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BRS Year 2 > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

anatomical contributions to LOS

A

3/4cm distal oesophagus within abdomen

Diaphragm surrounds LO

An intact phrenoesophageal ligament: has 2 limbs: 1 attached to the oesophagus and other attached to diaphragm- allows movement of oesophagus and diaphragm

Angle of His- between abdominal oesophagus and fundus of stomach- stops acid reflux

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2
Q

stages of swallowing

A 
4 (0-3)
oral
pharyngeal
upper oesophageal
lower oesophageal
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3
Q

how to determine motility of oesophagus

A

manometry- pressure measurements

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4
Q

functional disorders of the oesophagus

A
  • abnormal oesophageal contraction (hypomobility, hypermobility and disordered coordination)
  • failure of protective mechanisms of reflux
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5
Q

dysphagia

A

difficulty in swallowing

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6
Q

What do we call pain on swallowing?

A

odynophagia

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7
Q

regurgitation

A

return of oesophageal content from above an obstruction (functional or mechanical)

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8
Q

reflux

A

passive return of gastroduodenal contents to the mouth

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9
Q

is reflux the same as vomiting?

A

no

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10
Q

example of oseophageal hypermotility and causes?

A

achalasia
- Due to loss of ganglion cell in Aurebach’s myenteric plexus
Primary cause aetiology is unknown
Secondary cause:
-Diseases causing oesophageal motor abnormalities similar to primary achalasia
• Chagas’ Disease
• Protozoa infection
• Amyloid/Sarcoma/Eosinophilic Oesophagitis

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11
Q

features of achalaisa hypermotility

A
  • increased resting pressure of LOS
  • receptive relaxation sets in late and is too weak -> during reflex phase, pressure in LOS is markedly higher than stomach
  • swallowed food collects in the oesophagus causing increased pressure throughout with dilation of the oesophagus
  • Propagation of peristaltic wave ceases
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12
Q

disease course of achalasia

A
  • insidious onset: symptoms for years without seeking help
  • without treatment you get progressive oesophageal dilation
  • oesophageal cancer risk increased 28-fold
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13
Q

treatment of achalasia

A

pneumatic dilation (PD) to stretch muscles of the LOS:
-uses endoscopy, guide wire with PD
-balloon inserted and inflated to expand LO
- restored flow in LO
Efficacy of 90%, but usually relapses

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14
Q

surgical treatment of achalasia and risks?

A
  • heller’s myotomy : myotomy (muscle cut) for 6cm of oesophagus and 3cm of stomach
  • Dor fundopilation: anterior fundus folded over oesophagus and sutured to right side of myotomy

Risks include:

  • Esophageal and gastric perforation
  • Division of vagus nerve
  • splenic injury
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15
Q

What is an example of a cause of oesophageal hypomotility ?

A

Scleroderma-autoimmune disease
Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases
Decreased resting pressure of LOS
Leads to development of GORD- often associated with CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia)

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16
Q

treatment of scleroderma

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics
Once peristaltic failure occurs, this is usually irreversible - may have to have oesophagus removed

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17
Q

conditions causing disordered coordination

A

corkscrew oesophagus
Incoordinate contractions → dysphagia & chest pain
• Pressures of 400-500 mmHg
• Marked hypertrophy of circular muscle
• Corkscrew oesophagus seen on Barium x-ray scan

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18
Q

treating corkscrew oesophagus

A

forceful PD of cardia

results not as predictable as achalasia

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19
Q

What are causes of oesophageal perforation (most common to least common?

A 
latrogenic - usually due to OGD (Oesophago-Gastro-Duodenoscopy)
Spontaneous (Boerhaave's)
Foreign body
Trauma
Intraoperative
Malignant
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20
Q

what causes spontaneous oesophageal perforation

A

aka. Boerhaave’s
Sudden increase in intraesophageal pressure with negative intrathoracic pressure
Vomiting against a closed glottis
Usually left posterolateral aspect of distal oesophagus

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21
Q

foreign bodies causing oesophageal perforation

A

Disk batteries is growing problem- cause electrical burns if impact in mucosa

  • magnets
  • sharp objects
  • dishwasher tablets
  • acid/alkali
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22
Q

oesophageal perforation from trauma signs

A

Neck - caused by penetrating trauma
Thorax - caused by blunt force

Symptoms:

  • dysphagia
  • blood in saliva
  • haematemsis
  • surgical emphysema
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23
Q

surgeries that can cause oesophageal perforation

A
  • hiatus hernia repair
  • hellers myotomy
  • pulmonary surgery
  • thyroid surgery
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24
Q

investigating oesophageal perfortion

A
  • CXR
  • CT
  • Swallow (gastrograffin)
  • OGD
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25
Q

initial management of oesophageal perforation

A 
NBM (nil by mouth)
IV fluids
Broadspec AB and antifungal
Bloods
ICU/ HDU level care
tertiary care (specialist) referral
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26
Q

definitive management of the oesophageal perforation

A

Perforation is a surgical emergency (2x increase in morality if 24hr delay in diagnosis)

Operative management is default unless:
-there's minimal contamination
-it's contained
-patient unfit
In this case you can use conservative management with a covered metal stent
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27
Q

why is LOS normally closed?

A

barrier against reflux to protect from gastric juice

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28
Q

is sporadic reflux normal?

A

yes, occurs when:
pressure on full stomach
swallowing
transient sphincter opening (spontaneous)

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29
Q

3 mechanisms for protection following reflux

A
  • volume clearance (oesophageal peristalsis reflex)
  • pH clearance (saliva)
  • epithelial barrier properties
30
Q

what are failed protective mechanisms against reflux and what can this cause?

A

Decreased sphincter pressure
Transient sphincter opening
Decreased saliva production- leads to decreased pH clearance
Decreased buffering capacity of saliva (e.g. by smoking) - leads to decreased pH clearance
Abnormal peristalsis- leads to decreased volume clearance
Hiatus hernia
Defective mucosal protective mechanism

These can lead to
GORD -> reflux oesophagitis -> epithelial metaplasia -> carcinoma

31
Q

what often happens with GORD?

A

sliding hiatus hernia- Ligament gives way and stomach slides up

32
Q

rolling hiatus hernia

A

Bit of stomach squeezes through next to oesphagus

33
Q

how to investigate GORD

A 
OGD
- exclude other cause like cancer
- look for oesophagitis, peptic stricture and barrett's oesophagus
Oesophageal manometry
24 hr oesophageal pH recording
34
Q

types of gastritis

A
  • erosive and hemorrhagic
  • nonerosive chronic active gastritis
  • atrophic gastritis
  • reactive gastritis
35
Q

What are causes of nonerosive, chronic active gastritis, what does it lead to and what is treatment?

A

helicobacter pylori in the antrum
Leads to increased gastrin and inc/normal acid secretion -> gastric and duodenal ulcer -> reactive gastritis -> epithelial metaplasia -> carcinoma

Treatment:
triple therapy - amoxicillin and clarithromycin and a PPI for up to 14 days

36
Q

cause of atrophic gastritis

A

autoantibodies attacking gastric receptor/ carbonic anhydrase/ H+/K+NATPase/ IF
Atrophic gastritis leads to dec pepsinogen, dec acid secretion (-> inc gastrin -> ECL cell hyperplasia -> carcinoid OR G-cell hyperplasia -> carcinoma) and dec IF secretion (-> dec cobalamin absorption -> cobalamin deficiency -> pernicious anaemia)

37
Q

What are causes of erosive and hemorrhagic gastritis and what does it lead to?

A 
NSAIDs
Alcohol
Multi-organ failure
Trauma
Ischaemia

Leads to acute ulcer- gastric bleeding and perforation

38
Q

methods of mucosal protection (4)

A
  1. mucus film
  2. HCO3- secretion
  3. Epithelial barrier
  4. mucosal blood perfusion
39
Q

What are the stages of epithelial repair and wound healing?

A

Migration
Gap closed by cell growth
Acute wound healing

40
Q

How does H Pylori cause virulence? (8)

A

Urease: to neutralise gastric acid
Flagella: for mobility and chemotaxis
Lipopolysaccharides: adhere to host cells and inflammation
Outer proteins: Adhere to host cell
Exotoxins: vacuolating toxin for gastric mucosal injury
Secretory enzymes: mucinase, protease, lipase for gastric mucosal injury
Type IV secretion system: for injection of effectors
Effectors: for actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition

41
Q

neural stimulation of gastric secretion?

A

ACh -> postganglionic transmitter of vagal parasympathetic fibres

42
Q

endocrine stimulation of gastric secretion?

A

Gastrin (G cells of antrum)

43
Q

paracrine stimulation of gastric secretion?

A

Histamine (from ECL cells & mast cells of gastric wall)

44
Q

endocrine inhibition of gastric secretion?

A

Secretin (small intestine)

45
Q

paracrine inhibition of gastric secretion?

A

Somatostatin (SIH)

46
Q

paracrine and autocrine inhibition of gastric secretion?

A

Prostaglandins (E2 & I2), TGF-α &

adenosine

47
Q

What occurs in the migration stage of epithelial repair and wound healing

A

• Adjacent epithelial cells flatten to close gap

via sideward migration along BM

48
Q

gap closed by cell stage of epithelial repair and wound healing

A

• Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin

49
Q

acute wound healing by cell stage of epithelial repair and wound healing

A
  • BM destroyed - attraction of leukocytes &
    macrophages; phagocytosis of necrotic cells;
    angiogenesis; regeneration of ECM after repair
    of BM
  • epithelial closure by restitution & cell division.
50
Q

What factors contribute to ulcer formation?

look at slide on this and slide after!!

A
  • helicobater pylori
  • secretion of gastric juice increased
  • HCO3- secretion decreased
  • cell formation decreased
  • blood prefusion decreased
51
Q

primarily medical treatment ulcer

A
  • PPI or H2 blocker
    • Triple Rx (amoxicillin, clarithromycin,
    pantoprazole) for 7-14 days)
52
Q

Elective Surgical Rx for ulcers

A 
Rare - most uncomplicated ulcers heal
within 12 weeks
• If don’t, change medication, observe
additional 12 weeks
• Check serum gastrin (antral G-cell
hyperplasia or gastrinoma [ZollingerEllison syndrome])
• OGD: biopsy all 4 quadrants of ulcer
(rule out malignant ulcer) if refractory
53
Q

surgical indication ulcers

A
  • Intractability (after medical therapy)
  • Haemorrhage
    -Obstruction
    -Perforation
    -Relative: continuous requirement of
    steroid therapy/NSAIDs
54
Q

main disorders of the stomach (8)

A 
• Failure of protective mechanisms
• Gastrooesophageal reflux (GORD)
• Hiatus hernia
• Gastritis
• Failure in regulation of gastric secretion, mucosal
protection & epithelial repair
• GIT ulcer formation
• H. pylori
• Treatment
55
Q

What happens in the oral phase of swallowing?

A
  • Chewing & saliva prepare bolus

* Both oesophageal sphincters constricted

56
Q

What happens in the pharyngeal phase of swallowing?

A

• Pharyngeal musculature guides food bolus towards oesophagus
• Upper oesophageal sphincter opens reflexly
• LOS opened by vasovagal reflex (receptive relaxation
reflex)

57
Q

What happens in the upper oesophageal phase of swallowing?

A

• Upper sphincter closes
• Superior circular muscle rings contract & inferior rings
dilate
• Sequential contractions of longitudinal muscle

58
Q

What happens in the lower oesophageal phase of swallowing?

A

• Lower sphincter closes as food passes through

59
Q

What is the pressure of a normal oesophagus during a peristaltic wave?

A

40 mmhg

60
Q

What is the lower oesophageal resting pressure normally and how does this change with receptive relaxation?

A

20 mmhg

decreased by 5 mmhg during receptive relaxation

61
Q

What mediates the pressure within the oesophagus?

A

Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

62
Q

How is dysphagia classified?

A

Location: cricopharyngeal sphincter or distal

Type of dysphasia: solids or fluids/ intermittent or progressive/ precise or vague in precision

63
Q

What is an endoscopic treatment of achalasia?

A

Peroral endoscopic myotomy (POEM):

  1. Mucosal incision mae
  2. Submucosal tunnel is creates
  3. Myotomy
  4. Closure of mucosal tunnel
64
Q

What are iatrogenic causes of oesophageal perforation?

A

Usually occurs at OGD

Incidence (low to high)

OGD alone
Stricture dilatation
Sclerotherapy
Achalasia dilatation

65
Q

How do you treat malignancies that cause esophageal perforation?

A

• Radiotherapy
• Dilatation
• Stenting
Has poor prognosis

66
Q

What are symptoms of oesophageal perforation?

A

Pain
Fever
Dysphagia
Emphysema

67
Q

What surgery would be used to repair an oesophageal perforation?

A

Primary repair is optimina:
• +/- Vascularised pedicle flap
• +/- Gastric fundus buttressing
(e.g. Dor)
Oesophagaectomy is a definitive soloution:
- With reconstruction or oesophagostomy & delayed reconstruction

68
Q

What are things that can increase LOS pressure and what is their effect?

A

Acetylcholine, α-adrenergic agonists, hormones, protein-rich food, histamine, high intra-abdominal pressure, PGF2α, etc.
Inhibit reflux

69
Q

What are things that can decrease LOS pressure and what is their effect?

A

VIP, β-adrenergic agonists, hormones, dopamine, NO, PGI2 , PGE2 , chocolate, acid gastric juice, fat, smoking, etc.

Promote reflux

70
Q

What are treatments of GORD?

A

Medical:

  • lifestyle changes (wt loss, smoking)
  • PPIs

Surgical:

  • Dilatation peptic strictures
  • Laparoscopic Nissen’s fundoplication (close where stomach enters diaphragm and wrap fundus around oesophagus)
71
Q

What are the clinical outcomes of a H Pylori infection?

A 
Asymptomatic or chronic gastritis
e.g. Chronic atrophic gastritis
Intestinal metaplasia
Gastric or duodenal ulcer
Gastric cancer
e.g MALT lymphoma

BRS Year 2 (110 decks)

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