1b// Upper GI Tract Flashcards
What are the sphincters of the oesophagus?
upper and lower
Label.
Where does the oesophagus start?
C5, trachea
Which side does the aorta lie to compared to the oesophagus?
to the left
Where does the oesophagus end?
T10, diaphragm
How is the oesophagus split into 2?
thoracic and abdominal oesophagus
What is the arterial and venous supply to the thoracic oesophagus?
arterial supply from the branches of the thoracic aorta and the inferior thyroid artery
Venous drainage into the systemic circulation occurs via branches of the azygous veins and the inferior thyroid vein.
What is the arterial and venous supply of the abdominal oesophagus?
The abdominal oesophagus is supplied by the left gastric artery (a branch of the coeliac trunk) and left inferior phrenic artery.
This part of the oesophagus has a mixed venous drainage via two routes: To the portal circulation via left gastric vein. To the systemic circulation via the azygous vein.
What are the 2 plexuses in the oesophagus?
myenteric and meissner
What are the anatomical contributions to the lower oesophageal sphincter? (4)
- 3-4 cm distal oesophagus within abdomen
- Diaphragm surrounds LOS (Leftt & Right crux)
- An intact phrenoesophageal ligament
- Angle of His
What are the stages of swallowing?
stage 0= oral phase
stage 1= pharyngeal phase
stage 2= upper oesophageal phase
stage 3= lower oesophageal phase
What happens in stage 0 of swallowing?
all in mouth
- Chewing & saliva prepare bolus
- Both oesophageal sphincters constricted
What happens in stage 1 of swallowing?
- Pharyngeal musculature guides food bolus towards oesophagus
- circular and longitudinal muscle
- Upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
What happens in stage 2 of swallowing?
- Upper sphincter closes
- Superior circular muscle rings contract & inferior rings
dilate - Sequential contractions of longitudinal muscle
What happens in stage 3 of swallowing?
- Lower sphincter closes as food passes through
What determines oesophageal motility?
determined by pressure measurements (manometry)
What is the pressure roughly of peristaltic waves?
40mmHg
What is the LOS resting pressure?
roughly 20mmHg
When does LOS pressure decrease?
decreases 5mmHg during receptive relaxation (when the bolus goes down)
What mediates the decrease in pressure of the LOS?
mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurones of the myenteric plexus
What does the myenteric plexus do?
motility, allows relaxation
What does Meissner’s plexus do?
helps with secretions, and blood supply to oesophagus
What is the major cause of functional disorders of the oesophagus?
absence of structure
What causes the absence of structure in the oesophagus leading to disorders? (2)
abnormal oesophageal contraction
failure of protective mechanisms for reflux
What are examples that cause abnormal oesophageal contraction?
hypermotility
hypomotility
disordered coordination
What is an example that causes failure of protective mechanisms for reflux?
GastroOesophageal Reflux Disease (GORD)
What is dysphagia?
difficulty swallowing
Why is localisation important for dysphagia?
it can be high or low dysphagia
high= cricopharyngeal sphincter (aka UOS)
low= distal sphincter (aka LOS)
What are the types of dysphagia?
for solids or fluids
intermittent or progressive (e.g., cancer)
precised or vague in appreciation
What is odynophagia?
pain on swallowing
What is regurgitation?
Regurgitation refers to return of oesophageal contents from above an obstruction
May be functional or mechanical
What is reflux?
Reflux is passive return of gastroduodenal contents to the mouth
I.e., acidic contents
What is an example of hypermotility?
Achalasia
What causes Achalasia?
- Due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
→ decreased activity of inhibitory NCNA neurones
What is the aetiology of primary achalasia?
unk
What is the aetiology of secondary achalasia? (4)
- Diseases causing oesophageal motor abnormalities similar to primary achalasia
- Chagas’ Disease (a parasitic infection)
- Protozoa infection
- Amyloid/Sarcoma/Eosinophilic
Oesophagitis
How could you check for secondary achalasia cause?
serum blood sample
Do you understand this proposed model for achalasia?
What happens to the pressure of the LOS in hypermotility/ achalasia?
increased resting pressure
during reflex phase pressure in LOS is markedly higher than stomach
What happens to the oesophagus during hypermotility/ achalasia?
swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
What happens to the “waves” in achalasia/ hypermotility?
propagation of peristaltic waves cease
What are the symptoms of achalasia/ hypermotility and why? (5+extra)
weight loss
trouble swallowing
pain
esophagitis
pneumonia
during swallowing, due to achalasia, excitation of the NCNA (nonadrenergic noncholinergic) neurones decrease
causing the sphincter pressure to be too high
What is the disease course of achalasia/ hypermotility?
has insidious onset- symptoms for years prior to seeking help
without treatment=> progressive oesophageal dilation of oesophagus
risk of oesophageal cancer increased x28
What is a non-surgical treatment for achalasia/ hypermotility?
pneumatic dilation (PD)
What does pneumatic dilation do?
PD weakens LOS by circumferential stretching and in some cases, tearing of its muscle fibres
What is the efficacy of pneumatic dilation?
71-90% of patients respond initially but many patients subsequently relapse, need repeat dilation
it is almost never a definite treatment
Can achalasia/ hypermotility be treated surgically?
yes
How do you treat achalasia/ hypermotility surgically?
Heller’s Myotomy and then Dor fundoplication
What is Heller’s Myotomy?
a continuous myotomy performed for 6cm on the oesophagus and 3cm onto the stomach
What is Dor fundiplication?
anterior fundus folded over oesophagus and sutured to right side of myotomy
What type of surgery is it normally for achalasia/ hypermotility?
laparoscopic
What is the risk of surgery for achalasia/ hypermotility?
oesophageal and gastric perforation
division of vagus nerve- rare
splenic injury
What is a type of hypomotility called?
scleroderma
What is 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 altogether
What happens to the pressure of the LOS in scleroderma and what does it lead to?
decreased resting pressure of LOS
leading to gastrooesophageal reflux disease develops
- often associated with CREST syndrome
What is the mechanism of scleroderma?
neuronal defects
-> muscle atrophia
-> no peristalsis in smooth muscles
-> hypomotility
-> gostrooesophageal reflux disease
What is the treatment for slceroderma?
- Exclude organic obstruction 40
- Improve force of peristalsis with prokinetics (cisapride)
- Once peristaltic failure occurs → usually irreversible
What is an example of a disorders coordination disease?
corkscrew oesophagus
What does corkscrew oesophagus cause?
diffuse oesophageal spasm
What does diffuse oesophageal spasm cause?
- Incoordinate contractions → dysphagia & chest pain
- Pressures of 400-500 mmHg
- Marked hypertrophy of circular muscle
- Corkscrew oesophagus on Barium
What is the treatment for corkscrew oesophagus?
may respond to forceful pneumatic dilation of cardia
results not as predictable as achalasia
How do you see a corkscrew oesophagus?
endoscopy
What is the anatomy of oesophageal perforation?
3x areas of anatomical constriction
Pathological narrowing (cancer, foreign body, physiological dysfunction)
What are the 3 areas of constriction in the oesophagus?
cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphincter constriction
What is the aetiology of oesophageal perforations?
- iatrogenic (OGD) >50%
- Spontaneous (Boerhaave’s)- normally secondary to alcohol intake - 15%
- Foreign body - 12%
- Trauma - 9%
- Intraoperative - 2%
- Malignant - 1%
What is the most common cause of iatrogenic oesophageal perforation?
OGD OesophagoGastroDuodenoscopy
- more common in presence of diverticula or cancer
What happens in Boerhaave’s (oesophageal perforation)?
sudden increase in intra-oesophageal pressure with negative intrathoracic pressure
vomiting against a closed glottis
left posterolateral aspect of the distal oesophagus
What can the foreign bodies be for foreign body oesophageal perforation?
- Disk batteries growing problem
- Cause electrical burns if embeds in mucosa
- Magnets
- Sharp objects
- Dishwasher tablets
- Acid/Alkali
*risk of attaching to mucosa= perforation
*mostly in children
What type of trauma causes oesophageal perforation in the neck?
penetrating
What type of trauma causes oesophageal perforation in the thorax?
blunt force
What are symptoms of oesophageal perforation caused by trauma?
*can be difficult to diagnose
dysphagia
blood in saliva
haematemesis (vomiting blood)
surgical emphysema
What is the presentation of oesophageal perforation? (4)
- Pain 95 %
- Fever 80 %
- Dysphagia 70 %
- Emphysema 35 %
What type of imaging do you do for oesophageal perforation?
chest x ray
CT (computed tomography) scan
swallow gastrografin (contrast dye)
OGD
(OesophagoGastroDuodenoscopy)
What is the primary management of oesophageal perforation?
Surgical emergency (2x increased mortality if 24h delay in diagnosis)
What is the initial management of oesophageal perforation?
Nil by mouth (NBM)
IV fluids
Broad spectrum anti-b and antifungals
ITU (intensive unit)/ HDU (high dependency unit) level care
bloods (including G&S Group and Save is the sample processing that determines the patient blood group (ABO and RhD) and screens for any atypical antibodies)
tertiary referral centre
What is the definitive management of oesophageal perforation?
conservative management with covered metal stent (completely blocks off hole and patient can still eat)
What is the default for oesophageal perforation?And what is the surgery called?
operative management
primary repair is optimal
oesophagectomy- definitive solution
What is a protective mechanism against reflux?
LOS usually closed as barrier against reflux of harmful gastric juice (pepsin and HCl)
What is a risk factor that increases LOS pressure?
obesity
What decreases LOS pressure?
Smoking
What type of reflux is normal?
sporadic reflux
What is sporadic reflux?
1)pressure on full stomach
2)swallowing
3)transient sphincter opening
What are mechanisms to protect after reflux? (3)
- Volume clearance - oesophageal peristalsis reflex
- pH clearance - saliva
- Epithelium - barrier properties
What in the stomach promotes and inhibits reflux? (that picture w lots of info)
What does the failure of the protective mechanisms for reflux cause?
GORD (gastro oesophageal reflux disease)
What is the major thing that GORD can lead to?
carcinoma
What two things from GORD causes carcinomas?
reflux oesophagitis
Epithelial metaplasia
Do you understand these mechanisms for GORD?
What types of hernias are there?
sliding and rolling
sliding hiatus hernia
and
rolling/ paraoesophageal hiatus hernia
Picture of sliding hernia
picture of rolling hernia
What types of imaging and tests do you do for GORD and why?
OGD
- To exclude cancer
- Oesophagitis, peptic stricture & Barretts
oesophagus confirm narrowing
Oesophageal manometry
24-hr oesophageal pH recording
What is prescribed for GORD?
Medical:
Lifestyle changes (wt loss, smoking, EtOH)
PPIs
Surgical:
- Dilatation peptic strictures
- Laparoscopic Nissen’s fundoplication
What is the function of the stomach?
- Breaks food into smaller particles (acid & pepsin)
- Holds food, releasing it in controlled steady rate into duodenum
- Kills parasites & certain bacteria
What do different areas of the stomach do?
Cardia & Pyloric Region: Mucus only
Body & Fundus: Mucus, HCl, pepsinogen
Antrum: Gastrin (G cells)
What is gastritis?
Gastritis is when the lining of your stomach becomes irritated (inflamed)
What are the types of gastritis?
erosive and hemorrhagic gastritis
nonerosive, chronic gastritis
atrophic (fundal gland) gastritis
reactive gastritis
What is erosive and hemorrhagic gastritis?
Numerous causes
acute ulcer- gastric bleeding and perforation
What is nonerosive, chronic active gastritis?
Antrum
Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7
What is atrophic (fundal gland) gastritis?
- Fundus
- Autoantibodies vs parts & products of parietal cells
- Parietal cells atrophy
- ↓acid & IF (intrinsic factor) secretion
DO you understand this diagram of the mechanism of gastritis?
What is the stimulatory regulation of gastric juices?
Neural
Endocrine
Paracrine
What is the neural stimulation of gastric juices?
ACh- postganglionic transmitter of vagal parasympathetic fibres
What is the endocrine stimulation of gastric juices?
gastrin (G cells of antrum)
What is the paracrine stimulation of gastric juices?
histamine (ECL (Enterochromaffin-like) cells and mast cells of gastric wall)
What are the inhibitory regulations of gastric regulation?
Endocrine
Paracrine
Paracrine and Autocrine
What is the endocrine inhibition of gastric secretion?
secretin (small intestine)
What is the paracrine inhibition of gastric secretion?
somatostatin (SIH)
- secreted by delta cells
- pyloric antrum, the duodenum and the pancreatic islets
What is the paracrine and autocrine inhibition of gastric juices?
- PGs (E2 & I2), TGF-α & adenosine
Do you understand this diagram?
Yes
Do you understand this diagram of mucosal protection, How is the mucosa protected?
- epithelial barrier
- mucus film
- bicarbonate
What needs to happen after ulcer for your body?
epithelial repair and wound healing
What are the mechanisms repairing epithelial defects?
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.
What happens to the epithelial layer during an ulcer?
breaks mucosal epithelial layer
What can cause gastric ulcers?
Do you understand this diagram?
yes
What are the clinical outcomes of infections of H.Pylori? (4)
What are the treatments for Ulcers?
primarily medical
Elective Surgical prescription
What is the medical treatment for ulcers?
- PPI or H2 blocker
- Triple Rx (amoxicillin, clarithromycin,
pantoprazole) for 7-14 days)
What do you do before surgical treatment of 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 [Zollinger- Ellison syndrome])
- OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
What are the surgical indications of ulcers?
Intractability aka hard to control/ manage (after medical therapy)
Relative: continuous requirement of
steroid therapy/NSAIDs
What are the complications of ulcer surgery?
haemorrhage
obstruction
perforation
What do you measure to check pancreas function?
amylase
