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Semester 3 > GI Session 4 > Flashcards

GI Session 4 Flashcards

1
Q

What are gastric pits?

A

Indentations on gastric mucosa which denote entrances to tubular gastric glands

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2
Q

Where are tubular gastric glands deepest?

A

Pylorus

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3
Q

What cell types make up tubular gastric glands?

A

Mucus neck
Parietal/oxyntic
Chief
Enteroendocrine

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4
Q

What cells are found between gastric pits?

A

Endocrine

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5
Q

What is secreted by each cell type in the gastric pit?

A

Surface and neck mucus cells secrete mucus and alkali

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6
Q

What do the endocrine cells between gastric pits secrete?

A

Gastrin

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7
Q

What is secreted by the cell types in the gastric gland?

A

Parietal –> acid

Chief –> enzymes

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8
Q

How is acid secreted by parietal cells in the gastric glands?

A

Mitochondria split H2O –> H+ and OH- releasing ATP and CO2
OH-+CO2 –> HCO3- flows down concentration gradient into ECF
H+ actively pumped out of cell using ATP released

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9
Q

What is the canaliculus of a parietal cell?

A

Invagination of cell wall with proton pump

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10
Q

What shape are the parietal cells?

A

Triangular

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11
Q

What are the 3 main factors which overlap to control gastric acid c
Secretion?

A

Gastrin
Histamine
ACh

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12
Q

How does gastrin control gastric acid secretion?

A

Secreted by G-cells –> blood –> surface receptor on parietal cells –> secondary messenger –> acid and intrinsic factor secretion

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13
Q

How does a lack of gastrin release from G-cells lead to aneamia?

A

Lack of intrinsic factor secretion stimulation from parietal cells so vitamin B12 cannot be absorbed

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14
Q

How does histamine control gastric acid secretion?

A

Local release from mast cells scattered in gastric mucosa like endocrine cells –> H2 receptor on parietal cells –> cAMP –> acid secretion

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15
Q

What is different about the histamine receptors in the stomach?

A

H2 compared to H1 elsewhere, therefore H2 are almost unique to stomach parietal cells

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16
Q

How does ACh control gastric acid secretion?

A

Local release from post-ganglionic parasympathetic neurones of stomach wall plexuses –> muscarinic receptor on parietal cell–> secondary messenger –> acid secretion

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17
Q

What do G-cells sense and why?

A

Peptides and low pH due to proximity to surface of mucosa

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18
Q

What stimulates mast cells in the stomach to amplify the original signal for acid secretion?

A

Gastrin

ACh

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19
Q

What antagonises histamine action on parietal cells and therefore provides an effective mechanism of decreased acid secretion?

A

Cimetidine

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20
Q

What can activate intrinsic neurones to release ACh to act directly on parietal cells to stimulate acid secretion?

A

Distension on stretch receptors

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21
Q

What are the three phases of acid secretion control?

A

Cephalic
Gastric
Intestinal

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22
Q

What happens in the cephalic phase of acid secretion control?

A

Smelling/tasting/chewing food causes brainstem to use ANS to fire efferent impulses –> ACh stimulates parietal cells directly and indirectly via histamine to secrete acid

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23
Q

What happens in the initial surge of the gastric phase of acid secretion control?

A

Food bolus reaches stomach –> buffers stomach acid due to alkaline saliva and amine groups covering food –> increases stomach pH –> G-cells release gastrin –> stimulates acid secretion

Stomach distends –> intrinsic nerves –> ACh

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24
Q

What happens in the secondary surge of gastric phase of acid secretion control?

A

Initial digestion releases peptides –> gastrin released –> acts with previously released ACh –> histamine release

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25
Q

What ensures acid secretion continues when buffering and distension are acting at max stimulatory effect?

A

Secondary surge in gastric phase of acid secretion control

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26
Q

What happens in the intestinal phase of acid secretion control?

A

Stomach slowly empties chyme into duodenum –> G-cells stimulate further gastrin secretion in duodenum –> rapidly counteracted by duodenal hormones –> signal stomach function is complete

Accumulation of acid in empty inhibits gastrin secretion

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27
Q

What is the characteristic history of stomach ulcer?

A

Epigastric pain at 2-3am eased by eating

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28
Q

How does the mucus in the stomach compare to that in the saliva?

A

Much more viscous

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29
Q

What halogens to the mucus layer of the stomach when it is disrupted?

A

Self-heals

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30
Q

What is the unstirred layer in the stomach?

A

Surface epithelial cells secrete mucus and HCO3- which absorb and react with H+ to prevent damage to cells

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31
Q

What do H+ react with in the unstirred layer?

A

HCO3- and basic groups on mucus glycoproteins

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32
Q

What causes stimulation of secretion of the components of the unstirred mucus layer?

A

Prostaglandins which are promoted by most factors that stimulate acid secretion so defences match attack

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33
Q

What are the stomach secretions for defence against self-digestion?

A

Mucus and HCO3-

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34
Q

What causes persistent alcoholic gastritis?

A

Ongoing alcohol consumption causing mucus to be repeatedly dissolved

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35
Q

How does H.pylori infection lead to gastritis at least and peptic ulcer at worst?

A

Inhibits self-healing mechanisms of mucus

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36
Q

How can NSAIDs breach stomach defences?

A

Inhibit prostaglandins so decrease mucus and alkali secretion
Some converted into benign non-ionised form by stomach acid so they can pass through mucosa and be re-ionised in surface epithelial cells and become harmful

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37
Q

What are the stages of stomach motility?

A

Relax to accommodate food –> rhythmically contract to break down large particles –> slow delivery of chyme to duodenum

38
Q

How is receptive relaxation of the stomach brought about?

A

On swallowing a neural reflex via the vagus nerve and nerve plexuses –> active relaxation of tension in stomach wall

39
Q

What is the purpose of receptive relaxation in the stomach?

A

Prevent pressure increase within the stomach to reflux is limited

40
Q

How is the wave of peristalsis in the stomach brought about?

A

Pacemaker in the cardia region fires about 3x a minute to cause contraction of longitudinal and circular muscle

41
Q

How does the wave of peristalsis change as it moves across the stomach?

A

Slow at top where the stomach is wider as more cells have to be stimulated –> antrum accelerates as fewer cells

42
Q

What does the acceleration of the wave of peristalsis across the stomach cause to happen to the stomach contents?

A

Inertia or larger lumps means they are overtaken by the wave and pushed back into fundus

43
Q

How is chyme delivered slowly to the duodenum?

A

Initially Pylorus is open so a small squirt of chyme is ejected but the peristaltic wave shuts Pylorus so chyme is returned to the stomach

44
Q

How is the control of gastric emptying exerted?

A

Intestinal hormones signal to stomach how much chyme it can facilitate and rate of peristaltic wave acceleration is altered to change the volume of chyme ejected

45
Q

What is detected in the duodenum which causes it to signal to the stomach that it can accommodate a large volume of chyme?

A

Fat
Low pH
Hypertonicity

46
Q

Is the frequency of peristaltic wave in the stomach constant?

A

Yes

47
Q

Why does the midgut have to make a loop as it develops?

A

Runs out of space due to the rapid enlargement of itself and the liver

48
Q

What does the midgut use as its axis when forming a loop?

A

SMA connected to the yolk sac via the vitelline duct

49
Q

What does the formation of a loop by the midgut result in?

A

Cranial and caudal limbs

50
Q

Does the cranial or caudal midgut limb elongate more?

A

Cranial

51
Q

What are the adult derivatives of the cranial midgut limb?

A

Distal duodenum
Jejunum
Proximal ileum

52
Q

What are the adult derivatives of the caudal midgut limb?

A 
Distal ileum
Caecum
Appendix
Ascending colon
Proximal 2/3 transverse colon
53
Q

What happens in physiological herniation in the 8th week of development?

A

Intestinal loops –> umbilical cord during which small intestinal loops and caecum form

54
Q

When do the cranial and caudal limbs of the midgut form during development?

A

Week 6

55
Q

How does the midgut rotate during physiological herniation?

A

3x90 degree rotations counter clockwise

56
Q

What happens during the first 90 degree rotation of the midgut?

A

During herniation results in limbs running parallel –> cranial limb elongates and child to form large jejunal loops

57
Q

What happens during the second 90 degree rotation of the midgut?

A

During hernia resolution caudal limb moves in front of cranial so caudal derivatives lie anteriorly

58
Q

What happens during the third 90 degree rotation of the midgut?

A

During hernia resolution the cranial limb with extensive looping retracts to the L side first as ceacal bud stops caudal limb –> transverse colon anterior to duodenum

59
Q

What is the ceacal bud?

A

Small conical dilation of the caudal limb of the primary intestinal loop

60
Q

What is the last part to enter the abdominal cavity on hernia resolution?

A

Ceacal bud

61
Q

How is the appendix formed?

A

Distal end of ceacal bud forms a narrow diverticulum

62
Q

What causes the ascending colon and hepatic flexure to be in the R side?

A

Movement of caecal bud from directly below R lobe of liver in RUQ –> RIF

63
Q

What is sub-hepatic caecum?

A

Where the caecal bud does not move during development leading to a short p/absent ascending colon

64
Q

What is the clinical relevance of sub-hepatic caecum?

A

In acute appendicitis tenderness is not located at McBurney’s point

65
Q

What happens in incomplete rotation of the midgut?

A

Midgut loop only makes one 90 degree rotation –> L sided colon as colon and caecum return first and late loops must move to R

66
Q

What happens in reversed rotation of the midgut?

A

Midgut loop makes one 90 degree rotation clockwise –> transverse colon posterior to duodenum lying posterior to SMA

67
Q

What is a major complication of midgut abnormalities?

A

Volvulus due to abnormal mobility

SMA compression of transverse colon

68
Q

What can persistence of the vitelline duct result in?

A

Vitelline cyst or fistula

69
Q

What causes increased risk of volvulus in Meckel’s diverticulum?

A

Attachment by fibrous cord

70
Q

What is the difference between atresia and stenosis?

A

Atresia-lumen obliterated

Stenosis-lumen narrowed

71
Q

When can atresia or stenosis occur during development of the GI tract?

A

When recanalisation of the oesophagus, bile duct or small intestine is wholly or partially unsuccessful

72
Q

Describe the incidence of aterisa/stenosis in the duodenum, jejunum, ileum and colon.

A

Duodenum>jejunum=ileum>colon

73
Q

What is atresia/stenosis of the upper duodenum most likely to be due to?

A

Failure of recanalisation

74
Q

What is atresia/stenosis of the lower duodenum most likely to be due to?

A

Vascular accident leading to tissue necrosis

75
Q

What is pyloric stenosis?

A

Hypertrophy of pyloric sphincter circular muscle

76
Q

Is pyloric stenosis a failure of recanalisation?

A

No

77
Q

What is the characteristic presentation of pyloric stenosis?

A

Projectile vomiting in neonate

78
Q

Why does omphalocoele have a lower survival rate than gastroschisis?

A

Associated with other abnormalities and chromosomal disorders

79
Q

Why does tissue above the pectinate line have poorly localised pain?

A

Organisation of afferents giving visceral innervation

80
Q

What happens to the hindgut at 6 weeks?

A

Has swollen into cloaca which undergoes anteroposterior subdivision to give rise to the urogenital sinus and anorectal canal

81
Q

Describe the process that leads to perforation of the anus.

A

Urogenital septum grows down to meet cloacal membrane and proctodeum ectoderm pushes up to meet gut tube –> perineal body forms as urogenital septum reaches cloacal membrane –> anus perforates with perineal body anteriorly

82
Q

What is the importance of the perineal body?

A

Crucial for integrity of the pelvic floor

83
Q

Which organs retain their mesenteries?

A 
Jejunum
Ileum
Appendix
Transverse colon
Sigmoid colon
84
Q

Which organs develop fixed mesenteries?

A

Duodenum
Ascending colon
Descending colon
Rectum

85
Q

Where is there no peritoneal covering in the rectum?

A

Distal 1/3

86
Q

What is the fate of the dorsal mesentery?

A 
Greater omentum
Gastrolineal ligament
Lineorenal ligament
Mesocolon
Mesentery proper
Jejejunal and ileal loops
87
Q

What is the fate of the ventral mesentery?

A

Lesser omentum

Falciform ligament

88
Q

What gives innervation to the midgut?

A

PS: vagus
S: superior mesenteric ganglion and plexus

89
Q

What gives innervation to the hindgut?

A

PS: pelvic (S2-4)
S: inferior mesenteric ganglion and plexus

90
Q

When do the primordia of the liver, pancreas and trachea appear?

A

Week 4

91
Q

When do the pancreatic buds fuse?

A

Week 7

92
Q

When is adult disposition of abdominal viscera achieved?

A

Week 10

Semester 3 (50 decks)

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