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Gastroenterology > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

(54 cards)

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1
Q

Oesophagus anatomical landmark

A

Start - C5

End - T10

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2
Q

Oesophageal motility determined by

A

Pressure measurements

Manometry

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3
Q

Peristaltic waves

A

~40 mmHg

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4
Q

LOS resting pressure

A

~20 mmHg
Decreases by more then 5 mmHg during receptive relaxation
Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

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5
Q

Disorders of oesophagus

A

Absence of stricture

Caused by

  • abnormal oesophageal contraction - hypermotility, hypomotility, disordered coordination
  • failure of protective mechanism for reflux - gastroesophageal reflux disease (GORD)
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6
Q

Dysphagia

A

Difficulty in swallowing

-localisation is important - cricopharyngeal sphincter or distal

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7
Q

Types of dysphagia

A

For solids or fluids
Intermittent or progressive
Precise or vague in appreciation

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8
Q

Odynophagia

A

Pain on swallowing

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9
Q

Regurgitation

A

Return of oesophageal contents from above an obstruction - may be functional or mechanical

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10
Q

Reflux

A

Passive return of gastroduodenal contents to mouth

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11
Q

Achalasia pathophysiology

A

Hypermotility
Loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
Decreased activity of inhibitory NCNA neurones

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12
Q

Primary and secondary achalasia

A

-Aetiology unknown

-diseases causing oesophageal motor abnormalities similar to primary achalasia
—Chagas’ disease
—Protozoa infection
—amyloid/sarcoma/eosinophilic oesophagitis

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13
Q

Achalasia effects

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 oesophagus causing increased pressure throughout with dilation of oesophagus

Propagation of peristaltic waves cease

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14
Q

Achalasia disease course

A

Insidious onset - symptoms for years prior to seeking help

Without treatment - progressive oesophageal dilation of oesophagus

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15
Q

Achalasia risk of oesophageal cancer

A

Increased 28 fold

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16
Q

Achalasia treatment

A

Pneumatic dilation
Weakens LOS by circumferential stretching and in some cases, tearing of its muscle fibres
Efficacy - 71-90% but many relapse

Surgery
Heller’s myotomy - continuous myotomy for 6cm on oesophagus and 3cm onto stomach
Dor fundoplication - anterior Fundus folded over oesophagus and sutured to right side of myotomy

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17
Q

Treatment risks

A

Surgery

  • oesophageal and gastric perforation 10-16%
  • division of vagus nerve - rare
  • splenic injury - 1-5%
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18
Q

Scleroderma

A

Hypomotility
Autoimmune
Neuronal defects - atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases altogether
Decreased resting pressure of LOS
Gastroesophageal reflux disease develops - often associated with CREST syndrome

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19
Q

Scleroderma treatment

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristalsis failure occurs - usually irreversible

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20
Q

Corkscrew oesophagus

A 
Disordered coordination 
Diffuse oesophageal spams
Incoordinate contractions - dysphagia and chest pain 
Pressures of 400-500 mmHg
Marked hypertrophy of circular muscle 
Corkscrew oesophagus on Barium
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21
Q

Corkscrew oesophagus treatment

A

May respond to forceful PD of cardia

Results not as predictable as achalasia

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22
Q

Anatomy of oesophageal perforation

Study These Flashcards
A 
3x areas of anatomical construction - cricopharyngeal, aortic and bronchial, diaphragmatic and ‘sphincter’ 
Pathological narrowing (cancer, foreign body, physiological dysfunction)
23
Q

Iatrogenic oesophageal perforation

Study These Flashcards
A

Usually at OGD - more common in presence of diverticula or cancer

24
Q

Boerhaave’s oesophageal perforation

Study These Flashcards
A

Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
-vomiting against closed glottis

Usually at left posterolateral aspect of distal oesophagus

25
Foreign body oesophageal perforation
``` Disk batteries growing problem - cause electrical burns if embeds in mucosa Magnets Sharp objects Dishwater tablets Acid/alkali ```
26
Trauma oesophageal perforation
Neck - penetrating Thorax - blunt force Can be difficult to diagnose - dysphagia - blood in saliva - haematemesis - surgical emphysema
27
Oesophageal perforation presentation
Pain 95% Fever 80% Dysphagia 70% Emphysema 35%
28
Oesophageal perforation investigations
Chest x ray CT Swallowing gastrograffin OGD
29
Oesophageal perforation initial management
Surgical emergency - 2x mortality if 24h delay in diagnosis ``` Initial management -Nil by mouth -IV fluids -broad spectrum antibiotic and antifungal ITU/HDU level care Bloods (including G&S) Tertiary referral centre ```
30
Oesophageal perforation conservative management
Covered metal stent
31
Oesophageal perforation definitive management
Operative management is default Primary repair is optimal Oesophagectomy - definitive solution
32
Stomach mechanism against reflux
LOS closed as barrier against reflux of harmful gastric juice (pepsin and HCl) Sporadic reflux is normal - pressure on full stomach - swallowing - transient sphincter opening Mechanisms protect following reflux - volume clearance - oesophageal peristalsis reflex - pH clearance - saliva - epithelium - barrier properties
33
LOS pressure increased by
Acetylcholine Hormones Prostaglandin Inhibits reflux
34
LOS pressure decreased by
Eating fat Smoking Nitrous oxide Promotes reflux
35
Failure of protective mechanism against reflux
GORD Decreased sphincter pressure Increased sphincter opening Decreased volume clearance - from abnormal peristalsis Slowed pH clearance - from decreased saliva production or decreased buffering capacity of saliva Hiatus hernia Defective mucosal protective mechanism Could lead to epithelial metaplasia and then carcinoma
36
Sliding hiatus hernia
Peritoneal reflection Ligament holding stomach gives way Stomach slides up to chest
37
Rolling hiatus hernia
Portion of stomach slips up the side Can be strangulated - blood flow compromised Surgical emergency
38
GORD investigation
OGD to exclude cancer. Oesophagitis, peptic stricture and Barretts oesophagus confirm Oesophageal manometry 24 hour oesophageal pH recording
39
GORD treatment
Medical - lifestyle changes - PPIs Surgical - dilation peptic stricture - laparoscopic Nissen’s fundoplication (definitive)
40
Stomach functions
Break food into smaller particles (acids and pepsin) Holds food, releasing it in controlled steady rate into duodenum Kills parasites and certain bacteria
41
Stomach productions
Cardia and pyloric region - mucus only Body and Fundus - mucus, HCl, pepsinogen Antrum - gastrin
42
Erosive and haemorrhagic gastritis
``` Numerous causes (NSAIDs, stress, alcohol) Commonest cause of acute ulcer - gastric bleeding and perforation ```
43
Nonerosive chronic active gastritis
Antrum Helicobacter pylori - triple treatment with amoxicillin, clarithromycin, pantoprazole for one to two weeks Increased gastrin - increased acid secretion Can lead to reactive gastritis
44
Atrophic (fundal gland) gastritis
Fundus Autoantibodies vs parts and products of parietal cells like gastrin receptor, carbonic anhydrase intrinsic factor Decreased acid secretion lead to G cell hyperplasia and epithelial metaplasia - carcinoma, and also increased gastrin and ECL cell hyperplasia - carcinoid Decreased intrinsic factor leads to decreased cobalamine absorption and deficiency
45
Parietal cell secretion
Hydrogen ions
46
Chief cells secretion
Pepsinogen
47
Gastric secretion stimulation
Neural -acetylcholine - postganglionic transmitter of a gal parasympathetic fibres Endocrine -gastrin - G cells of antrum Paracrine -histamine - ECL cells and mast cells of gastric wall
48
Gastric secretion inhibition
Endocrine -secretin - small intestine Paracrine -somatostatin - SIH Paracrine and aurocrine - Prostaglandins - PGE2, PGI2 - adenosine - TGF-alpha
49
Mucosal protection
Mucus film protects against pepsin and hydrogen ion Epithelial cell produce bicarbonates (propagated by prostaglandins) which buffers hydrogen ions Epithelial barrier and tight junction prevent penetration of hydrogen ions Good mucosal blood perfusion so that hydrogen ions get taken away if they do get through
50
Mechanisms repairing epithelial defects
Migration -adjacent epithelial cells flatten to close gap via sideward migration along basement membrane Gap closed by cell growth -stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin Acute wound healing - basement membrane destroyed - attraction of leukocytes and macrophages, phagocytosis of necrotic cells, angiogenesis, regeneration of ECM after repair of basement membrane - epithelial closure by restitution and cell division
51
Ulcer formation
Due to increased chemical aggression or barrier function disturbed ``` Helicobacter pylori - gastritis - barrier function disturbed Increased secretion of gastric juice Decreased bicarbonate secretion Decreased cell formation Decreased blood perfusion ``` NSAIDs and smoking - decreased prostaglandin synthesis - decreased mucosal protection - barrier function disturbed Psychogenic components and gastrinoma - increased hydrogen and pepsinogen secretion - chemical aggression
52
Outcomes of Helicobacter pylori
>80% asymptomatic or chronic gastritis 15-20% chronic atrophic gastritis or intestinal metaplasia and gastric or duodenal ulcers <1% gastric cancer or MALT lymphoma
53
Ulcer treatment
Primarily medical - PPI or H2 blocker - amoxicillin, clarithromycin, pantaprazole for one to two weeks Elective surgery - rare - most heal within 12 weeks - if not, change medication, observe additional 12 weeks - check serum gastrin (natural G cell hyperplasia or gastrinoma -Zollinger-Ellison syndrome) - OGD - biopsy all 4 quadrants of ulcer (rule out malignant)
54
Ulcer surgery indications
``` Intractability after medical therapy Relative - continuous requirement of steroid therapy/NSAIDs Complications -haemorrhage -obstruction -perforation ```

Gastroenterology (11 decks)

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