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Gastroenterology > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

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

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

A

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

24
Q

Boerhaave’s oesophageal perforation

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
Q

Foreign body oesophageal perforation

A 
Disk batteries growing problem - cause electrical burns if embeds in mucosa 
Magnets
Sharp objects 
Dishwater tablets 
Acid/alkali
26
Q

Trauma oesophageal perforation

A

Neck - penetrating
Thorax - blunt force

Can be difficult to diagnose

  • dysphagia
  • blood in saliva
  • haematemesis
  • surgical emphysema
27
Q

Oesophageal perforation presentation

A

Pain 95%
Fever 80%
Dysphagia 70%
Emphysema 35%

28
Q

Oesophageal perforation investigations

A

Chest x ray
CT
Swallowing gastrograffin
OGD

29
Q

Oesophageal perforation initial management

A

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
Q

Oesophageal perforation conservative management

A

Covered metal stent

31
Q

Oesophageal perforation definitive management

A

Operative management is default
Primary repair is optimal
Oesophagectomy - definitive solution

32
Q

Stomach mechanism against reflux

A

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
Q

LOS pressure increased by

A

Acetylcholine
Hormones
Prostaglandin

Inhibits reflux

34
Q

LOS pressure decreased by

A

Eating fat
Smoking
Nitrous oxide

Promotes reflux

35
Q

Failure of protective mechanism against reflux

A

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
Q

Sliding hiatus hernia

A

Peritoneal reflection
Ligament holding stomach gives way
Stomach slides up to chest

37
Q

Rolling hiatus hernia

A

Portion of stomach slips up the side
Can be strangulated - blood flow compromised

Surgical emergency

38
Q

GORD investigation

A

OGD to exclude cancer. Oesophagitis, peptic stricture and Barretts oesophagus confirm
Oesophageal manometry
24 hour oesophageal pH recording

39
Q

GORD treatment

A

Medical

  • lifestyle changes
  • PPIs

Surgical

  • dilation peptic stricture
  • laparoscopic Nissen’s fundoplication (definitive)
40
Q

Stomach functions

A

Break food into smaller particles (acids and pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites and certain bacteria

41
Q

Stomach productions

A

Cardia and pyloric region - mucus only
Body and Fundus - mucus, HCl, pepsinogen
Antrum - gastrin

42
Q

Erosive and haemorrhagic gastritis

A 
Numerous causes (NSAIDs, stress, alcohol) 
Commonest cause of acute ulcer - gastric bleeding and perforation
43
Q

Nonerosive chronic active gastritis

A

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
Q

Atrophic (fundal gland) gastritis

A

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
Q

Parietal cell secretion

A

Hydrogen ions

46
Q

Chief cells secretion

A

Pepsinogen

47
Q

Gastric secretion stimulation

A

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
Q

Gastric secretion inhibition

A

Endocrine
-secretin - small intestine

Paracrine
-somatostatin - SIH

Paracrine and aurocrine

  • Prostaglandins - PGE2, PGI2
  • adenosine
  • TGF-alpha
49
Q

Mucosal protection

A

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
Q

Mechanisms 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, 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
Q

Ulcer formation

A

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
Q

Outcomes of Helicobacter pylori

A

> 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
Q

Ulcer treatment

A

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
Q

Ulcer surgery indications

A 
Intractability after medical therapy
Relative - continuous requirement of steroid therapy/NSAIDs
Complications 
-haemorrhage 
-obstruction 
-perforation

Gastroenterology (11 decks)

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