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Gastroenterology > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

Outline the oesophageal anatomy.

A

upper oesopahgeal sphincter > cervical oesophagus (skeletal) > upper/middle thoracic (skeletal/smooth) > lower thoracic (smooth) > lower oesophageal sphincter

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2
Q

oesophagus starts at what vertebral level?

A

C5

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3
Q

oesophagus ends at what vertebral level?

A

T10

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4
Q

anatomical contributions to LOS

A

3-4cm distal oesophagus within abdo, surrounded by diaphragm, intact phrenoesophageal ligament, angle of His

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5
Q

List the phases of swallowing.

A

oral phase
pharyngeal phase
upper oesophageal
lower oesophageal

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6
Q

oral phase

A

chewing/saliva prepare bolus

both sphincters constricted

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7
Q

pharyngeal phase

A

muscles guide bolus to oesophagus > UOS opens reflexively > LOS opened by vasovagal reflex (receptive relaxation reflex)

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8
Q

upper pharyngeal phase

A

UOS closes > superior circular muscle rings contract and inferior rings dilate > sequential contraction of longitudinal muscle

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9
Q

lower oesophageal phase

A

lower sphincter closes as food passes through

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10
Q

oesophageal motility determined by?

A

manometry

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11
Q

pressure of peristaltic waves?

A

40mmHg

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12
Q

LOS resting pressure?

A

20mmHg

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13
Q

LOS pressure during receptive relaxation?

A

decreases <5mmHg

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14
Q

LOS relaxation is mediated by?

A

inhibitory noncholinergic non adrenergic neurons of myenteric plexus

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15
Q

absence of a stricture caused by?

A 
abnormal contraction (hyper/hypomotility, disordered coordination)
failure of protective mechanisms for reflux (GORD)
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16
Q

dysphagia

A

difficulty in swallowing

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17
Q

classify dysphagia

A

localisation (cricopharyngeal sphincter or distal)

type (solids or fluids, intermittent or progressive, precise or vague)

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18
Q

odynophagia

A

pain on swallowing

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19
Q

regurgitation

A

return of oesophageal contents from above a obstruction

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20
Q

regurgitation may be _____ or ______

A

functional

mechanical

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21
Q

reflux

A

passive return of gastroduodenal contents to the mouth

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22
Q

Hypermotility-achalasia due to?

A

loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall > decreased activity in inhibitory NCNA neurons

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23
Q

aetiology of primary achalasia

A

unknown

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24
Q

what diseases can cause secondary achalasia?

A

Chagas’ disease
protozoa infection
amyloid/sarcoma/eosinophilic oesophagitis

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25
proposed model of achalasia pathophysiology
environ. trigger > genetic predisposition > ^non autoimmune inflammatory infiltrates > ^extracellular turnover/wound repair/fibrosis > loss of immunological tolerance > apoptosis of neurons > humoral response
26
hypermotility causes?
LOS pressure too high > food collects in oesophagus > cease propagation of peristaltic waves
27
disease course in hypermotility - achalasia
insidious onset - symptoms for years before seeking help, without treatment > progressive oesophageal dilatation
28
how does risk of oesophageal cancer increase with hypermotility?
increased 28 fold
29
treatment options for hypermotility
pneumatic dilatation heller's myotomy dor fundoplication peroral endoscopic myotomy
30
efficacy of pneumatic dilatation
71-90% respond initially but many patients subsequently relapse
31
risks to heller's myotomy/dor fundoplication
oesophageal+gastric perforation division of vagus nerve splenic injury
32
peroral endoscopic myotomy
mucosal incision > creation of submucosal tunnel > myotomy > closure of mucosal incision
33
dor fundoplication
anterior fundus folded over oesophagus and sutured to right side of myotomy
34
heller's myotomy
continuous myotomy performed for 6cm on the oesophagus and 3cm onto the stomach
35
scleroderma
autoimmune disease
36
hypomotility
neuronal defects > atrophy of smooth muscle
37
What happens to peristalsis in the distal portion of the oesophagus in hypomotility?
ultimately ceases altogether
38
What develops after hypomotility?
gastroesophageal reflux disease (often associated with CREST syndrome)
39
Treatment for hypomotility
exclude organic obstruction, improve force of peristalsis with prokinetics (cisapride)
40
In hypomotility, once peristaltic failure occurs is it irreversible or reversible?
irreversible
41
Give an example of disordered coordination.
corkscrew oesophagus
42
outline what occurs with disordered coordination
incoordinate contractions > dysphagia and chest pain | marked hypertrophy of circular muscle
43
treatment for disordered coordination
may respond to forceful PD of cardia
44
give examples of vascular anomalies causing dysphagia
dysphagia lusoria | double aortic arch
45
anatomy of oesophageal perforations
3x areas of anatomical constriction, pathological narrowing (cancer foreign body, physiological dysfunction
46
aetiology of oesophageal perforation
``` latrogenic (OGD) spontaneous (Boerhaave's) foreign body trauma inoperative malignant ```
47
latrogenic oesophageal perforation
usually at OGD, more common in presence of the diverticula or cancer
48
Boerhaave's oesophageal perforation
sudden increase in intra-oesophageal pressure with negative intrathoracic pressure, vomiting against a closed glottis
49
foreign body oesophageal perforation
disk batteries growing problem, magnets, sharp objects, dishwasher tablet
50
trauma oesophageal perforation
neck = penetrating, thorax = blunt force
51
intraoperative oesophageal perforation
hiatus hernia repair heller's cardiomyotomy pulmonary surgery thyroid surgery
52
malignant oesophageal perforation
``` advanced cancers radiotherapy dilatation stenting poor prognosis ```
53
presentation of oesophageal perforation
pain fever dysphagia emphysema
54
investigations for oesophageal perforation
CXR CT swallow (gastrograffin) OGD
55
initial management of oesophageal perforation
``` NBM IV fluids broad spectrum AB and antifungals ITU/HDU level care tertiary referral ```
56
in oesophageal perforation, operative management should be default unless?
minimal contamination contained unfit
57
surgical options for oesophageal perforation include
primary repair: vascularised pedicle flap, gastric fundus buttressing drains oesophagectomy
58
sporadic reflux is normal due to?
pressure on full stomach, swallowing, transient sphincter opening
59
list mechanisms that protect following reflux
``` volume clearance (peristalsis reflex) pH clearance (saliva) epithelium (barrier properties) ```
60
examples of failure of protective mechanisms of reflux
transient sphincter opening, decreased saliva production, abnormal peristalsis, hiatus hernia, defective mucosal protective mechanism
61
list examples of hiatus hernia
sliding | rolling/paraoesophageal
62
investigations for reflux
OGD oesophageal manometry 24hr oesophageal pH recording
63
Treatment for reflux conditions
lifestyle changes (weight loss, smoking), PPIs, surgery
64
what is produced in the cardia and pyloric regions of the stomach?
mucus only
65
what is produced in the body and fundus regions of the stomach?
mucus HCl pepsinogen
66
what is produced in the antrum regions of the stomach?
gastrin
67
list examples of gastritis
erosive and haemorhhagic nonerosive, chronic active gastritis atrophic gastritis reactive gastritis
68
causes of erosive and haemorrhagic gastritis
numerous, acute ulcer
69
where does nonerosive, chronic active gastritis occur?
antrum
70
cause of nonerosive, chronic active gastritis
H. pylori
71
where does atrophic gastritis occur?
fundus
72
causes of | atrophic gastritis
autoantibodies vs parts and products of parietal cells
73
describe stimulation of gastric secretion
acetylcholine gastrin histamine
74
describe inhibition of gastric secretion
``` secretin somatostatin PGE2/PGI2 TGF-alpha adenosine ```
75
mechanisms repairing epithelial defects
adjacent migration to close gap cell growth acute wound healing
76
How does H. pylori lead to ulcer formation?
increases secretion of gastric juice > decrease HCO3- secretion > decrease cell formation > decrease blood perfusion
77
H. pylori factors associated with virulence
urease exotoxin secretory enzymes
78
clinical outcomes of H. pylori infections
asymptomatic/chronic gastritis chronic atrophic gastritis or intestinal metaplasia gastric or duodenal cancer gastric cancer MALT lymphoma
79
primarily medical treatment for ulcer
``` PPI or H2 blocker triple Rx (amoxicillin, clarithromycin, pantoprazole for 7-14 days) ```
80
surgical indications for ulcer
``` intractability haemorrhage obstruction perforation relative: continuous requirement of steroid therapy/NSAIDs ```

Gastroenterology (9 decks)

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