Upper GI tract Flashcards
anatomical contributions to LOS
3/4cm distal oesophagus within abdomen
Diaphragm surrounds LO
An intact phrenoesophageal ligament: has 2 limbs: 1 attached to the oesophagus and other attached to diaphragm- allows movement of oesophagus and diaphragm
Angle of His- between abdominal oesophagus and fundus of stomach- stops acid reflux
stages of swallowing
4 (0-3) oral pharyngeal upper oesophageal lower oesophageal
how to determine motility of oesophagus
manometry- pressure measurements
functional disorders of the oesophagus
- abnormal oesophageal contraction (hypomobility, hypermobility and disordered coordination)
- failure of protective mechanisms of reflux
dysphagia
difficulty in swallowing
What do we call pain on swallowing?
odynophagia
regurgitation
return of oesophageal content from above an obstruction (functional or mechanical)
reflux
passive return of gastroduodenal contents to the mouth
is reflux the same as vomiting?
no
example of oseophageal hypermotility and causes?
achalasia
- Due to loss of ganglion cell in Aurebach’s myenteric plexus
Primary cause aetiology is unknown
Secondary cause:
-Diseases causing oesophageal motor abnormalities similar to primary achalasia
• Chagas’ Disease
• Protozoa infection
• Amyloid/Sarcoma/Eosinophilic Oesophagitis
features of achalaisa hypermotility
- 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 the oesophagus causing increased pressure throughout with dilation of the oesophagus
- Propagation of peristaltic wave ceases
disease course of achalasia
- insidious onset: symptoms for years without seeking help
- without treatment you get progressive oesophageal dilation
- oesophageal cancer risk increased 28-fold
treatment of achalasia
pneumatic dilation (PD) to stretch muscles of the LOS:
-uses endoscopy, guide wire with PD
-balloon inserted and inflated to expand LO
- restored flow in LO
Efficacy of 90%, but usually relapses
surgical treatment of achalasia and risks?
- heller’s myotomy : myotomy (muscle cut) for 6cm of oesophagus and 3cm of stomach
- Dor fundopilation: anterior fundus folded over oesophagus and sutured to right side of myotomy
Risks include:
- Esophageal and gastric perforation
- Division of vagus nerve
- splenic injury
What is an example of a cause of oesophageal hypomotility ?
Scleroderma-autoimmune disease
Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases
Decreased resting pressure of LOS
Leads to development of GORD- often associated with CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia)
treatment of scleroderma
Exclude organic obstruction
Improve force of peristalsis with prokinetics
Once peristaltic failure occurs, this is usually irreversible - may have to have oesophagus removed
conditions causing disordered coordination
corkscrew oesophagus
Incoordinate contractions → dysphagia & chest pain
• Pressures of 400-500 mmHg
• Marked hypertrophy of circular muscle
• Corkscrew oesophagus seen on Barium x-ray scan
treating corkscrew oesophagus
forceful PD of cardia
results not as predictable as achalasia
What are causes of oesophageal perforation (most common to least common?
latrogenic - usually due to OGD (Oesophago-Gastro-Duodenoscopy) Spontaneous (Boerhaave's) Foreign body Trauma Intraoperative Malignant
what causes spontaneous oesophageal perforation
aka. Boerhaave’s
Sudden increase in intraesophageal pressure with negative intrathoracic pressure
Vomiting against a closed glottis
Usually left posterolateral aspect of distal oesophagus
foreign bodies causing oesophageal perforation
Disk batteries is growing problem- cause electrical burns if impact in mucosa
- magnets
- sharp objects
- dishwasher tablets
- acid/alkali
oesophageal perforation from trauma signs
Neck - caused by penetrating trauma
Thorax - caused by blunt force
Symptoms:
- dysphagia
- blood in saliva
- haematemsis
- surgical emphysema
surgeries that can cause oesophageal perforation
- hiatus hernia repair
- hellers myotomy
- pulmonary surgery
- thyroid surgery
investigating oesophageal perfortion
- CXR
- CT
- Swallow (gastrograffin)
- OGD
initial management of oesophageal perforation
NBM (nil by mouth) IV fluids Broadspec AB and antifungal Bloods ICU/ HDU level care tertiary care (specialist) referral
definitive management of the oesophageal perforation
Perforation is a surgical emergency (2x increase in morality if 24hr delay in diagnosis)
Operative management is default unless: -there's minimal contamination -it's contained -patient unfit In this case you can use conservative management with a covered metal stent
why is LOS normally closed?
barrier against reflux to protect from gastric juice
is sporadic reflux normal?
yes, occurs when:
pressure on full stomach
swallowing
transient sphincter opening (spontaneous)
3 mechanisms for protection following reflux
- volume clearance (oesophageal peristalsis reflex)
- pH clearance (saliva)
- epithelial barrier properties
what are failed protective mechanisms against reflux and what can this cause?
Decreased sphincter pressure
Transient sphincter opening
Decreased saliva production- leads to decreased pH clearance
Decreased buffering capacity of saliva (e.g. by smoking) - leads to decreased pH clearance
Abnormal peristalsis- leads to decreased volume clearance
Hiatus hernia
Defective mucosal protective mechanism
These can lead to
GORD -> reflux oesophagitis -> epithelial metaplasia -> carcinoma
what often happens with GORD?
sliding hiatus hernia- Ligament gives way and stomach slides up
rolling hiatus hernia
Bit of stomach squeezes through next to oesphagus
how to investigate GORD
OGD - exclude other cause like cancer - look for oesophagitis, peptic stricture and barrett's oesophagus Oesophageal manometry 24 hr oesophageal pH recording
types of gastritis
- erosive and hemorrhagic
- nonerosive chronic active gastritis
- atrophic gastritis
- reactive gastritis
What are causes of nonerosive, chronic active gastritis, what does it lead to and what is treatment?
helicobacter pylori in the antrum
Leads to increased gastrin and inc/normal acid secretion -> gastric and duodenal ulcer -> reactive gastritis -> epithelial metaplasia -> carcinoma
Treatment:
triple therapy - amoxicillin and clarithromycin and a PPI for up to 14 days
cause of atrophic gastritis
autoantibodies attacking gastric receptor/ carbonic anhydrase/ H+/K+NATPase/ IF
Atrophic gastritis leads to dec pepsinogen, dec acid secretion (-> inc gastrin -> ECL cell hyperplasia -> carcinoid OR G-cell hyperplasia -> carcinoma) and dec IF secretion (-> dec cobalamin absorption -> cobalamin deficiency -> pernicious anaemia)
What are causes of erosive and hemorrhagic gastritis and what does it lead to?
NSAIDs Alcohol Multi-organ failure Trauma Ischaemia
Leads to acute ulcer- gastric bleeding and perforation
methods of mucosal protection (4)
- mucus film
- HCO3- secretion
- Epithelial barrier
- mucosal blood perfusion
What are the stages of epithelial repair and wound healing?
Migration
Gap closed by cell growth
Acute wound healing
How does H Pylori cause virulence? (8)
Urease: to neutralise gastric acid
Flagella: for mobility and chemotaxis
Lipopolysaccharides: adhere to host cells and inflammation
Outer proteins: Adhere to host cell
Exotoxins: vacuolating toxin for gastric mucosal injury
Secretory enzymes: mucinase, protease, lipase for gastric mucosal injury
Type IV secretion system: for injection of effectors
Effectors: for actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition
neural stimulation of gastric secretion?
ACh -> postganglionic transmitter of vagal parasympathetic fibres
endocrine stimulation of gastric secretion?
Gastrin (G cells of antrum)
paracrine stimulation of gastric secretion?
Histamine (from ECL cells & mast cells of gastric wall)
endocrine inhibition of gastric secretion?
Secretin (small intestine)
paracrine inhibition of gastric secretion?
Somatostatin (SIH)
paracrine and autocrine inhibition of gastric secretion?
Prostaglandins (E2 & I2), TGF-α &
adenosine
What occurs in the migration stage of epithelial repair and wound healing
• Adjacent epithelial cells flatten to close gap
via sideward migration along BM
gap closed by cell stage of epithelial repair and wound healing
• Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin
acute wound healing by cell stage of epithelial repair and 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.
What factors contribute to ulcer formation?
look at slide on this and slide after!!
- helicobater pylori
- secretion of gastric juice increased
- HCO3- secretion decreased
- cell formation decreased
- blood prefusion decreased
primarily medical treatment ulcer
- PPI or H2 blocker
• Triple Rx (amoxicillin, clarithromycin,
pantoprazole) for 7-14 days)
Elective Surgical Rx for ulcers
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 [ZollingerEllison syndrome]) • OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
surgical indication ulcers
- Intractability (after medical therapy)
- Haemorrhage
-Obstruction
-Perforation
-Relative: continuous requirement of
steroid therapy/NSAIDs
main disorders of the stomach (8)
• Failure of protective mechanisms • Gastrooesophageal reflux (GORD) • Hiatus hernia • Gastritis • Failure in regulation of gastric secretion, mucosal protection & epithelial repair • GIT ulcer formation • H. pylori • Treatment
What happens in the oral phase of swallowing?
- Chewing & saliva prepare bolus
* Both oesophageal sphincters constricted
What happens in the pharyngeal phase of swallowing?
• Pharyngeal musculature guides food bolus towards oesophagus
• Upper oesophageal sphincter opens reflexly
• LOS opened by vasovagal reflex (receptive relaxation
reflex)
What happens in the upper oesophageal phase of swallowing?
• Upper sphincter closes
• Superior circular muscle rings contract & inferior rings
dilate
• Sequential contractions of longitudinal muscle
What happens in the lower oesophageal phase of swallowing?
• Lower sphincter closes as food passes through
What is the pressure of a normal oesophagus during a peristaltic wave?
40 mmhg
What is the lower oesophageal resting pressure normally and how does this change with receptive relaxation?
20 mmhg
decreased by 5 mmhg during receptive relaxation
What mediates the pressure within the oesophagus?
Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
How is dysphagia classified?
Location: cricopharyngeal sphincter or distal
Type of dysphasia: solids or fluids/ intermittent or progressive/ precise or vague in precision
What is an endoscopic treatment of achalasia?
Peroral endoscopic myotomy (POEM):
- Mucosal incision mae
- Submucosal tunnel is creates
- Myotomy
- Closure of mucosal tunnel
What are iatrogenic causes of oesophageal perforation?
Usually occurs at OGD
Incidence (low to high)
OGD alone
Stricture dilatation
Sclerotherapy
Achalasia dilatation
How do you treat malignancies that cause esophageal perforation?
• Radiotherapy
• Dilatation
• Stenting
Has poor prognosis
What are symptoms of oesophageal perforation?
Pain
Fever
Dysphagia
Emphysema
What surgery would be used to repair an oesophageal perforation?
Primary repair is optimina:
• +/- Vascularised pedicle flap
• +/- Gastric fundus buttressing
(e.g. Dor)
Oesophagaectomy is a definitive soloution:
- With reconstruction or oesophagostomy & delayed reconstruction
What are things that can increase LOS pressure and what is their effect?
Acetylcholine, α-adrenergic agonists, hormones, protein-rich food, histamine, high intra-abdominal pressure, PGF2α, etc.
Inhibit reflux
What are things that can decrease LOS pressure and what is their effect?
VIP, β-adrenergic agonists, hormones, dopamine, NO, PGI2 , PGE2 , chocolate, acid gastric juice, fat, smoking, etc.
Promote reflux
What are treatments of GORD?
Medical:
- lifestyle changes (wt loss, smoking)
- PPIs
Surgical:
- Dilatation peptic strictures
- Laparoscopic Nissen’s fundoplication (close where stomach enters diaphragm and wrap fundus around oesophagus)
What are the clinical outcomes of a H Pylori infection?
Asymptomatic or chronic gastritis e.g. Chronic atrophic gastritis Intestinal metaplasia Gastric or duodenal ulcer Gastric cancer e.g MALT lymphoma
