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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
phrenoesophageal ligament
angle of His

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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

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4
Q

functional disorders of the oesophagus

A

Abnormal contractions: Hypermobility
Hypomobility
Disordered coordination
Failure of protective mechanisms: GORD

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5
Q

regurgitation vs reflux

A

return of oesophageal content from above an obstruction (functional or mechanical) (regurg)
passive return of gastroduodenal contents to the mouth (reflux)

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6
Q

achalasia hypermotility pathophysiology

A

Increasing rested pressure of LOS
Receptive relaxation sets in late and is too weak (during reflex phase pressure in LOS is much higher than stomach)
Swallowed food collects in oesophagus (Increases oesophageal pressure)
Dilatation of the oesophagus
Peristalsis ceases

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7
Q

What is the angle of his

A

Angle between distal oesophagus and the fundus

Compresses distal oesophagus from lateral to medial

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8
Q

What is the relaxation of the LOS mediated by

A

Mediated by inhibitory neurons of myenteric plexus

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9
Q

What causes Achalasia

A

Loss of ganglion cells in aurebach’s myenteric plexus in LOS wall
decreased inhibitory neuron activity (non-cholinergic, non-adrenergic)

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10
Q

What diseases is hypermotility seen in

A 
Chagas disease
Protozoa
Amyloid
Sarcoma
Eosinophilic oesophagitis
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11
Q

disease course of achalasia

A
  • insidious onset,
  • enlarged oesophagus
  • oesophageal cancer increased 28-fold
  • aspiration pneumonia is a risk
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12
Q

treatment of achalasia

A

pneumatic dilation to stretch muscles of the LOS

SURGICAL - hellers myotomy, dor fundoplication

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13
Q

What is pneumatic dilatation

A

Weakens LOS by circumferential stretching and in some cases, tearing of its muscles fibres
may relapse

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14
Q

What is Heller’s myotomy

A

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

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15
Q

What is dor fundoplication

A

anterior fundus folded over oesophagus and sutured to right side

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16
Q

what type of disease is scleroderma

A 
autoimmune disease - hypomotility
neuronal defects (atrophy of smooth muscle)
peristalsis in the distal oesophagus stops
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17
Q

name for pain on swallowing

A

odynophagia

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18
Q

treatment of scleroderma

A

exclude organic obstruction first

  • prokinetics
  • can use pneumotatic dilatation
  • usually irreversible - may have to have oesophagus removed
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19
Q

conditions causing disordered coordination

A

corkscrew oesophagus

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20
Q

What is scleroderma?

A 
Autoimmune disease
Hypomotility due to neuronal defects
Atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ceases
Decreases LOS resting pressure
GORD develops
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21
Q

corkscrew oesophagus treatment

A

forceful pneumatic dilation of cardia

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22
Q

Where are iatrogenic oeseophgeal perforations normally

A

cricopharyngeal constriction

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23
Q

where are the areas of oesophagus prone to perforation

A

cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphincter constriction

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24
Q

What is Boerhaave’s

A

Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
Vomiting against a close glottis
usually left posterolateral aspect of distal oesophagus

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25
Q

what foreign bodies may cause oesophageal perforation

A 
Disk batteries
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali
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26
Q

What operations can cause perforations

A

Hiatus hernia repair
Hellers cardiomyotomy
Pulmonary surgery
Thyroid surgery

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27
Q

signs of trauma causing oesophageal perforation

A

dysphagia
blood in saliva
haematemesis
surgical emphysema

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28
Q

investigations for perforated oesophagus

A

CXR
CT
swallow gastrograffin
OGD

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29
Q

presentation of oesophageal perforation

A

pain
fever
dysphagia
emphysema

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30
Q

what to avoid doing for a suspected oesophageal perforation

A

endoscopy

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31
Q

initial management of oesophageal perforation

A 
nil by mouth
IV fluids
broad spectrum ABs
ITU
bloods taken
transferral to tertiary care
32
Q

management of oesophageal perforation

A

primary repair 1st line
oesophagectomy - definitive solution
conservatively - metal stent

33
Q

3 mechanisms that protect against reflux

A

Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium - barrier properties

34
Q

What increases LOS pressure

A 
Acetylcholine
Alpha-adrenergic agonists
Hormones
Protein-rich food
Histamine
High intra-abdominal pressure
INHIBITS REFLUX
35
Q

what decreases LOS pressure and promotes reflux

A

acidic food
fats
NO
smoking

36
Q

Why is sporadic reflux normal

A

Pressure on full stomach
Swallowing
Transient sphincter opening

37
Q

What are sliding hiatus hernias

A

Portion of stomach herniated

Squeezes through diaphragm

38
Q

What is a rolling hiatus hernia

A

Junction is in place and the stomach herniates alongside the oesophagus

39
Q

How do you investigate GORD

A

OGD - to exclude cancer
or confirm oesophagitis, peptic stricture and barretts
Oesophageal manometry
24hr oesophageal pH recording

40
Q

treatments for GORD

A 
Lifestyle changes (weight loss, smoking, EtOH)
PPIs
41
Q

surgical treatments are available for GORD

A

Dilation peptic strictres

Laparascopic Nissen’s fundoplication

42
Q

which is worse sliding or rolling hiatus hernia

A

rolling

risk of strangulation greater

43
Q

What are the different types of gastritis

A

erosive and haemorrhagic
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis

44
Q

features of erosive and haemorrhagic gastritis

A

Numerous causes, NSAIDs, ischaemia, vasculitis, stress etc

Acute ulcer - gastric bleeding and perforation

45
Q

What are the features of Nonerosive, chronic active gastritis

A

Antrum usually

Helicobacter pylori - treat with amoxcillin, clarithromyocin, pantoporzole for 7-14 days

46
Q

features of Atrophic (fundal gland) gastritis

A

Fundus
Autoantibodies vs parts and products of parietal cells
Parietal cells atrophy
Decreased acid and IF secretion

47
Q

methods of mucosal protection in stomach

A

Mucus film
HCO3- secretion
Epithelial barrier (tight junctions, strong apical membrane)
Mucosal blood perfusion (good blood supply can get rid of H+ quickly)

48
Q

functions of stomach

A

breaks food into smaller particles
holds food, releases it at steady rate
kills parasites and bacteria

49
Q

what is produced in the cardia and pyloric region

A

mucus

50
Q

what is produced in the body and fundus

A

mucus

HCl pepsinogen

51
Q

what is produced in the antrum

A

gastrin

52
Q

stimulation of gastric secretion

A

ACh - vagal parasympathetic fibres
gastrin from G cells of antrum
histamine from ECL cells and mast cells

53
Q

chemicals for inhibition of gastric secretion

A

secretin - small intestine
somatostatin
PGs, TGF-a + adenosine

54
Q

mechanisms repairing epithelila defects in stomach

A

Migration
Gap closed by cell growth
Acute would healing

55
Q

How does migration repair epithelium

A

Adjacent epithelial cells flatten to close gap

via sideward migration along BM

56
Q

stages of epithelial repair and wound healing

A

migration - Adjacent epithelial cells flatten to close gap
via sideward migration along BM
gap closed by cell growth - Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin
acute wound healing - BM destroyed - attraction of leukocytes &
macrophages; phagocytosis of necrotic cells;
angiogenesis; regeneration of ECM after repair
of BM. epithelial closure by restitution & cell division

57
Q

How are ulcers formed

A 
H. Pylori
Increased gastric juice secretion
Decreased bicarbonate secretion
Decreased cell formation
Decreased blood perfusion
58
Q

primary medical treatment ulcer

A 
PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
59
Q

indications for surgery for ulcers

A 
Intractability (after medical therapy)
Haemorrhage
Obstruction
Perforation
Relative: continuous requirement of steroid therapy/NSAIDs
60
Q

When would you opt for elective surgery for ulcers

A

Rare - most uncomplicated ulcers heal within 12 weeks
if not - change medication, observe additional 12 weeks
Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory

61
Q

how to distinguish mechanical from neurological cause of dysphagia

A

liquids and solids hard to swallow - likely neuro

solids difficult/painful alone or solids first and then slowly liquids got harder to swallow - likely mechanical

62
Q

how to distinguish mechanical from neurological cause of dysphagia

A

liquids and solids hard to swallow - likely neuro

solids difficult/painful alone or solids first and then slowly liquids got harder to swallow - likely mechanical

63
Q

what is riglers sign

A

free air under diaphragm/intraperitoneal air

64
Q

most common site of perforation of duodenum

A

anterior/superior surface of first part of duodenum (D1)

65
Q

where in the gut is most likely to perforate

A

duodenum - 10x more than stomach

66
Q

what subsequent infection is likely after abdominal surgery

A

pneumonia

taking deep breaths after surgery is painful, so not filling with air
lungs fill with fluid, gets infected, get chest infection

67
Q

what is an intraabdominal collection

A

fluid from lavage during surgery hasn’t been fully washed out
causes a collection of contaminated fluid, subsequent infection

68
Q

what score is used for severity of pancreatitis

A

modified glasgow criteria

PANCREAS

69
Q

modified glasgow criteria

A 
pancreatitis scoring (PANCREAS)
Po2
Age (>55)
Neutrophil/WBC
Calcium (low)
Renal (urea increased)
Enzymes AST, LDH
Albumin low
Sugar high
70
Q

what are the indicators for severe pancreatitis

A

over 3 modified glasgow within 48hrs

or CRP over 200

71
Q

principles of management of pancreatitis

A

ABC

Fluid resuscitation (iv fluids, monitoring)
Analgesia
Pancreatic rest (NJ feeding, TPN)
Determine underlying cause
go to HDU if severe
72
Q

investigation for gallstones

A

ultrasound

then if issue persists, MRCP (not ERCP as is too invasive, too risky)

73
Q

intervention for persistent pancreatitis due to gallstones

A

ERCP once confirmed by MRCP

74
Q

what is murphys sign

A

cholecystitis - inflammation of gallbladder

palpation of right costal margin upon holding a deep breath elicits pain (hand comes into contact with gallbladder)

75
Q

what structures need to be divided and removed for a laparoscopic cholecystectomy

A

cystic duct and cystic artery

76
Q

investigation of suspected achalasia

A

oesophageal manometry

BRS Year 2 (67 decks)

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