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S3 GI > Introuduction To The Stomach > Flashcards

Introuduction To The Stomach Flashcards

1
Q

Describe the journey of hormones secreted from endocrine cells to their target location?

A

Peptides released from endocrine cells

Pass into portal circulation (portal vein)

Through liver

Systemic circulation (IVC, aorta, Celiac/ superior mesenteric/ IM)

Back to near where they were secreted

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2
Q

What is a paracrine hormone, give an example?

A

Relating to a hormone which has effect only in the vicinity of the gland secreting it

E.g. acid in antrum stimulates somatostatin release(D cells) to inhibit gastrin secretion(G cells)

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3
Q

What is neurocrine secretion, give an example?

A

Peptides released by neurones after AP

E.g. sight of food/ chewing -> gastrin releasing peptide (post-ganglionic fibres vagus N) increases gastrin release(G cells)

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4
Q

What are the two broad categories of gastrointestinal hormones and give two examples for each category?

A

Gastrin family:

  • Gastrin (G cells antrum of stomach)
  • Cholecystokinin (I cells duodenum/gallbladder)

Secretion family:

  • secretin (s cells duodenum)
  • gastric inhibitory polypeptide (duodenum & jejunum)
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5
Q

What is gastrin? Where is it secreted and what is it’s function? What stimulates its release?

A

A gastrin hormone

G cells antrum stomach

Increases gastric acid secretion

Stimulated by: peptides/ AAs in stomach, vagal stimulation of Ach , gastrin-releasing peptide

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6
Q

What is cholecystokinin? Where is it secreted, what’s its function and what stimulates its secretion?

A

gastrointestinal gastrin hormone

I cells duodenum and jejunum

Increases pancreatic and gallbladder secretions

Stimulated by fat and protein

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7
Q

What is secretin? Where is it released? What is it stimulated by? What it’s function?

A

Secretion hormone

S cells duodenum

Stimulated by H+ and Fa

Increases HCO3 (bicarbonate) from pancreas/ gallbladder ~ neutralises acidic chyme entering duodenum from stomach (also made in RBC/ PCT/ DCT compensatory mechanism) 
& decreases gastric acid secretion
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8
Q

What is gastric inhibitory polypeptide? Where is it secreted, what stimulates it and what is it’s function?

A

A gastrointestinal secretin hormone

Cells in duodenum and jejunum

Stimulated by sugars, aa, fa

Increases insulin and decreases gastric acid secretion

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9
Q

Main functions of the stomach

A

Short term storage food

Vigorous contractions of smooth muscle to increase SA food

Continue digestion - swallow amylase/ lipase, add proteases

Disinfect- acidity/ enzymes

Activate (renature) proteases
Chief cells in gastric glands-> Pepsinogen (activated by HCl)-> pepsin

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10
Q

Anatomy of the stomach, areas, curves and sphincters

A

Fundus- top

Cardia- near oesophagus entrance (above heart)

Body- main part

Antrum- end

Greater (lateral) and lesser curve (medial)

Lower oesophageal
Sphincter

Pylorus sphincter into duodenum

Rugae - mucosal and submucosal folds increase SA

Many little holes - gastric pits with gastric glands below

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11
Q

Epithelium of the gut

A

Stratified squamous in oesophagus and distal anus, everything between is simple columnar

Stratified squamous is more protective against abrasion

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12
Q

Types of epithelium cells in the stomach and their function

Other cell types in the stomach and their function

A

All simple columnar

Mucous cells- mucous lines stomach under acid layer

Parietal cells- secrete HCL and intrinsic factor (absorption V12)

Chief cells- proteases (pepsinogen and chymosin)

G cells- gastrin

Inferior to epithelium:
Enterochromaffin like cells- histamine (induces production of gastric acid)

D cells -> somatostatin (inhibits G cells)

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13
Q

Name of the stomach smooth muscle and function

A

Extra oblique layer of muscle

Mix/grind contents
Move contents along

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14
Q

Compare stomach contractions in the upper and lower stomach? How does the shape of the stomach aid movement of contents? How often is chyme ejected and where?

A

Upper- sustained contraction which create basal tone

Lower- strong peristalsis mixes contents, coordinated movements, contractions every 20seconds proximal to distal

Stomach is larger proximally so contents are accelerated and lumps left behind

Liquid chyme ejected into duodenum 3 times a minute

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15
Q

Branches of the coeliac trunk

A

Coeliac trunk (first branch of abdominal aorta)

  • > left gastric
  • > splenic: -> superior aspect pancreas, short gastric, left gastroepiploic
  • > common hepatic (-> gastroduodenal -> anterior superior pancreaticoduodenal + right gastroepiploic) -> proper hepatic -> left hepatic + right hepatic -> cystic

Look in notebook

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16
Q

Abdominal aorta branches

A

Superior-> inferior

Coeliac trunk (foregut)
Superior mesenteric artery (midgut)
Testicular/ ovarian
Inferior mesenteric (hindgut)
Bifurcation:
Left common iliac-> external & internal
Right common iliac -> external & internal

17
Q

Venous drainage of the foregut, midgut and hindgut

A

ALL drain into portal vein which drains into IVC

Foregut veins -> portal

Midgut-> superior mesenteric -> splenic vein -> portal

Hindgut -> inferior mesenteric -> portal

18
Q

Venous drainage of the stomach

A

Right gastric
Left gastric
Middle gastric
-> portal

Short gastric
Left gastroomental 
Right gastroomental 
-> superior mesenteric vein
-> portal
19
Q

What is receptive relaxation of the stomach and why does it need to occur?

A

Receptive relaxation of fundus of stomach as food enters through the distal oesophageal sphincter vagally mediated

Allows food to enter without raising intra-gastric pressure too much and prevents reflux

Gastric mucosa folds (rugae) allow distension

20
Q

What cell type predominantly makes up the cardia?

A

Mucous cells

21
Q

What cell types predominately make up the fundus & body and so what secretions?

A

Mucous cells

Parietal cells -> HCL

Chief cells -> pepsinogen

22
Q

What cell types predominately make up the pylorus and so what secretions?

A

G cells -> gastrin

D cells -> somatostatin

23
Q

What are the 3 stimulants of the parietal cell to secrete H+?

A

G cells (sight/ smell of food/ stretch/ peptides or AA from stomach lumen) -> gastrin though CCK channel

Entero-chromaffin like cells -> histamine through H2 channel (amplifies gastrin)

Parasympathetic vagus Nerve-> signal

24
Q

What happens once food leaves the stomach to turn off the digestive mechanisms?

A

Food acts as a buffer so once it leaves the PH drops

This activates D cells to secrete somatostatin which inhibits G cells and entero-chromaffin like cells

25
Q

What is the ‘alkaline tide’ and what is it’s function?

A

Durin HCL poorudction parietal cells extract CL-, CO2, H2O & Na from blood plasma

After eating partial cells secrete HCO3- bicarbonate through their basolateral membrane into the blood to maintain the electrical balance

Lasts until acids in food absorbed in the small intestine reunite with the bicarbonate (usually under 2 hours)

26
Q

Explain how HCl is produced in parietal cells

A

Anion antiport protein on basolateral membrane - Cl- in and HCO3- out

Cl- transcellular diffuses to Cl- channel protein on apical membrane

CO2 diffuses through basolateral combines with OH- from H2O to form HCO3- (which antiport with CL-)

H20 also produces H+ which goes through H+/K+ ATPase on apical membrane

(k+ channel protein apical where K+ diffuses out to create concert grad)

Slide 30

27
Q

What are the 3 stages of digestion and what percent is each responsible for total HCL production?

A
  1. Cephalic- 30%
  2. Gastric - 60%
  3. Intestinal - 10%
28
Q

What stimulates the cephalic phase of digestion and what does it cause?

A

Parasympathetic stimuli e.g. smell/ taste/ chewing/ swallowing

Direct stimulation of parietal cells by vagus Nerve

And G cells by vagus (GRP released)

Also slightly increases gastric motility

29
Q

What occurs in the gastric phase of digestion?

A

Distension of stomach stimulates vagus -> stimulates parietal and G cells

At this stage food is acting as buffer so gastrin is not inhibited

Enteric Ns and gastrin cause strong smooth muscle contractions

30
Q

What occurs in the intestinal phase of digestion?

A

Chyme initially stimulates gastrin secretion

Partially digested proteins detected in duodenum

Short Phase as soon overtaken by inhibition of G cells

Presence of lipids activates enterogastric reflux (stretching wall duodenum) -> Reduces vagal stimulation

Chyme stimulates CCK and secretin (helps suppress HcL secretion)

31
Q

How does the stomach protect itself from self-digestion?

A

Foveolar cells secrete mucin which forms a viscous mucus layer that adheres to epithelium and prevents physical damage from food

HCO3 ions are secreted into mucus to provide a neutral barrier against the stomach acid

Rich blood supply to gastric mucosa can remove and buffer acid that has breached the mucus layer

Prostaglandins promote above processes

High turnover of epithelial cells to remove damaged cells

Inactivation of proteases

Parietal and G cell inhibition when food has left

32
Q

Why should you eat before taking NSAIDS?

A

Decrease prostaglandin release which promotes protective process for the stomach e.g HCO3/ mucus secretion

If not could get a stomach ulcer and bleed

33
Q

Name some damaging factors to the stomach

A

H+
Pepsin
H.Pylori-> chronic active gastritis -> ulcers (1/2 of us have in normal flora)
NSAIDs inhibit prostaglandins
Physiological Stress (3rd degree burns/ head trauma)
Smoking
Alcohol dissolves mucus layer -> gastritis

S3 GI (16 decks)

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