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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
Q

proposed model of achalasia pathophysiology

A

environ. trigger > genetic predisposition > ^non autoimmune inflammatory infiltrates > ^extracellular turnover/wound repair/fibrosis > loss of immunological tolerance > apoptosis of neurons > humoral response

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26
Q

hypermotility causes?

A

LOS pressure too high > food collects in oesophagus > cease propagation of peristaltic waves

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27
Q

disease course in hypermotility - achalasia

A

insidious onset - symptoms for years before seeking help, without treatment > progressive oesophageal dilatation

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28
Q

how does risk of oesophageal cancer increase with hypermotility?

A

increased 28 fold

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29
Q

treatment options for hypermotility

A

pneumatic dilatation
heller’s myotomy
dor fundoplication
peroral endoscopic myotomy

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30
Q

efficacy of pneumatic dilatation

A

71-90% respond initially but many patients subsequently relapse

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31
Q

risks to heller’s myotomy/dor fundoplication

A

oesophageal+gastric perforation
division of vagus nerve
splenic injury

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32
Q

peroral endoscopic myotomy

A

mucosal incision > creation of submucosal tunnel > myotomy > closure of mucosal incision

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33
Q

dor fundoplication

A

anterior fundus folded over oesophagus and sutured to right side of myotomy

34
Q

heller’s myotomy

A

continuous myotomy performed for 6cm on the oesophagus and 3cm onto the stomach

35
Q

scleroderma

A

autoimmune disease

36
Q

hypomotility

A

neuronal defects > atrophy of smooth muscle

37
Q

What happens to peristalsis in the distal portion of the oesophagus in hypomotility?

A

ultimately ceases altogether

38
Q

What develops after hypomotility?

A

gastroesophageal reflux disease (often associated with CREST syndrome)

39
Q

Treatment for hypomotility

A

exclude organic obstruction, improve force of peristalsis with prokinetics (cisapride)

40
Q

In hypomotility, once peristaltic failure occurs is it irreversible or reversible?

A

irreversible

41
Q

Give an example of disordered coordination.

A

corkscrew oesophagus

42
Q

outline what occurs with disordered coordination

A

incoordinate contractions > dysphagia and chest pain

marked hypertrophy of circular muscle

43
Q

treatment for disordered coordination

A

may respond to forceful PD of cardia

44
Q

give examples of vascular anomalies causing dysphagia

A

dysphagia lusoria

double aortic arch

45
Q

anatomy of oesophageal perforations

A

3x areas of anatomical constriction, pathological narrowing (cancer foreign body, physiological dysfunction

46
Q

aetiology of oesophageal perforation

A 
latrogenic (OGD)
spontaneous (Boerhaave's)
foreign body
trauma
inoperative
malignant
47
Q

latrogenic oesophageal perforation

A

usually at OGD, more common in presence of the diverticula or cancer

48
Q

Boerhaave’s oesophageal perforation

A

sudden increase in intra-oesophageal pressure with negative intrathoracic pressure, vomiting against a closed glottis

49
Q

foreign body oesophageal perforation

A

disk batteries growing problem, magnets, sharp objects, dishwasher tablet

50
Q

trauma oesophageal perforation

A

neck = penetrating, thorax = blunt force

51
Q

intraoperative oesophageal perforation

A

hiatus hernia repair
heller’s cardiomyotomy
pulmonary surgery
thyroid surgery

52
Q

malignant oesophageal perforation

A 
advanced cancers
radiotherapy
dilatation
stenting
poor prognosis
53
Q

presentation of oesophageal perforation

A

pain
fever
dysphagia
emphysema

54
Q

investigations for oesophageal perforation

A

CXR
CT
swallow (gastrograffin)
OGD

55
Q

initial management of oesophageal perforation

A 
NBM
IV fluids
broad spectrum AB and antifungals
ITU/HDU level care
tertiary referral
56
Q

in oesophageal perforation, operative management should be default unless?

A

minimal contamination
contained
unfit

57
Q

surgical options for oesophageal perforation include

A

primary repair: vascularised pedicle flap, gastric fundus buttressing
drains
oesophagectomy

58
Q

sporadic reflux is normal due to?

A

pressure on full stomach, swallowing, transient sphincter opening

59
Q

list mechanisms that protect following reflux

A 
volume clearance (peristalsis reflex)
pH clearance (saliva)
epithelium (barrier properties)
60
Q

examples of failure of protective mechanisms of reflux

A

transient sphincter opening, decreased saliva production, abnormal peristalsis, hiatus hernia, defective mucosal protective mechanism

61
Q

list examples of hiatus hernia

A

sliding

rolling/paraoesophageal

62
Q

investigations for reflux

A

OGD
oesophageal manometry
24hr oesophageal pH recording

63
Q

Treatment for reflux conditions

A

lifestyle changes (weight loss, smoking), PPIs, surgery

64
Q

what is produced in the cardia and pyloric regions of the stomach?

A

mucus only

65
Q

what is produced in the body and fundus regions of the stomach?

A

mucus
HCl
pepsinogen

66
Q

what is produced in the antrum regions of the stomach?

A

gastrin

67
Q

list examples of gastritis

A

erosive and haemorhhagic
nonerosive, chronic active gastritis
atrophic gastritis
reactive gastritis

68
Q

causes of erosive and haemorrhagic gastritis

A

numerous, acute ulcer

69
Q

where does nonerosive, chronic active gastritis occur?

A

antrum

70
Q

cause of nonerosive, chronic active gastritis

A

H. pylori

71
Q

where does atrophic gastritis occur?

A

fundus

72
Q

causes of

atrophic gastritis

A

autoantibodies vs parts and products of parietal cells

73
Q

describe stimulation of gastric secretion

A

acetylcholine
gastrin
histamine

74
Q

describe inhibition of gastric secretion

A 
secretin
somatostatin
PGE2/PGI2
TGF-alpha
adenosine
75
Q

mechanisms repairing epithelial defects

A

adjacent migration to close gap
cell growth
acute wound healing

76
Q

How does H. pylori lead to ulcer formation?

A

increases secretion of gastric juice > decrease HCO3- secretion > decrease cell formation > decrease blood perfusion

77
Q

H. pylori factors associated with virulence

A

urease
exotoxin
secretory enzymes

78
Q

clinical outcomes of H. pylori infections

A

asymptomatic/chronic gastritis
chronic atrophic gastritis or intestinal metaplasia
gastric or duodenal cancer
gastric cancer MALT lymphoma

79
Q

primarily medical treatment for ulcer

A 
PPI or H2 blocker
triple Rx (amoxicillin, clarithromycin, pantoprazole for 7-14 days)
80
Q

surgical indications for ulcer

A 
intractability
haemorrhage
obstruction
perforation
relative: continuous requirement of steroid therapy/NSAIDs

Gastroenterology (9 decks)

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