Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do the greater and lesser omentum attach?

A

Lesser Omentum - Lesser Curvature

Greater Omentum - Greater curvature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pyloric sphincter a Landmark for?

A

The trans-pyloric plane (in X-rays)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mucus production - cells and function

A

Mucus -

  • protective (1mm surface, bicarb)
  • lubricate
  • neck cells and surfae epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
CCK - cell, receptor, what stimulates release, what inhibits
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
GIP- cell, receptor, what stimulates release, what inhibits
Cell: K cells in upper intestine Function: decrease gastric emptying and increase insulin production Stimulated by: FA and AA Inhibited by:
27
Describe the cephalic phase
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
Describe the Gastric Phase
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 3. Food neutralises HCl = increases pH Increases Gastrin and Histamine 60% acid secretion
29
Describe the Intestinal phase
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
What stimulates gastric emptying
stretch - mechanoreceptors proteins - chemoreceptors = Parasympathetic reaction - long and short reflexes
31
How does the vasovagal reflex work? what cells does it work on?
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
What is the result of the parasympathetic nervous system on gastric emptying?
Stomach Relaxation - Receptive relaxation in body and fundus ( allow storage of food) Peristaltic Waves from pyloric Antrum
33
What causes stomach relaxation?
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
How does it travel from longitudinal to circular layer
GAP junctions to circular layer and rest of the stomach
35
Mechanical digestion in the stomach
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
Regulation of the Basal electrical rhythm
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
Receptors on parietal cell and result of binding
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
What is a peptic ulcer and where are they commonly found
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
RF for Peptic Ulcer and causes of Peptic Ulcer
RF - Male - Smoker - Stressed - increased acid production - Diet - Alcohol - Aspirin/ increased NSAIDs - Caffeine
40
Symptoms of Peptic Ulcer
``` 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
Pathophysiology of peptic ulcers
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
List Treatment of peptic ulcer
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
Treatment for H. pylori infection
First Line: Omeprazole, metronidazole and amoxycillin 2nd Line: OP, amoxycillin and clarythromycin Allergy to penicillin and Clarythromycin
44
Diagnostic tests for Peptic ulcers and H pylori infection
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
Pathophysiology of H. pylori infection causing gastric cancer
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
Epidemiology of peptic ulcer disease
Related to socioeconomic conditions as kid (where get H pylori infection) younger kis are much less likely to have infection now than older.
47
Protective function of H pylori infection
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions