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Year 1 GI > 6. Gut Reaction To Food > Flashcards

6. Gut Reaction To Food Flashcards

1
Q

Describe distribution of striated and smooth muscle down oesophagus wall

Func of striated vs smooth

A

Pharynx: striated
UOS-muscle
Oesophageal body-proximal 1/3=striated; distal 2/3 smooth
LOS- muscle

Striated-voluntary contraction
Smooth-involuntary

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2
Q

Describe first phase of deglutition

1) name
2) voluntary or involuntary
3) What happens (3)

Describe 2nd phase of deglutition

1) name
2) voluntary or involuntary
3) What happens (3)

Describe 3rd phase of deglutition

1) name
2) voluntary/invol
3) what happens (3)

A

1) Oral
2) Voluntary (bc striated muscle)
3) Food bolus made from mastication;
Tongue moves up and back;
Soft palate rises to close nasal cavity

1) Pharyngeal
2)Involuntary
3) Soft palate rises (close nasal cav);
Epiglottis closes;
Tactile/distention receptors in pharynx wall tell brain stem via CNXII (hypoglossus) to relax upper oral sphincter/cricopharyngeal sphincter relaxes

1) oesophageal
2) involuntary
3) UOS contract; bolus moved by peristalsis; LOS relaxes

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3
Q 
Describe entry of food into stomach
(6)
1
2
3
4a
4b
4c
5
6
A
  1. Food comes down oesophagus
  2. Tactile/distention receptors detect & send signal to brain stem via vagal afferent fibre
  3. Brain stem>efferent>phrenic and vagus
    4a. Phrenic contracts diaphragm by acetylcholine (open up hiatus)
    4b. Vagus excitatory fibres switched off
    4c. Vagus inhibitory fibres stimulated and release relaxing factors (NO&vasoactive intestinal peptide)
  4. LOS open
  5. After release, reflex contraction of LOS to stop blackflow
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4
Q 
Regions of stomach involved in digestion
Role of them
3
9,4
6
7,6
7,9
A

1 LOS-control entry of food
2 Pacemaker zone (side of greater curvature)-sense distention/tactile stimuli & increase amplitude and freq of peristaltic contractions
3 Corpus-body of stomach; has acid secreting cells
4 Pyloric antrum-muscular pump to mix contents; endocrine cells that release gastric
5 Pyloric sphincter-causes retropulsion when shuts

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5
Q

How we accommodate large meal

A
  1. Distention detected
  2. Signal via vagal afferent nerve>nodose ganglion>brain stem
  3. Vagal efferent fibres: increase VIP/NO release; decrease Ach release
  4. Relaxation of corpus
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6
Q

Feeling full process

A
  1. Fats digest last; fatty acids/proteins stimulate intestine cell
  2. Cholecystokinin (CCK) released Into blood
  3. acts on vagal afferent fibres; cck receptors coming down to sense.
  4. Signals travel up via nodose ganglion to brain stem>relax stomach/reduce gastric motility & satiety centre activated(lower appetite and food intake)
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7
Q

These empty slower/delay gastric emptying

Rate of emptying controlled by ?

A 
Solids slower than liquids
Fat rich
Hypertonic/salty/high saline
Acidic meal->inhibit motility**
High viscosity
High carb

Rate of emptying controlled by duodenum and pyloric sphincter

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8
Q
  1. List gastric mucosal cells of fundus ()1
  2. List those of corpus (4)
  3. List those of antrum (4)

LIST ROLES (total 6 different cells)

A
  1. Surface epithelial cell
  2. Surf ep
    Chief/zymogen
    Parietal
    ECL (enterochromaffin-like)
  3. Surf ep
    Chief/zymogen (less than corpus)
    G cells
    D cells
  • Surf ep: mucus, HCO3- barrier
  • Zymogen: pepsinogen (pepsin precursor, activated by pepsin and H+)
  • Parietal: HCl secretion and intrinsic factor for B12 absorption
  • ECL: histamine (helps to make HCl)
  • G cell: gastrin (+histamine) secretion
  • D cell: somatostatin (inhibits everything)
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9
Q

Draw cells of gastric corpus cells (arrangement in gland)

A
  1. Surf ep at top of loop of gland
  2. Proliferating cells
  3. Parietal cells
  4. ECL distal to lumen with chief cells proximal to gland lumen (layer them)
  5. Chief cells at bottom of lumen
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10
Q

Draw resting vs stimulated parietal cell

A

(Check pp& screencast)

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11
Q

Describe how parietal cell secretes HCl
Total 6 channels
3 on each side
Stimulators for HCl secretion (4)

A

In tubulovesicular system?

Note H+ & HCO3- come from resp products>carbonic anhydrase>carbonic acid (h2co3)>h+ and HCO3-

Lumenal/apical side:
1 H+/K+ATPase (H+ out)
2 K+ channel (k+ out)
3 Cl- out (so HCl; maintain electro neutrality

Basolateral side (blood)
1 HCO3-/Cl- exchanger (H+ pumped out so build up of HCO3- inside>pumped out)
2 Na+/K+ATPase (facilitates HCO3- exchanger>sodium bicarb out)
3 K+ channel 
Food
Neural receptors
Histamine
Gastric receptors 
(All open k+ channel wider)
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12
Q

Describe first (classical) phase of gastric acid secretion
1a name
1b nerve involved
2 stimulated by
3 Results in (1 neuro, 1 paracrine, 1 endocrine)

A 
1A. Cephalic
1b. CNX 
2. Thought, sight, smell, taste, anticipation
3 neural stimulation: Ach, GRP
Paracrine: Ach>histamine
Endo: GRP>gastrin
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13
Q 
Describe second classic phase of gastric acid secretion
1 name
2 stimulated by
3 Results in 
4. Nerve involved
A
  1. Gastric
  2. Distension/detection of food in stomach by chemoreceptors
  3. Neuro: Release Ach at parietal level
    Endocrine: Gastrin release
    Paracrine: Ach&gastrin both>histamine
    »»more HCl secreted
  4. CNX
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14
Q

Describe third classic phase of gastric secretion

  1. Name
  2. Stimulated by
  3. Results in (1 neural, 1 endo, 2 paracrine)
  4. Nerve involved
A
  1. Intestinal
  2. Distension/chemoreceptors detect food in duodenum
  3. Neuro: Ach
    Endo: Gastrin (duodenal G cell)
    Paracrine: Ach&gastrin>histamine
  4. Vagus
    Secretin**
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15
Q

How acid secretion is controlled

  1. How (by what)
  2. Reason to stop acid secretion
A
  1. D cell secrete somatostatin, causes cells to stop releasing H+
  2. Damage in stomach
    Full
    Nor/adrenaline/SNS/fight or flight
    CCK
    VIP
    CGRP (calcitonin G related peptide)
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16
Q

Control of antral G cell function

  1. Stimulated by
  2. Inhibited by
  3. What happens to gastrin
A
  1. Stimulated by protein/peptide/aa; GRP in cephalic phase
  2. Too much H+ cause D cell to release somatostatin>inhibit G cell releasing gastrin
  3. Goes to circulation>stomach corpus>Stimulate ECL/parietal to secrete histamine/parietal to secrete H+
17
Q

Acid inhibitory therapy:
Which cell
Different ways this can be done (2 main, describe and e.g. of a drug of each)

A

Parietal cell

  1. H2/Histamine receptor: use competitive antagonist of histamine for this receptor e.g. Zantac/Tagamet/Pepcid AC
  2. Proton pump (H+/K+ATPase) inhibited/permanently blocked e.g. omeprazole/losec/nexium
18
Q

Bacteria; biological carcinogen; in antrum associated with ?; in antrum&corpus associated with ?
H(+11) p(+5) [12,6]

A

Helicobacter pylori
In antrum=low somatostatin secretion, hypergastrinaemia, increase acid secretion; duodenal&peptic ulcer disease

Antrum&corpus=hypergastrinaemia & low acid secretion; atrophic gastritis, gastric cancer

Year 1 GI (14 decks)

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