Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GIT physiology > Stomach > Flashcards

Stomach Flashcards

You may prefer our related Brainscape-certified flashcards:
Git Commands flashcards
1
Q

What happens when the bolus of food passes into stomach

A

Lower oesophageal sphincter hypercontracts to prevent reflux

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

What do specialised cells in the stomach do

A

Synthesise and secrete mucous fluid, enzyme precursors, HCl, hormones

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

What is responsible for gastric motility

A

Abundant SM in the stomach

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

Name for “food” in the stomach

A

Chyme

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

What secretes gastric juice

A

Cells of gastric mucosa

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

HCl (contained in gastric juice)

A

Cleans food

Protein digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pepsinogen

A

Precursor to pepsin

Digests protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Intrinsic factor

A

Vitamin B12 absorption in the ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mucus

A

Protects gastric mucosa from acidic environment (H+ - pH 1-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PARIETAL CELLS

  1. Location
  2. Secretion
A
  1. Body
  2. HCl and intrinsic factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CHIEF CELLS

  1. Location
  2. Secretion
A
  1. body
  2. Pepsinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

G CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Gastrin INTO CIRCULATION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MUCOUS CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Mucus and pepsinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

D CELLS

  1. Location
  2. Secretion
A
  1. Antrum
  2. Somatostatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is gastrin unusual

A

Secretion is not into the lumen but into bloodstream

PARACRINE secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 types of secretion

A
  1. EXOCRINE - outside of body (going to outer space)
  2. ENDOCRINE - with G cells (radio broadcast, signal to whole body but only people tuning in will listen to the message)
  3. PARACRINE - somatostatin (talking to the neighbours -conc of message decreases to the power of 3 as you move out from source - communicates 10 cells width)
  4. AUTOCRINE - acid secretion (singing to yourself)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are gastric pits similar to

A

salivary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the pits lined with

A

Parietal cells

Chief cells

G cells

D cells

Mucus neck cells (secrete mucus and bicarbonate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where do regional differences exist

  1. Secretions near lower oesophagus/pyloric sphincter
  2. Secretions in rest of stomach
A

in the number of cell types lining a gastric pit

  1. Mucus, HCO3-
  2. Digestive secretions (H+, pepsinogen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2 functions of HCl

A
  1. Clean food - make it aseptic, but becteria and viruses can still get through
  2. Denature proteins and break protein bonds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is HCl secreted

A

At apical membrane, H+ is secreted into lumen of stomach via primary active transport

Cl- follows H+ into the lumen

However, at basolateral membrane, HCO3- is moved into interstitial space in exchange for Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If the pH of the cell increases, what happens

A

Encourages the disintegration of carbonic acid to H2O and CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Stimulation of H+ secretion by gastric parietal cells

A

PNS stimulation starts at Vagus (Gs)

HISTAMINE is released from enterochromaffin-like cells in gastric mucosa, binds to nearby PARIETAL cells, binds to H2 receptor, Gs protein, cAMP, PKA increases ATPase activity

** ALL 3 involve PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are ulcers

What was first used to treat it

A

Injury to gastric mucosa, with acid going into it

Atropine - muscarinic antagonist

Now omeprazole - directly inhibitd the H+ K+ ATPase pump

  • reduces acid secretion, prevents acidic environment in the stomach, extremely effective against acid reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Inhibition of the H+ K+ ATPase pump - SOMATOSTATIN (D cells)

A

Direct pathway

  • inhibits parietal cells, bind to receptor, Gi, reduced cAMP, reduced H+ secretion
  • Inhibits G cells

Indirect pathway

  • Inhibits histamine release from ECL cells
  • Inhibits gastrin release from G cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is HCl secreted into stomach nerve-wise

A

Vagus nerve innervation - parietal cells directly (ACh) => HCl release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Role G cells play in HCl secretion

A

G cells (Gastrin-Releasing Peptide) release gastrin into circulation in response to proteins in the meal

Carried in bloodstream to parietal cells - HCl is then released via this indirect route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does atropine (muscarinic blocking agent) not fully block

A

HCl secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CEPHALIC PHASE

  1. How much of total HCl secretion does it account for
  2. What are the stimuli
  3. What sort of reflex is it
  4. What are the mechanisms
A
  1. Accounts for 30% total HCl secretion
  2. Smell, taste
  3. Conditioned reflex - in anticipation of food
  4. Direct and indirect mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

GASTRIC PHASE

  1. How much of total HCl secretion does it account for
  2. What are the stimuli
  3. Mechanisms
A
  1. Accounts for 60% of total HCl secretion
  2. Distension of stomach and presence of AAs and small peptides
  3. DISTENSION - direct and indirect vagal stimulation of parietal cells (gastrin): AA AND PEPTIDES - direct effect on G cells (gastrin)

** all converge on G cells and act on an endocrine signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where do majority of stimuli come from

A

Lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

INTESTINAL PHASE

  1. How much of total HCl secretion does it account for
  2. What is its major function
  3. Stimulus
A
  1. Accounts for 10% of total HCl secretion
  2. Major function is to inhibit acid secretion from stomach and protect SI from acid
  3. AAs and peptides stimulate G cells to release gastrin - parietal cells - HCl secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name the 5 protective factors

A
  1. HCO3-
  2. Mucus
  3. Prostaglandins - slightly inhibit gastric secretions)
  4. Mucosal blood flow
  5. Growth factors
34
Q

Name the 7 damaging factors

A
  1. H+
  2. Pepsin - would also digest mucosa
  3. NSAIDs e.g. aspirin
  4. stress
  5. smoking
  6. alcohol
  7. Helicobacter pylori - ONLY PATHOGEN NECESSARY FOR GASTRIC ULCERS
35
Q

Why must the gastric mucosa be protected

A

Mammalian cells cannot survive in an acidic environment as they will denature their own proteins

36
Q

Describe mucosal blood flow

A

quite high - high buffering capacity - high turnover rate of gastric mucosa

37
Q

Helicobacter pylori

How does it damage the mucus layer

A

One of the few pathogens that can live in the human GIT

Uses flagella to embed itself into mucus layer, secretes alkaline substances to neutralise acid, creates a little pocket for itself, doing that means it breaks the mucosa layer and creates a passage for acid to go into and attack cells

38
Q

How does the prevalence of H pylori infection differ between developed and developing countries

A

NB H pylori is essential for ulcers

39
Q

what does 13C-urea produce

A

alkaline agents

40
Q

Explain this graph

A

Black line is control

Blue (2) is a patient - 13CO2 will rise as urea is being metabolised by enzyme urease (not in our biome)

Graph 3 is normal

41
Q

What does the body do to overcome the noxious effect of pepsin

A

Chief cell secretes pepsinogen, a precursor to pepsin

42
Q

how is pepsinogen activated

A

By HCl in lumen of stomach

43
Q

Where does the breakdown of proteins to short peptides by pepsin happen

A

In lumen, away from mucosa

44
Q

+ve feedback loop of pepsin and pepsinogen

A

So beginning of meal, HCl stimulates pepsinogen to form pepsin, but then pepsin takes over and controls pepsinogen itself

Any pepsinogen rapidly becomes pepsin and action of protease in lumen is intrinsically high - no inactive pepsinogen in stomach

45
Q

2 functions of pepsin

A
  1. Breakdown of proteins, IC matrixes and release nutrients so we’re not just producing peptides but breaking down the whole organism together
  2. PROTECTION - pepsin is noxious on surface of bacteria, viruses, parasites, shave EC matrix by digesting EC protein, disrupt ion balance and homeostasis, break down any living organism getting into the stomach
46
Q

What does the intrinsic factor do

A

Binds vitamin B12

Protects it from damage it may suffer in the stomach and LI

47
Q

Where does the B12 and intrinsic factor complex eventually get absorbed

A

In the ileum

48
Q

What is B12 a co-factor in

A

Formation of RBCs in bone marrow

49
Q

What is pernicious anaemia

A

Formation of RBCs is not sufficient which could be as a result of a gastric problem with intrinsic factor

50
Q

Name the 3 reflexes that regulate the relaxation of the gastric reservoir

A
  1. Receptive - feed-forward mechanism, mostly distension but also nutrient sensing from gastric wall, triggering of a vagal vagal reflex
  2. Adaptive
  3. Feedback-relaxation - nutrients in duodenum cause vagal vagal reflex through tension receptors and release of CCK on vagal afferent neurons
51
Q

Relationship between pressure and vol (derived from Law of Laplace)

A

P = 2T/R

R is proportional to the square root of V

so T is proportional to P x Square root of V

52
Q

What does tetrodotoxin do

A

Binds to site on Na+ VG channel

53
Q

What happens to pressure as vol of stomach increases

A

The increase in pressure is smaller and smaller

54
Q

Effect of TTX and truncal vagotomy on pressure and vol

A

The cutting of the vagal nerve shows evidence that we need vagus transmission (neural) to generate gastric relaxation reflex

55
Q

Contribution of different triggers to the gastric accommodation reflex in humans

A
56
Q

Difference in function between body and antrum

A

BODY - storage

ANTRUM - pump

57
Q

Retention of a viscous meal

A
58
Q

Plasma glucose over time

A

Insulin drives glucose out of the bloodstream and into adipose tissue, liver and mostly muscle

59
Q

Relationship between gastric retention and how much glucose entered the blood stream

A

Retaining the food prevents glucose entering the bloodstream

High retention, low plasma glucose

60
Q

Regions of the stomach

A
61
Q

How is digesta moved from the gastric reservoir into the antral pump

A
  1. Tonic contractions - if tension is high, food will move quickly to the antrum
  2. Peristaltic waves
62
Q

Poiseuille’s equation for blood flow

A

n is viscosity of blood

lamda (upside down Y) is length of blood vessel

ALSO BF = difference in P/Resistance

=> R = 8nλ/πr4

(radius of pyloric sphincter changes greatly - major regulator of gastric emptying)

63
Q

3 phases of the function of the gastric pump

A
  1. Phase of propulsion
  2. Phase of emptying
  3. Phase of retropulsion
64
Q

Phase of propulsion

A

Contraction of proximal antrum

Propulsion of chyme into relaxing terminal antrum and duodenal contraction

pyloric sphincter - diameter 1mm

2-3 of these contractions per min after a meal

65
Q

Phase of emptying

A

Contraction of middle antrum

transpyloric and retrograde flow

Duodenal relaxation

66
Q

Phase of retropulsion

A

Contraction of terminal antrum

Jet-like back-flow with grinding

Duodenal contraction

67
Q

Sieving function

A

Lipids and small particles leave the stomach more rapidly than large particles

68
Q

How do we grind solid particles

A

Forceful jet-like retropulsion through the small orifice of the terminal antral contraction

69
Q

Antro-duodenal co-ordination

A

Proximal duodenum is silenced when the pyloric sphincter is open

When stomach is emptying, duodenum is relaxed and accepting this chyme

70
Q

Balance between gastric reservoir and antral pump

What do the 2 reflexes ensure

A

regulation of rate of delivery of food from body to pump

71
Q

What is pyloric activity modulated by

A

Antral inhibitory and duodenal excitatory reflexes

72
Q

What is an additional function of the pyloric sphincter

A

Prevent duodeno-gastric reflux

73
Q

Factors that influence the rate of flow

A

Viscosity

Nutrient density - if energy content of meal is higher it will empty more slowly

high osmolality of chyme will delay gastric emptying

acidity delays gastric emptying

74
Q

Rate of flow of pyloric sphincter is proportional to

Which part of the duodenum has low pressure

A

Pressure diff (stomach - duodenum) divided by R (diameter of pyloric sphincter)

duodenal bulb has low P

75
Q

What happens when oleic acid and bile is added

A

Pyloric sphincter not only contracts and stays contracted for the whole period after the fat is added, it is HYPERCONTRACTED

=> presence of fat closes pyloric sphincter more strongly than when it was closed before - stays closed for a couple of mins

76
Q

What do the duodenal bulbs do

A

Show brief spikes

  • peristatic waves
  • strong segmentation contractions
  1. Reduces drive of pressure in the stomach
  2. Increases the pressure in the duodenum
  3. Increases R
77
Q

Macronutrients that are best at regulating motility

A

Fat > protein > CHOs > osmotic load (signals within lumen of GIT)

78
Q

Factors of gastric and duodenal motility that co-operate and modulate gastric emptying

A
79
Q

How are solids and liquids of the gastric chyme emptied with different velocities

A

Emptying of liquids is exponential

Emptying of large solid particles only begins after sufficient grinding (lag phase)

Viscous chyme is then mainly emptied in a linear fashion

80
Q

Differences between a non-caloric and caloric meal

A
81
Q

Mediation of mechanisms that allow gastric emptying

A

Nutrients - LCFAs, Aas, peptides from lumen of duodenum stimulating 2 types of receptors

Neuronal cells that signal to afferent vagal neurons

Stimulate afferent CCK secreting cells that stimulate afferent vagal neurons going to vagal centre and 3 different outputs come out

Gastric accommodation reflex - mainly NO

Stimulating cholinergic vagal fibres that increase stimulation to pyloric sphincter and ACh release onto antrum to reduce contraction of antrum

White arrow - internal reflex contracting pyloric sphincter without needing vagal afferents

82
Q

What impact would a high fat breakfast have on lunch

A

Lunch would be emptied more slowly

Not just responding to the content of the meal, but also the meal preceding it

GIT physiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions