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Gastro Yr 2 > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

What marks the borders of upper GI

A

upper oesophageal sphincter to lower oesophageal sphincter

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2
Q

Anatomical contributions to lower oesophageal sphincter

A

3-4cm distal part of oesophagus is in abdomen

Diaphragm surrounds the sphincter (contracts against the sphincter)

Intact phreno-oesophageal ligament

Angle of His

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3
Q

How does the angle of His prevent reflux

A

The angle of His is an acute angle between the great curvature of the stomach and the oesophagus, and acts as an anti-reflux barrier by functioning like a valve

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4
Q

Why is an Intact phreno-oesphageal ligament important

A

ligament allows independent movement of the diaphragm and oesophagus during respiration and swallowing

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5
Q

4 stages of swallowing

A

Oral phase
Pharyngeal phase
Upper oesophageal phase
Lower oesophageal phase

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6
Q

Oral phase

A

Chewing + saliva prepare bolus

Both sphincter constricted

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7
Q

What is manometry

A

Way to record pressure of contractions of oesophagus + get an idea of its motility

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8
Q

what allows for relaxation of the sphincter - check this!

A

decreases LOS pressure - mediated by inhibitory noncholinergic noradrenergic neurons of myenteric plexus

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9
Q

What is absence of a stricture caused by

A

abnormal oesophageal contraction (hypermotility, hypomotility, disordered coordination)

Failure of protective mechanism for reflux (GORD)

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10
Q

Questions to ask about dysphagia

A

Location is important

Type of dyaphagia

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11
Q

Questions to ask abut dysphagia

A

Location is important (cricopharyngeal sphincter or distal)

Type of dysphagia (for solids fluids/ intermittent or progressive/ precise or vague)

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12
Q

Odynophagia

A

Pain on swallowing

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13
Q

what is oesophageal perforation?

A

hole in the oesophagus

3 areas of anatomical constriction (more vulnerable areas)

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14
Q

What is Boerhaave’s

A

sudden increase in intra-oesophageal pressure (vomit against closed glottis)

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15
Q

which foreign bodies cause a oesophageal perforation?

A

sharp objects
disk batteries (cause elctrical burns)
magnets
acid/ alkali

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16
Q

Trauma in the neck oesophageal perforation presentation?

A

dysphagia
haematemesis
surgical empysema
blood in saliva

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17
Q

what is GORD

A

acid from the stomach leaks up into the oesophagus

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18
Q

what does the antrum produce

A

gastrin

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19
Q

oesophageal perforation initial management?

A

IV fluids
Broad spectrum Antibiotics
Nil by mouth

20
Q

oesophageal definitive management?

A

conservative management with covered metal stent

21
Q

Protective mechanisms against reflux in the stomach

A

LOS usually closed as a barrier against reflux

22
Q

what contributes to increasing LOS reflux

A

acetylcholine
hormones
protein-rich food
histamine

23
Q

what contributes to decreasing LOS reflux

A

beta adrenergic agonists
dopamine
acid gastric juice
smoking

24
Q

Protective mechanism following reflux

A

volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
epithelium - barrier properties

25
Q

Causes of failure of protective mechanism

A

decreased vol clearance (abnormal peril-stasis)
Slowed ph clearance ( not producing enough saliva)
Smoking - decrease buffering capacity of saliva

26
Q

Sliding hiatus hernia mechanism

A

gastro- oesophageal junction, and part of the stomach protrude into the chest

27
Q

Rolling hiatus hernia

A

part of the stomach pushes up through the hole in the diaphragm next to the oesophagus (portion of stomach slips up the side)

28
Q

Mechanism to repair epothelial defects

A

migration
gap closed by cell growth
acute wound healing

29
Q

what do the body and fundus produce

A

mucus, HCl, pepsinogen

30
Q

what is erosive + haemorrhagic gastritis

A

acute ulcer - gastric bleeding + perforation

31
Q

what is nonerosive, chronic active gastritis

A

variety of histologic abnormalities that are mainly the result of Helicobacter pylori infection

32
Q

what is atrophic gastritis

A

chronic inflammation of the gastric mucosa with loss of the gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue

33
Q

reactive gastritis

A

long-term contact with substances that irritate the stomach lining

34
Q

Cause of erosive gastritis

A

NSAIDS
multi-organ failure
trauma
ischaemia

35
Q

what is reflux

A

passive return of gastroduodenal contents to the mouth

36
Q

Mechanism to repair epithelial defects

A

migration - adjacent epithelial cells flatten to close gap
gap closed by cell growth
acute wound healing - epithelial closure by restitution + cell division

37
Q

Why do you get ulcers

A

increased chemical aggression (anything that increases gastric juice secretion)

barrier function disturbed (h. pylori)

38
Q

what causes secondary hypermotility

A

chagas’ disease
protozoa infection
amyloid/ sarcoma/ eosinophilic oesophagitis

39
Q

what is the onset of hypermotility

A

insidious onset - symptoms for years prior to seeking help/ risk of oesophageal cancer increased 28 fold

40
Q

how is hypermotility treated

A

PD - pneumatic dilatation (balloon inserted + inflated to resume flow)
90% of patients respond initially but many relapse

41
Q

how is hyper-motility treated

A

PD - pneumatic dilatation (balloon inserted + inflated to resume flow)
90% of patients respond initially but many relapse

42
Q

what is heller’s myotomy

A

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

43
Q

dor fundoplication

A

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

44
Q

what is scleroderma

A

autoimmune hypomotility disease

45
Q

what is the cause of scleroderma

A

early stages - due to neuronal defects + atrophy of smooth muscle of oesophagus

46
Q

what is disordered coordination

A

incoordinate contractions which lead to dysphagia + chest pain

marked hypertrophy of circular muscle

47
Q

what are the causes of oesophageal perforation

A

cancer, foreign body, physiological dysfunction

Gastro Yr 2 (7 decks)

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