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upper gastrointestinal tract Flashcards

1
Q

what anatomical landmark marks start of oesophagus

A

c5

coincides with upper oesophageal sphincter

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2
Q

what are some anatomical contributions to lower oesophageal sphincter

A
  • 3-4cm distal oesophagus within abdomen
  • diaphragm surrounds LOS ( L and R crux)
  • intact phrenosophageal ligament ( extension of inferior diaphragmatic fascia)
  • angle of his
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3
Q

what is stage 0/ oral phase of swallowing

A

chewing and saliva prepare bolus

both sphincters constricted

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4
Q

what happens during stage 1/ pharyngeal phase

A

pharyngeal musculature guides food bolus towards oesophagus
UOS opens reflexly
LOS opened by vasovagal reflex = receptive relaxation reflex

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5
Q

what happens during stage 2/ upper oesophageal phase

A

upper sphincter closes
superior circular muscle rings contract and inferior rings dilate
sequential contractions of longitudinal muscle

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6
Q

what happens during stage 3/ lower oesophageal phase

A

lower sphincter closes as food passes through

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7
Q

how to measure swallowing

A

manometry - tube passed through nose down into oesophagus and measure pressure of contractions

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8
Q

what is the pressure created by peristaltic waves

A

40 mmhg

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9
Q

what is the normal resting pressure of LOS

A

20mmHg

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10
Q

what is the pressure of the LOS during receptive relaxation

A

> 5 mmHg

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11
Q

what is the LOS receptive relaxation mediated by

A

inhibitory noncholinergic nonadrenergic (ncna) neurons of myenteric plexus

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12
Q

what are some functional disorders of oesophagus

A
  • first look for absence of stricture = commenest,
    then caused by abnormal oesophageal contraction(hyper/hypomobility and disordered coordination)
    or by failure of protective mechanisms for reflux (gord)
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13
Q

what is dysphagia

A 
difficulty in swallowing
localisation is important 
for solids/liquids
intermittent/ progressive
precise/vague
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14
Q

odynophagia

A

pain on swallowing

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15
Q

what is regurgitation

A

return of oesophageal contents from above an obstruction

can be functional/mechanical

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16
Q

what is reflux

A

passive return of gastroduodenal contents to mouth

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17
Q

what is achalasia

A

hyper-motility issue

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18
Q

what causes achalasia

A

loss of ganglion cells in aurebachs myenteric plexus in LOS wall
leads to decreased activity of inhibitory NCNA neurones

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19
Q

what is the aetiology of primary achalasia

A

unknown

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20
Q

what is the proposed model of achalasia pathophysiology

A

environmental trigger e.g infection combined with genetic predisposition ( DQb1,DQa1…) leads to non autoimmune inflammatory infiltrates -> extracellular turnover wound repair ->loss of immunological tolerance -> apoptosis of neurons ->humoral response

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21
Q

what are some other diseases which cause oesophageal motor abnormalities similar to primary achalasia

A

chagas disease - caused by parasite
protozoa infection
amyloid/sarcoma/eosinophilic oesophagitis

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22
Q

what does hypermobility do to the resting pressure of LOS

A

increases the pressure

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23
Q

what happens in oesophagus during achalasia

A

receptive relaxation sets in late and is too weak
during reflex phase, pressure in LOS in much greater than in stomach therefore food collects in oesophagus causing increases pressure throughout with dilation
- propagation of peristaltic waves cease over time

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24
Q

what symptoms can achalasia form

A 
weightloss
trouble swallowing 
pain
regurgitate food
retrospective pain
can cause oesophagitis and pneumonia
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25
Q

what is the risk of oesophageal cancer in those with achalasia

A

increased 28x fold

annual incidence approx 0.34%

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26
Q

how to treat achalasia

A

pneumatic dilatation -

pd weakens LOS by circumferential stretching and in some cases tearing of muscle fibres

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27
Q

how effective if pneumatic dilatation

A

71-90% of patients respond initially but many patients subsequently relapse

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28
Q

what is the more effective treatment for achalasia

A

surgery

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29
Q

whats is hellers myotomy

A

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

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30
Q

what is dor fundoplication

A

follows myotomy and

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

31
Q

what are the risks of hellers myotomy and dor fundoplication

A

oesophageal and gastric perforations (10-16%)
division of vagus nerve - rare
splenic injury

32
Q

what is scleroderma

A

autoimmune disease causing hypomotility due to neuronal defects

33
Q

what does neuronal defects in scleroderma cause

A 
atrophy of smooth muscle in oesophagus
peristalsis in distal portion stops
decreased pressure in LOS
GORD develops
often associated with CREST syndrome
34
Q

what is the treatment for scleroderma

A

exclude organic obstruction
improve force of peristalsis with prokinetics - cisapride
once peristalsis failure occures usually irreversible

35
Q

what is an example of disordered coordination

A

corkscrew oesophagus

36
Q

what is corkscrew oesophagus

A 
incoordinate contractions
dysphagia
chest pain
pressure of 400-500
marked hypertrophy of circular muscle
37
Q

treatment for corkscrew oesophagus

A

may respond to forceful PD of cardia

results not as predictable as achalasia

38
Q

what are the 3 areas of anatomical constriction in oesophageal perforation

A

cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphinter constriction

39
Q

what causes pathological narrowing in oesophageal perforation

A

cancer
foreign body
physiological dysfunction

40
Q

what is the aetiology of oesophageal perforation

A 
iatrogenic >50%
spontaneous (boerhaaves) -15%
foreign body - 12%
trauma - 9%
intraoperative - 2%
malignant - 1%
41
Q

what is boerhaaves

A

spontaneous perforations

increase in intra oesophageal pressure with negative intra thoracic pressure - vomitting again closed glottis

42
Q

how does oesophageal perforation present in patients

A

pain - 95%
fever - 80 %
dysphagia - 70 %
emphysema - 35%

43
Q

what investigation can be done if oesophageal perforation suspected

A

chest x ray
ct
swallow -gastrograffin
ogd - Oesophago-Gastro-Duodenoscopy

44
Q

primary management for oesophageal perforation

A

surgical emerygency - 2x increase in mortality if 24h delay

45
Q

what is the initial management for oesophageal perforation

A 
nbm
iv fluids
broad spectrum antibiotics and antifungals
itu/hdu level care
bloods - including g and s
referred to tertiary centre
46
Q

definitive management for oesophageal perforation

A

conservation management with metal stent
operative management should be default:
- primary repair is optimal
- oesophagectomy - definitive solution

47
Q

what is the stomachs protective mechanisms against reflux

A

LOS usually closed as barrier against reflux of pepsin and hcl

48
Q

sporadic reflux is normal but what can it be caused by

A

pressure on full stomach
swallowing
transient sphincter opening

49
Q

what are the 3 mechanism to protect following reflux

A

volume clearance - oesophageal peristalsis reflex
ph clearance - saliva
epithelium - skin barrier

50
Q

what are the cause of failure of protective mechanisms

A 
GORD
decreased sphincter pressure
increased transient sphincter opening
decreased saliva production and buffering
abnormal peristalsis
hiatus hernia
defective mucosal protective mechanism
decreases volume and ph clearance
51
Q

what does failure of protective mechanisms lead to

A

reflux oesophagitis
epithelial metaplasia
leading to carcinoma

52
Q

what is a sliding hiatus hernia

A

stomach slides up within chest

53
Q

what is a rolling/paraoesophageal hiatus hernia

A

stomach slips up the side

= emergency

54
Q

investigations for gord

A

ogd - to exclude cancer
oesophagitis,peptic strictutre and barretts oesophagus confirmed
oesophageal manometry
24hr oesophageal ph recording

55
Q

treatment for gord

A

lifestly echanges - diet, smoking

ppis

56
Q

surgery that can be used for gord

A

dilation of peptic strictures

larascopic nissens fundoplication

57
Q

what is the function of the stomach

A

break food into smaller particles using acid and pepsin

holds food, releasing in controlled, steady state into duodenum

58
Q

whats found in cardia and pyloric region

A

mucus only

59
Q

what is found in body and fundus of stomach

A

mucus, hcl, pepsinogen

60
Q

what is found in antrum of stomach

A

gastrin

61
Q

what is erosive and haemorrhagic gastritis

A

numerous causes -

acute ulcer - gastric bleeding and perforation

62
Q

what is nonerosive, chronic active gastritis

A

takes place in antrum

caused by helicobacter pylori - amoxicillin, clarithromycin and pantoprazole for 7-14 days

63
Q

what is atrophic (fundal gland) gastritis

A 
takes place in fundus
autoantibodies vs parts and products of parietal cells
parietal cells atrophy
decreased acid - increased gastrin
decreased if secretion
64
Q

what is reactive gastritis

A

long term contact with substances that irritate lining

65
Q

what do parietal cells produce

A

H ions

66
Q

what is the role of chief cells

A

enrich secretion with pepsinogen

67
Q

what is the neural stimulation of stomach

A

ach - post ganglionic transmitter of vagal parasympathetic fibres

68
Q

what is the endocrine stimulation of stomach

A

gastrin - g cells of antrum

69
Q

what is the paracrine stimulation of stomach

A

histamine - ecl cell and mast cells of gastric walls

70
Q

what causes inhibition of stomach gastric secretions

A

endocrine - secretin in small intestine
paracrine - somatostatin (sih)
paracrine and autocrine pge2 and pgi2, tgf alpha and adenosine

71
Q

what are the mechanisms for repairing epithelial defects

A

> migration - adjacent epithelial cells flatten to close gap via sideward migration along basement membrane
gap closed by cell growth- stimulated by egf, tgf alpha, igf1,grp and gastrin
acute wound healing - attraction of leukocytes and macrophages: phagocytosis of necrotic cells, angiogenesis, regeneration of ecm after repair of bm
epithelial closure by restitution and cell division

72
Q

how does ulcer form?

A 
helicobacter pylori? - disturbs mucosal barrier
secretion of gastric juice
hco3 secretion
cell formation
blood formation
73
Q

treatment for ulcer

A 
ppi/h2 blocker
all 3 antibiotics
elective surgical 
rare - most ulcers heal within 12 weeks
change meds if see no change
check serum gastrin
ogd and biopsies
74
Q

what are some surgical indications

A

intractability - after medical therapy
continuous use of NSAIDs
complication - haemorrhage, obstruction, perforation

brs2 (65 decks)

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