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Gastroenterology > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

Where does the esophagus start and end?

A

starts at C6 and ends at T11

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2
Q

Where does the oesophagus pass the aorta?

A

T5

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3
Q

Where does the esophagus enter the diaphragm?

A

T10

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4
Q

Describe the anatomical contributions of the lower oesophageal sphincter

A
  • 3-4 cm distal oesophagus within abdomen
  • Diaphragm surrounds LOS (Lt & Rt crux)
  • An intact phrenoesophageal ligament
  • Angle of His (angle between the abdominal esophagus and the fundus of the stomach at the esophagogastric junction- prevents reflux)
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5
Q

Describe the process of swallowing

A

1 .Stage 0: Oral phase
- Chewing & saliva prepare bolus
- Both oesophageal sphincters constricted
2. Stage 1: Pharyngeal phase
- Pharyngeal musculature guides food bolus towards oesophagus
- Upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
3. Stage 2: Upper oesophageal phase
- Upper sphincter closes
- Superior circular muscle rings contract & inferior rings dilate
- Sequential contractions of longitudinal muscle
4. Stage 3: Lower oesophageal phase
Lower sphincter closes as food passes through

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6
Q

What factors affect the motility of the oesophagus?

A
  • Oesophageal motility determined by pressure measurements
  • Pressure is measured via manometry: A tube is usually inserted through the nose and passed into the esophagus.
  • The pressure of the sphincter muscle is recorded and also the contraction waves of swallowing are recorded
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7
Q

What are the normal pressures of the sphincter muscle and contraction waves of swallowing?

A
  1. Peristaltic waves ~ 40 mmHg
  2. LOS resting pressure ~ 20 mmHg
    ↓<5 mmHg during receptive relaxation
    Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
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8
Q

What are the causes of functional disorders of the oesophagus?

A

functional not mechanical: symptoms due to activity/ posture not obstruction; “absence of a stricture”
Caused by:
1. Abnormal oesophageal contraction:
- Hypermotility
- Hypomotility
- Disordered coordination

  1. Failure of protective mechanisms for reflux:
    - GastroOesophageal Reflux Disease (GORD)
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9
Q

What is dysphagia? what types of dysphagia can you have?

A

Dysphagia is difficulty in swallowing (different from pain)

Type of dysphagia:
- For solids or fluids
- Intermittent or progressive
- Precise or vague in appreciation

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10
Q

What is odynophagia?

A

Odynophagia is pain on swallowing

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11
Q

What is regurgitation?

A

Regurgitation refers to return of oesophageal contents from above an obstruction
- May be functional or mechanical

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12
Q

What is meant by “reflux”?

A

Reflux is passive return of gastroduodenal contents to the mouth

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13
Q

What is Achalasia?

A
  • Achalasia is a rare disorder in which damaged nerves in your esophagus prevent it from working as it should:
  • Muscles at the lower end of your esophagus fail to allow food to enter your stomach
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14
Q

Describe the pathophysiology of Achalasia?

A
  • Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
    → ↓ed activity of inhibitory NCNA neurones.
  • Receptive relaxation sets in late & is too weak
  • Swallowed food collects in oesophagus causing ↑ pressure throughout with dilation of the oesophagus
  • During reflex phase pressure in LOS is markedly ↑er than stomach
  • Propagation of peristaltic waves cease
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15
Q

What is the primary cause of achalasia?

A

aetiology unknown

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16
Q

What are the secondary causes of achalasia?

A

(Primary cause unknown)
secondary causes:
Diseases causing oesophageal motor abnormalities similar to 1o achalasia
- Chagas’ Disease
- Protozoa infection
- Amyloid/Sarcoma/Eosinophilic Oesophagitis

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17
Q

Describe the pathophysiology of Achalasia?

A
  • Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
    → ↓ed activity of inhibitory NCNA neurones.
  • Receptive relaxation sets in late & is too weak
  • Swallowed food collects in oesophagus causing ↑ pressure throughout with dilation of the oesophagus
  • During reflex phase pressure in LOS is markedly ↑er than stomach
  • Propagation of peristaltic waves cease
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18
Q

Describe the course/ onset of Achalasia

A
  1. Course:
    Has insidious onset (comes on slowly) - symptoms for years prior to seeking help
    Without treatment → progressive oesophageal dilatation of oesophagus.
  2. Risk of oesophageal cancer ↑ed 28-fold annual incidence only 0.34%
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19
Q

What is an Imaging feature very characteristic of Achalasia?

A

“Birds peak” appearance of the distal part (end of) the esophagus:
- dilated esophagus/ tapering of distal esophagus
- Late feature of Achalasia (so not the best tool for diagnosis)

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20
Q

How is Achalasia treated?

A
  1. “Pneumatic Dilation” (PD)
    PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
    Efficacy of PD— 71 - 90% of patients respond initially but many patients subsequently relapse (not v. effective)
  2. Surgery:
    - Heller’s Myotomy - A continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach
    - Dor fundoplication – anterior fundus folded over oesophagus and sutured to right side of myotomy
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21
Q

What are the risks of treating Achalasia with surgery?

A

Oesophageal & gastric perforation (10 – 16%)
Division of vagus nerve – rare
Splenic injury – 1 – 5%

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22
Q

What is Scleroderma?

A
  • Scleroderma - autoimmune disease
  • Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
  • causes inflammation, and the body makes too much collagen, leading to scleroderma
  • Peristalsis in the distal portion ultimately ceases altogether.
    ↓ed resting pressure of LOS
    → gastroesophageal reflux disease develops.
    Often associated with CREST syndrome
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23
Q

What is CREST syndrome?

A

CREST syndrome is characterized by: Calcinosis: Calcium skin deposits

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24
Q

How is Scleroderma treated?

A
  • Exclude organic obstruction
  • Improve force of peristalsis with prokinetics (cisapride)
  • Once peristaltic failure occurs → usually irreversible
25
Q

What is “Corkscrew oesophagus”?

A

It is a classic appearance of distal oesophageal spasm on a barium swallow:
- Incoordinate (disordered) contractions → dysphagia & chest pain
- Pressures of 400-500 mmHg
- Marked hypertrophy of circular muscle

26
Q

How is Corkscrew oesophagus treated?

A
  • May respond to forceful PD of cardia
  • Results not as predictable as achalasia
27
Q

What are the key areas vulnerable of oseophageal perforation?

A
  • 3x areas of anatomical constriction:
    1. cervical constriction: due to cricoid cartilage at the level of C5/6.
    2. thoracic constriction: due to aortic arch at the level of T4/5.
    3. abdominal constriction: at esophageal hiatus at T10/11.
  • Pathological narrowing (cancer, foreign body, physiological dysfunction)
28
Q

What are the causes of Oesophageal perforation?

A

Iatrogenic (OGD) >50%
Spontaneous (Boerhaave’s) - 15%
Foreign body - 12%
Trauma - 9%
Intraoperative - 2%
Malignant - 1%
iatrogenic (illness caused by medical examination or treatment):
- Usually at OGD
- Caused by an endescope perforating Killian’s triangle (muscles at OGD)
- More common in presence of diverticula or cancer

29
Q

What is Boerhaave’s ?

A
  • a rupture of your esophagus caused by tremendous stress
  • Sudden ↑ in intra-oesophageal pressure with negative intra thoracic pressure
  • Vomiting against a closed glottis
  • Left posterolateral aspect of the distal oesophagus
30
Q

What are some typical examples of foreign bodies that cause perforation of the esophagus?

A
  • Disk batteries growing problem (Cause electrical burns if embeds in mucosa)
  • Magnets
  • Sharp objects
  • Dishwasher tablets
  • Acid/Alkali
31
Q

What kind of trauma typically happens in the neck causing oesophageal perforation?

A

Penetrating

32
Q

What kind of trauma typically happens in the thorax causing oesophageal perforation?

A

Blunt force

33
Q

How is oesophageal perforation caused by trauma usually diagnosed?

A

Can be difficult to diagnose:
Dysphagia
Blood in saliva
Haematemesis
Surgical empysema

34
Q

What are common presentations for oseophageal perforation?

A

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

35
Q

What investigations are used to monitor oesophageal perforation?

A

CXR
CT
Swallow (gastrograffin)
OGD: OesophagoGastroDuodenoscopy (this one is the gold standard test)

36
Q

What is oesophageal perforation?

A

“a hole in the esophagus”
- Surgical emergency
2x ↑mortality if 24h delay in diagnosis

37
Q

How is an oesophageal perforation initially managed?

A

NBM
IV fluids
Broad spectrum A/Bs & Antifungals
ITU/HDU level care
Bloods (including G&S)
Tertiary referral centre

38
Q

What imaging features are characteristic of oesophageal perforation?

A

X-RAY OF THORAX:
- “White”= fluid: fluid collection in the thorax (GI contents leaking into the chest)
- “Black” areas near the oesophagus= air around the oesophagus
- Borders of the mediastinum no longer visible

39
Q

What is the definitive management of an oesophageal perforation?

A
  1. Conservative management with covered metal stent
    (chest must be drained first)
  2. Operative management should be default
    - Primary repair is optimal
    - Oesophagectomy - definitive solution
40
Q

What are the protective mechanisms against reflux?

A

LOS usually closed as barrier against reflux of harmful gastric juice (pepsin & HCl):
- LOS Pressure
- 3x mechanisms protect following reflux
* Volume clearance - oesophageal peristalsis reflex
* pH clearance - saliva
* Epithelium - barrier properties

41
Q

What factors affect the pressure of the lower oesophageal sphincter? how do these factors change the pressure?

A

LOS pressure ↑ed by:
- Acetylcholine
- α-adrenergic
- agonists
- hormones
- protein-rich food
- histamine
- high intra-abdominalpressure
- PGF2α
(Increased pressure in esophageal sphincter inhibits reflux)

LOS pressure ↓ed by:
- VIP
- β-adrenergic agonists
- hormones
- dopamine
- NO
- PGI2
- PGE2
- chocolate
- acid gastric juice
- fat
- smoking
(Decreased pressure in esophageal sphincter promotes reflux)

42
Q

What mechanisms are at risk of failing and, therefore, causing a loss in our protective mechanisms against reflux?

A
  • Sphincter pressure reduced
  • Transient sphincter increased opening
  • decreased saliva production
  • abnormal peristalsis= decreased volume clearance
  • decreased buffering capacity of saliva= decreased pH clearance
  • Hiatus hernia
  • Defective mucosal protective mechanism (e.g. alcohol)

ALL leads to reflux esophagitis (increases risk of cancer), epithelial metaplasia, carcinoma

43
Q

What imaging would you order to check for perforation of GI? what sign indicates perforation?

A

X Ray:
Rigler’s sign=
The Rigler sign, or double-wall sign, is an indication of free air enclosed within the peritoneal cavity. You can see the outline of the bowels

Spontaneous causes include peptic perforation, ischemia, bowel obstruction (benign or malignant), toxic megacolon, and inflammatory conditions (appendicitis, tuberculosis, necrotizing enterocolitis). Traumatic causes can be blunt or penetrating, either of which can result in bowel perforation

44
Q

What investigations are used to monitor GORD?

A

OGD “camera”
Oesophageal manometry “pressure”
24 hr oesophageal pH recording

45
Q

What is the management of GORD?

A

Medical:
- lifestyle changes
- PPIs
Surgical:
- Dilatation peptic strictures
- Disection and closure of hiatus
- Laparoscopic Nissen’s fundoplication (wrap fundus of stomach around oesophagus and stapple close)

46
Q

What is the function of the stomach?

A
  • Breaks food into smaller particles (acid & pepsin)
  • Hold food, releasing it in a controlled steady rate into the duodenum
  • Kills parasites & certain bacteria
47
Q

What is released from the cardia & pyloric region of the stomach

A

Mucus only

48
Q

What is released from the body & fundus of the stomach?

A

Mucus, HCL, pepsinogen

49
Q

What is released from the antrum of the stomach?

A

Gastrin

50
Q

What are the 4 types of gastritis you can have?

A

Erosive & haemorrhagic gastritis

Nonerosive, chronic active gastritis

Atrophic (fundal gland) gastritis

Reactive gastritis

51
Q

What is erosive & haemorrhagic gastritis?

A

gastric mucosal erosion caused by acute ulcer- gastric bleeding & perforation

52
Q

What is Nonerosive, chronic active gastritis?

A

Inflammation of the stomach lining without erosion or compromising the stomach lining cuased by H pylori in the antrum (antral gastritis)

53
Q

What is atrophic gastritis?

A

chronic inflammation of the gastric mucosa with loss of the gastric glandular cells in the fundus (replaced by intestinal and fibrous tissue)- caused by autoantibodies attacking parts & products of parietal cells (reduced HCL)

54
Q

What is the process of repairing epithelial damage in the stomach?

A
  1. Migration
    Adjacent epithelial cells flatten to close gap via sideward migration along basement membrane
  2. Gap closed by cell growth
    Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin
  3. Acute wound healing
    - Basement membrane destroyed - attraction of leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of basement membrane
    - epithelial closure by restitution & cell division.
55
Q

What are the consequences of gastric ulcer?

A

bleeding at the site of the ulcer. the stomach lining at the site of the ulcer splitting open (perforation) the ulcer blocking the movement of food through the digestive system (gastric obstruction)

Break in stomach epithelium:
- increased secretion of gastric juice
- reduced secretion of bicarbonate
- reduced cell formation
- reduced blood perfusion

56
Q

What are the clinical outcomes of H pylori?

A
  1. Asymptomatic or chronic gastritis
  2. Chronic atrophic gastritis & Intestinal metaplasia
  3. Gastric or duodenal ulcer
  4. Gastric cancer- MALT lymphoma
57
Q

What is the primary/ medical treatment of a an ulcer?

A

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

58
Q

What elective surgery is used to treat ulcer?

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 [Zollinger-Ellison syndrome])
OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory

59
Q

What are the possible consequences of doing surgery on an ulcer?

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

Gastroenterology (9 decks)

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