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GI Tract > GI - Stomach > Flashcards

GI - Stomach Flashcards

1
Q

Important Anatomy of the Stomach

A

Cardiac Sphincter (physiological sphincter)
Fundus
Cardia
Body
Pyloric Antrum
Pyloric Canal
Pyloric Sphincter (anatomical sphincter - thick SM)
Lumen
Angular Notch (Start of the pyloric Region)

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2
Q

What is the importance of the cardiac sphincter?

A
  • start of the oblique layer of muscle

- Area of the intrinsic and extrinsic lower oesophageal sphincter

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3
Q

Where do the greater and lesser omentum attach?

A

Lesser Omentum - Lesser Curvature

Greater Omentum - Greater curvature

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4
Q

What is the importance of the arrangement of blood vessels of the stomach?

A

Anastomoses allows the stomach to move as diaphragm moves up and down

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5
Q

What Glands are found in the regions of the stomach, and what is the main role of these regions?

A

Fundus - Fundic/ Oxyntic Glands. Release HCl and Pepsinogen - Digestion
Cardia - Cardiac Glands. Protection - Produce Mucus
Body - Fundic/ Oxyntic glands. HCl and Pepsin - Digestion
Pyloric Antrum - Pyloric Glands. Produce Mucus, gastrin, somatostatin. Regulate acid production

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6
Q

What is the pyloric sphincter a Landmark for?

A

The trans-pyloric plane (in X-rays)

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7
Q

Blood supply to the Stomach?

A

Short Gastric A (from splenic)
Left Gastric A Left Gastroepiploic A
R Gastric A R. Gastroepiploic A

Gastroepiploic - from splenic or Gastroduodenal
L gastric - from cephalic trunk
R gastric - from hepatic

All drain to portal vein system

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8
Q

Special histology of stomach

A
  • simple columnar epithelia
  • Mucosa in rugae
  • Gastric pits extending to lamina propria, with glands at the bottom

submucosal plexus - secretory cell control

Muscularis externa - longitudinal, circular, oblique

Myenteric plexus between longitudinal and circular - controls motility

Mesothelium (simple squamous) around serosa - peritoneal lining

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9
Q

Secretory cells in Different Glands of stomach

A

Fundic/ Oxyntic Glands - Parietal cell (HCl), Chief cell (pepsinogen), some G cells (Gastrin) and ECL (histamine) cells.

Cardiac- surface epithelium and neck cells - both produce mucus

Pyloric - mucus secreting cells, G cells and D cells

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10
Q

Position of secretory cells in glands

A 
Mucus Neck cells - top of gastric gland 
Parietal cells - next
Chief cells - next
ECL Cells - bottom 
Gastrin - Bottom
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11
Q

Innervation of Stomach

A

Parasympathetic - Vagus nerve. Increase secretion/ motility of stomach

Sympathetic - thoracolumbar. Decrease Secretion/Motility.

Connect to ENS or directly to smooth muscle or gland.

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12
Q

Parietal Gland - Function, Histology

A
  • Produces HCl and IF
  • Activates pepsinogen
  • kills microbes
  • denatures proteins

Highly regulated

Structure

  • Many mitochondria - must lower lumen from pH8 -> pH2
  • Caniculli for proton pumps to release H+ in to
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13
Q

Mucus production - cells and function

A

Mucus -

  • protective (1mm surface, bicarb)
  • lubricate
  • neck cells and surfae epithelium
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14
Q

Chief cells - Histology and Function

A 
Release Pepsinogen (zymogen) 
- Regulated similarly to HCl
Activated by pH 0.8-3.5
Endopeptidase 
Irreversibly inactivated in duodenum 
Digest 20% protein
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15
Q

What ions are released to the stomach by parietal cells and how?

A

K+, H+, Cl-, H2O

Make H+ by splitting Water
- OH joins CO2 from blood to make HCO3, which is antiported to blood for CL

H+ enters lumen through H+/K+ ATPase antiporter
Cl to lumen through channel

K+ to lumen through channel, from blood through K+/Na+ ATPase antiporter

H2O diffuses across

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16
Q

Histamine - cell, receptor, what stimulates release, what inhibits

A

Cell - ECL cells
Receptor - H2 receptor on parietal cell
Stimulated by: Ach
Inhibited by: SST

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17
Q

Gastrin - cell, receptor, what stimulates release, what inhibits

A 
Cell - G cell 
Receptor - CCK 2 on parietal cell
Systemically released 
Stimulated by: raised pH, GRP (from PS neurons), directly by proteins/distention, 
Inhibited by:  Secretin, lowered pH, SST
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18
Q

Somatostatin- cell, receptor, what stimulates release, what inhibits

A

Cell - D cell
Receptor - SST receptor on parietal cell
Inhibits Gastrin, Histamine, Secretin, CCK release
Stimulated by: Gastrin, secretin, lowered pH
Inhibited by: ACh

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19
Q

What makes up the gastric barrier? What damages it?

A

TJs and surface mucus

Aspirin and Alcohol damage GB through mucosal damage

20
Q

Regulation of Gastric Secretion - stimulators and inhibitors

A

Stimulators

  • Gastrin
  • Histamine
  • ACh

Inhibitors

  • Somatostatin
  • Secretin (Acid/ Fat)
  • Low pH
  • CCK (FA/ AA)
  • GIP (FA and AA)
21
Q

What are the 3 Gastric Acid Phases

A

Cephalic, Gastric and Intestinal

22
Q

Describe the role of the PSNS in gastric secretion of the stomach - cells act on, nerve, receptors, what it stimulates to be released

A

Vagus innervation - Long vasovagal reflex
ENS - short reflex
acts on M3 Receptors - Parietal cells, chief cells and mucus cells
- Gastric Secretion and Gastric Emptying

23
Q

What effect does lowered pH have on the stomach?

A

Inhibits gastrin directly
Stim somatostatin
Occurs 1 hr after digestion

24
Q

Secretin - cell, receptor, what stimulates release, what inhibits

A

Cell - S cells (neuroendocrine cell in intestine)
Function: Increase pepsin secretion, decrease acid secretion and gastrin secretion, increases SST increases bicarb production in biliary system and pancreas
Stimulated by: Acid, Fat
Inhibited by: SST

25
Q

CCK - cell, receptor, what stimulates release, what inhibits

A

Cell - I cells (NEC in SI)
Function
- Increases contraction of the gall bladder, exocrine secretion of pancreas
- Decrease appetite (Vagus afferents) and Gastric emptying

Stimulated by: FA, acid, AA
Inhibited by: SST

26
Q

GIP- cell, receptor, what stimulates release, what inhibits

A

Cell: K cells in upper intestine
Function: decrease gastric emptying and increase insulin production
Stimulated by: FA and AA
Inhibited by:

27
Q

Describe the cephalic phase

A

Stimulated by sight/ smell/ taste/ thinking of food

  1. Vagus innervation
    from cerebral cortex and appetite centers of amydala/ hypothalamus
  2. ACh release: Gastrin, Histamine, Acid release and pepsinogen release

Moderate stimulation = 30% Acid released

28
Q

Describe the Gastric Phase

A

Stimulated on protein detection and distention

  1. Mechanoreceptors and chemoreceptors triggered, by stretch and proteins.
    - Cause vasovagal long reflex and ENS short reflex
    - Release of HCl, Gastrin, Histamine and Pepsinogen

2 Gastrin triggered by proteins/ peptides/ coffee/ Ca

  1. Food neutralises HCl = increases pH
    Increases Gastrin and Histamine

60% acid secretion

29
Q

Describe the Intestinal phase

A

Food in duodenum

Presence of Acid/ Distention/AA/ FA

Acid = Secretin
- increases SST, decreases Gastrin and Acid secretion in stomach = Less Acid

Lipids/ FA/ AA= CCK

  • Less gastric emptying and appetite
  • increase gallbladder and pancreatic exocrine secretions

Lipids/ FA/ AA = Peptide YY

  • Less gastric emptying and appetite
  • increased water and electrolyte absorption

AA/ FA = GIP

  • less gastric emptying
  • increased insulin
30
Q

What stimulates gastric emptying

A

stretch - mechanoreceptors
proteins - chemoreceptors

= Parasympathetic reaction - long and short reflexes

31
Q

How does the vasovagal reflex work? what cells does it work on?

A

Controlled by the medulla
Signals through vagus nerve
Causes ACh release
Acts on SM pacemaker cells (Cells of Cajal) in the longitudinal muscle

Cells of Cajal control the BER of the stomach (3 depol/repol waves per minute) - these are quite weak
Increased AP frequency (in response to signals) = increased chance of reaching threshold for AP signal = stronger contractions

Causes Receptive relaxation of stomach

32
Q

What is the result of the parasympathetic nervous system on gastric emptying?

A

Stomach Relaxation - Receptive relaxation in body and fundus ( allow storage of food)

Peristaltic Waves from pyloric Antrum

33
Q

What causes stomach relaxation?

A

Short ENS reflexes cause ACh release (also long VV reflex)
Causes NO and Serotonin release
Receptive relaxation of fundus and body (Increased volume with no increased pressure)

34
Q

How does it travel from longitudinal to circular layer

A

GAP junctions to circular layer and rest of the stomach

35
Q

Mechanical digestion in the stomach

A

Churning motions - mix luminal contents
Retropulsion against the closed pyloric sphincter (closed in contractions) - force of food disperses chyme

to get to duodenum must be liquid

36
Q

Regulation of the Basal electrical rhythm

A

Neural and Hormonal stimuli = increase AP to reach threshold = increased strength contraction

Fasting BER is weak

+ Gastrin (increase force and movement)
+ PS stimulation

  • increased acidity (secretin) / distention (CCK) / AA (CCK)/ FA in duodenum
  • Peptide YY, GIP
  • Hypertonic Solution
  • Sympathetic stimulation
37
Q

Receptors on parietal cell and result of binding

A

Cause Ca release = expression of H+/K+ ATPAse on cell surface

  • M3 - Ach
  • CCK2 - Gastrin

Effects cAMP through GPCR

  • H2 - Histamine, cause cAMP prod and expression of H+/K+ ATPAse
  • SSTR - inhibits cAMP through AC
38
Q

What is a peptic ulcer and where are they commonly found

A

Ulcer caused by the action of pepsin and stomach acid - causes mucosal damage through increased acid production (usually) and erodes away stomach/ duodenum

Commonly found in stomach. More commonly in duodenum - undergoes metaphasia to stomach columnar cell in response to increased acid, then gets ulcer.

39
Q

RF for Peptic Ulcer and causes of Peptic Ulcer

A

RF

  • Male
  • Smoker
  • Stressed
  • increased acid production
  • Diet
  • Alcohol
  • Aspirin/ increased NSAIDs
  • Caffeine
40
Q

Symptoms of Peptic Ulcer

A 
Pain, particularly after meals 
Reflux is other common side effect of increased acid
weight loss
Nausea/ vomiting 
Bloating 
Easily full
Heartburn

Erodes to hit major BV = haemorrhage and vomiting blood (haematymysis)/ occult stool

Erode all the way through = acute peritonitis (patient will collapse)
Only treatment is surgery here

41
Q

Pathophysiology of peptic ulcers

A

Usually caused by H. pylori

H. pylori

  • makes urease, converts urea to ammonia to regulate pH to allow it to survive in stomach
  • if colonises antrum, alkaline cloud covers G cells and D cells, preventing low pH detection and SST release from D cells
  • unregulated increased Acid production - increased risk acid in duodenum and increased risk ulcer.

Increased Duodenal Acid load
- increased gastric metaplasia and H. pylori infection and ulceration of duodenum

-H pylori infection causes gastritis, can also cause D cell atrophy = less somatostatin

More prevalent in Cag +ve individual (more westerners) = more inflammation

42
Q

List Treatment of peptic ulcer

A

Surgical
- Vagotomy, Subtotal gastrectomy, anterectomy

Medical
H2RA - block H2R
PPI - Act directly on parietal cells
- not good, control not cure and expensive

Sucralfate and bismuth salt seem to be curative

AB for H pylori infection is most effective treatment

43
Q

Treatment for H. pylori infection

A

First Line: Omeprazole, metronidazole and amoxycillin
2nd Line: OP, amoxycillin and clarythromycin
Allergy to penicillin and Clarythromycin

44
Q

Diagnostic tests for Peptic ulcers and H pylori infection

A

Urea Breath Test- urea labelled with C13/ C14 - in 10-30 mins test to see if radiolabelled CO2 breathed out

Urease Slide test
- biopsy of mucosa in gastroscopy and then CLO test ( urea to see if urease converts to NH3 and CO2) pH indicator phenyl red turns red if present

Blood - Antibodies 
Foecal - antigens 
- Urine 
Endoscopy and biopsy 
- microscopy
- serology 
- culture
45
Q

Pathophysiology of H. pylori infection causing gastric cancer

A

Presents with - weight loss, anorexia , anaemia and usually uncurable
Mostly attributed to H pylori (some to AD genetics condition)

If infection at bottom of stomach

  • inflammation can cause atrophic gastritis (G cell atrpohy = less gastrin = less acid - hypochlorohydria
  • Chronic atrophic gastritis
  • metaplasia that becomes dysplastic

Summary: H pylori → superficial gastritis → (mediated by host genetics, bacterial strain + Environmental factors) atrophic gastritis + hypochlorhydria → (Mediated by gender + Environmental factors) Dysplasia + Cancer.

Risk high in China and Japan
If get peptic ulcer, less likely to get H pylori mediated gastric cancer

46
Q

Epidemiology of peptic ulcer disease

A

Related to socioeconomic conditions as kid (where get H pylori infection) younger kis are much less likely to have infection now than older.

47
Q

Protective function of H pylori infection

A

Raises pH of in stomach in general population, especially as people age and secretory cells get less effective anyway = protective for GORD and oesophageal cancer

GI Tract (4 decks)

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