appearance
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12
Q

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

Apearance of Esophagus?

A

Corkscrew Esophagus

‘Corkscrew’ or Rosary bead appearance of disordered peristalsis
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13
Q

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

A

Gastro Oesophageal Reflux Disease ( GORD)

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14
Q

Anatomomical Regions (4)
Histological Regions (3)

A
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15
Q

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

Function?

A

Fundus

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

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16
Q

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

A

Body/Corpus

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17
Q

Part of stomach which is mainly mucus and highly muscular?

A

Pylorus

18
Q

Stomach cell that secretes mucus and bicarbonate?

Location/Role of this cell?

A

Surface Mucous Cell

Protects Stomach from Acid in Lumen

19
Q

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

Location/Characterisitics of this cell?

A

Mucous Neck Cell

Less columnar - rounded nuclei

20
Q

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

A

Parietal cell

Strong eosinophilic staining

21
Q

Where are Chief Cells located and what do they Produce?

A

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

22
Q

What is Pepsinogen

From where is it secreted?

A

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)

23
Q

Gastrin/5HT producing cells in pylous?

A

Enteroendocrine cells (G-Cells)

24
Q

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

A

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

25
Q

Process of Gastric Mucous Production?

A
26
Q

Mucous secretion is ____________ by prostaglandins

A

Mucous secretion is stimulated by prostaglandins

NSAIDS can inhibit prostaglandins and thus limit surface mucous production

27
Q

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

A

Proteins

Carbohydrates/Lipids primiarily digested later on

28
Q

How is protein Digested in stomach?

A

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

29
Q

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?

A

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

30
Q

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
A
  • 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
31
Q

Why do Parietal Cells have an abundance of mitochondira?

A

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

32
Q

What is Intrinsic Factor Required for?

Where is it produced? Optimum pH?

A

Intrinsic Factor: Protein required for takeup of vitamin B12

Parietal Cells - pH 7

33
Q

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?

A
  • 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

34
Q

Clinical condiiton associated with loss of parietal cells?

A

Pernicious Anaemia

autoimmune disease

Loss of Parietal Cells => Amount of intrinsic factor is compromised => cant absorb B12 as effectively in small intestine => deficiency of B12 => erythropoiesis is compromised

35
Q

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

A

Triggerrs: ACh, Gastrin Secretin

Releases: Pepsinogen, Gastric Lipase, Rennin

Pepsinogen is a pro-enzyme released by Chief cells -> pepsin in stomach

36
Q

Enzyme Producing Cell of Stomach?

A

Chief Cells (Pepsinogen/ Gastric Lipase)

37
Q

Hormone Producing Cells of Stomach?

Role of each?

A

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

38
Q

What do G-Cells do?

What Type of Cell are they?

A

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

Enteroendocrine cell

39
Q

What do D-Cells do?

What Type of Cell are they?

A

Secretion of Somatostatin
Inhibition of other G cells

Enteroendocrine cell

40
Q

What do Enterochromaffin (EC) Cells do?

A

Secretion of Serotonin and Substance P
Promotion of gut motility

41
Q

Oxyntic Glands vs. Pyloric Glands?

Region and cell types of each

A

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

Sem3: PHYS30240 GI and Renal Physiology (24 decks)

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